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Sample records for aldehydes acrolein crotonaldehyde

  1. Hydrogenation of the alpha,beta-Unsaturated Aldehydes Acrolein, Crotonaldehyde, and Prenal over Pt Single Crystals: A Kinetic and Sum-Frequency Generation Vibrational Spectroscopy Study

    Energy Technology Data Exchange (ETDEWEB)

    Kliewer, C.J.; Somorjai, G.A.

    2008-11-26

    Sum-frequency generation vibrational spectroscopy (SFG-VS) and kinetic measurements using gas chromatography have been used to study the surface reaction intermediates during the hydrogenation of three {alpha},{beta}-unsaturated aldehydes, acrolein, crotonaldehyde, and prenal, over Pt(111) at Torr pressures (1 Torr aldehyde, 100 Torr hydrogen) in the temperature range of 295K to 415K. SFG-VS data showed that acrolein has mixed adsorption species of {eta}{sub 2}-di-{sigma}(CC)-trans, {eta}{sub 2}-di-{sigma}(CC)-cis as well as highly coordinated {eta}{sub 3} or {eta}{sub 4} species. Crotonaldehyde adsorbed to Pt(111) as {eta}{sub 2} surface intermediates. SFG-VS during prenal hydrogenation also suggested the presence of the {eta}{sub 2} adsorption species, and became more highly coordinated as the temperature was raised to 415K, in agreement with its enhanced C=O hydrogenation. The effect of catalyst surface structure was clarified by carrying out the hydrogenation of crotonaldehyde over both Pt(111) and Pt(100) single crystals while acquiring the SFG-VS spectra in situ. Both the kinetics and SFG-VS showed little structure sensitivity. Pt(100) generated more decarbonylation 'cracking' product while Pt(111) had a higher selectivity for the formation of the desired unsaturated alcohol, crotylalcohol.

  2. Mercapturic Acids Derived from the Toxicants Acrolein and Crotonaldehyde in the Urine of Cigarette Smokers from Five Ethnic Groups with Differing Risks for Lung Cancer.

    Science.gov (United States)

    Park, Sungshim L; Carmella, Steven G; Chen, Menglan; Patel, Yesha; Stram, Daniel O; Haiman, Christopher A; Le Marchand, Loic; Hecht, Stephen S

    2015-01-01

    The Multiethnic Cohort epidemiology study has clearly demonstrated that, compared to Whites and for the same number of cigarettes smoked, African Americans and Native Hawaiians have a higher risk for lung cancer whereas Latinos and Japanese Americans have a lower risk. Acrolein and crotonaldehyde are two important constituents of cigarette smoke which have well documented toxic effects and could play a role in lung cancer etiology. Their urinary metabolites 3-hydroxypropylmercapturic acid (3-HPMA) and 3-hydroxy-1-methylpropylmercapturic acid (HMPMA), respectively, are validated biomarkers of acrolein and crotonaldehyde exposure. We quantified levels of 3-HPMA and HMPMA in the urine of more than 2200 smokers from these five ethnic groups, and also carried out a genome wide association study using blood samples from these subjects. After adjusting for age, sex, creatinine, and total nicotine equivalents, geometric mean levels of 3-HPMA and HMPMA were significantly different in the five groups (P acrolein and crotonaldehyde may be involved in lung cancer etiology, and that their divergent levels may partially explain the differing risks of Native Hawaiian and Latino smokers. No strong signals were associated with 3-HPMA in the genome wide association study, suggesting that formation of the glutathione conjugate of acrolein is mainly non-enzymatic, while the top significant association with HMPMA was located on chromosome 12 near the TBX3 gene, but its relationship to HMPMA excretion is not clear.

  3. Adverse health effects of cigarette smoke: aldehydes Crotonaldehyde, butyraldehyde, hexanal and malonaldehyde

    NARCIS (Netherlands)

    Andel I van; Sleijffers A; Schenk E; Rambali B; Wolterink G; Werken G van de; Aerts LAGJM van; Vleeming W; Amsterdam JGC van; TOX

    2006-01-01

    Crotonaldehyde in cigarette smoke can be concluded to induce airway damage in humans. This is one conclusion derived from the existing data found in the literature and reported here in the discussion on adverse health effects and possible addictive effects due to the exposure of crotonaldehyde,

  4. Mercapturic Acids Derived from the Toxicants Acrolein and Crotonaldehyde in the Urine of Cigarette Smokers from Five Ethnic Groups with Differing Risks for Lung Cancer.

    Directory of Open Access Journals (Sweden)

    Sungshim L Park

    Full Text Available The Multiethnic Cohort epidemiology study has clearly demonstrated that, compared to Whites and for the same number of cigarettes smoked, African Americans and Native Hawaiians have a higher risk for lung cancer whereas Latinos and Japanese Americans have a lower risk. Acrolein and crotonaldehyde are two important constituents of cigarette smoke which have well documented toxic effects and could play a role in lung cancer etiology. Their urinary metabolites 3-hydroxypropylmercapturic acid (3-HPMA and 3-hydroxy-1-methylpropylmercapturic acid (HMPMA, respectively, are validated biomarkers of acrolein and crotonaldehyde exposure. We quantified levels of 3-HPMA and HMPMA in the urine of more than 2200 smokers from these five ethnic groups, and also carried out a genome wide association study using blood samples from these subjects. After adjusting for age, sex, creatinine, and total nicotine equivalents, geometric mean levels of 3-HPMA and HMPMA were significantly different in the five groups (P < 0.0001. Native Hawaiians had the highest and Latinos the lowest geometric mean levels of both 3-HPMA and HMPMA. Levels of 3-HPMA and HMPMA were 3787 and 2759 pmol/ml urine, respectively, in Native Hawaiians and 1720 and 2210 pmol/ml urine in Latinos. These results suggest that acrolein and crotonaldehyde may be involved in lung cancer etiology, and that their divergent levels may partially explain the differing risks of Native Hawaiian and Latino smokers. No strong signals were associated with 3-HPMA in the genome wide association study, suggesting that formation of the glutathione conjugate of acrolein is mainly non-enzymatic, while the top significant association with HMPMA was located on chromosome 12 near the TBX3 gene, but its relationship to HMPMA excretion is not clear.

  5. Use of In Vivo and In Vitro Data to Derive a Chronic Reference Value for Crotonaldehyde Based on Relative Potency to Acrolein.

    Science.gov (United States)

    Grant, Roberta L; Jenkins, Allison F

    2015-01-01

    The Texas Commission on Environmental Quality (TCEQ) conducted a chronic inhalation noncancer toxicity assessment for crotonaldehyde (CRO). Since there were limited toxicity data for CRO, a reference value (ReV) was derived using a relative potency factor (RPF) approach with acrolein as the index chemical. Both CRO and acrolein are α,β-unsaturated carbonyls and share common steps in their mode of action (MOA). Only studies that investigated the effects of CRO and acrolein in the same study were used to calculate a CRO:acrolein RPF. In vivo findings measuring both 50% respiratory depression in rats and two species of mice and subcutaneous 50% lethality in rats and mice were used to calculate an RPF of 3 (rounded to one significant figure). In vitro data were useful to compare the MOA of CRO and acrolein and to support the RPF determined using in vivo data. In vitro cell culture studies investigating cytotoxicity in normal human lung fibroblast cultures using the propidium iodide cytotoxicity assay and in mouse lymphocyte cultures using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) cytotoxicity assay were used to calculate an in vitro RPF of 3, which supports the in vivo RPF. The chronic ReV for acrolein of 1.2 ppb derived by TCEQ was multiplied by the RPF of 3 to calculate the ReV for CRO of 3.6 ppb (10 μg/m(3)). The ReV for CRO was developed to protect the general public from adverse health effects from chronic exposure to CRO in ambient air.

  6. Chronic oral exposure to the aldehyde pollutant acrolein induces dilated cardiomyopathy

    Science.gov (United States)

    Ismahil, Mohamed Ameen; Hamid, Tariq; Haberzettl, Petra; Gu, Yan; Chandrasekar, Bysani; Srivastava, Sanjay; Bhatnagar, Aruni

    2011-01-01

    Environmental triggers of dilated cardiomyopathy are poorly understood. Acute exposure to acrolein, a ubiquitous aldehyde pollutant, impairs cardiac function and cardioprotective responses in mice. Here, we tested the hypothesis that chronic oral exposure to acrolein induces inflammation and cardiomyopathy. C57BL/6 mice were gavage-fed acrolein (1 mg/kg) or water (vehicle) daily for 48 days. The dose was chosen based on estimates of human daily unsaturated aldehyde consumption. Compared with vehicle-fed mice, acrolein-fed mice exhibited significant (P acrolein adduct formation indicative of physical translocation of ingested acrolein to the heart. Acrolein also induced myocyte hypertrophy (∼2.2-fold increased myocyte area, P acrolein-exposed hearts, along with upregulated gene expression of proinflammatory cytokines tumor necrosis factor-α and interleukin-1β. Long-term oral exposure to acrolein, at an amount within the range of human unsaturated aldehyde intake, induces a phenotype of dilated cardiomyopathy in the mouse. Human exposure to acrolein may have analogous effects and raise consideration of an environmental, aldehyde-mediated basis for heart failure. PMID:21908791

  7. Elevated levels of mercapturic acids of acrolein and crotonaldehyde in the urine of Chinese women in Singapore who regularly cook at home.

    Directory of Open Access Journals (Sweden)

    Stephen S Hecht

    Full Text Available Lung cancer is unusually common among non-smoking women in Southeastern Asia but the causes of this frequently fatal disease are not well understood. Several epidemiology studies indicate that inhalation of fumes from high temperature Chinese style cooking with a wok may be a cause. Only one previous study investigated uptake of potential toxicants and carcinogens by women who cook with a wok. We enrolled three-hundred twenty-eight non-smoking women from Singapore for this study. Each provided a spot urine sample and answered a questionnaire concerning their cooking habits and other factors. The urine samples were analyzed by liquid chromatography-tandem mass spectrometry for mercapturic acid metabolites of acrolein (3-hydroxypropylmercapturic acid, crotonaldehyde (3-hydroxy-1-methylpropylmercapturic acid, and benzene (S-phenylmercapturic acid, accepted biomarkers of uptake of these toxic and carcinogenic compounds. We observed statistically significant effects of wok cooking frequency on levels of 3-hydroxypropylmercapturic acid and 3-hydroxy-1-methylpropylmercapturic acid, but not S-phenylmercapturic acid. Women who cooked greater than 7 times per week had a geometric mean of 2600 (95% CI, 2189-3090 pmol/mg creatinine 3-hydroxypropylmercapturic acid compared to 1901 (95% CI, 1510-2395 pmol/mg creatinine when cooking less than once per week (P for trend 0.018. The corresponding values for 3-hydroxy-1-methylpropylmercapturic acid were 1167 (95% CI, 1022-1332 and 894 (95% CI, 749-1067 pmol/mg creatinine (P for trend 0.008. We conclude that frequent wok cooking leads to elevated exposure to the toxicants acrolein and crotonaldehyde, but not benzene. Kitchens should be properly ventilated to decrease exposure to potentially toxic and carcinogenic fumes produced during Chinese style wok cooking.

  8. Reductive detoxification of acrolein as a potential role for aldehyde reductase (AKR1A) in mammals.

    Science.gov (United States)

    Kurahashi, Toshihiro; Kwon, Myoungsu; Homma, Takujiro; Saito, Yuka; Lee, Jaeyong; Takahashi, Motoko; Yamada, Ken-Ichi; Miyata, Satoshi; Fujii, Junichi

    2014-09-12

    Aldehyde reductase (AKR1A), a member of the aldo-keto reductase superfamily, suppresses diabetic complications via a reduction in metabolic intermediates; it also plays a role in ascorbic acid biosynthesis in mice. Because primates cannot synthesize ascorbic acid, a principle role of AKR1A appears to be the reductive detoxification of aldehydes. In this study, we isolated and immortalized mouse embryonic fibroblasts (MEFs) from wild-type (WT) and human Akr1a-transgenic (Tg) mice and used them to investigate the potential roles of AKR1A under culture conditions. Tg MEFs showed higher methylglyoxal- and acrolein-reducing activities than WT MEFs and also were more resistant to cytotoxicity. Enzymatic analyses of purified rat AKR1A showed that the efficiency of the acrolein reduction was about 20% that of glyceraldehyde. Ascorbic acid levels were quite low in the MEFs, and while the administration of ascorbic acid to the cells increased the intracellular levels of ascorbic acid, it had no affect on the resistance to acrolein. Endoplasmic reticulum stress and protein carbonylation induced by acrolein treatment were less evident in Tg MEFs than in WT MEFs. These data collectively indicate that one of the principle roles of AKR1A in primates is the reductive detoxification of aldehydes, notably acrolein, and protection from its detrimental effects. Copyright © 2014 Elsevier Inc. All rights reserved.

  9. Reactions of CH-acids with α,β-unsaturated aldehydes in ionic liquids

    DEFF Research Database (Denmark)

    Kryshtal, G. V.; Zhdankina, G. M.; Astakhova, Irina Kira

    2004-01-01

    Metal carbonate-catalyzed reactions of CH-acids (diethyl malonate, ethyl acetoacetate, ethyl cyanoacetate, and ethyl 2-acetyl- and 2-ethoxycarbonyl-5,9- dimethyldeca-4,8-dienoates) with α,β-unsaturated aldehydes (acrolein, crotonaldehyde, citral) were studied in an ionic liquid, 1-butyl-3......- methylimidazolium hexafluorophosphate [bmim][PF 6], and in a 1-butyl-3-methylimidazolium bromide ([bmim][Br]) - benzene system. The reactions with acrolein and crotonaldehyde afforded Michael addition products, those with citral resulted in Knoevenagel addition products. Sonication increased the yields...

  10. Acrolein inhibits cytokine gene expression by alkylating cysteine and arginine residues in the NF-kappaB1 DNA binding domain.

    Science.gov (United States)

    Lambert, Cherie; Li, Jimei; Jonscher, Karen; Yang, Teng-Chieh; Reigan, Philip; Quintana, Megan; Harvey, Jean; Freed, Brian M

    2007-07-06

    Cigarette smoke is a potent inhibitor of pulmonary T cell responses, resulting in decreased immune surveillance and an increased incidence of respiratory tract infections. The alpha,beta-unsaturated aldehydes in cigarette smoke (acrolein and crotonaldehyde) inhibited production of interleukin-2 (IL-2), IL-10, granulocyte-macrophage colony-stimulating factor, interferon-gamma, and tumor necrosis factor-alpha by human T cells but did not inhibit production of IL-8. The saturated aldehydes (acetaldehyde, propionaldehyde, and butyraldehyde) in cigarette smoke were inactive. Acrolein inhibited induction of NF-kappaB DNA binding activity after mitogenic stimulation of T cells but had no effect on induction of NFAT or AP-1. Acrolein inhibited NF-kappaB1 (p50) binding to the IL-2 promoter in a chromatin immunoprecipitation assay by >99%. Using purified recombinant p50 in an electrophoretic mobility shift assay, we demonstrated that acrolein was 2000-fold more potent than crotonaldehyde in blocking DNA binding to an NF-kappaB consensus sequence. Matrix-assisted laser desorption/ionization time-of-flight and tandem mass spectrometry demonstrated that acrolein alkylated two amino acids (Cys-61 and Arg-307) in the DNA binding domain. Crotonaldehyde reacted with Cys-61, but not Arg-307, whereas the saturated aldehydes in cigarette smoke did not react with p50. These experiments demonstrate that aldehydes in cigarette smoke can regulate gene expression by direct modification of a transcription factor.

  11. α,β-Unsaturated aldehyde pollutant acrolein suppresses cardiomyocyte contractile function: Role of TRPV1 and oxidative stress.

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    Wu, Zhenbiao; He, Emily Y; Scott, Glenda I; Ren, Jun

    2015-01-01

    Air pollution is associated with an increased prevalence of heart disease and is known to trigger a proinflammatory response via stimulation of transient receptor potential vanilloid cation channels (TRPV1, also known as the capsaicin receptor). This study was designed to examine the effect of acrolein, an essential α,β-unsaturated aldehyde pollutant, on myocardial contractile function and the underlying mechanism involved with a focus on TRPV1 and oxidative stress. Cardiomyocyte mechanical and intracellular Ca(2+) properties were evaluated using an IonOptix MyoCam® system including peak shortening (PS), maximal velocity of shortening/relengthening (± dL/dt), time-to-PS (TPS), time-to-90% relengthening (TR90 ), fura-2 fluorescence intensity (FFI) and intracellular Ca(2+) decay. Changes in apoptosis and TRPV1 were evaluated using Western blot analysis. The degree of oxidative stress was assessed using the ratio between reduced and oxidized glutathione. Results obtained revealed that exposure of cardiomyocytes to acrolein acutely compromised contractile and intracellular Ca(2+) properties including depressed PS, ± dL/dt and ΔFFI, as well as prolonged TR90 and intracellular Ca(2+) decay. In addition, acrolein exposure upregulated TRPV1 associated with an increase in both apoptosis and oxidative stress. However, the acrolein-induced cardiomyocyte contractile and intracellular Ca(2+) anomalies, as well as apoptosis (as evidenced by Bcl-2, Bax, FasL, Caspase-3 and -8), were negated by the reactive oxygen species (ROS) scavenger glutathione or the TRPV1 antagonist capsazepine. Collectively these data suggest that the α,β-unsaturated aldehyde pollutant acrolein may play a role in the pathogenesis and sequelae of air pollution-induced heart disease via a TRPV1- and oxidative stress-dependent mechanism. © 2013 Wiley Periodicals, Inc.

  12. UTILIZING THE PAKS METHOD FOR MEASURING ACROLEIN AND OTHER ALDEHYDES IN DEARS

    Science.gov (United States)

    Acrolein is a hazardous air pollutant of high priority due to its high irritation potency and other potential adverse health effects. However, a reliable method is currently unavailable for measuring airborne acrolein at typical environmental levels. In the Detroit Exposure and A...

  13. Acrolein in cigarette smoke inhibits T-cell responses.

    Science.gov (United States)

    Lambert, Cherie; McCue, Jesica; Portas, Mary; Ouyang, Yanli; Li, JiMei; Rosano, Thomas G; Lazis, Alexander; Freed, Brian M

    2005-10-01

    Cigarette smoking inhibits T-cell responses in the lungs, but the immunosuppressive compounds have not been fully identified. Cigarette smoke extracts inhibit IL-2, IFN-gamma, and TNF-alpha production in stimulated lymphocytes obtained from peripheral blood, even when the extracts were diluted 100-fold to 1000-fold. The objective of these studies was to identify the immunosuppressive compounds found in cigarette smoke. Gas chromatography/mass spectroscopy and HPLC were used to identify and quantitate volatile compounds found in cigarette smoke extracts. Bioactivity was measured by viability and production of cytokine mRNA and protein levels in treated human lymphocytes. The vapor phase of the cigarette smoke extract inhibited cytokine production, indicating that the immunosuppressive compounds were volatile. Among the volatile compounds identified in cigarette smoke extracts, only the alpha,beta-unsaturated aldehydes, acrolein (inhibitory concentration of 50% [IC50] = 3 micromol/L) and crotonaldehyde (IC50 = 6 micromol/L), exhibited significant inhibition of cytokine production. Although the levels of aldehydes varied 10-fold between high-tar (Camel) and ultralow-tar (Carlton) extracts, even ultralow-tar cigarettes produced sufficient levels of acrolein (34 micromol/L) to suppress cytokine production by >95%. We determined that the cigarette smoke extract inhibited transcription of cytokine genes. The inhibitory effects of acrolein could be blocked with the thiol compound N-acetylcysteine. The vapor phase from cigarette smoke extracts potently suppresses cytokine production. The compound responsible for this inhibition appears to be acrolein.

  14. Structure of products of the condensation of α,β-unsaturated aldehydes with dimedone

    International Nuclear Information System (INIS)

    Yurchenko, O.I.; Pushkareva, K.S.; Zheldubovskaya, G.A.; Komarov, N.V.; Berkova, G.A.

    1987-01-01

    α,β-Acetylenic aldehydes and cinnamaldehyde in reaction with dimedone give the corresponding unsaturated bis(dimedonyl)methanes. In the case of acrolein and crotonaldehyde intramolecular cyclization occurs with the participation of hydroxyl of the dimedone fragment and the double bond with the formation of pyran systems. The PMR spectra were determined on Tesla BS-487C (80 MHz) and Tesla BS-467C (60 MHz) spectrometers in chloroform-d, pyridine-d 5 , and trifluoroacetic acid solutions. Internal standards HMDS and methylene chloride

  15. The health- and addictive effectes due to exposure to aldehydes of cigarette smoke. Part 1; Acetaldehyde, Formaldehyde, Acrolein and Propionaldehyde

    NARCIS (Netherlands)

    van Andel I; Schenk E; Rambali B; Wolterink G; van de Werken G; Stevenson H; van Aerts LAGJM; Vleeming W; LEO; LGM; LOC; CRV

    2003-01-01

    In deze literatuurstudie worden de gezondheids- en mogelijke verslavende effecten van blootstelling aan aldehyden ten gevolge van het roken van sigaretten beschreven. Dit literatuuronderzoek richt zich met name op acetaldehyde, formaldehyde, acrolein, en propionaldehyde. Alle aldehyden veroorzaken

  16. Acrolein health effects.

    Science.gov (United States)

    Faroon, O; Roney, N; Taylor, J; Ashizawa, A; Lumpkin, M H; Plewak, D J

    2008-08-01

    Acrolein is a chemical used as an intermediate reactive aldehyde in chemical industry. It is used for synthesis of many organic substances, methionine production, and methyl chloride refrigerant. The general population is exposed to acrolein via smoking, second-hand smoke, exposure to wood and plastic smoke. Firefighters and population living or working in areas with heavy automotive traffic may expose to higher level of acrolein via inhalation of smoke or automotive exhaust. Degradation of acrolein in all environmental media occurs rapidly, therefore, environmental accumulation is not expected. Acrolein degrade in 6A days when applied to surface water, and it has not been found as a contaminant in municipal drinking water. Acrolein vapor may cause eye, nasal and respiratory tract irritations in low level exposure. A decrease in breathing rate was reported by volunteers acutely exposed to 0.3A ppm of acrolein. At similar level, mild nasal epithelial dysplasia, necrosis, and focal basal cell metaplasia have been observed in rats. The acrolein effects on gastrointestinal mucosa in the animals include epithelial hyperplasia, ulceration, and hemorrhage. The severity of the effects is dose dependent. Acrolein induces the respiratory, ocular, and gastrointestinal irritations by inducing the release of peptides in nerve terminals innervating these systems. Levels of acrolein between 22 and 249 ppm for 10 min induced a dose-related decrease in substance P (a short-chain polypeptide that functions as a neurotransmitter or neuromodulator).

  17. Acrolein inhalation alters myocardial synchrony and performance at and below exposure concentrations that cause ventilatory responses

    Science.gov (United States)

    Acrolein is an irritating aldehyde generated during combustion of organic compounds. Altered autonomic activity has been documented following acrolein inhalation, possibly impacting myocardial synchrony and function. Given the ubiquitous nature of acrolein in the environment, we ...

  18. NMR investigation of acrolein stability in hydroalcoholic solution as a foundation for the valid HS-SPME/GC–MS quantification of the unsaturated aldehyde in beverages

    International Nuclear Information System (INIS)

    Kächele, Martin; Monakhova, Yulia B.; Kuballa, Thomas; Lachenmeier, Dirk W.

    2014-01-01

    Highlights: • Acrolein in hydroalcoholic solution degrades to 1,3,3-propanetriol and 3-hydroxypropionaldehyde. • Hydroquinone (0.2%) at pH 3.0 stabilizes acrolein solutions. • Quantitative HS-SPME/GC–MS determination of acrolein in alcoholic beverages was developed (LOD 14 μg L −1 ). • 6 of 117 samples had acrolein levels above the WHO threshold (1500 μg L −1 ). - Abstract: Acrolein (propenal) is found in many foods and beverages and may pose a health hazard due to its cytotoxicity. Considerable knowledge gaps regarding human exposure to acrolein exist, and there is a lack of reliable analytical methods. Hydroalcoholic dilutions prepared for calibration purposes from pure acrolein show considerable degradation of the compound and nuclear magnetic resonance (NMR) spectroscopy showed that 1,3,3-propanetriol and 3-hydroxypropionaldehyde are formed. The degradation can be prevented by addition of hydroquinone as stabilizer to the calibration solutions, which then show linear concentration-response behaviour required for quantitative analysis. The stabilized calibration solutions were used for quantitative headspace solid-phase microextraction/gas chromatography–mass spectrometry (HS-SPME/GC–MS) determination of acrolein in alcoholic beverages with a detection limit of 14 μg L −1 . Of 117 tested alcoholic beverages, 64 were tested positive with the highest incidence in grape marc spirits and whiskey (100%, mean 252 μg L −1 ), followed by fruit spirits (86%, mean 591 μg/L −1 ), tequila (86%, mean 404 μg L −1 ), Asian spirits (43%, mean 54 μg L −1 ) and wine (9%, mean 0.7 μg L −1 ). Acrolein could not be detected in beer, vodka, absinthe and bottled water. Six of the fruit and grape marc spirits had acrolein levels above the World Health Organization (WHO) provisional tolerable concentration of 1.5 mg L −1

  19. NMR investigation of acrolein stability in hydroalcoholic solution as a foundation for the valid HS-SPME/GC–MS quantification of the unsaturated aldehyde in beverages

    Energy Technology Data Exchange (ETDEWEB)

    Kächele, Martin [Chemisches und Veterinäruntersuchungsamt (CVUA) Karlsruhe, Weissenburger Strasse 3, D-76187 Karlsruhe (Germany); Hochschule Mannheim, Paul-Wittsack-Strasse 10, D-68163 Mannheim (Germany); Monakhova, Yulia B. [Chemisches und Veterinäruntersuchungsamt (CVUA) Karlsruhe, Weissenburger Strasse 3, D-76187 Karlsruhe (Germany); Bruker Biospin GmbH, Silbersteifen, 76287 Rheinstetten (Germany); Department of Chemistry, Saratov State University, Astrakhanskaya Street 83, 410012 Saratov (Russian Federation); Kuballa, Thomas [Chemisches und Veterinäruntersuchungsamt (CVUA) Karlsruhe, Weissenburger Strasse 3, D-76187 Karlsruhe (Germany); Lachenmeier, Dirk W., E-mail: lachenmeier@web.de [Chemisches und Veterinäruntersuchungsamt (CVUA) Karlsruhe, Weissenburger Strasse 3, D-76187 Karlsruhe (Germany); Ministry of Rural Affairs and Consumer Protection, Kernerplatz 10, 70182 Stuttgart (Germany)

    2014-04-01

    Highlights: • Acrolein in hydroalcoholic solution degrades to 1,3,3-propanetriol and 3-hydroxypropionaldehyde. • Hydroquinone (0.2%) at pH 3.0 stabilizes acrolein solutions. • Quantitative HS-SPME/GC–MS determination of acrolein in alcoholic beverages was developed (LOD 14 μg L⁻¹. • 6 of 117 samples had acrolein levels above the WHO threshold (1500 μg L⁻¹). Abstract: Acrolein (propenal) is found in many foods and beverages and may pose a health hazard due to its cytotoxicity. Considerable knowledge gaps regarding human exposure to acrolein exist, and there is a lack of reliable analytical methods. Hydroalcoholic dilutions prepared for calibration purposes from pure acrolein show considerable degradation of the compound and nuclear magnetic resonance (NMR) spectroscopy showed that 1,3,3-propanetriol and 3-hydroxypropionaldehyde are formed. The degradation can be prevented by addition of hydroquinone as stabilizer to the calibration solutions, which then show linear concentration-response behaviour required for quantitative analysis. The stabilized calibration solutions were used for quantitative headspace solid-phase microextraction/gas chromatography–mass spectrometry (HS-SPME/GC–MS) determination of acrolein in alcoholic beverages with a detection limit of 14 μg L⁻¹. Of 117 tested alcoholic beverages, 64 were tested positive with the highest incidence in grape marc spirits and whiskey (100%, mean 252 μg L⁻¹), followed by fruit spirits (86%, mean 591 μg/L⁻¹), tequila (86%, mean 404 μg L⁻¹), Asian spirits (43%, mean 54 μg L⁻¹) and wine (9%, mean 0.7 μg L⁻¹). Acrolein could not be detected in beer, vodka, absinthe and bottled water. Six of the fruit and grape marc spirits had acrolein levels above the World Health Organization (WHO) provisional tolerable concentration of 1.5 mg L⁻¹.

  20. Acrolein Can Cause Cardiovascular Disease: A Review.

    Science.gov (United States)

    Henning, Robert J; Johnson, Giffe T; Coyle, Jayme P; Harbison, Raymond D

    2017-07-01

    Acrolein is a highly reactive unsaturated aldehyde that is formed during the burning of gasoline and diesel fuels, cigarettes, woods and plastics. In addition, acrolein is generated during the cooking or frying of food with fats or oils. Acrolein is also used in the synthesis of many organic chemicals and as a biocide in agricultural and industrial water supply systems. The total emissions of acrolein in the United States from all sources are estimated to be 62,660 tons/year. Acrolein is classified by the Environmental Protection Agency as a high-priority air and water toxicant. Acrolein can exert toxic effects following inhalation, ingestion, and dermal exposures that are dose dependent. Cardiovascular tissues are particularly sensitive to the toxic effects of acrolein based primarily on in vitro and in vivo studies. Acrolein can generate free oxygen radical stress in the heart, decrease endothelial nitric oxide synthase phosphorylation and nitric oxide formation, form cytoplasmic and nuclear protein adducts with myocyte and vascular endothelial cell proteins and cause vasospasm. In this manner, chronic exposure to acrolein can cause myocyte dysfunction, myocyte necrosis and apoptosis and ultimately lead to cardiomyopathy and cardiac failure. Epidemiological studies of acrolein exposure and toxicity should be developed and treatment strategies devised that prevent or significantly limit acrolein cardiovascular toxicity.

  1. NMR investigation of acrolein stability in hydroalcoholic solution as a foundation for the valid HS-SPME/GC-MS quantification of the unsaturated aldehyde in beverages.

    Science.gov (United States)

    Kächele, Martin; Monakhova, Yulia B; Kuballa, Thomas; Lachenmeier, Dirk W

    2014-04-11

    Acrolein (propenal) is found in many foods and beverages and may pose a health hazard due to its cytotoxicity. Considerable knowledge gaps regarding human exposure to acrolein exist, and there is a lack of reliable analytical methods. Hydroalcoholic dilutions prepared for calibration purposes from pure acrolein show considerable degradation of the compound and nuclear magnetic resonance (NMR) spectroscopy showed that 1,3,3-propanetriol and 3-hydroxypropionaldehyde are formed. The degradation can be prevented by addition of hydroquinone as stabilizer to the calibration solutions, which then show linear concentration-response behaviour required for quantitative analysis. The stabilized calibration solutions were used for quantitative headspace solid-phase microextraction/gas chromatography-mass spectrometry (HS-SPME/GC-MS) determination of acrolein in alcoholic beverages with a detection limit of 14 μg L(-1). Of 117 tested alcoholic beverages, 64 were tested positive with the highest incidence in grape marc spirits and whiskey (100%, mean 252 μg L(-1)), followed by fruit spirits (86%, mean 591 μg/L(-1)), tequila (86%, mean 404 μg L(-1)), Asian spirits (43%, mean 54 μg L(-1)) and wine (9%, mean 0.7 μg L(-1)). Acrolein could not be detected in beer, vodka, absinthe and bottled water. Six of the fruit and grape marc spirits had acrolein levels above the World Health Organization (WHO) provisional tolerable concentration of 1.5 mg L(-1). Copyright © 2014 Elsevier B.V. All rights reserved.

  2. Dimercaprol is an acrolein scavenger that mitigates acrolein-mediated PC-12 cells toxicity and reduces acrolein in rat following spinal cord injury.

    Science.gov (United States)

    Tian, Ran; Shi, Riyi

    2017-06-01

    Acrolein is one of the most toxic byproducts of lipid peroxidation, and it has been shown to be associated with multiple pathological processes in trauma and diseases, including spinal cord injury, multiple sclerosis, and Alzheimer's disease. Therefore, suppressing acrolein using acrolein scavengers has been suggested as a novel strategy of neuroprotection. In an effort to identify effective acrolein scavengers, we have confirmed that dimercaprol, which possesses thiol functional groups, could bind and trap acrolein. We demonstrated the reaction between acrolein and dimercaprol in an abiotic condition by nuclear magnetic resonance spectroscopy. Specifically, dimercaprol is able to bind to both the carbon double bond and aldehyde group of acrolein. Its acrolein scavenging capability was further demonstrated by in vitro results that showed that dimercaprol could significantly protect PC-12 cells from acrolein-mediated cell death in a dose-dependent manner. Furthermore, dimercaprol, when applied systemically through intraperitoneal injection, could significantly reduce acrolein contents in spinal cord tissue following a spinal cord contusion injury in rats, a condition known to have elevated acrolein concentration. Taken together, dimercaprol may be an effective acrolein scavenger and a viable candidate for acrolein detoxification. © 2017 International Society for Neurochemistry.

  3. Polyamine modification by acrolein exclusively produces 1,5-diazacyclooctanes: a previously unrecognized mechanism for acrolein-mediated oxidative stress.

    Science.gov (United States)

    Tsutsui, Ayumi; Imamaki, Rie; Kitazume, Shinobu; Hanashima, Shinya; Yamaguchi, Yoshiki; Kaneda, Masato; Oishi, Shinya; Fujii, Nobutaka; Kurbangalieva, Almira; Taniguchi, Naoyuki; Tanaka, Katsunori

    2014-07-28

    Acrolein, a toxic unsaturated aldehyde generated as a result of oxidative stress, readily reacts with a variety of nucleophilic biomolecules. Polyamines, which produced acrolein in the presence of amine oxidase, were then found to react with acrolein to produce 1,5-diazacyclooctane, a previously unrecognized but significant downstream product of oxidative stress. Although diazacyclooctane formation effectively neutralized acrolein toxicity, the diazacyclooctane hydrogel produced through a sequential diazacyclooctane polymerization reaction was highly cytotoxic. This study suggests that diazacyclooctane formation is involved in the mechanism underlying acrolein-mediated oxidative stress.

  4. A Comparative study on VOCs and aldehyde-ketone emissions from a spark Ignition vehicle fuelled on compressed natural gas and gasoline

    International Nuclear Information System (INIS)

    Shah, A.N.

    2012-01-01

    In this work, an experimental study was conducted on a spark ignition (SI) vehicle fuelled on compressed natural gas (CNG), and gasoline to compare the unregulated emissions such as volatile organic compounds (VOCs) and aldehyde-ketones or carbonyls. In the meantime, ozone forming potential (OFP) of pollutants was also calculated on the basis of their specific reactivity (SR). The vehicle was run on a chassis dynamometer following the Chinese National Standards test scheduled for light duty vehicle (LDV) emissions. According to the results, total aldehyde-ketones were increased by 39.4% due to the substantial increase in formaldehyde and acrolein + acetone emissions, while VOCs and BTEX (benzene, toluene, ethyl benzene, and xylene) reduced by 85.2 and 86% respectively, in case of CNG fuelled vehicle as compared to gasoline vehicle. Although total aldehyde-ketones were higher with CNG relative to gasoline, their SR was lower due decrease in acetaldehyde, propionaldehyde, crotonaldehyde, and methacrolein species having higher maximum incremental reactivity (MIR) values. The SR of VOCs and aldehyde-ketones emitted from CNG fuelled vehicle was decreased by above 10% and 32% respectively, owing to better physicochemical properties and more complete burning of CNG as compared to gasoline. (author)

  5. Role of aldehyde chemistry and NOx concentrations in secondary organic aerosol formation

    Directory of Open Access Journals (Sweden)

    P. O. Wennberg

    2010-08-01

    Full Text Available Aldehydes are an important class of products from atmospheric oxidation of hydrocarbons. Isoprene (2-methyl-1,3-butadiene, the most abundantly emitted atmospheric non-methane hydrocarbon, produces a significant amount of secondary organic aerosol (SOA via methacrolein (a C4-unsaturated aldehyde under urban high-NOx conditions. Previously, we have identified peroxy methacryloyl nitrate (MPAN as the important intermediate to isoprene and methacrolein SOA in this NOx regime. Here we show that as a result of this chemistry, NO2 enhances SOA formation from methacrolein and two other α, β-unsaturated aldehydes, specifically acrolein and crotonaldehyde, a NOx effect on SOA formation previously unrecognized. Oligoesters of dihydroxycarboxylic acids and hydroxynitrooxycarboxylic acids are observed to increase with increasing NO2/NO ratio, and previous characterizations are confirmed by both online and offline high-resolution mass spectrometry techniques. Molecular structure also determines the amount of SOA formation, as the SOA mass yields are the highest for aldehydes that are α, β-unsaturated and contain an additional methyl group on the α-carbon. Aerosol formation from 2-methyl-3-buten-2-ol (MBO232 is insignificant, even under high-NO2 conditions, as PAN (peroxy acyl nitrate, RC(OOONO2 formation is structurally unfavorable. At atmospherically relevant NO2/NO ratios (3–8, the SOA yields from isoprene high-NOx photooxidation are 3 times greater than previously measured at lower NO2/NO ratios. At sufficiently high NO2 concentrations, in systems of α, β-unsaturated aldehydes, SOA formation from subsequent oxidation of products from acyl peroxyl radicals+NO2 can exceed that from RO2+HO2 reactions under the same inorganic seed conditions, making RO2+NO2 an important channel for SOA formation.

  6. Role of aldehyde chemistry and NOx concentrations in secondary organic aerosol formation

    Science.gov (United States)

    Chan, A. W. H.; Chan, M. N.; Surratt, J. D.; Chhabra, P. S.; Loza, C. L.; Crounse, J. D.; Yee, L. D.; Flagan, R. C.; Wennberg, P. O.; Seinfeld, J. H.

    2010-08-01

    Aldehydes are an important class of products from atmospheric oxidation of hydrocarbons. Isoprene (2-methyl-1,3-butadiene), the most abundantly emitted atmospheric non-methane hydrocarbon, produces a significant amount of secondary organic aerosol (SOA) via methacrolein (a C4-unsaturated aldehyde) under urban high-NOx conditions. Previously, we have identified peroxy methacryloyl nitrate (MPAN) as the important intermediate to isoprene and methacrolein SOA in this NOx regime. Here we show that as a result of this chemistry, NO2 enhances SOA formation from methacrolein and two other α, β-unsaturated aldehydes, specifically acrolein and crotonaldehyde, a NOx effect on SOA formation previously unrecognized. Oligoesters of dihydroxycarboxylic acids and hydroxynitrooxycarboxylic acids are observed to increase with increasing NO2/NO ratio, and previous characterizations are confirmed by both online and offline high-resolution mass spectrometry techniques. Molecular structure also determines the amount of SOA formation, as the SOA mass yields are the highest for aldehydes that are α, β-unsaturated and contain an additional methyl group on the α-carbon. Aerosol formation from 2-methyl-3-buten-2-ol (MBO232) is insignificant, even under high-NO2 conditions, as PAN (peroxy acyl nitrate, RC(O)OONO2) formation is structurally unfavorable. At atmospherically relevant NO2/NO ratios (3-8), the SOA yields from isoprene high-NOx photooxidation are 3 times greater than previously measured at lower NO2/NO ratios. At sufficiently high NO2 concentrations, in systems of α, β-unsaturated aldehydes, SOA formation from subsequent oxidation of products from acyl peroxyl radicals+NO2 can exceed that from RO2+HO2 reactions under the same inorganic seed conditions, making RO2+NO2 an important channel for SOA formation.

  7. Acrolein-detoxifying isozymes of glutathione transferase in plants.

    Science.gov (United States)

    Mano, Jun'ichi; Ishibashi, Asami; Muneuchi, Hitoshi; Morita, Chihiro; Sakai, Hiroki; Biswas, Md Sanaullah; Koeduka, Takao; Kitajima, Sakihito

    2017-02-01

    Acrolein is a lipid-derived highly reactive aldehyde, mediating oxidative signal and damage in plants. We found acrolein-scavenging glutathione transferase activity in plants and purified a low K M isozyme from spinach. Various environmental stressors on plants cause the generation of acrolein, a highly toxic aldehyde produced from lipid peroxides, via the promotion of the formation of reactive oxygen species, which oxidize membrane lipids. In mammals, acrolein is scavenged by glutathione transferase (GST; EC 2.5.1.18) isozymes of Alpha, Pi, and Mu classes, but plants lack these GST classes. We detected the acrolein-scavenging GST activity in four species of plants, and purified an isozyme showing this activity from spinach (Spinacia oleracea L.) leaves. The isozyme (GST-Acr), obtained after an affinity chromatography and two ion exchange chromatography steps, showed the K M value for acrolein 93 μM, the smallest value known for acrolein-detoxifying enzymes in plants. Peptide sequence homology search revealed that GST-Acr belongs to the GST Tau, a plant-specific class. The Arabidopsis thaliana GST Tau19, which has the closest sequence similar to spinach GST-Acr, also showed a high catalytic efficiency for acrolein. These results suggest that GST plays as a scavenger for acrolein in plants.

  8. Inhibition by acrolein of light-induced stomatal opening through inhibition of inward-rectifying potassium channels in Arabidopsis thaliana.

    Science.gov (United States)

    Islam, Md Moshiul; Ye, Wenxiu; Matsushima, Daiki; Khokon, Md Atiqur Rahman; Munemasa, Shintaro; Nakamura, Yoshimasa; Murata, Yoshiyuki

    2015-01-01

    Acrolein is a reactive α,β-unsaturated aldehyde derived from lipid peroxides, which are produced in plants under a variety of stress. We investigated effects of acrolein on light-induced stomatal opening using Arabidopsis thaliana. Acrolein inhibited light-induced stomatal opening in a dose-dependent manner. Acrolein at 100 μM inhibited plasma membrane inward-rectifying potassium (Kin) channels in guard cells. Acrolein at 100 μM inhibited Kin channel KAT1 expressed in a heterologous system using Xenopus leaves oocytes. These results suggest that acrolein inhibits light-induced stomatal opening through inhibition of Kin channels in guard cells.

  9. Acrolein consumption induces systemic dyslipidemia and lipoprotein modification

    International Nuclear Information System (INIS)

    Conklin, Daniel J.; Barski, Oleg A.; Lesgards, Jean-Francois; Juvan, Peter; Rezen, Tadeja; Rozman, Damjana; Prough, Russell A.; Vladykovskaya, Elena; Liu, SiQi; Srivastava, Sanjay; Bhatnagar, Aruni

    2010-01-01

    Aldehydes such as acrolein are ubiquitous pollutants present in automobile exhaust, cigarette, wood, and coal smoke. Such aldehydes are also constituents of several food substances and are present in drinking water, irrigation canals, and effluents from manufacturing plants. Oral intake represents the most significant source of exposure to acrolein and related aldehydes. To study the effects of short-term oral exposure to acrolein on lipoprotein levels and metabolism, adult mice were gavage-fed 0.1 to 5 mg acrolein/kg bwt and changes in plasma lipoproteins were assessed. Changes in hepatic gene expression related to lipid metabolism and cytokines were examined by qRT-PCR analysis. Acrolein feeding did not affect body weight, blood urea nitrogen, plasma creatinine, electrolytes, cytokines or liver enzymes, but increased plasma cholesterol and triglycerides. Similar results were obtained with apoE-null mice. Plasma lipoproteins from acrolein-fed mice showed altered electrophoretic mobility on agarose gels. Chromatographic analysis revealed elevated VLDL cholesterol, phospholipids, and triglycerides levels with little change in LDL or HDL. NMR analysis indicated shifts from small to large VLDL and from large to medium-small LDL with no change in the size of HDL particles. Increased plasma VLDL was associated with a significant decrease in post-heparin plasma hepatic lipase activity and a decrease in hepatic expression of hepatic lipase. These observations suggest that oral exposure to acrolein could induce or exacerbate systemic dyslipidemia and thereby contribute to cardiovascular disease risk.

  10. Acrolein consumption induces systemic dyslipidemia and lipoprotein modification

    Energy Technology Data Exchange (ETDEWEB)

    Conklin, Daniel J., E-mail: dj.conklin@louisville.ed [Diabetes and Obesity Center, University of Louisville, Louisville, KY 40202 (United States); Barski, Oleg A; Lesgards, Jean-Francois [Diabetes and Obesity Center, University of Louisville, Louisville, KY 40202 (United States); Juvan, Peter; Rezen, Tadeja; Rozman, Damjana [Centre for Functional Genomics and Bio-Chips (CFGBC), Institute of Biochemistry, Faculty of Medicine, University of Ljubljana, Zaloska 4, SI-1000 Ljubljana (Slovenia); Prough, Russell A [Department of Biochemistry and Molecular Biology, University of Louisville, Louisville, KY 40202 (United States); Vladykovskaya, Elena; Liu, SiQi; Srivastava, Sanjay [Diabetes and Obesity Center, University of Louisville, Louisville, KY 40202 (United States); Bhatnagar, Aruni [Diabetes and Obesity Center, University of Louisville, Louisville, KY 40202 (United States); Department of Biochemistry and Molecular Biology, University of Louisville, Louisville, KY 40202 (United States)

    2010-02-15

    Aldehydes such as acrolein are ubiquitous pollutants present in automobile exhaust, cigarette, wood, and coal smoke. Such aldehydes are also constituents of several food substances and are present in drinking water, irrigation canals, and effluents from manufacturing plants. Oral intake represents the most significant source of exposure to acrolein and related aldehydes. To study the effects of short-term oral exposure to acrolein on lipoprotein levels and metabolism, adult mice were gavage-fed 0.1 to 5 mg acrolein/kg bwt and changes in plasma lipoproteins were assessed. Changes in hepatic gene expression related to lipid metabolism and cytokines were examined by qRT-PCR analysis. Acrolein feeding did not affect body weight, blood urea nitrogen, plasma creatinine, electrolytes, cytokines or liver enzymes, but increased plasma cholesterol and triglycerides. Similar results were obtained with apoE-null mice. Plasma lipoproteins from acrolein-fed mice showed altered electrophoretic mobility on agarose gels. Chromatographic analysis revealed elevated VLDL cholesterol, phospholipids, and triglycerides levels with little change in LDL or HDL. NMR analysis indicated shifts from small to large VLDL and from large to medium-small LDL with no change in the size of HDL particles. Increased plasma VLDL was associated with a significant decrease in post-heparin plasma hepatic lipase activity and a decrease in hepatic expression of hepatic lipase. These observations suggest that oral exposure to acrolein could induce or exacerbate systemic dyslipidemia and thereby contribute to cardiovascular disease risk.

  11. Acrolein Inhalation Suppresses Lipopolysaccharide-Induced Inflammatory Cytokine Production but Does Not Affect Acute Airways Neutrophilia1

    OpenAIRE

    Kasahara, David Itiro; Poynter, Matthew E.; Othman, Ziryan; Hemenway, David; van der Vliet, Albert

    2008-01-01

    Acrolein is a reactive unsaturated aldehyde that is produced during endogenous oxidative processes and is a major bioactive component of environmental pollutants such as cigarette smoke. Because in vitro studies demonstrate that acrolein can inhibit neutrophil apoptosis, we evaluated the effects of in vivo acrolein exposure on acute lung inflammation induced by LPS. Male C57BL/6J mice received 300 μg/kg intratracheal LPS and were exposed to acrolein (5 parts per million, 6 h/day), either befo...

  12. Acrolein acts as a neurotoxin in the nigrostriatal dopaminergic system of rat: involvement of ?-synuclein aggregation and programmed cell death

    OpenAIRE

    Wang, Yi-Ting; Lin, Hui-Ching; Zhao, Wei-Zhong; Huang, Hui-Ju; Lo, Yu-Li; Wang, Hsiang-Tsui; Maan-Yuh Lin, Anya

    2017-01-01

    Clinical studies report significant increases in acrolein (an ?,?-unsaturated aldehyde) in the substantia nigra (SN) of patients with Parkinson?s disease (PD). In the present study, acrolein-induced neurotoxicity in the nigrostriatal dopaminergic system was investigated by local infusion of acrolein (15, 50, 150?nmoles/0.5??l) in the SN of Sprague-Dawley rats. Acrolein-induced neurodegeneration of nigrostriatal dopaminergic system was delineated by reductions in tyrosine hydroxylase (TH) leve...

  13. Acrolein-mediated injury in nervous system trauma and diseases

    Science.gov (United States)

    Shi, Riyi; Rickett, Todd; Sun, Wenjing

    2012-01-01

    Acrolein, an α,β-unsaturated aldehyde, is a ubiquitous pollutant that is also produced endogenously through lipid peroxidation. This compound is hundreds of times more reactive than other aldehydes such as 4-hydroxynonenal, is produced at much higher concentrations, and persists in solution for much longer than better known free radicals. It has been implicated in disease states known to involve chronic oxidative stress, particularly spinal cord injury and multiple sclerosis. Acrolein may overwhelm the anti-oxidative systems of any cell by depleting glutathione reserves, preventing glutathione regeneration, and inactivating protective enzymes. On the cellular level, acrolein exposure can cause membrane damage, mitochondrial dysfunction, and myelin disruption. Such pathologies can be exacerbated by increased concentrations or duration of exposure, and can occur in normal tissue incubated with injured spinal cord, showing that acrolein can act as a diffusive agent, spreading secondary injury. Several chemical species are capable of binding and inactivating acrolein. Hydralazine in particular can reduce acrolein concentrations and inhibit acrolein-mediated pathologies in vivo. Acrolein scavenging appears to be a novel effective treatment which is primed for rapid translation to the clinic. PMID:21823221

  14. Effects of acrolein on leukotriene biosynthesis in human neutrophils.

    Science.gov (United States)

    Berry, Karin A Zemski; Henson, Peter M; Murphy, Robert C

    2008-12-01

    Acrolein is a toxic, highly reactive alpha,beta-unsaturated aldehyde that is present in high concentrations in cigarette smoke. In the current study, the effect of acrolein on eicosanoid synthesis in stimulated human neutrophils was examined. Eicosanoid synthesis in neutrophils was initiated by priming with granulocyte-macrophage colony-stimulating factor (GM-CSF) and subsequent stimulation with formyl-methionyl-leucyl-phenylalanine (fMLP) and 5-lipoxygenase (5-LO) products in addition to small amounts of cyclooxygenase (COX) products were detected using LC/MS/MS. A dose-dependent decrease in the formation of 5-LO products was observed in GM-CSF/fMLP-stimulated neutrophils when acrolein (0-50 microM) was present with almost complete inhibition at > or = 25 microM acrolein. The production of COX products was not affected by acrolein in these cells. The effect of acrolein was examined on key parts of the eicosanoid pathway, such as arachidonic acid release, intracellular calcium ion concentration, and adenosine production. In addition, the direct effect of acrolein on 5-LO enzymatic activity was probed using a recombinant enzyme. Some of these factors were affected by acrolein but did not completely explain the almost complete inhibition of 5-LO product formation in GM-CSF/fMLP-treated cells with acrolein. In addition, the effect of acrolein on different stimuli that initiate the 5-LO pathway [platelet-activating factor (PAF)/fMLP, GM-CSF/PAF, opsonized zymosan, and A23187] was examined. Acrolein had no significant effect on the leukotriene production in neutrophils stimulated with PAF/fMLP, GM-CSF/ PAF, or OPZ. Additionally, 50% inhibition of the 5-LO pathway was observed in A23187-stimulated neutrophils. Our results suggest that acrolein has a profound effect on the 5-LO pathway in neutrophils, which may have implications in disease states, such as chronic obstructive pulmonary disease and other pulmonary disease, where both activated neutrophils and acrolein are

  15. Proteomic analysis of rat cerebral cortex following subchronic acrolein toxicity.

    Science.gov (United States)

    Rashedinia, Marzieh; Lari, Parisa; Abnous, Khalil; Hosseinzadeh, Hossein

    2013-10-01

    Acrolein, a member of reactive α,β-unsaturated aldehydes, is a major environmental pollutant. Acrolein is also produced endogenously as a toxic by-product of lipid peroxidation. Because of high reactivity, acrolein may mediate oxidative damages to cells and tissues. It has been shown to be involved in a wide variety of pathological states including pulmonary, atherosclerosis and neurodegenerative diseases. In this study we employed proteomics approach to investigate the effects of subchronic oral exposures to 3mg/kg of acrolein on protein expression profile in the brain of rats. Moreover effects of acrolein on malondialdehyde (MDA) levels and reduced glutathione (GSH) content were investigated. Our results revealed that treatment with acrolein changed levels of several proteins in diverse physiological process including energy metabolism, cell communication and transport, response to stimulus and metabolic process. Interestingly, several differentially over-expressed proteins, including β-synuclein, enolase and calcineurin, are known to be associated with human neurodegenerative diseases. Changes in the levels of some proteins were confirmed by Western blot. Moreover, acrolein increases the level of MDA, as a lipid peroxidation biomarker and decreased GSH concentrations, as a non-enzyme antioxidant in the brain of acrolein treated rats. These findings suggested that acrolein induces the oxidative stress and lipid peroxidation in the brain, and so that may contribute to the pathophysiology of neurological disorders. Copyright © 2013 Elsevier Inc. All rights reserved.

  16. Acrolein-Induced Dyslipidemia and Acute Phase Response Independenly of HMG-CoA Reductase

    Science.gov (United States)

    Conklin, Daniel J.; Prough, Russell A.; Juvan, Peter; Rezen, Tadeja; Rozman, Damjana; Haberzettl, Petra; Srivastava, Sanjay; Bhatnagar, Aruni

    2012-01-01

    Scope Aldehydes are ubiquitous natural constituents of foods, water and beverages. Dietary intake represents the greatest source of exposure to acrolein and related aldehydes. Oral acrolein induces dyslipidemia acutely and chronically increases atherosclerosis in mice, yet the mechanisms are unknown. Because lipid synthesis and trafficking are largely under hepatic control, we examined hepatic genes in murine models of acute and chronic oral acrolein exposure. Methods and results Changes in hepatic gene expression were examined using a Steroltalk microarray. Acute acrolein feeding modified plasma and hepatic proteins and increased plasma triglycerides within 15 min. By 6h, acrolein altered hepatic gene expression including Insig1, Insig2 and Hmgcr genes and stimulated an acute phase response (APR) with up-regulation of serum amyloid A genes (Saa) and systemic hypoalbuminemia. To test if decreased HMG-CoA reductase activity could modify acrolein-induced dyslipidemia or the APR, mice were pretreated with simvastatin. Statin treatment, however, did not alter acrolein-induced dyslipidemia or hypoalbuminemia associated with an APR. Few hepatic genes were dysregulated by chronic acrolein feeding in apoE-null mice. These studies confirmed that acute acrolein exposure altered expression of hepatic genes involved with lipid synthesis and trafficking and APR, and thus, indicated a hepatic locus of acrolein-induced dyslipidemia and APR that was independent of HMG CoA-reductase. Conclusion Dietary intake of acrolein could contribute to cardiovascular disease risk by disturbing hepatic function. PMID:21812109

  17. Effects of Acrolein on Leukotriene Biosynthesis in Human Neutrophils

    OpenAIRE

    Zemski Berry, Karin A.; Henson, Peter M.; Murphy, Robert C.

    2008-01-01

    Acrolein is a toxic, highly reactive α,β-unsaturated aldehyde that is present in high concentrations in cigarette smoke. In the current study, the effect of acrolein on eicosanoid synthesis in stimulated human neutrophils was examined. Eicosanoid synthesis in neutrophils was initiated by priming with granulocyte-macrophage colony-stimulating factor (GM-CSF) and subsequent stimulation with formyl-methionyl-leucyl-phenylalanine (fMLP) and 5-LO products in addition to small amounts of COX produc...

  18. Alda-1 Protects Against Acrolein-Induced Acute Lung Injury and Endothelial Barrier Dysfunction.

    Science.gov (United States)

    Lu, Qing; Mundy, Miles; Chambers, Eboni; Lange, Thilo; Newton, Julie; Borgas, Diana; Yao, Hongwei; Choudhary, Gaurav; Basak, Rajshekhar; Oldham, Mahogany; Rounds, Sharon

    2017-12-01

    Inhalation of acrolein, a highly reactive aldehyde, causes lung edema. The underlying mechanism is poorly understood and there is no effective treatment. In this study, we demonstrated that acrolein not only dose-dependently induced lung edema but also promoted LPS-induced acute lung injury. Importantly, acrolein-induced lung injury was prevented and rescued by Alda-1, an activator of mitochondrial aldehyde dehydrogenase 2. Acrolein also dose-dependently increased monolayer permeability, disrupted adherens junctions and focal adhesion complexes, and caused intercellular gap formation in primary cultured lung microvascular endothelial cells (LMVECs). These effects were attenuated by Alda-1 and the antioxidant N-acetylcysteine, but not by the NADPH inhibitor apocynin. Furthermore, acrolein inhibited AMP-activated protein kinase (AMPK) and increased mitochondrial reactive oxygen species levels in LMVECs-effects that were associated with impaired mitochondrial respiration. AMPK total protein levels were also reduced in lung tissue of mice and LMVECs exposed to acrolein. Activation of AMPK with 5-aminoimidazole-4-carboxamide-1-β-4-ribofuranoside blunted an acrolein-induced increase in endothelial monolayer permeability, but not mitochondrial oxidative stress or inhibition of mitochondrial respiration. Our results suggest that acrolein-induced mitochondrial dysfunction may not contribute to endothelial barrier dysfunction. We speculate that detoxification of acrolein by Alda-1 and activation of AMPK may be novel approaches to prevent and treat acrolein-associated acute lung injury, which may occur after smoke inhalation.

  19. Proteomic analysis of rat cerebral cortex following subchronic acrolein toxicity

    Energy Technology Data Exchange (ETDEWEB)

    Rashedinia, Marzieh; Lari, Parisa [Department of Pharmacodynamics and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad (Iran, Islamic Republic of); Abnous, Khalil, E-mail: Abnouskh@mums.ac.r [Pharmaceutical Research Center, Department of Medicinal Chemistry, Mashhad University of Medical Sciences, Mashhad (Iran, Islamic Republic of); Hosseinzadeh, Hossein, E-mail: Hosseinzadehh@mums.ac.ir [Pharmaceutical Research Center, Department of Pharmacodynamics and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad (Iran, Islamic Republic of)

    2013-10-01

    Acrolein, a member of reactive α,β-unsaturated aldehydes, is a major environmental pollutant. Acrolein is also produced endogenously as a toxic by-product of lipid peroxidation. Because of high reactivity, acrolein may mediate oxidative damages to cells and tissues. It has been shown to be involved in a wide variety of pathological states including pulmonary, atherosclerosis and neurodegenerative diseases. In this study we employed proteomics approach to investigate the effects of subchronic oral exposures to 3 mg/kg of acrolein on protein expression profile in the brain of rats. Moreover effects of acrolein on malondialdehyde (MDA) levels and reduced glutathione (GSH) content were investigated. Our results revealed that treatment with acrolein changed levels of several proteins in diverse physiological process including energy metabolism, cell communication and transport, response to stimulus and metabolic process. Interestingly, several differentially over-expressed proteins, including β-synuclein, enolase and calcineurin, are known to be associated with human neurodegenerative diseases. Changes in the levels of some proteins were confirmed by Western blot. Moreover, acrolein increases the level of MDA, as a lipid peroxidation biomarker and decreased GSH concentrations, as a non-enzyme antioxidant in the brain of acrolein treated rats. These findings suggested that acrolein induces the oxidative stress and lipid peroxidation in the brain, and so that may contribute to the pathophysiology of neurological disorders. - Highlights: • Acrolein intoxication increased lipid peroxidation and deplete GSH in rat brain. • Effect of acrolein on protein levels of cerebral cortex was analyzed by 2DE-PAGE. • Levels of a number of proteins with different biological functions were increased.

  20. Proteomic analysis of rat cerebral cortex following subchronic acrolein toxicity

    International Nuclear Information System (INIS)

    Rashedinia, Marzieh; Lari, Parisa; Abnous, Khalil; Hosseinzadeh, Hossein

    2013-01-01

    Acrolein, a member of reactive α,β-unsaturated aldehydes, is a major environmental pollutant. Acrolein is also produced endogenously as a toxic by-product of lipid peroxidation. Because of high reactivity, acrolein may mediate oxidative damages to cells and tissues. It has been shown to be involved in a wide variety of pathological states including pulmonary, atherosclerosis and neurodegenerative diseases. In this study we employed proteomics approach to investigate the effects of subchronic oral exposures to 3 mg/kg of acrolein on protein expression profile in the brain of rats. Moreover effects of acrolein on malondialdehyde (MDA) levels and reduced glutathione (GSH) content were investigated. Our results revealed that treatment with acrolein changed levels of several proteins in diverse physiological process including energy metabolism, cell communication and transport, response to stimulus and metabolic process. Interestingly, several differentially over-expressed proteins, including β-synuclein, enolase and calcineurin, are known to be associated with human neurodegenerative diseases. Changes in the levels of some proteins were confirmed by Western blot. Moreover, acrolein increases the level of MDA, as a lipid peroxidation biomarker and decreased GSH concentrations, as a non-enzyme antioxidant in the brain of acrolein treated rats. These findings suggested that acrolein induces the oxidative stress and lipid peroxidation in the brain, and so that may contribute to the pathophysiology of neurological disorders. - Highlights: • Acrolein intoxication increased lipid peroxidation and deplete GSH in rat brain. • Effect of acrolein on protein levels of cerebral cortex was analyzed by 2DE-PAGE. • Levels of a number of proteins with different biological functions were increased

  1. Atmospheric measurements of hydroperoxides and aldehydes during field campaigns : new results due to improvement of measurements techniques

    Science.gov (United States)

    François, S.; Sowka, I.; Poulain, L.; Monod, A.; Wortham, H.

    2003-04-01

    Hydroperoxides and aldehydes are considered as atmospheric reservoirs of OH, HO_2 and RO_2 radicals and can reflect the oxidizing levels of the atmosphere. They are considered as important gas phase photo-oxidants present in the atmosphere. However, the atmospheric role of these compounds can vary from one species to another, therefore it is essential to investigate their measurement and speciation in the atmosphere. Atmospheric measurements were realized during two different field campaigns in the Marseilles area (France). Hydroperoxides were trapped in aqueous phase, with a glass coil and analyzed by HPLC/fluorescence detector with post column derivatization. Aldehydes were trapped in a liquid phase containing 2-4 DNPH, with a mist chamber and analyzed by HPLC/UV. The analytical techniques provided individual separation and quantification of seven hydroperoxides (hydrogen peroxide, hydroxymethyl hydroperoxide, bis(hydroxymethyl) peroxide, 1-hydroxyethyl hydroperoxide, methyl hydroperoxide, ethyl hydroperoxide and peroxyacetic acid) and eleven volatile aldehydes (formaldehyde, acetaldehyde, acrolein, acetone, propionaldehyde, crotonaldehyde, butyraldehyde, benzaldehyde, glyoxal, valeraldehyde and methylglyoxal). The first field campaign was part of the ESCOMPTE project (June 4th to July 16th 2001). During this campaign five different sampling sites, at low altitudes (<= 285 m), were investigated (maritime, urban, sub-industrial, biogenic and rural sites) and atmospheric measurements were realized during photochemical air pollution events. The second field campaign was part of the BOND project (July 2nd to July 14th 2002). Atmospheric measurements of hydroperoxides were carried out on one biogenic site, at altitude 690 m. The measurement system was improved allowing online sampling and analysis. During these field campaigns collection efficiencies were better than 96% for hydroperoxides, and from 78% to 96% for aldehydes. Detection limits were between 7,3× 10-3

  2. Acrolein induction of oxidative stress and degranulation in mast cells.

    Science.gov (United States)

    Hochman, Daniel J; Collaco, Christopher R; Brooks, Edward G

    2014-08-01

    Increases in asthma worldwide have been associated epidemiologically with expanding urban air pollution. The mechanistic relationship between airway hyper-responsiveness, inflammation, and ambient airborne triggers remains ambiguous. Acrolein, a ubiquitous aldehyde pollutant, is a product of incomplete combustion reactions. Acrolein is abundant in cigarette smoke, effluent from industrial smokestacks, diesel exhaust, and even hot oil cooking vapors. Acrolein is a potent airway irritant and can induce airway hyper-responsiveness and inflammation in the lungs of animal models. In the present study, we utilized the mast cell analog, RBL-2H3, to interrogate the responses of cells relevant to airway inflammation and allergic responses as a model for the induction of asthma-like conditions upon exposure to acrolein. We hypothesized that acrolein would induce oxidative stress and degranulation in airway mast cells. Our results indicate that acrolein at 1 ppm initiated degranulation and promoted the generation of reactive oxygen species (ROS). Introduction of antioxidants to the system significantly reduced both ROS generation and degranulation. At higher levels of exposure (above 100 ppm), RBL-2H3 cells displayed signs of severe toxicity. This experimental data indicates acrolein can induce an allergic inflammation in mast cell lines, and the initiation of degranulation was moderated by the application of antioxidants. Copyright © 2012 Wiley Periodicals, Inc., a Wiley company.

  3. Acrolein detection: potential theranostic utility in multiple sclerosis and spinal cord injury.

    Science.gov (United States)

    Tully, Melissa; Zheng, Lingxing; Shi, Riyi

    2014-06-01

    Oxidative stress has been implicated as a major pathological process underlying CNS disease and trauma. More specifically, acrolein, an unsaturated aldehyde, produced by way of lipid peroxidation, has been shown to play a crucial role in initiating and perpetuating detrimental effects associated with multiple sclerosis and spinal cord injury. In light of these findings, quantification of acrolein levels both systemically and locally could allow for the use of acrolein as a biomarker to aid in diagnosis and guide treatment regimens. The three main approaches currently available are acrolein derivatization followed by LC/GC-MS, application of an acrolein antibody and subsequent immunoblotting, and the 3-hydroxypropylmercapturic acid-based method. Of these three strategies, the 3-hydroxypropylmercapturic acid-based method is the least invasive allowing for rapid translation of acrolein detection into a clinical setting.

  4. OPTIMIZING THE PAKS METHOD FOR MEASURING AIRBORNE ACROLEIN

    Science.gov (United States)

    Airborne acrolein is produced from the combustion of fuel and tobacco and is of concern due to its potential for respiratory tract irritation and other adverse health effects. DNPH active-sampling is a method widely used for sampling airborne aldehydes and ketones (carbonyls); ...

  5. ORAL EXPOSURE TO ACROLEIN EXACERBATES ATHEROSCLEROSIS IN APO E-NULL MICE

    Science.gov (United States)

    Srivastava, Sanjay; Sithu, Srinivas D.; Vladykovskaya, Elena; Haberzettl, Petra; Hoetker, David J.; Siddiqui, Maqsood A.; Conklin, Daniel J.; D'Souza, Stanley E.; Bhatnagar, Aruni

    2011-01-01

    Background Acrolein is a dietary aldehyde that is present in high concentrations in alcoholic beverages and foods including cheese, donuts and coffee. It is also abundant in tobacco smoke, automobile exhaust and industrial waste and is generated in vivo during inflammation and oxidative stress. Objectives The goal of this study was to examine the effects of dietary acrolein on atherosclerosis. Methods Eight-week old male apoE-null mice were gavage-fed acrolein (2.5 mg/kg/day) for 8 weeks. Atherosclerotic lesion formation and composition and plasma lipids and platelet factor 4 (PF4) levels were measured. Effects of acrolein and PF4 on endothelial cell function was measured in vitro. Results Acrolein feeding increased the concentration of cholesterol in the plasma. NMR analysis of the lipoproteins showed that acrolein feeding increased the abundance of small and medium VLDL particles. Acrolein feeding also increased atherosclerotic lesion formation in the aortic valve and the aortic arch. Immunohistochemical analysis showed increased macrophage accumulation in the lesions of acrolein-fed mice. Plasma PF4 levels and accumulation of PF4 in atherosclerotic lesions was increased in the acrolein-fed mice. Incubation of endothelial cells with the plasma of acrolein-fed mice augmented transmigration of monocytic cells, which was abolished by anti-PF4 antibody treatment. Conclusions Dietary exposure to acrolein exacerbates atherosclerosis in apoE-null mice. Consumption of foods and beverages rich in unsaturated aldehydes such as acrolein may be a contributing factor to the progression of atherosclerotic lesions. PMID:21371710

  6. Acrolein inhalation causes myocardial strain delay and decreased cardiac performance as detected by high-frequency echocardiography in mice

    Science.gov (United States)

    Acrolein, an unsaturated aldehyde found in air pollution, impairs Ca2+ flux and contraction in cardiomyocytes in vitro. To better define direct and delayed functional cardiac effects, we hypothesized that a single exposure to acrolein would modify myocardial strain and performanc...

  7. Toxicity of formaldehyde and acrolein mixtures : in vitro studies using nasal epithelial cells

    NARCIS (Netherlands)

    Cassee, F.R.; Stenhuis, W.S.; Groten, J.P.; Feron, V.J.

    1996-01-01

    In vitro studies with human and rat nasal epithelial cells were carried out to investigate the combined toxicity of formaldehyde and acrolein and the role of aldehyde dehydrogenases in this process. These studies showed that the toxic effect of mixtures of aldehydes was additive. In addition,

  8. Acrolein involvement in sensory and behavioral hypersensitivity following spinal cord injury in the rat.

    Science.gov (United States)

    Due, Michael R; Park, Jonghyuck; Zheng, Lingxing; Walls, Michael; Allette, Yohance M; White, Fletcher A; Shi, Riyi

    2014-03-01

    Growing evidence suggests that oxidative stress, as associated with spinal cord injury (SCI), may play a critical role in both neuroinflammation and neuropathic pain conditions. The production of the endogenous aldehyde acrolein, following lipid peroxidation during the inflammatory response, may contribute to peripheral sensitization and hyperreflexia following SCI via the TRPA1-dependent mechanism. Here, we report that there are enhanced levels of acrolein and increased neuronal sensitivity to the aldehyde for at least 14 days after SCI. Concurrent with injury-induced increases in acrolein concentration is an increased expression of TRPA1 in the lumbar (L3-L6) sensory ganglia. As proof of the potential pronociceptive role for acrolein, intrathecal injections of acrolein revealed enhanced sensitivity to both tactile and thermal stimuli for up to 10 days, supporting the compound's pro-nociceptive functionality. Treatment of SCI animals with the acrolein scavenger hydralazine produced moderate improvement in tactile responses as well as robust changes in thermal sensitivity for up to 49 days. Taken together, these data suggest that acrolein directly modulates SCI-associated pain behavior, making it a novel therapeutic target for preclinical and clinical SCI as an analgesic. Following spinal cord injury (SCI), acrolein involvement in neuropathic pain is likely through direct activation and elevated levels of pro-nociceptive channel TRPA1. While acrolein elevation correlates with neuropathic pain, suppression of this aldehyde by hydralazine leads to an analgesic effect. Acrolein may serve as a novel therapeutic target for preclinical and clinical SCI to relieve both acute and chronic post-SCI neuropathic pain. © 2013 International Society for Neurochemistry.

  9. Acrolein cytotoxicity in hepatocytes involves endoplasmic reticulum stress, mitochondrial dysfunction and oxidative stress

    Science.gov (United States)

    Mohammad, Mohammad K; Avila, Diana; Zhang, Jingwen; Barve, Shirish; Arteel, Gavin; McClain, Craig; Joshi-Barve, Swati

    2012-01-01

    Acrolein is a common environmental, food and water pollutant and a major component of cigarette smoke. Also, it is produced endogenously via lipid peroxidation and cellular metabolism of certain amino acids and drugs. Acrolein is cytotoxic to many cell types including hepatocytes; however the mechanisms are not fully understood. We examined the molecular mechanisms underlying acrolein hepatotoxicity in primary human hepatocytes and hepatoma cells. Acrolein, at pathophysiological concentrations, caused a dose-dependent loss of viability of hepatocytes. The death was apoptotic at moderate and necrotic at high concentrations of acrolein. Acrolein exposure rapidly and dramatically decreased intracellular glutathione and overall antioxidant capacity, and activated the stress-signaling MAP-kinases JNK, p42/44 and p38. Our data demonstrate for the first time in human hepatocytes, that acrolein triggered endoplasmic reticulum (ER) stress and activated eIF2α, ATF-3 and -4, and Gadd153/CHOP, resulting in cell death. Notably, the protective/adaptive component of ER stress was not activated, and acrolein failed to up-regulate the protective ER-chaperones, GRP78 and GRP94. Additionally, exposure to acrolein disrupted mitochondrial integrity/function, and led to the release of pro-apoptotic proteins and ATP depletion. Acrolein-induced cell death was attenuated by N-acetyl cysteine, phenyl-butyric acid, and caspase and JNK inhibitors. Our data demonstrate that exposure to acrolein induces a variety of stress responses in hepatocytes, including GSH depletion, oxidative stress, mitochondrial dysfunction and ER stress (without ER-protective responses) which together contribute to acrolein toxicity. Our study defines basic mechanisms underlying liver injury caused by reactive aldehyde pollutants such as acrolein. PMID:23026831

  10. Aldose reductase regulates acrolein-induced cytotoxicity in human small airway epithelial cells

    Science.gov (United States)

    Yadav, Umesh CS; Ramana, KV; Srivastava, SK

    2013-01-01

    Aldose reductase (AR), a glucose metabolizing enzyme, reduces lipid aldehydes and their glutathione conjugates with more than 1000-fold efficiency (Km aldehydes 5-30μM) than glucose. Acrolein, a major endogenous lipid peroxidation product as well as component of environmental pollutant and cigarette smoke, is known to be involved in various pathologies including atherosclerosis, airway inflammation, COPD, and age-related disorders but the mechanism of acrolein-induced cytotoxicity is not clearly understood. We have investigated the role of AR in acrolein-induced cytotoxicity in primary human small airway epithelial cells SAECs. Exposure of SAECs to varying concentrations of acrolein caused cell-death in a concentration- and time-dependent manner. AR inhibition by fidarestat prevented the low (5 to 10 μM) but not high (>10 μM) concentrations of acrolein-induced SAECs cell death. AR inhibition protected SAECs from low dose (5 μM) acrolein-induced cellular reactive oxygen species (ROS). Inhibition of acrolein-induced apoptosis by fidarestat was confirmed by decreased condensation of nuclear chromatin, DNA fragmentation, comet tail-moment, and annexin-V fluorescence. Further, fidarestat inhibited acrolein-induced translocation of pro-apoptotic proteins Bax and Bad from cytosol to the mitochondria, and that of Bcl2 and BclXL from mitochondria to cytosol. Acrolein-induced cytochrome c release from mitochondria was also prevented by AR inhibition. The mitogen-activated protein kinases (MAPK) such as extracellular signal-regulated kinases 1 and 2 (ERK1/2), stress-activated protein kinases/c-jun NH2-terminal kinases (SAPK/JNK) and p38MAPK, and c-jun were transiently activated in airway epithelial cells by acrolein in a concentration and time-dependent fashion, which were significantly prevented by AR inhibition. These results suggest that AR inhibitors could prevent acrolein-induced cytotoxicity in the lung epithelial cells. PMID:23770200

  11. Aldose reductase regulates acrolein-induced cytotoxicity in human small airway epithelial cells.

    Science.gov (United States)

    Yadav, Umesh C S; Ramana, K V; Srivastava, Satish K

    2013-12-01

    Aldose reductase (AR), a glucose-metabolizing enzyme, reduces lipid aldehydes and their glutathione conjugates with more than 1000-fold efficiency (Km aldehydes 5-30 µM) relative to glucose. Acrolein, a major endogenous lipid peroxidation product as well as a component of environmental pollutants and cigarette smoke, is known to be involved in various pathologies including atherosclerosis, airway inflammation, COPD, and age-related disorders, but the mechanism of acrolein-induced cytotoxicity is not clearly understood. We have investigated the role of AR in acrolein-induced cytotoxicity in primary human small airway epithelial cells (SAECs). Exposure of SAECs to varying concentrations of acrolein caused cell death in a concentration- and time-dependent manner. AR inhibition by fidarestat prevented the low-dose (5-10 µM) but not the high-dose (>10 µM) acrolein-induced SAEC death. AR inhibition protected SAECs from low-dose (5 µM) acrolein-induced cellular reactive oxygen species (ROS). Inhibition of acrolein-induced apoptosis by fidarestat was confirmed by decreased condensation of nuclear chromatin, DNA fragmentation, comet tail moment, and annexin V fluorescence. Further, fidarestat inhibited acrolein-induced translocation of the proapoptotic proteins Bax and Bad from the cytosol to the mitochondria and that of Bcl2 and BclXL from the mitochondria to the cytosol. Acrolein-induced cytochrome c release from mitochondria was also prevented by AR inhibition. The mitogen-activated protein kinases (MAPKs), such as extracellular signal-regulated kinases 1 and 2, stress-activated protein kinase/c-Jun NH2-terminal kinase, and p38MAPK, and c-Jun were transiently activated in airway epithelial cells by acrolein in a concentration- and time-dependent fashion, which was significantly prevented by AR inhibition. These results suggest that AR inhibitors could prevent acrolein-induced cytotoxicity in the lung epithelial cells. Copyright © 2013 Elsevier Inc. All rights

  12. Acute effects of acrolein in human volunteers during controlled exposure.

    Science.gov (United States)

    Dwivedi, Aishwarya M; Johanson, Gunnar; Lorentzen, Johnny C; Palmberg, Lena; Sjögren, Bengt; Ernstgård, Lena

    2015-01-01

    Acrolein is a reactive aldehyde mainly formed by combustion. The critical effect is considered to be irritation of the eyes and airways; however, the scarce data available make it difficult to assess effect levels. The aim of the study was to determine thresholds for acute irritation for acrolein. Nine healthy volunteers of each sex were exposed at six occasions for 2 h at rest to: clean air, 15 ppm ethyl acetate (EA), and 0.05 ppm and 0.1 ppm acrolein with and without EA (15 ppm) to mask the potential influence of odor. Symptoms related to irritation and central nervous system effects were rated on 100-mm Visual Analogue Scales. The ratings of eye irritation were slightly but significantly increased during exposure to acrolein in a dose-dependent manner (p acrolein alone but not during any of the other five exposure conditions. Based on subjective ratings, the present study showed minor eye irritation by exposure to 0.1 ppm acrolein.

  13. Neuroprotective role of hydralazine in rat spinal cord injury-attenuation of acrolein-mediated damage

    Science.gov (United States)

    Park, Jonghyuck; Zheng, Lingxing; Marquis, Andrew; Walls, Michael; Duerstock, Brad; Pond, Amber; Alvarez, Sascha Vega; He, Wang; Ouyang, Zheng; Shi, Riyi

    2014-01-01

    Acrolein, an α,β-unsaturated aldehyde and a reactive product of lipid peroxidation, has been suggested as a key factor in neural post-traumatic secondary injury in SCI, mainly based on in vitro and ex vivo evidence. Here we demonstrate an increase of acrolein up to 300%; the elevation lasted at least two weeks in a rat SCI model. More importantly, hydralazine, a known acrolein scavenger can provide neuroprotection when applied systemically. Besides effectively reducing acrolein, hydralazine treatment also resulted in significant amelioration of tissue damage, motor deficits, and neuropathic pain. This effect was further supported by demonstrating the ability of hydralazine to reach spinal cord tissue at a therapeutic level following intraperitoneal application. This suggests that hydralazine is an effective neuroprotective agent not only in vitro, but in a live animal model of SCI as well. Finally, the role of acrolein in SCI was further validated by the fact that acrolein injection into the spinal cord caused significant SCI-like tissue damage and motor deficits. Taken together, available evidence strongly suggests a critical causal role of acrolein in the pathogenesis of spinal cord trauma. Since acrolein has been linked to a variety of illness and conditions, we believe that acrolein-scavenging measures have the potential to be expanded significantly ensuring a broad impact on human health. PMID:24286176

  14. Neuroprotective role of hydralazine in rat spinal cord injury-attenuation of acrolein-mediated damage.

    Science.gov (United States)

    Park, Jonghyuck; Zheng, Lingxing; Marquis, Andrew; Walls, Michael; Duerstock, Brad; Pond, Amber; Vega-Alvarez, Sasha; Wang, He; Ouyang, Zheng; Shi, Riyi

    2014-04-01

    Acrolein, an α,β-unsaturated aldehyde and a reactive product of lipid peroxidation, has been suggested as a key factor in neural post-traumatic secondary injury in spinal cord injury (SCI), mainly based on in vitro and ex vivo evidence. Here, we demonstrate an increase of acrolein up to 300%; the elevation lasted at least 2 weeks in a rat SCI model. More importantly, hydralazine, a known acrolein scavenger can provide neuroprotection when applied systemically. Besides effectively reducing acrolein, hydralazine treatment also resulted in significant amelioration of tissue damage, motor deficits, and neuropathic pain. This effect was further supported by demonstrating the ability of hydralazine to reach spinal cord tissue at a therapeutic level following intraperitoneal application. This suggests that hydralazine is an effective neuroprotective agent not only in vitro, but in a live animal model of SCI as well. Finally, the role of acrolein in SCI was further validated by the fact that acrolein injection into the spinal cord caused significant SCI-like tissue damage and motor deficits. Taken together, available evidence strongly suggests a critical causal role of acrolein in the pathogenesis of spinal cord trauma. Since acrolein has been linked to a variety of illness and conditions, we believe that acrolein-scavenging measures have the potential to be expanded significantly ensuring a broad impact on human health. © 2013 International Society for Neurochemistry.

  15. Acrolein stimulates eicosanoid release from bovine airway epithelial cells

    International Nuclear Information System (INIS)

    Doupnik, C.A.; Leikauf, G.D.

    1990-01-01

    Injury to the airway mucosa after exposure to environmental irritants is associated with pulmonary inflammation and bronchial hyperresponsiveness. To better understand the relationships between mediator release and airway epithelial cell injury during irritant exposures, we studied the effects of acrolein, a low-molecular-weight aldehyde found in cigarette smoke, on arachidonic acid metabolism in cultured bovine tracheal epithelial cells. Confluent airway epithelial cell monolayers, prelabeled with [3H]arachidonic acid, released significant levels of 3H activity when exposed (20 min) to 100 microM acrolein. [3H]arachidonic acid products were resolved using reverse-phase high-performance liquid chromatography. Under control conditions the released 3H activity coeluted predominantly with the cyclooxygenase product, prostaglandin (PG) E2. After exposure to acrolein, significant peaks in 3H activity coeluted with the lipoxygenase products 12-hydroxyeicosatetraenoic acid (HETE) and 15-HETE, as well as with PGE2, PGF2 alpha, and 6-keto-PGF1 alpha. Dose-response relationships for acrolein-induced release of immunoreactive PGF2 alpha and PGE2 from unlabeled epithelial monolayers demonstrated 30 microM acrolein as the threshold dose, with 100 microM acrolein inducing nearly a fivefold increase in both PGF2 alpha and PGE2. Cellular viability after exposure to 100 microM acrolein, determined by released lactate dehydrogenase activity, was not affected until exposure periods were greater than or equal to 2 h. These results implicate the airway epithelial cell as a possible source of eicosanoids after exposure to acrolein

  16. Activation versus inhibition of microsomal glutathione S-transferase activity by acrolein. Dependence on the concentration and time of acrolein exposure.

    Science.gov (United States)

    Sthijns, Mireille M J P E; den Hartog, Gertjan J M; Scasso, Caterina; Haenen, Jan P; Bast, Aalt; Haenen, Guido R M M

    2017-09-25

    The toxicity of acrolein, an α,β-unsaturated aldehyde, is due to its soft electrophilic nature and primarily involves the adduction of protein thiols. The thiol glutathione (GSH) forms the first line of defense against acrolein. The present study confirms that acrolein added to isolated rat liver microsomes can increase microsomal GSH transferase (MGST) activity 2-3 fold, which can be seen as a direct adaptive increase in the protection against acrolein. At a relatively high exposure level, acrolein appeared to inhibit MGST. The activation is due to adduction of thiol groups, and the inactivation probably involves adduction of amino groups in the enzyme by acrolein. The preference of acrolein to react with thiol groups over amino groups can explain why the enzyme is activated at a low exposure level and inhibited at a high exposure level of acrolein. These opposite forms of direct adaptation on the level of enzyme activity further narrow the thin line between survival and promotion of cell death, governed by the level of exposure. Copyright © 2017 The Authors. Published by Elsevier B.V. All rights reserved.

  17. Role of TRPA1 in acute cardiopulmonary toxicity of inhaled acrolein.

    Science.gov (United States)

    Conklin, Daniel J; Haberzettl, Petra; Jagatheesan, Ganapathy; Kong, Maiying; Hoyle, Gary W

    2017-06-01

    Acrolein is a highly toxic, volatile, unsaturated aldehyde generated during incomplete combustion as in tobacco smoke and indoor fires. Because the transient receptor potential ankyrin 1 (TRPA1) channel mediates tobacco smoke-induced lung injury, we assessed its role in high-level acrolein-induced toxicity in mice. Acrolein (100-275ppm, 10-30min) caused upper airway epithelial sloughing, bradypnea and oral gasping, hypothermia, cardiac depression and mortality. Male wild-type mice (WT, C57BL/6; 5-52weeks) were significantly more sensitive to high-level acrolein than age-matched, female WT mice. Both male and female TRPA1-null mice were more sensitive to acrolein-induced mortality than age- and sex-matched WT mice. Acrolein exposure increased lung weight:body weight ratios and lung albumin and decreased plasma albumin to a greater extent in TRPA1-null than in WT mice. Lung and plasma protein-acrolein adducts were not increased in acrolein-exposed TRPA1-null mice compared with WT mice. To assess TRPA1-dependent protective mechanisms, respiratory parameters were monitored by telemetry. TRPA1-null mice had a slower onset of breathing rate suppression ('respiratory braking') than WT mice suggesting TRPA1 mediates this protective response. Surprisingly, WT male mice treated either with a TRPA1 antagonist (HC030031; 200mg/kg) alone or with combined TRPA1 (100mg/kg) and TRPV1 (capsazepine, 10mg/kg) antagonists at 30min post-acrolein exposure (i.e., "real world" delay in treatment) were significantly protected from acrolein-induced mortality. These data show TRPA1 protects against high-level acrolein-induced toxicity in a sex-dependent manner. Post-exposure TRPA1 antagonism also protected against acrolein-induced mortality attesting to a complex role of TRPA1 in cardiopulmonary injury. Copyright © 2016 Elsevier Inc. All rights reserved.

  18. Acrolein scavengers, cysteamine and N-benzylhydroxylamine, reduces the mouse liver damage after acetaminophen overdose.

    Science.gov (United States)

    Koyama, Ryo; Mizuta, Ryushin

    2017-01-10

    Our previous study suggested that the highly toxic α,β-unsaturated aldehyde acrolein, a byproduct of oxidative stress, plays a major role in acetaminophen-induced liver injury. In this study, to determine the involvement of acrolein in the liver injury and to identify novel therapeutic options for the liver damage, we examined two putative acrolein scavengers, a thiol compound cysteamine and a hydroxylamine N-benzylhydroxylamine, in cell culture and in mice. Our results showed that cysteamine and N-benzylhydroxylamine effectively prevented the cell toxicity of acrolein in vitro and acetaminophen-induced liver injury in vivo, which suggested that acrolein is involved in the liver damage, and these two drugs can be potential therapeutic options for this condition.

  19. Acrolein involvement in sensory and behavioral hypersensitivity following spinal cord injury in the rat

    OpenAIRE

    Due, Michael R.; Park, Jonghyuck; Zheng, Lingxing; Walls, Michael; Allette, Yohance M.; White, Fletcher A.; Shi, Riyi

    2013-01-01

    Growing evidence suggests that oxidative stress, as associated with spinal cord injury (SCI), may play a critical role in both neuroinflammation and neuropathic pain conditions. The production of the endogenous aldehyde acrolein, following lipid peroxidation during the inflammatory response, may contribute to peripheral sensitization and hyperreflexia following SCI via the TRPA1-dependent mechanism. Here we report that there are enhanced levels of acrolein and increased neuronal sensitivity t...

  20. Aldehyde-sequestering drugs: tools for studying protein damage by lipid peroxidation products.

    Science.gov (United States)

    Burcham, Philip C; Kaminskas, Lisa M; Fontaine, Frank R; Petersen, Dennis R; Pyke, Simon M

    2002-12-27

    Elevated levels of reactive alpha,beta-unsaturated aldehydes (e.g. malondialdehyde, 4-hydroxynonenal and acrolein) in the affected tissues of various degenerative conditions suggest these substances are active propagators of the disease process. One experimental approach to attenuating damage by these intermediates employs 'aldehyde-sequestering drugs' as sacrificial nucleophiles, thereby sparing cell macromolecules and perhaps slowing disease progression. Drugs with demonstrated trapping activity toward lipid-derived aldehydes include various amine compounds such as aminoguanidine, carnosine and pyridoxamine. We have focused on identifying scavengers of acrolein, perhaps the most toxic aldehyde formed during lipid peroxidation cascades. Various phthalazine compounds (hydralazine and dihydralazine) were found to trap acrolein readily, forming hydrazone derivatives in a rapid Schiff-type reaction. These compounds strongly protect against acrolein-mediated toxicity in isolated hepatocytes.

  1. Acrolein cytotoxicity in hepatocytes involves endoplasmic reticulum stress, mitochondrial dysfunction and oxidative stress

    International Nuclear Information System (INIS)

    Mohammad, Mohammad K.; Avila, Diana; Zhang, Jingwen; Barve, Shirish; Arteel, Gavin; McClain, Craig; Joshi-Barve, Swati

    2012-01-01

    Acrolein is a common environmental, food and water pollutant and a major component of cigarette smoke. Also, it is produced endogenously via lipid peroxidation and cellular metabolism of certain amino acids and drugs. Acrolein is cytotoxic to many cell types including hepatocytes; however the mechanisms are not fully understood. We examined the molecular mechanisms underlying acrolein hepatotoxicity in primary human hepatocytes and hepatoma cells. Acrolein, at pathophysiological concentrations, caused a dose-dependent loss of viability of hepatocytes. The death was apoptotic at moderate and necrotic at high concentrations of acrolein. Acrolein exposure rapidly and dramatically decreased intracellular glutathione and overall antioxidant capacity, and activated the stress-signaling MAP-kinases JNK, p42/44 and p38. Our data demonstrate for the first time in human hepatocytes, that acrolein triggered endoplasmic reticulum (ER) stress and activated eIF2α, ATF-3 and -4, and Gadd153/CHOP, resulting in cell death. Notably, the protective/adaptive component of ER stress was not activated, and acrolein failed to up-regulate the protective ER-chaperones, GRP78 and GRP94. Additionally, exposure to acrolein disrupted mitochondrial integrity/function, and led to the release of pro-apoptotic proteins and ATP depletion. Acrolein-induced cell death was attenuated by N-acetyl cysteine, phenyl-butyric acid, and caspase and JNK inhibitors. Our data demonstrate that exposure to acrolein induces a variety of stress responses in hepatocytes, including GSH depletion, oxidative stress, mitochondrial dysfunction and ER stress (without ER-protective responses) which together contribute to acrolein toxicity. Our study defines basic mechanisms underlying liver injury caused by reactive aldehyde pollutants such as acrolein. -- Highlights: ► Human primary hepatocytes and cultured cell lines are used. ► Multiple cell death signaling pathways are activated by acrolein. ► Novel finding of

  2. Acrolein cytotoxicity in hepatocytes involves endoplasmic reticulum stress, mitochondrial dysfunction and oxidative stress

    Energy Technology Data Exchange (ETDEWEB)

    Mohammad, Mohammad K. [Department of Medicine, University of Louisville (United States); Alcohol Research Center, University of Louisville (United States); Avila, Diana [Department of Medicine, University of Louisville (United States); Department of Pharmacology and Toxicology, University of Louisville (United States); Alcohol Research Center, University of Louisville (United States); Zhang, Jingwen [Department of Medicine, University of Louisville (United States); Alcohol Research Center, University of Louisville (United States); Barve, Shirish [Department of Medicine, University of Louisville (United States); Department of Pharmacology and Toxicology, University of Louisville (United States); Alcohol Research Center, University of Louisville (United States); Arteel, Gavin [Department of Pharmacology and Toxicology, University of Louisville (United States); Alcohol Research Center, University of Louisville (United States); McClain, Craig [Department of Medicine, University of Louisville (United States); Department of Pharmacology and Toxicology, University of Louisville (United States); Alcohol Research Center, University of Louisville (United States); Robley Rex VAMC, Louisville, KY (United States); Joshi-Barve, Swati, E-mail: s0josh01@louisville.edu [Department of Medicine, University of Louisville (United States); Department of Pharmacology and Toxicology, University of Louisville (United States); Alcohol Research Center, University of Louisville (United States)

    2012-11-15

    Acrolein is a common environmental, food and water pollutant and a major component of cigarette smoke. Also, it is produced endogenously via lipid peroxidation and cellular metabolism of certain amino acids and drugs. Acrolein is cytotoxic to many cell types including hepatocytes; however the mechanisms are not fully understood. We examined the molecular mechanisms underlying acrolein hepatotoxicity in primary human hepatocytes and hepatoma cells. Acrolein, at pathophysiological concentrations, caused a dose-dependent loss of viability of hepatocytes. The death was apoptotic at moderate and necrotic at high concentrations of acrolein. Acrolein exposure rapidly and dramatically decreased intracellular glutathione and overall antioxidant capacity, and activated the stress-signaling MAP-kinases JNK, p42/44 and p38. Our data demonstrate for the first time in human hepatocytes, that acrolein triggered endoplasmic reticulum (ER) stress and activated eIF2α, ATF-3 and -4, and Gadd153/CHOP, resulting in cell death. Notably, the protective/adaptive component of ER stress was not activated, and acrolein failed to up-regulate the protective ER-chaperones, GRP78 and GRP94. Additionally, exposure to acrolein disrupted mitochondrial integrity/function, and led to the release of pro-apoptotic proteins and ATP depletion. Acrolein-induced cell death was attenuated by N-acetyl cysteine, phenyl-butyric acid, and caspase and JNK inhibitors. Our data demonstrate that exposure to acrolein induces a variety of stress responses in hepatocytes, including GSH depletion, oxidative stress, mitochondrial dysfunction and ER stress (without ER-protective responses) which together contribute to acrolein toxicity. Our study defines basic mechanisms underlying liver injury caused by reactive aldehyde pollutants such as acrolein. -- Highlights: ► Human primary hepatocytes and cultured cell lines are used. ► Multiple cell death signaling pathways are activated by acrolein. ► Novel finding of

  3. Acrolein - a pulmonary hazard.

    Science.gov (United States)

    Bein, Kiflai; Leikauf, George D

    2011-09-01

    Acrolein is a respiratory irritant that can be generated during cooking and is in environmental tobacco smoke. More plentiful in cigarette smoke than polycyclic aromatic hydrocarbons (PAH), acrolein can adduct tumor suppressor p53 (TP53) DNA and may contribute to TP53-mutations in lung cancer. Acrolein is also generated endogenously at sites of injury, and excessive breath levels (sufficient to activate metalloproteinases and increase mucin transcripts) have been detected in asthma and chronic obstructive pulmonary disease (COPD). Because of its reactivity with respiratory-lining fluid or cellular macromolecules, acrolein alters gene regulation, inflammation, mucociliary transport, and alveolar-capillary barrier integrity. In laboratory animals, acute exposures have lead to acute lung injury and pulmonary edema similar to that produced by smoke inhalation whereas lower concentrations have produced bronchial hyperreactivity, excessive mucus production, and alveolar enlargement. Susceptibility to acrolein exposure is associated with differential regulation of cell surface receptor, transcription factor, and ubiquitin-proteasome genes. Consequent to its pathophysiological impact, acrolein contributes to the morbidly and mortality associated with acute lung injury and COPD, and possibly asthma and lung cancer. Copyright © 2011 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim.

  4. Acrolein involvement in sensory and behavioral hypersensitivity following spinal cord injury in the rat

    Science.gov (United States)

    Zheng, Lingxing; Walls, Michael; Allette, Yohance M.; White, Fletcher A.; Shi, Riyi

    2013-01-01

    Growing evidence suggests that oxidative stress, as associated with spinal cord injury (SCI), may play a critical role in both neuroinflammation and neuropathic pain conditions. The production of the endogenous aldehyde acrolein, following lipid peroxidation during the inflammatory response, may contribute to peripheral sensitization and hyperreflexia following SCI via the TRPA1-dependent mechanism. Here we report that there are enhanced levels of acrolein and increased neuronal sensitivity to the aldehyde for at least 14 days after SCI. Concurrent with injury-induced increases in acrolein concentration is an increased expression of TRPA1 in the lumbar (L3-L6) sensory ganglia. As proof of the potential pronociceptive role for acrolein, intrathecal injections of acrolein revealed enhanced sensitivity to both tactile and thermal stimuli for up to 10 days, supporting the compound’s pro-nociceptive functionality. Treatment of SCI animals with the acrolein scavenger hydralazine produced moderate improvement in tactile responses as well as robust changes in thermal sensitivity for up to 49 days. Taken together, these data suggests that acrolein directly modulates SCI-associated pain behavior, making it a novel therapeutic target for preclinical and clinical SCI as an analgesic. PMID:24147766

  5. Environmental risk limits for acrolein

    NARCIS (Netherlands)

    Bodar CWM; SEC

    2008-01-01

    Dit rapport geeft milieurisicogrenzen voor acroleine in (grond)water, bodem en lucht. Milieurisicogrenzen zijn de technisch-wetenschappelijke advieswaarden voor de uiteindelijke milieukwaliteitsnormen in Nederland. De milieurisicogrenzen voor acroleine zijn gebaseerd op de uitkomsten van de EU

  6. Role of TRPA1 in acute cardiopulmonary toxicity of inhaled acrolein

    International Nuclear Information System (INIS)

    Conklin, Daniel J.; Haberzettl, Petra; Jagatheesan, Ganapathy; Kong, Maiying; Hoyle, Gary W.

    2017-01-01

    Acrolein is a highly toxic, volatile, unsaturated aldehyde generated during incomplete combustion as in tobacco smoke and indoor fires. Because the transient receptor potential ankyrin 1 (TRPA1) channel mediates tobacco smoke-induced lung injury, we assessed its role in high-level acrolein-induced toxicity in mice. Acrolein (100–275 ppm, 10–30 min) caused upper airway epithelial sloughing, bradypnea and oral gasping, hypothermia, cardiac depression and mortality. Male wild-type mice (WT, C57BL/6; 5–52 weeks) were significantly more sensitive to high-level acrolein than age-matched, female WT mice. Both male and female TRPA1-null mice were more sensitive to acrolein-induced mortality than age- and sex-matched WT mice. Acrolein exposure increased lung weight:body weight ratios and lung albumin and decreased plasma albumin to a greater extent in TRPA1-null than in WT mice. Lung and plasma protein-acrolein adducts were not increased in acrolein-exposed TRPA1-null mice compared with WT mice. To assess TRPA1-dependent protective mechanisms, respiratory parameters were monitored by telemetry. TRPA1-null mice had a slower onset of breathing rate suppression (‘respiratory braking’) than WT mice suggesting TRPA1 mediates this protective response. Surprisingly, WT male mice treated either with a TRPA1 antagonist (HC030031; 200 mg/kg) alone or with combined TRPA1 (100 mg/kg) and TRPV1 (capsazepine, 10 mg/kg) antagonists at 30 min post-acrolein exposure (i.e., “real world” delay in treatment) were significantly protected from acrolein-induced mortality. These data show TRPA1 protects against high-level acrolein-induced toxicity in a sex-dependent manner. Post-exposure TRPA1 antagonism also protected against acrolein-induced mortality attesting to a complex role of TRPA1 in cardiopulmonary injury. - Highlights: • TRPA1 protects mice against toxicity and mortality of inhaled high-level acrolein. • TRPA1 protection against inhaled high-level acrolein is sex

  7. Role of TRPA1 in acute cardiopulmonary toxicity of inhaled acrolein

    Energy Technology Data Exchange (ETDEWEB)

    Conklin, Daniel J., E-mail: dj.conklin@louisville.edu [Diabetes and Obesity Center, Institute of Molecular Cardiology, Division of Cardiovascular Medicine, Department of Medicine, School of Medicine, University of Louisville, Louisville, KY 40292 (United States); Haberzettl, Petra; Jagatheesan, Ganapathy [Diabetes and Obesity Center, Institute of Molecular Cardiology, Division of Cardiovascular Medicine, Department of Medicine, School of Medicine, University of Louisville, Louisville, KY 40292 (United States); Kong, Maiying [Department of Bioinformatics and Biostatistics, School of Public Health & Information Sciences, University of Louisville, Louisville, KY 40292 (United States); Hoyle, Gary W. [Department of Environmental and Occupational Health Sciences, School of Public Health & Information Sciences, University of Louisville, Louisville, KY 40292 (United States)

    2017-06-01

    Acrolein is a highly toxic, volatile, unsaturated aldehyde generated during incomplete combustion as in tobacco smoke and indoor fires. Because the transient receptor potential ankyrin 1 (TRPA1) channel mediates tobacco smoke-induced lung injury, we assessed its role in high-level acrolein-induced toxicity in mice. Acrolein (100–275 ppm, 10–30 min) caused upper airway epithelial sloughing, bradypnea and oral gasping, hypothermia, cardiac depression and mortality. Male wild-type mice (WT, C57BL/6; 5–52 weeks) were significantly more sensitive to high-level acrolein than age-matched, female WT mice. Both male and female TRPA1-null mice were more sensitive to acrolein-induced mortality than age- and sex-matched WT mice. Acrolein exposure increased lung weight:body weight ratios and lung albumin and decreased plasma albumin to a greater extent in TRPA1-null than in WT mice. Lung and plasma protein-acrolein adducts were not increased in acrolein-exposed TRPA1-null mice compared with WT mice. To assess TRPA1-dependent protective mechanisms, respiratory parameters were monitored by telemetry. TRPA1-null mice had a slower onset of breathing rate suppression (‘respiratory braking’) than WT mice suggesting TRPA1 mediates this protective response. Surprisingly, WT male mice treated either with a TRPA1 antagonist (HC030031; 200 mg/kg) alone or with combined TRPA1 (100 mg/kg) and TRPV1 (capsazepine, 10 mg/kg) antagonists at 30 min post-acrolein exposure (i.e., “real world” delay in treatment) were significantly protected from acrolein-induced mortality. These data show TRPA1 protects against high-level acrolein-induced toxicity in a sex-dependent manner. Post-exposure TRPA1 antagonism also protected against acrolein-induced mortality attesting to a complex role of TRPA1 in cardiopulmonary injury. - Highlights: • TRPA1 protects mice against toxicity and mortality of inhaled high-level acrolein. • TRPA1 protection against inhaled high-level acrolein is sex

  8. Glucose-stimulated acrolein production from unsaturated fatty acids.

    Science.gov (United States)

    Medina-Navarro, R; Duran-Reyes, G; Diaz-Flores, M; Hicks, J J; Kumate, J

    2004-02-01

    Glucose auto-oxidation may be a significant source of reactive oxygen species (ROS), and also be important in the lipid peroxidation process, accompanied by the release of toxic reactive products. We wanted to demonstrate that acrolein can be formed directly and actively from free fatty acids in a hyperglycemic environment. A suspension of linoleic and arachidonic acids (2.5 mM) was exposed to different glucose concentrations (5, 10 and 15 mmol/L) in vitro. The samples were extracted with organic solvents, partitioned, followed at 255-267 nm, and analysed using capillary electrophoresis and mass spectroscopy. The total release of aldehydes significantly (P products, acrolein (5% of total) and its condensing product, 4-hydroxy-hexenal, were identified. From the results presented here, it was possible to demonstrate the production of acrolein, probably as a fatty acid product, due to free radicals generated from the glucose auto-oxidation process. The results led us to propose that acrolein, which is one of the most toxic aldehydes, is produced during hyperglycemic states, and may lead to tissue injury, as one of the initial problems to be linked to high levels of glucose in vivo.

  9. Acrolein inhalation suppresses lipopolysaccharide-induced inflammatory cytokine production but does not affect acute airways neutrophilia.

    Science.gov (United States)

    Kasahara, David Itiro; Poynter, Matthew E; Othman, Ziryan; Hemenway, David; van der Vliet, Albert

    2008-07-01

    Acrolein is a reactive unsaturated aldehyde that is produced during endogenous oxidative processes and is a major bioactive component of environmental pollutants such as cigarette smoke. Because in vitro studies demonstrate that acrolein can inhibit neutrophil apoptosis, we evaluated the effects of in vivo acrolein exposure on acute lung inflammation induced by LPS. Male C57BL/6J mice received 300 microg/kg intratracheal LPS and were exposed to acrolein (5 parts per million, 6 h/day), either before or after LPS challenge. Exposure to acrolein either before or after LPS challenge did not significantly affect the overall extent of LPS-induced lung inflammation, or the duration of the inflammatory response, as observed from recovered lung lavage leukocytes and histology. However, exposure to acrolein after LPS instillation markedly diminished the LPS-induced production of several inflammatory cytokines, specifically TNF-alpha, IL-12, and the Th1 cytokine IFN-gamma, which was associated with reduction in NF-kappaB activation. Our data demonstrate that acrolein exposure suppresses LPS-induced Th1 cytokine responses without affecting acute neutrophilia. Disruption of cytokine signaling by acrolein may represent a mechanism by which smoking contributes to chronic disease in chronic obstructive pulmonary disease and asthma.

  10. Exogenous Acrolein intensifies sensory hypersensitivity after spinal cord injury in rat.

    Science.gov (United States)

    Butler, Breanne; Acosta, Glen; Shi, Riyi

    2017-08-15

    Acrolein, an α,β-unsaturated aldehyde associated with oxidative stress, is also a major toxic component of tobacco cigarette smoke, which has been reported in the clinic to coincide with the exacerbation of neuropathic pain after SCI. Previous reports have shown that acrolein involvement in spinal cord injury (SCI) is crucial to the development and persistence of neuropathic pain. Through the activation and upregulation of the transient receptor protein ankyrin-1 (TRPA1) cation channel, acrolein is capable of sensitizing the central nervous system in the acute and chronic stages of SCI. Here, we report that the acute or delayed nasal exposure of acrolein, apart from cigarette smoke but at concentrations similar to that found in cigarette smoke, resulted in increased neuropathic pain behaviors in a rat model of contusion SCI. We also found that this hyperalgesia occurred concurrently with an augmentation in systemic acrolein, detected by an acrolein-glutathione metabolite in the urine. The application of an acrolein scavenger, phenelzine, was shown to reduce the hyperalgesic effect of acrolein inhalation. The previously determined ability of acrolein to bind to and activate the TRPA1 channel and elicit algesic responses may be a mechanism of the phenomenon seen in this study. Upon the exposure to actual cigarette smoke after SCI, intensified neuropathic pain behaviors were also observed and persisted for at least 1week after the cessation of the exposure period. Taken together, these results indicate that cigarette smoke, through mechanisms involving acrolein, poses a threat to the vulnerable CNS after SCI and can contribute to neuropathic pain. This investigation also provides further evidence for the potential utility of acrolein scavengers as a therapeutic strategy in SCI-resultant neuropathic pain. Copyright © 2017. Published by Elsevier B.V.

  11. Acrolein exposure is associated with increased cardiovascular disease risk.

    Science.gov (United States)

    DeJarnett, Natasha; Conklin, Daniel J; Riggs, Daniel W; Myers, John A; O'Toole, Timothy E; Hamzeh, Ihab; Wagner, Stephen; Chugh, Atul; Ramos, Kenneth S; Srivastava, Sanjay; Higdon, Deirdre; Tollerud, David J; DeFilippis, Andrew; Becher, Carrie; Wyatt, Brad; McCracken, James; Abplanalp, Wes; Rai, Shesh N; Ciszewski, Tiffany; Xie, Zhengzhi; Yeager, Ray; Prabhu, Sumanth D; Bhatnagar, Aruni

    2014-08-06

    Acrolein is a reactive aldehyde present in high amounts in coal, wood, paper, and tobacco smoke. It is also generated endogenously by lipid peroxidation and the oxidation of amino acids by myeloperoxidase. In animals, acrolein exposure is associated with the suppression of circulating progenitor cells and increases in thrombosis and atherogenesis. The purpose of this study was to determine whether acrolein exposure in humans is also associated with increased cardiovascular disease (CVD) risk. Acrolein exposure was assessed in 211 participants of the Louisville Healthy Heart Study with moderate to high (CVD) risk by measuring the urinary levels of the major acrolein metabolite-3-hydroxypropylmercapturic acid (3-HPMA). Generalized linear models were used to assess the association between acrolein exposure and parameters of CVD risk, and adjusted for potential demographic confounders. Urinary 3-HPMA levels were higher in smokers than nonsmokers and were positively correlated with urinary cotinine levels. Urinary 3-HPMA levels were inversely related to levels of both early (AC133(+)) and late (AC133(-)) circulating angiogenic cells. In smokers as well as nonsmokers, 3-HPMA levels were positively associated with both increased levels of platelet-leukocyte aggregates and the Framingham Risk Score. No association was observed between 3-HPMA and plasma fibrinogen. Levels of C-reactive protein were associated with 3-HPMA levels in nonsmokers only. Regardless of its source, acrolein exposure is associated with platelet activation and suppression of circulating angiogenic cell levels, as well as increased CVD risk. © 2014 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.

  12. Acrolein impairs the cholesterol transport functions of high density lipoproteins.

    Science.gov (United States)

    Chadwick, Alexandra C; Holme, Rebecca L; Chen, Yiliang; Thomas, Michael J; Sorci-Thomas, Mary G; Silverstein, Roy L; Pritchard, Kirkwood A; Sahoo, Daisy

    2015-01-01

    High density lipoproteins (HDL) are considered athero-protective, primarily due to their role in reverse cholesterol transport, where they transport cholesterol from peripheral tissues to the liver for excretion. The current study was designed to determine the impact of HDL modification by acrolein, a highly reactive aldehyde found in high abundance in cigarette smoke, on the cholesterol transport functions of HDL. HDL was chemically-modified with acrolein and immunoblot and mass spectrometry analyses confirmed apolipoprotein crosslinking, as well as acrolein adducts on apolipoproteins A-I and A-II. The ability of acrolein-modified HDL (acro-HDL) to serve as an acceptor of free cholesterol (FC) from COS-7 cells transiently expressing SR-BI was significantly decreased. Further, in contrast to native HDL, acro-HDL promotes higher neutral lipid accumulation in murine macrophages as judged by Oil Red O staining. The ability of acro-HDL to mediate efficient selective uptake of HDL-cholesteryl esters (CE) into SR-BI-expressing cells was reduced compared to native HDL. Together, the findings from our studies suggest that acrolein modification of HDL produces a dysfunctional particle that may ultimately promote atherogenesis by impairing functions that are critical in the reverse cholesterol transport pathway.

  13. Molecular mechanisms of acrolein toxicity: relevance to human disease.

    Science.gov (United States)

    Moghe, Akshata; Ghare, Smita; Lamoreau, Bryan; Mohammad, Mohammad; Barve, Shirish; McClain, Craig; Joshi-Barve, Swati

    2015-02-01

    Acrolein, a highly reactive unsaturated aldehyde, is a ubiquitous environmental pollutant and its potential as a serious environmental health threat is beginning to be recognized. Humans are exposed to acrolein per oral (food and water), respiratory (cigarette smoke, automobile exhaust, and biocide use) and dermal routes, in addition to endogenous generation (metabolism and lipid peroxidation). Acrolein has been suggested to play a role in several disease states including spinal cord injury, multiple sclerosis, Alzheimer's disease, cardiovascular disease, diabetes mellitus, and neuro-, hepato-, and nephro-toxicity. On the cellular level, acrolein exposure has diverse toxic effects, including DNA and protein adduction, oxidative stress, mitochondrial disruption, membrane damage, endoplasmic reticulum stress, and immune dysfunction. This review addresses our current understanding of each pathogenic mechanism of acrolein toxicity, with emphasis on the known and anticipated contribution to clinical disease, and potential therapies. © The Author 2015. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.

  14. Alcohol, Aldehydes, Adducts and Airways

    Directory of Open Access Journals (Sweden)

    Muna Sapkota

    2015-11-01

    Full Text Available Drinking alcohol and smoking cigarettes results in the formation of reactive aldehydes in the lung, which are capable of forming adducts with several proteins and DNA. Acetaldehyde and malondialdehyde are the major aldehydes generated in high levels in the lung of subjects with alcohol use disorder who smoke cigarettes. In addition to the above aldehydes, several other aldehydes like 4-hydroxynonenal, formaldehyde and acrolein are also detected in the lung due to exposure to toxic gases, vapors and chemicals. These aldehydes react with nucleophilic targets in cells such as DNA, lipids and proteins to form both stable and unstable adducts. This adduction may disturb cellular functions as well as damage proteins, nucleic acids and lipids. Among several adducts formed in the lung, malondialdehyde DNA (MDA-DNA adduct and hybrid malondialdehyde-acetaldehyde (MAA protein adducts have been shown to initiate several pathological conditions in the lung. MDA-DNA adducts are pre-mutagenic in mammalian cells and induce frame shift and base-pair substitution mutations, whereas MAA protein adducts have been shown to induce inflammation and inhibit wound healing. This review provides an insight into different reactive aldehyde adducts and their role in the pathogenesis of lung disease.

  15. The effects of acetaldehyde and acrolein on muscle catabolism in C2 myotubes.

    Science.gov (United States)

    Rom, Oren; Kaisari, Sharon; Aizenbud, Dror; Reznick, Abraham Z

    2013-12-01

    The toxic aldehydes acetaldehyde and acrolein were previously suggested to damage skeletal muscle. Several conditions in which exposure to acetaldehyde and acrolein is increased were associated with muscle wasting and dysfunction. These include alcoholic myopathy, renal failure, oxidative stress, and inflammation. A main exogenous source of both acetaldehyde and acrolein is cigarette smoking, which was previously associated with increased muscle catabolism. Recently, we have shown that exposure of skeletal myotubes to cigarette smoke stimulated muscle catabolism via increased oxidative stress, activation of p38 MAPK, and upregulation of muscle-specific E3 ubiquitin ligases. In this study, we aimed to investigate the effects of acetaldehyde and acrolein on catabolism of skeletal muscle. Skeletal myotubes differentiated from the C2 myoblast cell line were exposed to acetaldehyde or acrolein and their effects on signaling pathways related to muscle catabolism were studied. Exposure of myotubes to acetaldehyde did not promote muscle catabolism. However, exposure to acrolein caused increased generation of free radicals, activation of p38 MAPK, upregulation of the muscle-specific E3 ligases atrogin-1 and MuRF1, degradation of myosin heavy chain, and atrophy of myotubes. Inhibition of p38 MAPK by SB203580 abolished acrolein-induced muscle catabolism. Our findings demonstrate that acrolein but not acetaldehyde activates a signaling cascade resulting in muscle catabolism in skeletal myotubes. Although within the limitations of an in vitro study, these findings indicate that acrolein may promote muscle wasting in conditions of increased exposure to this aldehyde. Copyright © 2013 Elsevier Inc. All rights reserved.

  16. Effects of acrolein on the production of corticosterone in male rats.

    Science.gov (United States)

    Yeh, Yung-Hsing; Chou, Jou-Chun; Weng, Ting-Chun; Lieu, Fu-Kong; Lin, Jou-Yu; Yeh, Chii-Chang; Hu, Sindy; Wang, Paulus S; Idova, Galina; Wang, Shyi-Wu

    2016-07-01

    Acrolein, an α, β-unsaturated aldehyde, exists in a wide range of sources. Acrolein can be not only generated from all types of smoke but also produced endogenously from the metabolism by lipid peroxidation. The cellular influence of acrolein is due to its electrophilic character via binding to and depleting cellular nucleophiles. Although the toxicity of acrolein has been extensively studied, there is relatively little information about its impact on hormone release. This study aimed at the effect of acrolein on hypothalamic-pituitary-adrenal (H-P-A) axis. In an in vivo study, male rats were administrated with acrolein for 1 or 3days. The plasma corticosterone in response to a single injection of adrenocorticotropic hormone (ACTH) increased slowly in acrolein-pretreated rats than in control rats. Further investigating the steroidogenic pathway, the protein expressions of steroidogenic acute regulatory protein (StAR) and the upper receptor-melanocortin 2 receptor (MC2R) were attenuated in acrolein-treated groups. Another experiment using trilostane showed less activity of P450scc in zona fasciculata-reticularis (ZFR) cells in acrolein-treated groups. In addition to the suppressed ability of corticosterone production in ZFR cells, acrolein even had extended influence at higher concentrations. The lower ACTH was observed in the plasma from acrolein-pretreated rats. In an in vitro study, ZFR cells were incubated with acrolein and the results showed that corticosterone concentrations in media were decreased in a dose-dependent manner. Acrolein also desensitized the response of the ZFR cells to ACTH. These results suggested that acrolein decreased the releasing ability of corticosterone via an inhibition on the response of ZFR cells to ACTH and the reduction of protein expressions of StAR and MC2R as well as the activity of P450scc in rat ZFR cells. The present evidences showed that the H-P-A axis was affected by the administration of acrolein. Copyright © 2016

  17. Mechanisms of CDDO-imidazolide-mediated cytoprotection against acrolein-induced neurocytotoxicity in SH-SY5Y cells and primary human astrocytes.

    Science.gov (United States)

    Speen, Adam; Jones, Colton; Patel, Ruby; Shah, Halley; Nallasamy, Palanisamy; Brooke, Elizabeth A S; Zhu, Hong; Li, Y Robert; Jia, Zhenquan

    2015-10-01

    Acrolein is a ubiquitous unsaturated aldehyde has been implicated in the pathogenesis of various neurological disorders. However, limited study has been conducted into potential therapeutic protection and underlying mechanism against acrolein-induced cytotoxicity via upregulation of cellular aldehyde-detoxification defenses. In this study we have utilized RA-differentiated human SH-SY5Y cells and primary human astrocytes to investigate the induction of glutathione (GSH) by the synthetic triterpenoid 2-cyano-3,12-dixooleana-1,9-dien-28-imidazolide (CDDO-Im) and the protective effects CDDO-Im-mediated antioxidant defenses on acrolein toxicity. Acrolein exposure to RA-differentiated SH-SY5Y cells resulted in a significant time dependent depletion of cellular GSH preceding a reduction in cell viability and LDH release. Further, we demonstrated the predominance of cellular GSH in protection against acrolein-induced cytotoxicity. Buthionine sulfoximine (BSO) at 25μM dramatically depleted GSH and significantly potentiated acrolein-induced cytotoxicity. Pretreatment of the cells with 100nM CDDO-Im afforded a dramatic protection against acrolein-induced cytotoxicity. Pretreatment of BSO and CDDO was found to prevent the CDDO-Im-mediated GSH induction and partially reversed the cytoprotective effects of CDDO-Im against acrolein cytotoxicity. Overall, this study represents for the first time the CDDO-Im mediated upregulation of GSH is a predominant mechanism against acrolein-induced neurotoxicity. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.

  18. Redox mechanism of neurotoxicity by a serotonin-acrolein polymeric melanoid.

    Science.gov (United States)

    Murphy, Meghan M; Miller, Elizabeth D; Fibuch, Eugene E; Seidler, Norbert W

    2011-02-01

    Postoperative cognitive dysfunction may be associated with the toxic products of lipid peroxidation, such as the α,β-unsaturated aldehyde acrolein, which accumulates in aging. We previously identified an acrolein-mediated, serotonin-derived melanoid product, or SDM. This study further characterizes this putative novel neuromelanin, which is not made from catecholamines. In addition to its strong protein-binding properties, we observed that SDM binds Fe(2+) readily and exhibits complex redox characteristics. SDM may exist as a two-dimensional network of polymers that coalesce into larger entities exhibiting electroactive properties. These observations suggest that SDM may contribute to the decline in cognition due to focal degeneration from SDM-mediated free-radical production. We know that inhalational anesthetics sequester acrolein, which is toxic to neurons, and we propose that the local increase in acrolein depletes serotonin levels and enhances neuronal vulnerability through the production of neuromelanin-like structures, such as SDM.

  19. Modification and inactivation of Cu,Zn-superoxide dismutase by the lipid peroxidation product, acrolein

    Directory of Open Access Journals (Sweden)

    Jung Hoon Kang

    2013-11-01

    Full Text Available Acrolein is the most reactive aldehydic product of lipidperoxidation and is found to be elevated in the brain whenoxidative stress is high. The effects of acrolein on the structureand function of human Cu,Zn-superoxide dismutase (SOD wereexamined. When Cu,Zn-SOD was incubated with acrolein, thecovalent crosslinking of the protein was increased, and the loss ofenzymatic activity was increased in a dose-dependent manner.Reactive oxygen species (ROS scavengers and copper chelatorsinhibited the acrolein-mediated Cu,Zn-SOD modification and theformation of carbonyl compound. The present study shows thatROS may play a critical role in acrolein-induced Cu,Zn-SODmodification and inactivation. When Cu,Zn-SOD that has beenexposed to acrolein was subsequently analyzed by amino acidanalysis, serine, histidine, arginine, threonine and lysine residueswere particularly sensitive. It is suggested that the modificationand inactivation of Cu,Zn-SOD by acrolein could be produced bymore oxidative cell environments. [BMB Reports 2013; 46(11:555-560

  20. Acrolein effects in pulmonary cells: relevance to chronic obstructive pulmonary disease.

    Science.gov (United States)

    Moretto, Nadia; Volpi, Giorgia; Pastore, Fiorella; Facchinetti, Fabrizio

    2012-07-01

    Acrolein (2-propenal) is a highly reactive α,β-unsaturated aldehyde and a respiratory irritant that is ubiquitously present in the environment but that can also be generated endogenously at sites of inflammation. Acrolein is abundant in tobacco smoke, which is the major environmental risk factor for chronic obstructive pulmonary disease (COPD), and elevated levels of acrolein are found in the lung fluids of COPD patients. Its high electrophilicity makes acrolein notorious for its facile reaction with biological nucleophiles, leading to the modification of proteins and DNA and depletion of antioxidant defenses. As a consequence, acrolein results in oxidative stress as well as altered intracellular signaling and gene transcription/translation. In pulmonary cells, acrolein, at subtoxic concentrations, can activate intracellular stress kinases, alter the production of inflammatory mediators and proteases, modify innate immune response, induce mucus hypersecretion, and damage airway epithelium. A better comprehension of the mechanisms underlying acrolein effects in the airways may suggest novel treatment strategies in COPD. © 2012 New York Academy of Sciences.

  1. Inhibition of NFkappaB activation and IL-8 expression in human bronchial epithelial cells by acrolein.

    Science.gov (United States)

    Valacchi, Giuseppe; Pagnin, Elisa; Phung, Anh; Nardini, Mirella; Schock, Bettina C; Cross, Carroll E; van der Vliet, Albert

    2005-01-01

    Lipid oxidation and environmental pollutants are major sources of alpha,beta-unsaturated aldehydes such as acrolein and 4-hydroxynonenal. Acrolein (2-propenal), a major product of organic combustion such as tobacco smoke, represents the most reactive alpha,beta-unsaturated aldehyde, with high reactivity toward nucleophilic targets such as sulfhydryl groups. To investigate how acrolein affects respiratory tract cell activation, we exposed either primary (NHBE) or immortalized human bronchial epithelial cells (HBE1) to 0-25 microM acrolein, and determined effects on basal and tumor necrosis factor-alpha (TNFalpha)-induced production of the chemokine interleukin (IL)-8. Cell exposure to acrolein dose-dependently suppressed IL-8 mRNA levels in HBE1 cells (26, 40, and 79% at 5, 10, and 25 microM acrolein concentrations, respectively) and resulted in corresponding decreases in IL-8 production. Studies of nuclear factor-kappaB (NFkappaB) activation, an essential event in IL-8 production, showed decreased TNFalpha-induced NFkappaB activation by acrolein, illustrated by inhibition of nuclear translocation of NFkappaB and reduced IkappaBalpha degradation. Immunochemical analysis of IkappaB kinase (IKK), a redox-sensitive regulator of NFkappaB activation, indicated direct modification of the IKK beta-subunit by acrolein, suggesting that acrolein may act directly on IKK. In summary, our results demonstrate that acrolein can suppress inflammatory processes in the airways by inhibiting epithelial IL-8 production through direct or indirect inhibitory effects on NFkappaB activation.

  2. Protection of HepG2 cells against acrolein toxicity by 2-cyano-3,12-dioxooleana-1,9-dien-28-imidazolide via glutathione-mediated mechanism.

    Science.gov (United States)

    Shah, Halley; Speen, Adam M; Saunders, Christina; Brooke, Elizabeth A S; Nallasamy, Palanisamy; Zhu, Hong; Li, Y Robert; Jia, Zhenquan

    2015-10-01

    Acrolein is an environmental toxicant, mainly found in smoke released from incomplete combustion of organic matter. Several studies showed that exposure to acrolein can lead to liver damage. The mechanisms involved in acrolein-induced hepatocellular toxicity, however, are not completely understood. This study examined the cytotoxic mechanisms of acrolein on HepG2 cells. Acrolein at pathophysiological concentrations was shown to cause apoptotic cell death and an increase in levels of protein carbonyl and thiobarbituric acid reactive acid substances. Acrolein also rapidly depleted intracellular glutathione (GSH), GSH-linked glutathione-S-transferases, and aldose reductase, three critical cellular defenses that detoxify reactive aldehydes. Results further showed that depletion of cellular GSH by acrolein preceded the loss of cell viability. To further determine the role of cellular GSH in acrolein-mediated cytotoxicity, buthionine sulfoximine (BSO) was used to inhibit cellular GSH biosynthesis. It was observed that depletion of cellular GSH by BSO led to a marked potentiation of acrolein-mediated cytotoxicity in HepG2 cells. To further assess the contribution of these events to acrolein-induced cytotoxicity, triterpenoid compound 2-cyano-3,12-dioxooleana-1,9-dien-28-imidazolide (CDDO-Im) was used for induction of GSH. Induction of GSH by CDDO-Im afforded cytoprotection against acrolein toxicity in HepG2 cells. Furthermore, BSO significantly inhibited CDDO-Im-mediated induction in cellular GSH levels and also reversed cytoprotective effects of CDDO-Im in HepG2 cells. These results suggest that GSH is a predominant mechanism underlying acrolein-induced cytotoxicity as well as CDDO-Im-mediated cytoprotection. This study may provide understanding on the molecular action of acrolein which may be important to develop novel strategies for the prevention of acrolein-mediated toxicity. © 2014 by the Society for Experimental Biology and Medicine.

  3. Determination of acrolein in serum by high-performance liquid chromatography with fluorescence detection after pre-column fluorogenic derivatization using 1,2-diamino-4,5-dimethoxybenzene.

    Science.gov (United States)

    Imazato, Takahiro; Kanematsu, Mariko; Kishikawa, Naoya; Ohyama, Kaname; Hino, Takako; Ueki, Yukitaka; Maehata, Eisuke; Kuroda, Naotaka

    2015-09-01

    Acrolein is a major unsaturated aldehyde that is generated during the lipid peroxidation process. The measurement of acrolein in biological samples should be useful to estimate the degree of lipid peroxidation and to evaluate the effect of hazardous properties of acrolein on human health. In this study, a highly sensitive and selective high-performance liquid chromatography with fluorescence detection method was developed for the determination of acrolein in human serum. The proposed method involves the pre-column fluorogenic derivatization of acrolein with 1,2-diamino-4,5-dimethoxybenzene (DDB) as a reagent. The fluorescent derivative of acrolein could be detected clearly without any interfering reagent blank peaks because DDB does not have intrinsic fluorescence itself, and the detection limit was 10 nM (signal-to-noise ratio = 3). The proposed method could selectively detect acrolein in human serum with a simple protein precipitation treatment. Copyright © 2015 John Wiley & Sons, Ltd.

  4. Acrolein, an I-κBα-independent downregulator of NF-κB activity, causes the decrease in nitric oxide production in human malignant keratinocytes.

    Science.gov (United States)

    Moon, Ki-Young

    2011-05-01

    Acrolein, a reactive electrophilic α, β-unsaturated aldehyde, is known to be an alkylating chemical carcinogen. The effect of acrolein on the activation of NF-κB in human malignant epidermal keratinocytes was examined to elucidate the molecular mechanism associated with this NF-κB-acrolein regulation and its consecutive sequence, nitric oxide (NO) production. Acrolein significantly downregulated the cellular NF-κB activity up to 60% compared with control as well as the lipopolysaccharide (LPS)-induced NO production in a dose response manner at concentrations of 10~30 μM. To investigate the regulatory mechanism associated with this NF-κB-acrolein downregulation, the relative level of phosphorylation of I-κBα (serines-32 and -36), a principle regulator of NF-κB activation, represented by acrolein, was quantified. Acrolein inhibited NF-κB activity without altering cellular levels of the phosphorylated and nonphosphorylated forms of I-κBα, implying that the downregulatory effect of acrolein on cellular NF-κB activity in human skin cells is an I-κBα-independent activation pathway. The results suggests that acrolein causes the decrease in nitric oxide production as an I-κBα-independent downregulator of NF-κB activity in human malignant keratinocytes, and acrolein-induced carcinogenesis may be associated with the modulation of cellular NF-κB activity.

  5. Mediating the potent ROS toxicity of acrolein in neurons with silica nanoparticles and a natural product approach

    Science.gov (United States)

    White-Schenk, Désirée.; Shi, Riyi; Leary, James F.

    2014-03-01

    Acrolein, a very reactive aldehyde, is a culprit in the biochemical cascade after primary, mechanical spinal cord injury (SCI), which leads to the destruction of tissue initially unharmed, referred to as "secondary injury". Additionally, in models of multiple sclerosis (MS) and some clinical research, acrolein levels are significantly increased. Due to its ability to make more copies of itself in the presence of tissue via lipid peroxidation, researchers believe that acrolein plays a role in the increased destruction of the central nervous system in both SCI and MS. Hydralazine, an FDAapproved hypotensive drug, has been shown to scavenge acrolein, but its side effects and short half life at the appropriate dose for acrolein scavenging must be improved for beneficial clinical translation. Therefore, a nanomedical approach has been designed using silica nanoparticles as a porous delivery vehicle hydralazine. The silica particles are formed in a one-step method that incorporates poly(ethylene) glycol (PEG), a stealth molecule, directly onto the nanoparticles. As an additional avenue for study, a natural product in green tea, epigallocatechin gallate (EGCG), has been explored for its ability to react with acrolein, disabling its reactive capabilities. Upon demonstration of attenuating acrolein, EGCG's delivery may also be improved using the nanomedical approach. The current work exposes the potential of using silica nanoparticles as a delivery vehicle and EGCG's antioxidant capabilities in B35 neuroblastoma cells exposed to acrolein. We also measure nanotoxicity to individual rat neurons using high-throughput image scanning cytometry.

  6. Gas-phase Hydrogenation of Crotonaldehyde Over Nickel-on-Kieselguhr Catalyst Pellets

    International Nuclear Information System (INIS)

    Uraz, C.; Atalay, F.; Atalay, S.

    2001-01-01

    Gas phase catalytic hydrogenation of crotonaldehyde to η-butanol was investigated. A nickel based commercial catalyst produced by Harshaw was used at constant temperatures ranging from 160 to 210deg; at pressures of 1.5, 2 , and 2.5 atm and at different crotonaldehyde to hydrogen feed ratios changing from 0.134 to 0.226. The conversion of crotonaldehyde at different operating conditions were determined and the reaction rates were calculated . The experimental results were fitted to ten langmuir-Hinshelwood/ Eley Rideal type models in addition to a homogeneous kinetics modal and the best modal was identified. The effects of external and internal mass transfer resistances were found to be negligible .(authors) refs 28., 2 figs , 4 tabs

  7. Research advances in the catalysts for the selective oxidation of ethane to aldehydes

    Institute of Scientific and Technical Information of China (English)

    ZHANG Zhe; ZHAO Zhen; XU Chunming

    2005-01-01

    Selective oxidation of ethane to aldehydes is one of the most difficult processes in the catalysis researches of low alkanes. The development of selective oxidation of ethane to aldehydes (formaldehyde, acetaldehyde and acrolein) is discussed. The latest progress of the catalysts, including bulk or supported metal oxide catalysts, highly dispersed and isolated active sites catalysts, and the photo-catalytic ethane oxidation catalysts, partial oxidation of ethane in the gas phase, and the proposed reaction pathways from ethane to aldehydes are involved.

  8. Isotope-labeling studies on the formation pathway of acrolein during heat processing of oils.

    Science.gov (United States)

    Ewert, Alice; Granvogl, Michael; Schieberle, Peter

    2014-08-20

    Acrolein (2-propenal) is classified as a foodborne toxicant and was shown to be present in significant amounts in heated edible oils. Up to now, its formation was mainly suggested to be from the glycerol part of triacylglycerides, although a clear influence of the unsaturation of the fatty acid moiety was also obvious in previous studies. To unequivocally clarify the role of the glycerol and the fatty acid parts in acrolein formation, two series of labeled triacylglycerides were synthesized: [(13)C(3)]-triacylglycerides of stearic, oleic, linoleic, and linolenic acid and [(13)C(54)]-triacylglycerides with labeled stearic, oleic, and linoleic acid, but with unlabeled glycerol. Heating of each of the seven intermediates singly in silicon oil and measurement of the formed amounts of labeled and unlabeled acrolein clearly proved the fatty acid backbone as the key precursor structure. Enzymatically synthesized pure linoleic acid and linolenic acid hydroperoxides were shown to be the key intermediates in acrolein formation, thus allowing the discussion of a radical-induced reaction pathway leading to the formation of the aldehyde. Surprisingly, although several oils contained high amounts of acrolein after heating, deep-fried foods themselves, such as donuts or French fries, were low in the aldehyde.

  9. Acrolein generation stimulates hypercontraction in isolated human blood vessels

    International Nuclear Information System (INIS)

    Conklin, D.J.; Bhatnagar, A.; Cowley, H.R.; Johnson, G.H.; Wiechmann, R.J.; Sayre, L.M.; Trent, M.B.; Boor, P.J.

    2006-01-01

    Increased risk of vasospasm, a spontaneous hyperconstriction, is associated with atherosclerosis, cigarette smoking, and hypertension-all conditions involving oxidative stress, lipid peroxidation, and inflammation. To test the role of the lipid peroxidation- and inflammation-derived aldehyde, acrolein, in human vasospasm, we developed an ex vivo model using human coronary artery bypass graft (CABG) blood vessels and a demonstrated acrolein precursor, allylamine. Allylamine induces hypercontraction in isolated rat coronary artery in a semicarbazide-sensitive amine oxidase activity (SSAO) dependent manner. Isolated human CABG blood vessels (internal mammary artery, radial artery, saphenous vein) were used to determine: (1) vessel responses and sensitivity to acrolein, allylamine, and H 2 O 2 exposure (1 μM-1 mM), (2) SSAO dependence of allylamine-induced effects using SSAO inhibitors (semicarbazide, 1 mM; MDL 72274-E, active isomer; MDL 72274-Z, inactive isomer; 100 μM), (3) the vasoactive effects of two other SSAO amine substrates, benzylamine and methylamine, and (4) the contribution of extracellular Ca 2+ to hypercontraction. Acrolein or allylamine but not H 2 O 2 , benzylamine, or methylamine stimulated spontaneous and pharmacologically intractable hypercontraction in CABG blood vessels that was similar to clinical vasospasm. Allylamine-induced hypercontraction and blood vessel SSAO activity were abolished by pretreatment with semicarbazide or MDL 72274-E but not by MDL 72274-Z. Allylamine-induced hypercontraction also was significantly attenuated in Ca 2+ -free buffer. In isolated aorta of spontaneously hypertensive rat, allylamine-induced an SSAO-dependent contraction and enhanced norepinephrine sensitivity but not in Sprague-Dawley rat aorta. We conclude that acrolein generation in the blood vessel wall increases human susceptibility to vasospasm, an event that is enhanced in hypertension

  10. Upregulation of endothelial heme oxygenase-1 expression through the activation of the JNK pathway by sublethal concentrations of acrolein.

    Science.gov (United States)

    Wu, C C; Hsieh, C W; Lai, P H; Lin, J B; Liu, Y C; Wung, B S

    2006-08-01

    Acrolein is a highly electrophilic alpha,beta-unsaturated aldehyde that is present in cigarette smoke. Heme oxygenase-1 (HO-1) is a cytoprotective enzyme activated by various such electrophilic compounds. In this study, the regulatory effects of acrolein upon the expression of HO-1 were investigated in endothelial cells (ECs). We demonstrate that acrolein induces the elevation of HO-1 protein levels, and subsequent enzyme activity, at non-cytotoxic concentrations. An additional alpha,beta-unsaturated aldehyde, cinnamaldehyde, was also found to increase HO-1 expression and have less cytotoxicity than acrolein. Moreover, acrolein-mediated HO-1 induction is abrogated in the presence of actinomycin D and cycloheximide. Nrf2 is a transcription factor involved in the induction of HO-1 through an antioxidant response element (ARE) in the promoter region of the HO-1 gene. We show that acrolein induces Nrf2 translocation and ARE-luciferase reporter activity. Acrolein was also found to induce the production of both superoxide and H2O2 at levels greater than 100 microM. However, with the exception of NAC, no antioxidant generated any effect upon acrolein-dependent HO-1 expression in ECs. Our present findings suggest that reactive oxygen species (ROS) may not be a major modulator for HO-1 induction. Using buthionine sulfoximine to deplete the intracellular GSH levels further enhanced the effects of acrolein. We also found that cellular GSH level was rapidly reduced after both 10 and 100 microM acrolein treatment. However, after 6 h of exposure to ECs, only 10 microM acrolein treatment increases GSH level. In addition, only the JNK inhibitor SP600125 and tyrosine kinase inhibitor genistein had any significant inhibitory impact upon the upregulation of HO-1 by acrolein. Pretreatment with a range of other PI3 kinase inhibitors, including wortmannin and LY294002, showed no effects. Hence, we show in our current experiments that a sublethal concentration of acrolein is in fact a

  11. Upregulation of endothelial heme oxygenase-1 expression through the activation of the JNK pathway by sublethal concentrations of acrolein

    International Nuclear Information System (INIS)

    Wu, C.C.; Hsieh, C.W.; Lai, P.H.; Lin, J.B.; Liu, Y.C.; Wung, B.S.

    2006-01-01

    Acrolein is a highly electrophilic α,β-unsaturated aldehyde that is present in cigarette smoke. Heme oxygenase-1 (HO-1) is a cytoprotective enzyme activated by various such electrophilic compounds. In this study, the regulatory effects of acrolein upon the expression of HO-1 were investigated in endothelial cells (ECs). We demonstrate that acrolein induces the elevation of HO-1 protein levels, and subsequent enzyme activity, at non-cytotoxic concentrations. An additional α,β-unsaturated aldehyde, cinnamaldehyde, was also found to increase HO-1 expression and have less cytotoxicity than acrolein. Moreover, acrolein-mediated HO-1 induction is abrogated in the presence of actinomycin D and cycloheximide. Nrf2 is a transcription factor involved in the induction of HO-1 through an antioxidant response element (ARE) in the promoter region of the HO-1 gene. We show that acrolein induces Nrf2 translocation and ARE-luciferase reporter activity. Acrolein was also found to induce the production of both superoxide and H 2 O 2 at levels greater than 100 μM. However, with the exception of NAC, no antioxidant generated any effect upon acrolein-dependent HO-1 expression in ECs. Our present findings suggest that reactive oxygen species (ROS) may not be a major modulator for HO-1 induction. Using buthionine sulfoximine to deplete the intracellular GSH levels further enhanced the effects of acrolein. We also found that cellular GSH level was rapidly reduced after both 10 and 100 μM acrolein treatment. However, after 6 h of exposure to ECs, only 10 μM acrolein treatment increases GSH level. In addition, only the JNK inhibitor SP600125 and tyrosine kinase inhibitor genistein had any significant inhibitory impact upon the upregulation of HO-1 by acrolein. Pretreatment with a range of other PI3 kinase inhibitors, including wortmannin and LY294002, showed no effects. Hence, we show in our current experiments that a sublethal concentration of acrolein is in fact a novel HO-1 inducer

  12. The effects of acrolein on peroxiredoxins, thioredoxins, and thioredoxin reductase in human bronchial epithelial cells

    International Nuclear Information System (INIS)

    Myers, Charles R.; Myers, Judith M.

    2009-01-01

    Inhalation is a common form of exposure to acrolein, a toxic reactive volatile aldehyde that is a ubiquitous environmental pollutant. Bronchial epithelial cells would be directly exposed to inhaled acrolein. The thioredoxin (Trx) system is essential for the maintenance of cellular thiol redox balance, and is critical for cell survival. Normally, thioredoxin reductase (TrxR) maintains the cytosolic (Trx1) and mitochondrial (Trx2) thioredoxins in the reduced state, and the thioredoxins keep the peroxiredoxins (Prx) reduced, thereby supporting their peroxidase function. The effects of acrolein on TrxR, Trx and Prx in human bronchial epithelial (BEAS-2B) cells were determined. A 30-min exposure to 5 μM acrolein oxidized both Trx1 and Trx2, although significant effects were noted for Trx1 at even lower acrolein concentrations. The effects on Trx1 and Trx2 could not be reversed by treatment with disulfide reductants. TrxR activity was inhibited 60% and >85% by 2.5 and 5 μM acrolein, respectively. The endogenous electron donor for TrxR, NADPH, could not restore its activity, and activity did not recover in cells during a 4-h acrolein-free period in complete medium. The effects of acrolein on TrxR and Trx therefore extend beyond the duration of exposure. While there was a strong correlation between TrxR inhibition and Trx1 oxidation, the irreversible effects on Trx1 suggest direct effects of acrolein rather than loss of reducing equivalents from TrxR. Trx2 did not become oxidized until ≥90% of TrxR was inhibited, but irreversible effects on Trx2 also suggest direct effects of acrolein. Prx1 (cytosolic) and Prx3 (mitochondrial) shifted to a largely oxidized state only when >90 and 100% of their respective Trxs were oxidized. Prx oxidation was readily reversed with a disulfide reductant, suggesting that Prx oxidation resulted from lack of reducing equivalents from Trx and not direct reaction with acrolein. The effects of acrolein on the thioredoxin system and

  13. The dimers of glyoxal and acrolein with H 2O and HF: Negative intramolecular coupling and blue-shifted C-H stretch

    Science.gov (United States)

    Karpfen, Alfred; Kryachko, Eugene S.

    2010-04-01

    The structures and the vibrational spectra of the hydrogen-bonded complexes: glyoxal-H 2O, glyoxal-HF, acrolein-H 2O, and acrolein-HF, are investigated within the MP2/aug-cc-pVTZ computational approach. It is demonstrated that the calculated blue shifts of the C-H stretching frequencies in the glyoxal-H 2O complexes are only indirectly pertinent to hydrogen bonding to the C-H group. The comparison with the glyoxal-HF and the acrolein-HF complexes reveals that these blue shifts are a direct consequence of a negative intramolecular coupling between vicinal C dbnd O and C-H bonds in the aldehyde groups of isolated glyoxal and acrolein molecules. To support this interpretation, the halogen-bonded complexes glyoxal-BrF and acrolein-BrF are discussed.

  14. Acrolein activates cell survival and apoptotic death responses involving the endoplasmic reticulum in A549 lung cells.

    Science.gov (United States)

    Tanel, André; Pallepati, Pragathi; Bettaieb, Ahmed; Morin, Patrick; Averill-Bates, Diana A

    2014-05-01

    Acrolein, a highly reactive α,β-unsaturated aldehyde, is a product of endogenous lipid peroxidation. It is a ubiquitous environmental pollutant that is generated mainly by smoke, overheated cooking oil and vehicle exhaust. Acrolein damages cellular proteins, which could lead to accumulation of aberrantly-folded proteins in the endoplasmic reticulum (ER). This study determines the mechanisms involved in acrolein-induced apoptosis mediated by the ER and possible links with the ER stress response in human A549 lung cells. The exposure of cells to acrolein (15-50μM) for shorter times of 15 to 30min activated several ER stress markers. These included the ER chaperone protein BiP and the three ER sensors: (i) the survival/rescue molecules protein kinase RNA (PKR)-like ER kinase (PERK) and eukaryotic initiation factor 2 alpha (eIF2α) were phosphorylated; (ii) cleavage of activating transcription factor 6 (ATF6) occurred, and (iii) inositol-requiring protein-1 alpha (IRE1α) was phosphorylated. Acrolein (25-50μM) caused apoptotic cell death mediated by the ER after 2h, which was characterised by the induction of CHOP and activation of ER proteases calpain and caspase-4. Calpain and caspase-7 were the initiating factors for caspase-4 activation in acrolein-induced apoptosis. These results increase our knowledge about cellular responses to acrolein in lung cells, which have implications for human health. Copyright © 2014 Elsevier B.V. All rights reserved.

  15. Acrolein inhalation alters arterial blood gases and triggers carotid body-mediated cardiovascular responses in hypertensive rats.

    Science.gov (United States)

    Perez, Christina M; Hazari, Mehdi S; Ledbetter, Allen D; Haykal-Coates, Najwa; Carll, Alex P; Cascio, Wayne E; Winsett, Darrell W; Costa, Daniel L; Farraj, Aimen K

    2015-01-01

    Air pollution exposure affects autonomic function, heart rate, blood pressure and left ventricular function. While the mechanism for these effects is uncertain, several studies have reported that air pollution exposure modifies activity of the carotid body, the major organ that senses changes in arterial oxygen and carbon dioxide levels, and elicits downstream changes in autonomic control and cardiac function. We hypothesized that exposure to acrolein, an unsaturated aldehyde and mucosal irritant found in cigarette smoke and diesel exhaust, would activate the carotid body chemoreceptor response and lead to secondary cardiovascular responses in rats. Spontaneously hypertensive (SH) rats were exposed once for 3 h to 3 ppm acrolein gas or filtered air in whole body plethysmograph chambers. To determine if the carotid body mediated acrolein-induced cardiovascular responses, rats were pretreated with an inhibitor of cystathionine γ-lyase (CSE), an enzyme essential for carotid body signal transduction. Acrolein exposure induced several cardiovascular effects. Systolic, diastolic and mean arterial blood pressure increased during exposure, while cardiac contractility decreased 1 day after exposure. The cardiovascular effects were associated with decreases in pO2, breathing frequency and expiratory time, and increases in sympathetic tone during exposure followed by parasympathetic dominance after exposure. The CSE inhibitor prevented the cardiovascular effects of acrolein exposure. Pretreatment with the CSE inhibitor prevented the cardiovascular effects of acrolein, suggesting that the cardiovascular responses with acrolein may be mediated by carotid body-triggered changes in autonomic tone. (This abstract does not reflect EPA policy.).

  16. Changes in the nasal epithelium of rats exposed by inhalation to mixtures of formaldehyde, acetaldehyde, and acrolein

    NARCIS (Netherlands)

    Cassee, F.R.; Groten, J.P.; Feron, V.J.

    1996-01-01

    Formaldehyde, acetaldehyde, and acrolein are well-known upper respiratory tract irritants and occur simultaneously as pollutants in many indoor and outdoor environments. The upper respiratory tract, and especially the nose, is the prime target for inhaled aldehydes. To study possible additive or

  17. Acrolein with an alpha, beta-unsaturated Carbonyl Group Inhibits LPS-induced Homodimerization of Toll-like Receptor 4

    Science.gov (United States)

    Acrolein is a highly electrophilic a,ß-unsaturated aldehyde present in a number of environmental sources, especially cigarette smoke. It reacts strongly with the thiol groups of cysteine residues by Michael addition and has been reported to inhibit nuclear factor-kB (NF-kB) activation by lipopolysac...

  18. IRIS Toxicological Review of Acrolein (2003 Final)

    Science.gov (United States)

    EPA announced the release of the final report, Toxicological Review of Acrolein: in support of the Integrated Risk Information System (IRIS). The updated Summary for Acrolein and accompanying toxicological review have been added to the IRIS Database.

  19. A Comparative Study of Basic, Amphoteric, and Acidic Catalysts in the Oxidative Coupling of Methanol and Ethanol for Acrolein Production.

    Science.gov (United States)

    Lilić, Aleksandra; Wei, Tiantian; Bennici, Simona; Devaux, Jean-François; Dubois, Jean-Luc; Auroux, Aline

    2017-09-11

    The impact of acid/base properties (determined by adsorption microcalorimetry) of various catalysts on the cross-aldolization of acetaldehyde and formaldehyde leading to acrolein was methodically studied in oxidizing conditions starting from a mixture of methanol and ethanol. The aldol condensation and further dehydration to acrolein were carried out on catalysts presenting various acid/base properties (MgO, Mg-Al oxides, Mg/SiO 2 , NbP, and heteropolyanions on silica, HPA/SiO 2 ). Thermodynamic calculations revealed that cross-aldolization is always favored compared with self-aldolization of acetaldehyde, which leads to crotonaldehyde formation. The presence of strong basic sites is shown to be necessary, but a too high amount drastically increases CO x production. On strong acid sites, production of acrolein and carbon oxides (CO x ) does not increase with temperature. The optimal catalyst for this process should be amphoteric with a balanced acid/base cooperation of medium strength sites and a small amount (150 kJ mol -1 ). © 2017 Wiley-VCH Verlag GmbH & Co. KGaA, Weinheim.

  20. Sustainable Production of o-Xylene from Biomass-Derived Pinacol and Acrolein.

    Science.gov (United States)

    Hu, Yancheng; Li, Ning; Li, Guangyi; Wang, Aiqin; Cong, Yu; Wang, Xiaodong; Zhang, Tao

    2017-07-21

    o-Xylene (OX) is a large-volume commodity chemical that is conventionally produced from fossil fuels. In this study, an efficient and sustainable two-step route is used to produce OX from biomass-derived pinacol and acrolein. In the first step, the phosphotungstic acid (HPW)-catalyzed pinacol dehydration in 1-ethyl-3-methylimidazolium chloride ([emim]Cl) selectively affords 2,3-dimethylbutadiene. The high selectivity of this reaction can be ascribed to the H-bonding interaction between Cl - and the hydroxy group of pinacol. The stabilization of the carbocation intermediate by the surrounding anion Cl - may be another reason for the high selectivity. Notably, the good reusability of the HPW/[emim]Cl system can reduce the waste output and production cost. In the second step, OX is selectively produced by a Diels-Alder reaction of 2,3-dimethylbutadiene and acrolein, followed by a Pd/C-catalyzed decarbonylation/aromatization cascade in a one-pot fashion. The sustainable two-step process efficiently produces renewable OX in 79 % overall yield. Analogously, biomass-derived crotonaldehyde and pinacol can also serve as the feedstocks for the production of 1,2,4-trimethylbenzene. © 2017 Wiley-VCH Verlag GmbH & Co. KGaA, Weinheim.

  1. A Potential Role for Acrolein in Neutrophil-Mediated Chronic Inflammation.

    Science.gov (United States)

    Noerager, Brett D; Xu, Xin; Davis, Virginia A; Jones, Caleb W; Okafor, Svetlana; Whitehead, Alicia; Blalock, J Edwin; Jackson, Patricia L

    2015-12-01

    Neutrophils (PMNs) are key mediators of inflammatory processes throughout the body. In this study, we investigated the role of acrolein, a highly reactive aldehyde that is ubiquitously present in the environment and produced endogenously at sites of inflammation, in mediating PMN-mediated degradation of collagen facilitating proline-glycine-proline (PGP) production. We treated peripheral blood neutrophils with acrolein and analyzed cell supernatants and lysates for matrix metalloproteinase-9 (MMP-9) and prolyl endopeptidase (PE), assessed their ability to break down collagen and release PGP, and assayed for the presence of leukotriene A4 hydrolase (LTA4H) and its ability to degrade PGP. Acrolein treatment induced elevated production and functionality of collagen-degrading enzymes and generation of PGP fragments. Meanwhile, LTA4H levels and triaminopeptidase activity declined with increasing concentrations of acrolein thereby sparing PGP from enzymatic destruction. These findings suggest that acrolein exacerbates the acute inflammatory response mediated by neutrophils and sets the stage for chronic pulmonary and systemic inflammation.

  2. The Effects of Acrolein on the Thioredoxin System: Implications for Redox-Sensitive Signaling

    Science.gov (United States)

    Myers, Charles R.; Myers, Judith M.; Kufahl, Timothy D.; Forbes, Rachel; Szadkowski, Adam

    2012-01-01

    The reactive aldehyde acrolein is a ubiquitous environmental pollutant and is also generated endogenously. It is a strong electrophile and reacts rapidly with nucleophiles including thiolates. This review focuses on the effects of acrolein on thioredoxin reductase (TrxR) and thioredoxin (Trx), which are major regulators of intracellular protein thiol redox balance. Acrolein causes irreversible effects on TrxR and Trx, which are consistent with the formation of covalent adducts to selenocysteine and cysteine residues that are key to their activity. TrxR and Trx are more sensitive than some other redox-sensitive proteins, and their prolonged inhibition could disrupt a number of redox-sensitive functions in cells. Among these effects are the oxidation of peroxiredoxins and the activation of apoptosis signal regulating kinase (ASK1). ASK1 promotes MAP kinase activation, and p38 activation contributes to apoptosis and a number of other acrolein-induced stress responses. Overall, the disruption of the TrxR/Trx system by acrolein could be significant early and prolonged events that affects many aspects of redox-sensitive signaling and oxidant stress. PMID:21812108

  3. Chitosan nanoparticle-based neuronal membrane sealing and neuroprotection following acrolein-induced cell injury

    Directory of Open Access Journals (Sweden)

    Shi Riyi

    2010-01-01

    Full Text Available Abstract Background The highly reactive aldehyde acrolein is a very potent endogenous toxin with a long half-life. Acrolein is produced within cells after insult, and is a central player in slow and progressive "secondary injury" cascades. Indeed, acrolein-biomolecule complexes formed by cross-linking with proteins and DNA are associated with a number of pathologies, especially central nervous system (CNS trauma and neurodegenerative diseases. Hydralazine is capable of inhibiting or reducing acrolein-induced damage. However, since hydralazine's principle activity is to reduce blood pressure as a common anti-hypertension drug, the possible problems encountered when applied to hypotensive trauma victims have led us to explore alternative approaches. This study aims to evaluate such an alternative - a chitosan nanoparticle-based therapeutic system. Results Hydralazine-loaded chitosan nanoparticles were prepared using different types of polyanions and characterized for particle size, morphology, zeta potential value, and the efficiency of hydralazine entrapment and release. Hydralazine-loaded chitosan nanoparticles ranged in size from 300 nm to 350 nm in diameter, and with a tunable, or adjustable, surface charge. Conclusions We evaluated the utility of chitosan nanoparticles with an in-vitro model of acrolein-mediated cell injury using PC -12 cells. The particles effectively, and statistically, reduced damage to membrane integrity, secondary oxidative stress, and lipid peroxidation. This study suggests that a chitosan nanoparticle-based therapy to interfere with "secondary" injury may be possible.

  4. Time and dose effects of cigarette smoke and acrolein on protein carbonyl formation in HaCaT keratinocytes.

    Science.gov (United States)

    Avezov, K; Reznick, A Z; Aizenbud, D

    2015-01-01

    Cigarette smoke (CS) is an important environmental source of human exposure to a highly toxic and chemically active α,β-unsaturated aldehyde: acrolein. It is capable of causing protein carbonylation and dysfunction, especially in oral tissues of smokers, constantly exposed to CS toxic constituents. The foremost damage is considered to be cumulative, but even a short exposure can be potentially harmful. The objectives of the current study were to examine the short time and dose effects of direct CS and acrolein exposure on intracellular protein carbonylation in epithelial cells. HaCaT-keratinocytes were exposed to different doses of acrolein and whole phase CS using a unique smoking simulator apparatus that mimics the exposure in smokers. The rate of intracellular protein carbonyl modification was examined 10-60 min after the exposure by Western blot. In addition, the effect of pre-incubation with a thiol scavenger N-acetylcysteine (NAC) was also assessed. We found that intracellular protein carbonyls increased as fast as 10 min after CS exposure and their concentration doubled after 20 min, with a slight elevation afterwards. Also, carbonyl levels increased gradually as CS and acrolein doses were elevated. Addition of 1 mM NAC neutralized part of the damage. We conclude that CS and acrolein intracellular protein carbonylation is dose- and time- dependent. Even a short time exposure to CS and its aldehydic constituents can be potentially harmful.

  5. Acrolein enhances epigenetic modifications, FasL expression and hepatocyte toxicity induced by anti-HIV drug Zidovudine.

    Science.gov (United States)

    Ghare, Smita S; Donde, Hridgandh; Chen, Wei-Yang; Barker, David F; Gobejishvilli, Leila; McClain, Craig J; Barve, Shirish S; Joshi-Barve, Swati

    2016-09-01

    Zidovudine (AZT) remains the mainstay of antiretroviral therapy against HIV in resource-poor countries; however, its use is frequently associated with hepatotoxicity. Not all HIV patients on AZT develop hepatotoxicity, and the determining factors are unclear. Alcohol consumption and cigarette smoking are known risk factors for HIV hepatotoxicity, and both are significant sources of acrolein, a highly reactive and toxic aldehyde. This study examines the potential hepatotoxic interactions between acrolein and AZT. Our data demonstrate that acrolein markedly enhanced AZT-induced transcriptionally permissive histone modifications (H3K9Ac and H3K9Me3) allowing the recruitment of transcription factor NF-kB and RNA polymerase II at the FasL gene promoter, resulting in FasL upregulation and apoptosis in hepatocytes. Notably, the acrolein scavenger, hydralazine prevented these promoter-associated epigenetic changes and inhibited FasL upregulation and apoptosis induced by the combination of AZT and acrolein, as well as AZT alone. Our data strongly suggest that acrolein enhancement of promoter histone modifications and FasL upregulation are major pathogenic mechanisms driving AZT-induced hepatotoxicity. Moreover, these data also indicate the therapeutic potential of hydralazine in mitigating AZT hepatotoxicity. Copyright © 2016 Elsevier B.V. All rights reserved.

  6. Acrolein contributes to TRPA1 up-regulation in peripheral and central sensory hypersensitivity following spinal cord injury.

    Science.gov (United States)

    Park, Jonghyuck; Zheng, Lingxing; Acosta, Glen; Vega-Alvarez, Sasha; Chen, Zhe; Muratori, Breanne; Cao, Peng; Shi, Riyi

    2015-12-01

    Acrolein, an endogenous aldehyde, has been shown to be involved in sensory hypersensitivity after rat spinal cord injury (SCI), for which the pathogenesis is unclear. Acrolein can directly activate a pro-algesic transient receptor protein ankyrin 1 (TRPA1) channel that exists in sensory neurons. Both acrolein and TRPA1 mRNA are elevated post SCI, which contributes to the activation of TRPA1 by acrolein and consequently, neuropathic pain. In the current study, we further showed that, post-SCI elevation of TRPA1 mRNA exists not only in dorsal root ganglias but also in both peripheral (paw skin) and central endings of primary afferent nerves (dorsal horn of spinal cord). This is the first indication that pain signaling can be over-amplified in the peripheral skin by elevated expressions of TRPA1 following SCI, in addition over-amplification previously seen in the spinal cord and dorsal root ganglia. Furthermore, we show that acrolein alone, in the absence of physical trauma, could lead to the elevation of TRPA1 mRNA at various locations when injected to the spinal cord. In addition, post-SCI elevation of TRPA1 mRNA could be mitigated using acrolein scavengers. Both of these attributes support the critical role of acrolein in elevating TRPA1 expression through gene regulation. Taken together, these data indicate that acrolein is likely a critical causal factor in heightening pain sensation post-SCI, through both the direct binding of TRPA1 receptor, and also by boosting the expression of TRPA1. Finally, our data also further support the notion that acrolein scavenging may be an effective therapeutic approach to alleviate neuropathic pain after SCI. We propose that the trauma-mediated elevation of acrolein causes neuropathic pain through at least two mechanisms: acrolein stimulates the production of transient receptor protein ankyrin 1 (TRPA1) in both central and peripheral locations, and it activates TRPA1 channels directly. Therefore, acrolein appears to be a critical

  7. Ambient concentrations of aldehydes in relation to Beijing Olympic air pollution control measures

    Science.gov (United States)

    Gong, J. C.; Zhu, T.; Hu, M.; Zhang, L. W.; Cheng, H.; Zhang, L.; Tong, J.; Zhang, J.

    2010-08-01

    Aldehydes are ubiquitous constituents of the atmosphere. Their concentrations are elevated in polluted urban atmospheres. The present study was carried out to characterize three aldehydes of most health concern (formaldehyde, acetaldehyde, and acrolein) in a central Beijing site in the summer and early fall of 2008 (from June to October). Measurements were made before, during, and after the Beijing Olympics to examine whether the air pollution control measures implemented to improve Beijing's air quality during the Olympics had any impact on concentrations of the three aldehydes. Average concentrations of formaldehyde, acetaldehyde and acrolein were 29.34 ± 15.12 μg/m3, 27.09 ± 15.74 μg/m3 and 2.32 ± 0.95 μg/m3, respectively, for the entire period of measurements, all being the highest among the levels measured in cities around the world in photochemical smog seasons. Among the three measured aldehydes, only acetaldehyde had a substantially reduced mean concentration during the Olympic air pollution control period compared to the pre-Olympic period. Formaldehyde and acrolein followed the changing pattern of temperature and were each significantly correlated with ozone (a secondary product of photochemical reactions). In contrast, acetaldehyde was significantly correlated with several pollutants emitted mainly from local emission sources (e.g., NO2, CO, and PM2.5). These findings suggest that local direct emissions had a larger impact on acetaldehyde than formaldehyde and acrolein.

  8. Acrolein increases macrophage atherogenicity in association with gut microbiota remodeling in atherosclerotic mice: protective role for the polyphenol-rich pomegranate juice.

    Science.gov (United States)

    Rom, Oren; Korach-Rechtman, Hila; Hayek, Tony; Danin-Poleg, Yael; Bar, Haim; Kashi, Yechezkel; Aviram, Michael

    2017-04-01

    The unsaturated aldehyde acrolein is pro-atherogenic, and the polyphenol-rich pomegranate juice (PJ), known for its anti-oxidative/anti-atherogenic properties, inhibits macrophage foam cell formation, the hallmark feature of early atherosclerosis. This study aimed to investigate two unexplored areas of acrolein atherogenicity: macrophage lipid metabolism and the gut microbiota composition. The protective effects of PJ against acrolein atherogenicity were also evaluated. Atherosclerotic apolipoprotein E-deficient (apoE -/- ) mice that were fed acrolein (3 mg/kg/day) for 1 month showed significant increases in serum and aortic cholesterol, triglycerides, and lipid peroxides. In peritoneal macrophages isolated from the mice and in J774A.1 cultured macrophages, acrolein exposure increased intracellular oxidative stress and stimulated cholesterol and triglyceride accumulation via enhanced rates of their biosynthesis and over-expression of key regulators of cellular lipid biosynthesis: sterol regulatory element-binding proteins (SREBPs), 3-hydroxy-3-methyl-glutaryl-CoA reductase (HMGCR), and diacylglycerol acyltransferase1 (DGAT1). Acrolein-fed mice demonstrated a major shift in the gut microbiota composition, including a significant phylum-level change in increased Firmicutes and decreased Bacteroidetes. At the family level, acrolein significantly increased the prevalence of Ruminococcaceae and Lachnospiraceae of which the Coprococcus genus was significantly and positively correlated with serum, aortic and macrophage lipid levels and peroxidation. The pro-atherogenic effects of acrolein on serum, aortas, macrophages, and the gut microbiota were substantially abolished by PJ. In conclusion, these findings provide novel mechanisms by which acrolein increases macrophage lipid accumulation and alters the gut microbiota composition in association with enhanced atherogenesis. Moreover, PJ was found as an effective strategy against acrolein atherogenicity.

  9. Protective Effects of Olive Leaf Extract on Acrolein-Exacerbated Myocardial Infarction via an Endoplasmic Reticulum Stress Pathway

    Directory of Open Access Journals (Sweden)

    Yuyu Xu

    2018-02-01

    Full Text Available Many studies reported that air pollution particulate matter (PM exposure was associated with myocardial infarction (MI. Acrolein representing the unsaturated aldehydes, the main component of PM, derives from the incomplete combustion of wood, plastic, fossil fuels and the main constitute of cigarette smoking. However, the effect of acrolein on MI remains not that clear. In the current study, the effect of acrolein-exacerbated MI was investigated. In vivo, male Sprague–Dawley rats received olive leaf extract (OLE followed by acrolein, then isoprenaline (ISO was received by subcutaneous injection to induce MI. Results showed that the expression levels of GRP78 and CHOP, two major components of endoplasmic reticulum (ER stress were higher in the combination of acrolein and ISO than those in ISO treatment. The apoptosis marker, Bax, was also higher while the anti-apoptosis indicator, Bcl2 expression was lower both at protein and mRNA levels in the combination group. Also, the acrolein-protein adducts and myocardial pathological damage increased in the combination of acrolein and ISO relative to the ISO treatment. Besides, cardiac parameters, ejection fraction (EF and fractional shortening (FS were reduced more significantly when acrolein was added than in ISO treatment. Interestingly, all the changes were able to be ameliorated by OLE. Since hydroxytyrosol (HT and oleuropein (OP were the main components in OLE, we next investigated the effect of HT and OP on cardiomyocyte H9c2 cell apoptosis induced by acrolein through ER stress and Bax pathway. Results showed that GRP78, CHOP and Bax expression were upregulated, while Bcl2 expression was downregulated both at the protein and mRNA levels, when the H9c2 cells were treated with acrolein. In addition, pretreatment with HT can reverse the expression of GRP78, CHOP, Bax and Bcl2 on the protein and mRNA levels, while there was no effect of OP on the expression of GRP78 and CHOP on the mRNA levels

  10. Mechanism of catalytic action of oxide systems in reactions of aldehyde oxidation to carboxylic acids

    International Nuclear Information System (INIS)

    Andrushkevich, T.V.

    1997-01-01

    Mechanism of selective action of oxide catalysts (on the base of V 2 O 4 , MoO 3 ) of aldehyde oxidation to acids is considered, reaction acrolein oxidation to acrylic acid is taken as an example. Multistage mechanism of the process is established; it involves consequent transformation of coordination-bonded aldehyde into carbonyl-bonded aldehyde and symmetric carboxylate. Principles of active surface construction are formulated, they take into account the activity of stabilization center of concrete intermediate compound and bond energy of oxygen with surface. (author)

  11. Melatonin suppresses acrolein-induced IL-8 production in human pulmonary fibroblasts.

    Science.gov (United States)

    Kim, Gun-Dong; Lee, Seung Eun; Kim, Tae-Ho; Jin, Young-Ho; Park, Yong Seek; Park, Cheung-Seog

    2012-04-01

    Cigarette smoke (CS) causes harmful alterations in the lungs and airway structures and functions that characterize chronic obstructive pulmonary disease (COPD). In addition to COPD, active cigarette smoking causes other respiratory diseases and diminishes health status. Furthermore, recent studies show that, α, β-unsaturated aldehyde acrolein in CS induces the production of interleukin (IL)-8, which is known to be related to bronchitis, rhinitis, pulmonary fibrosis, and asthma. In addition, lung and pulmonary fibroblasts secrete IL-8, which has a chemotactic effect on leukocytes, and which in turn, play a critical role in lung inflammation. On the other hand, melatonin regulates circadian rhythm homeostasis in humans and has many other effects, which include antioxidant and anti-inflammatory effects, as demonstrated by the reduced expressions of iNOS, IL-1β, and IL-6 and increased glutathione (GSH) and superoxide dismutase activities. In this study, we investigated whether melatonin suppresses acrolein-induced IL-8 secretion in human pulmonary fibroblasts (HPFs). It was found that acrolein-induced IL-8 production was accompanied by increased levels of phosphorylation of Akt and extracellular signal-regulated kinases (ERK1/2) in HPFs, and that melatonin suppressed IL-8 production in HPFs. These results suggest that melatonin suppresses acrolein-induced IL-8 production via ERK1/2 and phosphatidylinositol 3-kinase (PI3K)/Akt signal inhibition in HPFs. © 2011 John Wiley & Sons A/S.

  12. Molecular mechanisms of acrolein-mediated myelin destruction in CNS trauma and disease

    Science.gov (United States)

    Shi, Riyi; Page, Jessica; Tully, Melissa

    2016-01-01

    Myelin is a critical component of the nervous system facilitating efficient propagation of electrical signals and thus communication between the central and peripheral nervous systems and organ systems they innervate throughout the body. In instances of neurotrauma and neurodegenerative disease, injury to myelin is a prominent pathological feature responsible for conduction deficits and leaves axons vulnerable to damage from noxious compounds. Although the pathological mechanisms underlying myelin loss have yet to be fully characterized, oxidative stress appears to play a prominent role. Specifically, acrolein, a neurotoxic aldehyde that is both a product and instigator of oxidative stress, has been observed in studies to elicit demyelination through calcium-independent and -dependent mechanisms and also by affecting glutamate uptake and promoting excitotoxicity. Furthermore, pharmacological scavenging of acrolein has demonstrated a neuroprotective effect in animal disease models by conserving myelin structural integrity and alleviating functional deficits. This evidence is indicative that acrolein may be a key culprit of myelin damage while acrolein scavenging could potentially be a promising therapeutic approach for patients suffering from nervous system trauma and disease. PMID:25879847

  13. Acrolein induces Hsp72 via both PKCdelta/JNK and calcium signaling pathways in human umbilical vein endothelial cells.

    Science.gov (United States)

    Misonou, Yoshiko; Takahashi, Motoko; Park, Yong Seek; Asahi, Michio; Miyamoto, Yasuhide; Sakiyama, Haruhiko; Cheng, Xinyao; Taniguchi, Naoyuki

    2005-05-01

    Acrolein is a highly electrophilic alpha,beta-unsaturated aldehydes to which humans are exposed in a variety of environment situations and is also a product of lipid peroxidation. Increased levels of unsaturated aldehydes play an important role in the pathogenesis of a number of human diseases such as Alzheimer's disease, atherosclerosis and diabetes. A number of studies have reported that acrolein evokes downstream signaling via an elevation in cellular oxidative stress. Here, we report that low concentrations of acrolein induce Hsp72 in human umbilical vein endothelial cells (HUVEC) and that both the PKCdelta/JNK pathway and calcium pathway were involved in the induction. The findings confirm that the production of reactive oxygen species (ROS) is not directly involved in the pathway. The induction of Hsp72 was not observed in other cells such as smooth muscle cells (SMC) or COS-1 cells. The results suggest that HUVEC have a unique defense system against cell damage by acrolein in which Hsp72 is induced via activation of both the PKCd/JNK and the calcium pathway.

  14. Update of the exploratory report Acrolein

    NARCIS (Netherlands)

    Slooff W; Bont PFH; Janus JA; Pronk MEJ; Ros JPM; ECO; PPCbv; ACT; LAE

    1994-01-01

    The report is an update of the exploratory report acrolein (Slooff et al., 1991) that served as a basis for the discussion during the exploratory meeting on acrolein in March 1992. The meeting supported the conclusion that priority should be given to the compartment air and to the risks to humans.

  15. Anthocyanins Protect SK-N-SH Cells Against Acrolein-Induced Toxicity by Preserving the Cellular Redox State.

    Science.gov (United States)

    Belkacemi, Abdenour; Ramassamy, Charles

    2016-01-01

    In Alzheimer's disease (AD) and in mild cognitive impairment (MCI) patients, by-products of lipid peroxidation such as acrolein accumulated in vulnerable regions of the brain. We have previously shown that acrolein is a highly reactive and neurotoxic aldehyde and its toxicity involves the alteration of several redox-sensitive pathways. Recently, protein-conjugated acrolein in cerebrospinal fluid has been proposed as a biomarker to distinguish between MCI and AD. With growing evidence of the early involvement of oxidative stress in AD etiology, one would expect that a successful therapy should prevent brain oxidative damage. In this regard, several studies have demonstrated that polyphenol-rich extracts exert beneficial effect on cognitive impairment and oxidative stress. We have recently demonstrated the efficacy of an anthocyanin formulation (MAF14001) against amyloid-β-induced oxidative stress. The aim of this study is to investigate the neuroprotective effect of MAF14001 as a mixture of anthocyanins, a particular class of polyphenols, against acrolein-induced oxidative damage in SK-N-SH neuronal cells. Our results demonstrated that MAF14001, from 5μM, was able to efficiently protect SK-N-SH cells against acrolein-induced cell death. MAF14001 was able to lower reactive oxygen species and protein carbonyl levels induced by acrolein. Moreover, MAF1401 prevented glutathione depletion and positively modulated, in the presence of acrolein, some oxidative stress-sensitive pathways including the transcription factors NF-κB and Nrf2, the proteins γ-GCS and GSK3β, and the protein adaptator p66Shc. Along with its proven protective effect against amyloid-β toxicity, these results demonstrate that MAF14001 could target multiple mechanisms and could be a promising agent for AD prevention.

  16. Acrolein Exposure in U.S. Tobacco Smokers and Non-Tobacco Users: NHANES 2005-2006.

    Science.gov (United States)

    Alwis, K Udeni; deCastro, B Rey; Morrow, John C; Blount, Benjamin C

    2015-12-01

    Acrolein is a highly reactive α,β unsaturated aldehyde and respiratory irritant. Acrolein is formed during combustion (e.g., burning tobacco or biomass), during high-temperature cooking of foods, and in vivo as a product of oxidative stress and polyamine metabolism. No biomonitoring reference data have been reported to characterize acrolein exposure for the U.S. Our goals were to a) evaluate two acrolein metabolites in urine--N-acetyl-S-(3-hydroxypropyl)-L-cysteine (3HPMA) and N-acetyl-S-(2-carboxyethyl)-L-cysteine (CEMA)--as biomarkers of exposure to acrolein for the U.S. population by age, sex, race, and smoking status; and b) assess tobacco smoke as a predictor of acrolein exposure. We analyzed urine from National Health and Nutrition Examination Survey (NHANES 2005-2006) participants ≥ 12 years old (n = 2,866) for 3HPMA and CEMA using ultra-high-performance liquid chromatography coupled with electrospray ionization tandem mass spectrometry (UPLC/ESI-MSMS). Sample-weighted linear regression models stratified for non-tobacco users versus tobacco smokers (as defined by serum cotinine and self-report) characterized the association of urinary 3HPMA and CEMA with tobacco smoke exposure, adjusting for urinary creatinine, sex, age, and race/ethnicity. 3HPMA and CEMA levels were higher among tobacco smokers (cigarettes, cigars, and pipe users) than among non-tobacco users. The median 3HPMA levels for tobacco smokers and non-tobacco users were 1,089 and 219 μg/g creatinine, respectively. Similarly, median CEMA levels were 203 μg/g creatinine for tobacco smokers and 78.8 μg/g creatinine for non-tobacco users. Regression analysis showed that serum cotinine was a significant positive predictor (p acrolein exposure in the U.S. population.

  17. Acrolein—an α,ß-Unsaturated Aldehyde: A Review of Oral Cavity Exposure and Oral Pathology Effects

    Directory of Open Access Journals (Sweden)

    Dror Aizenbud

    2016-07-01

    Full Text Available Acrolein is a highly reactive unsaturated aldehyde widely present in the environment, particularly as a product of tobacco smoke. Our previous studies indicated the adverse consequences of even short-term acrolein exposure and proposed a molecular mechanism of its potential harmful effect on oral cavity keratinocytic cells. In this paper we chose to review the broad spectrum of acrolein sources such as pollution, food, and smoking. Consequently, in this paper we consider a high level of oral exposure to acrolein through these sources and discuss the noxious effects it has on the oral cavity including on salivary quality and contents, oral resistance to oxidative stress, and stress mechanism activation in a variety of oral cells.

  18. Anticancer system created by acrolein and hydroxyl radical generated in enzymatic oxidation of spermine and other biochemical reactions.

    Science.gov (United States)

    Alarcon, R A

    2012-10-01

    A hypothesis suggesting the existence of a ubiquitous physiological anticancer system created by two highly reactive oxidative stress inducers with anticancer properties, acrolein and hydroxyl radical, is reported in this communication. Both components can originate separately or together in several biochemical interactions, among them, the enzymatic oxidation of the polyamine spermine, which appear to be their main source. The foundations of this hypothesis encompass our initial search for growth-inhibitors or anticancer compounds in biological material leading to the isolation of spermine, a polyamine that became highly cytotoxic through the generation of acrolein, when enzymatically oxidized. Findings complemented with pertinent literature data by other workers and observed anticancer activities by sources capable of producing acrolein and hydroxyl radical. This hypothesis obvious implication: spermine enzymatic oxidations or other biochemical interactions that would co-generate acrolein and hydroxyl radical, the anticancer system components, should be tried as treatments for any given cancer. The biochemical generation of acrolein observed was totally unexpected, since this aldehyde was known; as a very toxic and highly reactive xenobiotic chemical produced in the pyrolysis of fats and other organic material, found as an atmospheric pollutant, in tobacco smoke and car emissions, and mainly used as a pesticide or aquatic herbicide. Numerous studies on acrolein, considered after our work a biological product, as well, followed. In them, acrolein widespread presence, its effects on diverse cellular proteins, such as, growth factors, and its anticancer activities, were additionally reported. Regarding hydroxyl radical, the second component of the proposed anticancer system, and another cytotoxic product in normal cell metabolism, it co-generates with acrolein in several biochemical interactions, occurrences suggesting that these products might jointly fulfill some

  19. Inhibition of acrolein-stimulated MUC5AC production by fucoidan in human bronchial epithelial cells.

    Science.gov (United States)

    Pokharel, Yuba Raj; Yoon, Se Young; Kim, Sang Kyum; Li, Jian-Dong; Kang, Keon Wook

    2008-10-01

    Fucoidan, a marine sulfated polysaccharide has both antithrombotic and anti-inflammatory effects. We determined the effect of fucoidan on MUC5AC expression in a human bronchial epithelial cell line, NCI-H292. Reverse transcription-polymerase chain reaction (RT-PCR) analysis showed that fucoidan inhibited MUC5AC expression and protein secretion in cells stimulated with acrolein, a toxic aldehyde present in tobacco smoke. The activation of both nuclear factor-kappa B (NF-kappa B) and activator protein 1 (AP-1) are key steps in the transcriptional activation of MUC5AC. We found that the acrolein-mediated transactivation of MUC5AC was selectively dependent on AP-1 activation and was suppressed by fucoidan. Fucoidan-induced AP-1 inhibition and MUC5AC repression might be associated with fucoidan's protective effects against respiratory diseases.

  20. Protein modification by acrolein: Formation and stability of cysteine adducts

    OpenAIRE

    Cai, Jian; Bhatnagar, Aruni; Pierce, William M.

    2009-01-01

    The toxicity of the ubiquitous pollutant and endogenous metabolite, acrolein, is due in part to covalent protein modifications. Acrolein reacts readily with protein nucleophiles via Michael addition and Schiff base formation. Potential acrolein targets in protein include the nucleophilic side chains of cysteine, histidine, and lysine residues as well as the free amino terminus of proteins. Although cysteine is the most acrolein-reactive residue, cysteine-acrolein adducts are difficult to iden...

  1. Acrolein-induced activation of mitogen-activated protein kinase signaling is mediated by alkylation of thioredoxin reductase and thioredoxin 1.

    Science.gov (United States)

    Randall, Matthew J; Spiess, Page C; Hristova, Milena; Hondal, Robert J; van der Vliet, Albert

    2013-01-01

    Cigarette smoking remains a major health concern worldwide, and many of the adverse effects of cigarette smoke (CS) can be attributed to its abundant electrophilic aldehydes, such as acrolein (2-propenal). Previous studies indicate that acrolein readily reacts with thioredoxin reductase 1 (TrxR1), a critical enzyme involved in regulation of thioredoxin (Trx)-mediated redox signaling, by alkylation at its selenocysteine (Sec) residue. Because alkylation of Sec within TrxR1 has significant implications for its enzymatic function, we explored the potential importance of TrxR1 alkylation in acrolein-induced activation or injury of bronchial epithelial cells. Exposure of human bronchial epithelial HBE1 cells to acrolein (1-30 μM) resulted in dose-dependent loss of TrxR thioredoxin reductase activity, which coincided with its alkylation, as determined by biotin hydrazide labeling, and was independent of initial GSH status. To test the involvement of TrxR1 in acrolein responses in HBE1 cells, we suppressed TrxR1 using siRNA silencing or augmented TrxR1 by cell supplementation with sodium selenite. Acrolein exposure of HBE1 cells induced dose-dependent activation of the MAP kinases, extracellular regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38, and activation of JNK was markedly enhanced after selenite-mediated induction of TrxR1, and was associated with increased alkylation of TrxR1. Conversely, siRNA silencing of TrxR1 significantly suppressed the ability of acrolein to activate JNK, and also appeared to attenuate acrolein-dependent activation of ERK and p38. Alteration of initial TrxR1 levels by siRNA or selenite supplementation also affected initial Trx1 redox status and acrolein-mediated alkylation of Trx1, but did not significantly affect acrolein-mediated activation of HO-1 or cytotoxicity. Collectively, our findings indicate that alkylation of TrxR1 and/or Trx1 may contribute directly to acrolein-mediated activation of MAP kinases such as JNK, and

  2. Acrolein-induced activation of mitogen-activated protein kinase signaling is mediated by alkylation of thioredoxin reductase and thioredoxin 1

    Directory of Open Access Journals (Sweden)

    Matthew J. Randall

    2013-01-01

    Full Text Available Cigarette smoking remains a major health concern worldwide, and many of the adverse effects of cigarette smoke (CS can be attributed to its abundant electrophilic aldehydes, such as acrolein (2-propenal. Previous studies indicate that acrolein readily reacts with thioredoxin reductase 1 (TrxR1, a critical enzyme involved in regulation of thioredoxin (Trx-mediated redox signaling, by alkylation at its selenocysteine (Sec residue. Because alkylation of Sec within TrxR1 has significant implications for its enzymatic function, we explored the potential importance of TrxR1 alkylation in acrolein-induced activation or injury of bronchial epithelial cells. Exposure of human bronchial epithelial HBE1 cells to acrolein (1–30 μM resulted in dose-dependent loss of TrxR thioredoxin reductase activity, which coincided with its alkylation, as determined by biotin hydrazide labeling, and was independent of initial GSH status. To test the involvement of TrxR1 in acrolein responses in HBE1 cells, we suppressed TrxR1 using siRNA silencing or augmented TrxR1 by cell supplementation with sodium selenite. Acrolein exposure of HBE1 cells induced dose-dependent activation of the MAP kinases, extracellular regulated kinase (ERK, c-Jun N-terminal kinase (JNK, and p38, and activation of JNK was markedly enhanced after selenite-mediated induction of TrxR1, and was associated with increased alkylation of TrxR1. Conversely, siRNA silencing of TrxR1 significantly suppressed the ability of acrolein to activate JNK, and also appeared to attenuate acrolein-dependent activation of ERK and p38. Alteration of initial TrxR1 levels by siRNA or selenite supplementation also affected initial Trx1 redox status and acrolein-mediated alkylation of Trx1, but did not significantly affect acrolein-mediated activation of HO-1 or cytotoxicity. Collectively, our findings indicate that alkylation of TrxR1 and/or Trx1 may contribute directly to acrolein-mediated activation of MAP kinases

  3. Acrolein-induced activation of mitogen-activated protein kinase signaling is mediated by alkylation of thioredoxin reductase and thioredoxin 1☆☆☆

    Science.gov (United States)

    Randall, Matthew J.; Spiess, Page C.; Hristova, Milena; Hondal, Robert J.; van der Vliet, Albert

    2013-01-01

    Cigarette smoking remains a major health concern worldwide, and many of the adverse effects of cigarette smoke (CS) can be attributed to its abundant electrophilic aldehydes, such as acrolein (2-propenal). Previous studies indicate that acrolein readily reacts with thioredoxin reductase 1 (TrxR1), a critical enzyme involved in regulation of thioredoxin (Trx)-mediated redox signaling, by alkylation at its selenocysteine (Sec) residue. Because alkylation of Sec within TrxR1 has significant implications for its enzymatic function, we explored the potential importance of TrxR1 alkylation in acrolein-induced activation or injury of bronchial epithelial cells. Exposure of human bronchial epithelial HBE1 cells to acrolein (1–30 μM) resulted in dose-dependent loss of TrxR thioredoxin reductase activity, which coincided with its alkylation, as determined by biotin hydrazide labeling, and was independent of initial GSH status. To test the involvement of TrxR1 in acrolein responses in HBE1 cells, we suppressed TrxR1 using siRNA silencing or augmented TrxR1 by cell supplementation with sodium selenite. Acrolein exposure of HBE1 cells induced dose-dependent activation of the MAP kinases, extracellular regulated1 kinase (ERK), c-Jun N-terminal kinase (JNK), and p38, and activation of JNK was markedly enhanced after selenite-mediated induction of TrxR1, and was associated with increased alkylation of TrxR1. Conversely, siRNA silencing of TrxR1 significantly suppressed the ability of acrolein to activate JNK, and also appeared to attenuate acrolein-dependent activation of ERK and p38. Alteration of initial TrxR1 levels by siRNA or selenite supplementation also affected initial Trx1 redox status and acrolein-mediated alkylation of Trx1, but did not significantly affect acrolein-mediated activation of HO-1 or cytotoxicity. Collectively, our findings indicate that alkylation of TrxR1 and/or Trx1 may contribute directly to acrolein-mediated activation of MAP kinases such as JNK

  4. In vitro assessment of human airway toxicity from major aldehydes in automotive emissions

    Energy Technology Data Exchange (ETDEWEB)

    Grafstroem, R.C. [Karolinska Inst., Stockholm (Sweden). Inst. of Environmental Medicine

    1997-09-01

    Automotive exhausts can significantly contribute to the levels of reactive aldehydes, including formaldehyde, acetaldehyde and acrolein, in urban air. The use of alcohols as an alternative fuel for gasoline or diesel may further increase these emissions. Since it is unclear if aldehyde inhalation may induce pathological states, including cancer, in human airways, the toxic properties of the above-mentioned aldehydes were studied in cultured target cell types. Each aldehyde modified vital cellular functions in a dose-dependent manner, and invariably inhibited growth and induced abnormal terminal differentiation. Decreases of cellular thiols and increases of intracellular Ca{sup 2+} were observed, and moreover, variable types and amounts of short-lived or persistent genetic damage were induced. The concentrations required for specified levels of a particular type of injury varied up to 10000-fold among the aldehydes. Overall, distinctive patterns of cytopathological activity were observed, which differed both qualitatively and quantitatively among the aldehydes. Finally, aldehydes inhibited DNA repair processes and increased cytotoxicity and mutagenesis in synergy with other known toxicants, indicating that aldehydes may also enhance damage by other constituents in automotive exhausts. In summary, the aldehydes, notably {sup m}u{sup M}-mM formaldehyde, caused pathological effects and induced mechanisms that relate to acute toxicity and cancer development in airway epithelial cells. Since `no-effect` levels may not exist for carcinogenic agents, the overall results support a need for elimination of aldehydes in automotive exhausts. 41 refs

  5. Acrolein Modification Impairs Key Functional Features of Rat Apolipoprotein E: Identification of Modified Sites by Mass Spectrometry

    Science.gov (United States)

    Tran, Tuyen N.; Kosaraju, Malathi G.; Tamamizu-Kato, Shiori; Akintunde, Olayemi; Zheng, Ying; Bielicki, John K.; Pinkerton, Kent; Uchida, Koji; Lee, Yuan Yu; Narayanaswami, Vasanthy

    2014-01-01

    Apolipoprotein E (apoE), an anti-atherogenic apolipoprotein, plays a significant role in the metabolism of lipoproteins. It lowers plasma lipid levels by acting as a ligand for low-density lipoprotein receptor (LDLr) family of proteins, in addition to playing a role in promoting macrophage cholesterol efflux in atherosclerotic lesions. The objective of this study is to examine the effect of acrolein modification on the structure and function of rat apoE and to determine sites and nature of modification by mass spectrometry. Acrolein is a highly reactive aldehyde, which is generated endogenously as one of the products of lipid peroxidation and is present in the environment in pollutants such as tobacco smoke and heated oils. In initial studies, acrolein-modified apoE was identified by immunoprecipitation using an acrolein-lysine specific antibody, in the plasma of ten-week old male rats that were exposed to filtered air (FA) or low doses of environmental tobacco smoke (ETS). While both groups displayed acrolein-modified apoE in the lipoprotein fraction, the ETS group had higher levels in lipid-free fraction compared to the FA group. This observation provided the rationale to further investigate the effect of acrolein modification on rat apoE at a molecular level. Treatment of recombinant rat apoE with a 10-fold molar excess of acrolein resulted in: (i) a significant decrease in lipid-binding and cholesterol efflux abilities, (ii) impairment in the LDLr- and heparin-binding capabilities, and (iii) significant alterations in the overall stability of the protein. The disruption in the functional abilities is attributed directly or indirectly to acrolein modification yielding: an aldimine adduct at K149 and K155 (+38); a propanal adduct at K135 and K138 (+56); an Nε-(3-methylpyridinium)lysine (MP-lysine) at K64, K67 and K254 (+76), and Nε-(3-formyl-3,4-dehydropiperidino)lysine (FDP-lysine) derivative at position K68 (+94), as determined by Matrix-Assisted Laser

  6. Pyrolysis of D-Glucose to Acrolein

    Science.gov (United States)

    Shen, Chong; Zhang, Igor Ying; Fu, Gang; Xu, Xin

    2011-06-01

    Despite of its great importance, the detailed molecular mechanism for carbohydrate pyrolysis remains poorly understood. We perform a density functional study with a newly developed XYG3 functional on the processes for D-glucose pyrolysis to acrolein. The most feasible reaction pathway starts from an isomerization from D-glucose to D-fructose, which then undergoes a cyclic Grob fragmentation, followed by a concerted electrocyclic dehydration to yield acrolein. This mechanism can account for the known experimental results.

  7. Acrolein-Induced Oxidative Stress and Cell Death Exhibiting Features of Apoptosis in the Yeast Saccharomyces cerevisiae Deficient in SOD1.

    Science.gov (United States)

    Kwolek-Mirek, Magdalena; Zadrąg-Tęcza, Renata; Bednarska, Sabina; Bartosz, Grzegorz

    2015-04-01

    The yeast Saccharomyces cerevisiae is a useful eukaryotic model to study the toxicity of acrolein, an important environmental toxin and endogenous product of lipid peroxidation. The study was aimed at elucidation of the cytotoxic effect of acrolein on the yeast deficient in SOD1, Cu, Zn-superoxide dismutase which is hypersensitive to aldehydes. Acrolein generated within the cell from its precursor allyl alcohol caused growth arrest and cell death of the yeast cells. The growth inhibition involved an increase in production of reactive oxygen species and high level of protein carbonylation. DNA condensation and fragmentation, exposition of phosphatidylserine at the cell surface as well as decreased dynamic of actin microfilaments and mitochondria disintegration point to the induction of apoptotic-type cell death besides necrotic cell death.

  8. Crude glycerol combustion: Particulate, acrolein, and other volatile organic emissions

    KAUST Repository

    Steinmetz, Scott; Herrington, Jason S.; Winterrowd, Chris K.; Roberts, William L.; Wendt, Jost O L; Linak, William P.

    2013-01-01

    to be formed from the low temperature thermal decomposition of glycerol. Currently, there is no known reliable method for measuring acrolein in sources. Acrolein and emissions of other volatile organic compounds were characterized through the use of a SUMMA

  9. Interaction of α,β-unsaturated aldehydes with dienes in the presence of boron trifluoride etherate

    International Nuclear Information System (INIS)

    Gramenitskaya, V.N.; Golovkina, L.S.; Orach, V.S.

    1975-01-01

    The products of the acrolein reaction with divinyl, isoprene and chloroprene catalized by BF 3 xEt 2 O are corresponding 3-cyclohexenaldehydes trimerized under the catalyst influence. Mixtures of substituted 3-cyclohexealdehydes and Δ 3 -dihydropirines were produced as results of the reaction of croton aldehyde with 1,1,3-trimethilbutadiene at high temperature as well as at 20 deg C in presence of catalyst

  10. Acrolein: An Effective Biomarker for Tissue Damage Produced from Polyamines.

    Science.gov (United States)

    Igarashi, Kazuei; Uemura, Takeshi; Kashiwagi, Keiko

    2018-01-01

    It is thought that the major factor responsible for cell damage is reactive oxygen species (ROS), but our recent studies have shown that acrolein (CH 2 =CH-CHO) produced from spermine and spermidine is more toxic than ROS. Thus, (1) the mechanism of acrolein production during brain stroke, (2) one of the mechanisms of acrolein toxicity, and (3) the role of glutathione in acrolein detoxification are described in this chapter.

  11. A model of hemorrhagic cystitis induced with acrolein in mice

    Directory of Open Access Journals (Sweden)

    C.K.L.P. Batista

    2006-11-01

    Full Text Available Acrolein is a urinary metabolite of cyclophosphamide and ifosfamide, which has been reported to be the causative agent of hemorrhagic cystitis induced by these compounds. A direct cytotoxic effect of acrolein, however, has not yet been demonstrated. In the present study, the effects of intravesical injection of acrolein and mesna, the classical acrolein chemical inhibitor, were evaluated. Male Swiss mice weighing 25 to 35 g (N = 6 per group received saline or acrolein (25, 75, 225 µg intravesically 3, 6, 12, and 24 h before sacrifice for evaluation of bladder wet weight, macroscopic and histopathological changes by Gray's criteria, and 3 and 24 h for assessment of increase in vascular permeability. In other animals, mesna was administered intravesically (2 mg or systemically (80 mg/kg 1 h before acrolein. Intravesical administration of acrolein induced a dose- and time-dependent increase in vascular permeability and bladder wet weight (within 3 h: 2.2- and 21-fold increases in bladder wet weight and Evans blue dye exuded, respectively, at doses of 75 µg/bladder, as confirmed by Gray's criteria. Pretreatment with mesna (2-mercaptoethanesulfonic acid, which interacts with acrolein resulting in an inactive compound, inhibited all changes induced by acrolein. Our results are the first demonstration that intravesical administration of acrolein induces hemorrhagic cystitis. This model of acrolein-induced hemorrhagic cystitis in mice may be an important tool for the evaluation of the mechanism by which acrolein induces bladder lesion, as well as for investigation of new uroprotective drugs.

  12. Role of Lipid Peroxidation-Derived α, β-Unsaturated Aldehydes in Vascular Dysfunction

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    Seung Eun Lee

    2013-01-01

    Full Text Available Vascular diseases are the most prominent cause of death, and inflammation and vascular dysfunction are key initiators of the pathophysiology of vascular disease. Lipid peroxidation products, such as acrolein and other α, β-unsaturated aldehydes, have been implicated as mediators of inflammation and vascular dysfunction. α, β-Unsaturated aldehydes are toxic because of their high reactivity with nucleophiles and their ability to form protein and DNA adducts without prior metabolic activation. This strong reactivity leads to electrophilic stress that disrupts normal cellular function. Furthermore, α, β-unsaturated aldehydes are reported to cause endothelial dysfunction by induction of oxidative stress, redox-sensitive mechanisms, and inflammatory changes such as induction of cyclooxygenase-2 and cytokines. This review provides an overview of the effects of lipid peroxidation products, α, β-unsaturated aldehydes, on inflammation and vascular dysfunction.

  13. Acrolein coupling on reduced TiO 2(1 1 0): The effect of surface oxidation and the role of subsurface defects

    Science.gov (United States)

    Benz, Lauren; Haubrich, Jan; Quiller, Ryan G.; Friend, Cynthia M.

    2009-04-01

    Reactions of acrolein, water, and oxygen with the vacuum-reduced surface of TiO 2(1 1 0) are reported in a temperature programmed reaction study of the interaction of an aldehydic pollutant with a reducible metal oxide. A total of 25% of the acrolein that binds to the surface is converted to products. Notably, carbon-carbon coupling occurs with 86% selectivity for formation of C 6 products: C 6H 8, identified as 1,3-cyclohexadiene, in a peak at 500 K and benzene immediately thereafter at 530 K. Acrolein is evolved from the surface in three peaks: a peak independent of coverage at 495 K, attributed to decomposition of an intermediate that is partly converted to C 6H 8; a coverage-dependent peak that shifts from 370 K (low coverage) to 260 K (high coverage), which is attributed to adsorption at 5-fold coordinated Ti sites; and a multilayer state at 160 K. Water and acrolein compete for 5-fold coordinated titanium sites when dosed sequentially. The addition of water also opens a new reaction pathway, leading to the hydrogenation of acrolein to form propanal. Water has no effect on the yield of 1,3-cyclohexadiene. Exposure of the surface to oxygen prior to acrolein dosing quenches the evolution of acrolein at 495 K and concurrently eliminates the coupling. From these results, we propose that reduced subsurface defects such as titanium ion interstitials play a role in the reactions observed here. The notion that subsurface defects may contribute to the reactivity of organic molecules over reducible oxide substrates may prove to be general.

  14. Acrolein produces nitric oxide through the elevation of intracellular calcium levels to induce apoptosis in human umbilical vein endothelial cells: implications for smoke angiopathy.

    Science.gov (United States)

    Misonou, Yoshiko; Asahi, Michio; Yokoe, Shunichi; Miyoshi, Eiji; Taniguchi, Naoyuki

    2006-03-01

    Acrolein is a highly electrophilic alpha, beta-unsaturated aldehyde, the levels of which are increased in the blood of smokers. To determine if acrolein is involved in the pathology of smoke angiopathy, the effect of acrolein on human umbilical vein endothelial cells (HUVEC) was examined. Intracellular nitric oxide (NO) levels, determined using diaminofluorescein-2 diacetate (DAF-2 DA), an NO sensitive fluorescent dye, were found to be increased after treatment in HUVEC with 10 microM acrolein. The measurement of nitrite with 2,3-diaminonaphthalene and a Western blot analysis revealed that nitrite and S-nitroso-cysteine levels were increased in a dose-dependent manner, confirming that NO production is increased by acrolein. The increase was not reduced by treatment with 10mM N-acetyl-l-cysteine (NAC), an anti-oxidant, but was reduced with 10 microM of the intracellular calcium chelator, 1,2-bis (o-aminophenoxy) ethane-N,N,N',N'-tetraacetic acid tetra (acetoxymethyl) ester. Acrolein-stimulated NO production was significantly reduced by pretreatment with 1mM N(G)-nitro-l-arginine-methyl ester (L-NAME), an NO synthase inhibitor. The cytotoxicity of acrolein was reduced by pretreatment with 10 microM 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl 3-oxide (carboxy-PTIO), an intracellular NO scavenger, or 1mM L-NAME, whereas it was not reduced by 10mM NAC, 20 microM Curcumin, another peroxide scavenger, or 100 microM Mn(III)TMPyP, a superoxide dismutase mimic. Nuclear staining and a Western blot analysis using an anti-cleaved caspase 3 antibody revealed that the reduced viability of HUVEC by acrolein was due to apoptosis, which was reversed after pretreatment with 0.1mM carboxy-PTIO or 1mM L-NAME. Thus, acrolein increases intracellular calcium production to induce intracellular NO production by a calcium-dependent NO synthase, possibly eNOS, and the excess and rapid increase in NO might lead to the apoptosis of HUVEC. These data suggest that acrolein might be

  15. Do flavouring compounds contribute to aldehyde emissions in e-cigarettes?

    Science.gov (United States)

    Farsalinos, Konstantinos E; Voudris, Vassilis

    2018-05-01

    A recent study identified up to 10,000-fold higher aldehyde emissions from flavoured compared to unflavoured e-cigarette liquids. We set to replicate this study and also test similar flavourings with a new-generation e-cigarette device. Three liquids with the highest levels of aldehyde emissions in the previous study were tested (in standard and sweetened versions) using the same e-cigarette device and puffing patterns. Additionally, similar flavourings from a different manufacturer were tested using a new-generation e-cigarette device. Unflavoured samples were also tested. Low levels of formaldehyde (8.3-62 μg/g), acetaldehyde (12.1-26.0 μg/g) and acrolein (5.4-19.4 μg/g) were detected, lower by up to 589-fold compared to the previous report. Unflavoured liquid emitted 16.1 μg/g formaldehyde, 5.6 μg/g acetaldehyde and 2.4 μg/g acrolein, significantly lower compared to 2 liquids for formaldehyde and 1 for acrolein. Emissions from the new-generation device were even lower. Aldehyde emissions from all flavoured liquids were 79-99.8% lower than smoking and lower than commonly measured indoor levels and occupational and indoor safety limits. The e-cigarettes tested herein emit very low levels of aldehydes. Some flavourings may contribute to aldehyde emissions, but the absolute levels were minimal. Validated methods should be used when analysing e-cigarette emissions. Copyright © 2018 Elsevier Ltd. All rights reserved.

  16. The formation of rats' choroidal neovascularization induced by acrolein

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    Guan-Feng Wang

    2016-04-01

    Full Text Available AIM:To investigate the formation of rats' choroidal neovascularization(CNVinduced by acrolein. METHODS:Twelve Sprague-Dawley rats were randomly divided into three groups. Acrolein 200μL(2.5 mg/kg/dwas poured into the rats' stomach for 4wk as acrolein 4wk and for 8wk as acrolein 8wk group. The same volume of fresh water was also done to the rats as the control group. Remove all eye balls and embed into paraffin with HE staining.RESLUTS:The RPE-Bruch membrane was intact with no obvious abnormality in the control group and acrolein 4wk group. Lost in the continuity of RPE and the movement of choroidal neovascularization were found in the acrolein 8wk. CONCLUSION:The long time use of acrolein can induce the formation of choroial neovascularization in rats.

  17. INTERACTION OF ALDEHYDES DERIVED FROM LIPID PEROXIDATION AND MEMBRANE PROTEINS.

    Directory of Open Access Journals (Sweden)

    Stefania ePizzimenti

    2013-09-01

    Full Text Available A great variety of compounds are formed during lipid peroxidation of polyunsaturated fatty acids of membrane phospholipids. Among them, bioactive aldehydes, such as 4-hydroxyalkenals, malondialdehyde (MDA and acrolein, have received particular attention since they have been considered as toxic messengers that can propagate and amplify oxidative injury. In the 4-hydroxyalkenal class, 4-hydroxy-2-nonenal (HNE is the most intensively studied aldehyde, in relation not only to its toxic function, but also to its physiological role. Indeed, HNE can be found at low concentrations in human tissues and plasma and participates in the control of biological processes, such as signal transduction, cell proliferation and differentiation. Moreover, at low doses, HNE exerts an anti-cancer effect, by inhibiting cell proliferation, angiogenesis, cell adhesion and by inducing differentiation and/or apoptosis in various tumor cell lines. It is very likely that a substantial fraction of the effects observed in cellular responses, induced by HNE and related aldehydes, be mediated by their interaction with proteins, resulting in the formation of covalent adducts or in the modulation of their expression and/or activity. In this review we focus on membrane proteins affected by lipid peroxidation-derived aldehydes, under physiological and pathological conditions.

  18. Threshold photoelectron spectroscopy of acetaldehyde and acrolein

    International Nuclear Information System (INIS)

    Yencha, Andrew J.; Siggel-King, Michele R.F.; King, George C.; Malins, Andrew E.R.; Eypper, Marie

    2013-01-01

    Highlights: •High-resolution threshold photoelectron spectrum of acetaldehyde. •High-resolution threshold photoelectron spectrum of acrolein. •High-resolution total photoion yield spectrum of acetaldehyde. •High-resolution total photoion yield spectrum of acrolein. •Determination of vertical ionization potentials in acetaldehyde and acrolein. -- Abstract: High-resolution (6 meV and 12 meV) threshold photoelectron (TPE) spectra of acetaldehyde and acrolein (2-propenal) have been recorded over the valence binding energy region 10–20 eV, employing synchrotron radiation and a penetrating-field electron spectrometer. These TPE spectra are presented here for the first time. All of the band structures observed in the TPE spectra replicate those found in their conventional HeI photoelectron (PE) spectra. However, the relative band intensities are found to be dramatically different in the two types of spectra that are attributed to the different dominant operative formation mechanisms. In addition, some band shapes and their vertical ionization potentials are found to differ in the two types of spectra that are associated with the autoionization of Rydberg states in the two molecules

  19. Acrolein Induces Endoplasmic Reticulum Stress and Causes Airspace Enlargement

    Science.gov (United States)

    Hanaoka, Masayuki; Natarajan, Ramesh; Kraskauskas, Donatas; Voelkel, Norbert F.

    2012-01-01

    Background Given the relative abundance and toxic potential of acrolein in inhaled cigarette smoke, it is surprising how little is known about the pulmonary and systemic effects of acrolein. Here we test the hypothesis whether systemic administration of acrolein could cause endoplasmic reticulum (ER) stress, and lung cell apoptosis, leading to the enlargement of the alveolar air spaces in rats. Methods Acute and chronic effects of intraperitoneally administered acrolein were tested. Mean alveolar airspace area was measured by using light microscopy and imaging system software. TUNEL staining and immunohistochemistry (IHC) for active caspase 3 and Western blot analysis for active caspase 3, and caspase 12 were performed to detect apoptosis. The ER-stress related gene expression in the lungs was determined by Quantitative real-time PCR analysis. Acrolein-protein adducts in the lung tissue were detected by IHC. Results Acute administration of acrolein caused a significant elevation of activated caspase 3, upregulation of VEGF expression and induced ER stress proteins in the lung tissue. The chronic administration of acrolein in rats led to emphysematous lung tissue remodeling. TUNEL staining and IHC for cleaved caspase 3 showed a large number of apoptotic septal cells in the acrolein-treated rat lungs. Chronic acrolein administration cause the endoplasmic reticulum stress response manifested by significant upregulation of ATF4, CHOP and GADd34 expression. In smokers with COPD there was a considerable accumulation of acrolein-protein adducts in the inflammatory, airway and vascular cells. Conclusions Systemic administration of acrolein causes endoplasmic reticulum stress response, lung cell apoptosis, and chronic administration leads to the enlargement of the alveolar air spaces and emphysema in rats. The substantial accumulation of acrolein-protein adducts in the lungs of COPD patients suggest a role of acrolein in the pathogenesis of emphysema. PMID:22675432

  20. Exposure to acrolein by inhalation causes platelet activation

    International Nuclear Information System (INIS)

    Sithu, Srinivas D.; Srivastava, Sanjay; Siddiqui, Maqsood A.; Vladykovskaya, Elena; Riggs, Daniel W.; Conklin, Daniel J.; Haberzettl, Petra; O'Toole, Timothy E.; Bhatnagar, Aruni; D'Souza, Stanley E.

    2010-01-01

    Acrolein is a common air pollutant that is present in high concentrations in wood, cotton, and tobacco smoke, automobile exhaust and industrial waste and emissions. Exposure to acrolein containing environmental pollutants such as tobacco smoke and automobile exhaust has been linked to the activation of the coagulation and hemostasis pathways and thereby to the predisposition of thrombotic events in human. To examine the effects of acrolein on platelets, adult male C57Bl/6 mice were subjected acute (5 ppm for 6 h) or sub-chronic (1 ppm, 6 h/day for 4 days) acrolein inhalation exposures. The acute exposure to acrolein did not cause pulmonary inflammation and oxidative stress, dyslipidemia or induce liver damage or muscle injury. Platelet GSH levels in acrolein-exposed mice were comparable to controls, but acrolein-exposure increased the abundance of protein-acrolein adducts in platelets. Platelets isolated from mice, exposed to both acute and sub-chronic acrolein levels, showed increased ADP-induced platelet aggregation. Exposure to acrolein also led to an increase in the indices of platelet activation such as the formation of platelet-leukocyte aggregates in the blood, plasma PF4 levels, and increased platelet-fibrinogen binding. The bleeding time was decreased in acrolein exposed mice. Plasma levels of PF4 were also increased in mice exposed to environmental tobacco smoke. Similar to inhalation exposure, acrolein feeding to mice also increased platelet activation and established a pro-thrombotic state in mice. Together, our data suggest that acrolein is an important contributing factor to the pro-thrombotic risk in human exposure to pollutants such as tobacco smoke or automobile exhaust, or through dietary consumption.

  1. Exposure to acrolein by inhalation causes platelet activation

    Energy Technology Data Exchange (ETDEWEB)

    Sithu, Srinivas D [Department of Physiology and Biophysics, University of Louisville, Louisville, KY 40202 (United States); Diabetes and Obesity Center, University of Louisville, Louisville, KY 40202 (United States); Srivastava, Sanjay; Siddiqui, Maqsood A; Vladykovskaya, Elena; Riggs, Daniel W; Conklin, Daniel J; Haberzettl, Petra; O' Toole, Timothy E; Bhatnagar, Aruni [Diabetes and Obesity Center, University of Louisville, Louisville, KY 40202 (United States); D' Souza, Stanley E., E-mail: sedsou01@louisville.ed [Department of Physiology and Biophysics, University of Louisville, Louisville, KY 40202 (United States)

    2010-10-15

    Acrolein is a common air pollutant that is present in high concentrations in wood, cotton, and tobacco smoke, automobile exhaust and industrial waste and emissions. Exposure to acrolein containing environmental pollutants such as tobacco smoke and automobile exhaust has been linked to the activation of the coagulation and hemostasis pathways and thereby to the predisposition of thrombotic events in human. To examine the effects of acrolein on platelets, adult male C57Bl/6 mice were subjected acute (5 ppm for 6 h) or sub-chronic (1 ppm, 6 h/day for 4 days) acrolein inhalation exposures. The acute exposure to acrolein did not cause pulmonary inflammation and oxidative stress, dyslipidemia or induce liver damage or muscle injury. Platelet GSH levels in acrolein-exposed mice were comparable to controls, but acrolein-exposure increased the abundance of protein-acrolein adducts in platelets. Platelets isolated from mice, exposed to both acute and sub-chronic acrolein levels, showed increased ADP-induced platelet aggregation. Exposure to acrolein also led to an increase in the indices of platelet activation such as the formation of platelet-leukocyte aggregates in the blood, plasma PF4 levels, and increased platelet-fibrinogen binding. The bleeding time was decreased in acrolein exposed mice. Plasma levels of PF4 were also increased in mice exposed to environmental tobacco smoke. Similar to inhalation exposure, acrolein feeding to mice also increased platelet activation and established a pro-thrombotic state in mice. Together, our data suggest that acrolein is an important contributing factor to the pro-thrombotic risk in human exposure to pollutants such as tobacco smoke or automobile exhaust, or through dietary consumption.

  2. Gut Microbial Glycerol Metabolism as an Endogenous Acrolein Source

    Directory of Open Access Journals (Sweden)

    Jianbo Zhang

    2018-01-01

    Full Text Available Acrolein is a highly reactive electrophile causing toxic effects, such as DNA and protein adduction, oxidative stress, endoplasmic reticulum stress, immune dysfunction, and membrane damage. This Opinion/Hypothesis provides an overview of endogenous and exogenous acrolein sources, acrolein’s mode of action, and its metabolic fate. Recent reports underpin the finding that gut microbial glycerol metabolism leading to the formation of reuterin is an additional source of endogenous acrolein. Reuterin is an antimicrobial multicomponent system consisting of 3-hydroxypropionaldehyde, its dimer and hydrate, and also acrolein. The major conclusion is that gut microbes can metabolize glycerol to reuterin and that this transformation occurs in vivo. Given the known toxicity of acrolein, the observation that acrolein is formed in the gut necessitates further investigations on functional relevance for gut microbiota and the host.

  3. EXPOSURE TO ACROLEIN BY INHALATION CAUSES PLATELET ACTIVATION

    OpenAIRE

    Sithu, Srinivas D; Srivastava, Sanjay; Siddiqui, Maqsood A; Vladykovskaya, Elena; Riggs, Daniel W; Conklin, Daniel J; Haberzettl, Petra; O’Toole, Timothy E; Bhatnagar, Aruni; D’Souza, Stanley E

    2010-01-01

    Acrolein is a common air pollutant that is present in high concentrations in wood, cotton, and tobacco smoke, automobile exhaust and industrial waste and emissions. Exposure to acrolein containing environmental pollutants such as tobacco smoke and automobile exhaust has been linked to the activation of the coagulation and hemostasis pathways and thereby to the predisposition of thrombotic events in human. To examine the effects of acrolein on platelets, adult male C57Bl/6 mice were subjected ...

  4. Threshold photoelectron spectroscopy and photoionization total ion yield spectroscopy of simple organic acids, aldehydes, ketones and amines

    International Nuclear Information System (INIS)

    Yencha, Andrew J; Malins, Andrew E R; Siggel-King, Michele R F; Eypper, Marie; King, George C

    2009-01-01

    We have initiated a research program to investigate the ionization behavior of some simple organic molecules containing the carboxyl group (R 2 C=O), where R could be H, OH, NH 2 , or CH 3 or other aliphatic or aromatic carbon groups, using threshold photoelectron spectroscopy and photoionization total ion yield spectroscopy. We report here on the simplest organic acid, formic acid, and two simple aldehydes: acetaldehyde and the simplest unsaturated aldehyde, 2-propenal (acrolein). The objective of this study was to characterize the valence cationic states of these molecules with vibrational structural resolution.

  5. Intense correlation between brain infarction and protein-conjugated acrolein.

    Science.gov (United States)

    Saiki, Ryotaro; Nishimura, Kazuhiro; Ishii, Itsuko; Omura, Tomohiro; Okuyama, Shigeru; Kashiwagi, Keiko; Igarashi, Kazuei

    2009-10-01

    We recently found that increases in plasma levels of protein-conjugated acrolein and polyamine oxidases, enzymes that produce acrolein, are good markers for stroke. The aim of this study was to determine whether the level of protein-conjugated acrolein is increased and levels of spermine and spermidine, the substrates of acrolein production, are decreased at the locus of infarction. A unilateral infarction was induced in mouse brain by photoinduction after injection of Rose Bengal. The volume of the infarction was analyzed using the public domain National Institutes of Health image program. The level of protein-conjugated acrolein at the locus of infarction and in plasma was measured by Western blotting and enzyme-linked immunosorbent assay, respectively. The levels of polyamines at the locus of infarction and in plasma were measured by high-performance liquid chromatography. The level of protein-conjugated acrolein was greatly increased, and levels of spermine and spermidine were decreased at the locus of infarction at 24 hours after the induction of stroke. The size of infarction was significantly decreased by N-acetylcysteine, a scavenger of acrolein. It was also found that the increases in the protein-conjugated acrolein, polyamines, and polyamine oxidases in plasma were observed after the induction of stroke. The results indicate that the induction of infarction is well correlated with the increase in protein-conjugated acrolein at the locus of infarction and in plasma.

  6. Synthesis of Reactive Polymers for Acrolein Capture Using AGET ATRP.

    Science.gov (United States)

    Beringer, Laura T; Li, Shaohua; Gilmore, Gary; Lister, John; Averick, Saadyah

    2015-10-05

    Acrolein is a toxic metabolite of the anticancer agent cyclophosphamide (CP). Current strategies to mitigate acrolein toxicity are insufficient, and in this brief article, we report the synthesis of well-defined low molecular weight block copolymers using activators generated by electron transfer atom transfer radical polymerization (AGET ATRP) capable of reacting with the cytotoxic small molecule acrolein. Acrolein reactivity was introduced into the block copolymers via incorporation of either (a) aminooxy or (b) sulfhydryl groups. The cytoprotective effect of the polymers was compared to sodium 2-sulfanylethanesulfonate (mesna) the current gold standard for protection from CP urotoxicity, and we found that the polymers bearing sulfhydryl moieties demonstrated superior cytoprotective activity.

  7. New Insights in the Pathogenesis of Multiple Sclerosis—Role of Acrolein in Neuronal and Myelin Damage

    Directory of Open Access Journals (Sweden)

    Riyi Shi

    2013-10-01

    Full Text Available Multiple sclerosis (MS is an autoimmune disease of the central nervous system (CNS characterized by an inappropriate inflammatory reaction resulting in widespread myelin injury along white matter tracts. Neurological impairment as a result of the disease can be attributed to immune-mediated injury to myelin, axons and mitochondria, but the molecular mechanisms underlying the neuropathy remain incompletely understood. Incomplete mechanistic knowledge hinders the development of therapies capable of alleviating symptoms and slowing disease progression in the long-term. Recently, oxidative stress has been implicated as a key component of neural tissue damage prompting investigation of reactive oxygen species (ROS scavengers as a potential therapeutic option. Despite the establishment of oxidative stress as a crucial process in MS development and progression, ROS scavengers have had limited success in animal studies which has prompted pursuit of an alternative target capable of curtailing oxidative stress. Acrolein, a toxic β-unsaturated aldehyde capable of initiating and perpetuating oxidative stress, has been suggested as a viable point of intervention to guide the development of new treatments. Sequestering acrolein using an FDA-approved compound, hydralazine, offers neuroprotection resulting in dampened symptom severity and slowed disease progression in experimental autoimmune encephalomyelitis (EAE mice. These results provide promise for therapeutic development, indicating the possible utility of neutralizing acrolein to preserve and improve neurological function in MS patients.

  8. Product Analysis of the {OH} Oxidation of Acrolein and Methacrolein in the Presence of {NO}

    Science.gov (United States)

    Dransfield, T. J.; Sprengnether, M. M.; Huang, Y.; Donahue, N. M.; Demerjian, K. L.; Anderson, J. G.

    2002-12-01

    The oxidation of acrolein and methacrolein by OH in the presence of high NO was studied under "wall-less" conditions in Harvard's High Pressure Flow System. The experiment was conducted at 450 torr with a reaction time of several seconds. In the present work, first stage products are formed at 1013 molecules/cm3 levels and analyzed in-situ by FTIR spectroscopy. The use of Reaction Modulation Spectroscopy allows for accurate measurement of the very small(~1%) change in unsaturated aldehyde and NO reactants, in addition to product concentrations. Observed products from the acrolein oxidation include: formaldehyde(CH2O), glyoxal(CHOCHO), glycolaldehyde(CH2OHCHO), ketene(CH2CO), nitrogen dioxide, carbon dioxide and carbon monoxide. The methacrolein oxidation produces: formaldehyde, methylgyloxal(CH3COCHO), hydroxyacetone(CH2OHC(O)CH3), ketene, nitrogen dioxide, carbon dioxide and carbon monoxide. Both reactions also produce peroxynitrates and alkylnitrates that have proven difficult to spectrally resolve. We observe elevated yields of ketene relative to previously published experiments conducted on longer timescales. We interpret this as evidence of rapid ketene removal in these systems. The mechanisms for ketene formation are discussed.

  9. Selective Production of Toluene from Biomass-Derived Isoprene and Acrolein.

    Science.gov (United States)

    Dai, Tao; Li, Changzhi; Zhang, Bo; Guo, Haiwei; Pan, Xiaoli; Li, Lin; Wang, Aiqin; Zhang, Tao

    2016-12-20

    Toluene is a basic chemical that is currently produced from petroleum resources. In this paper, we report a new route for the effective synthesis of toluene from isoprene and acrolein, two reactants readily available from biomass, through a simple two-step reaction. The process includes Diels-Alder cycloaddition of isoprene and acrolein in a Zn-containing ionic liquid at room temperature to produce methylcyclohex-3-enecarbaldehydes (MCHCAs) as intermediates, followed by M (M=Pt, Pd, Rh)/Al 2 O 3 -catalyzed consecutive dehydrogenation-decarbonylation of the MCHCAs at 573 K to generate toluene with an overall yield up to 90.7 %. Model reactions indicated that a synergistic inductive effect of the C=C double bond and the aldehyde group in MCHCA plays a key role in initiating the consecutive dehydrogenation-decarbonylation, and that methyl benzaldehydes are the key intermediates in the gas-phase transformation of MCHCAs. Microcalorimetric adsorption of CO on different catalysts showed that decarbonylation of the substrate occurs more likely on the strong adsorption sites. To the best of our knowledge, it is the first report of Pt/Al 2 O 3 -catalyzed consecutive dehydrogenation-decarbonylation of a given compound in one reactor. This work provides a highly efficient and environmental friendly route to toluene by utilizing two compounds that can be prepared from biomass. © 2016 Wiley-VCH Verlag GmbH & Co. KGaA, Weinheim.

  10. Proteomic profiling of acrolein adducts in human lung epithelial cells

    Science.gov (United States)

    Spiess, Page C.; Deng, Bin; Hondal, Robert J.; Matthews, Dwight E.; van der Vliet, Albert

    2011-01-01

    Acrolein (2,3-propenal) is a major indoor and outdoor air pollutant originating largely from tobacco smoke or organic combustion. Given its high reactivity, the adverse effects of inhaled acrolein are likely due to direct interactions with the airway epithelium, resulting in altered epithelial function, but only limited information exists to date regarding the primary direct cellular targets for acrolein. Here, we describe a global proteomics approach to characterize the spectrum of airway epithelial protein targets for Michael adduction in acrolein-exposed bronchial epithelial (HBE1) cells, based on biotin hydrazide labeling and avidin purification of biotinylated proteins or peptides for analysis by LC-MS/MS. Identified protein targets included a number of stress proteins, cytoskeletal proteins, and several key proteins involved in redox signaling, including thioredoxin reductase, thioredoxin, peroxiredoxins, and glutathione S-transferase π. Because of the central role of thioredoxin reductase in cellular redox regulation, additional LC-MS/MS characterization was performed on purified mitochondrial thioredoxin reductase to identify the specific site of acrolein adduction, revealing the catalytic selenocysteine residue as the target responsible for enzyme inactivation. Our findings indicate that these approaches are useful in characterizing major protein targets for acrolein, and will enhance mechanistic understanding of the impact of acrolein on cell biology. PMID:21704744

  11. Conjugation vs hyperconjugation in molecular structure of acrolein

    Science.gov (United States)

    Shishkina, Svitlana V.; Slabko, Anzhelika I.; Shishkin, Oleg V.

    2013-01-01

    Analysis of geometric parameters of butadiene and acrolein reveals the contradiction between the Csp2-Csp2 bond length in acrolein and classical concept of conjugation degree in the polarized molecules. In this Letter the reasons of this contradiction have been investigated. It is concluded that the Csp2-Csp2 bond length in acrolein is determined by influence of the bonding for it π-π conjugation and antibonding n → σ∗ hyperconjugation between the oxygen lone pair and the antibonding orbital of the single bond. It was shown also this bond length depends on the difference in energy of conjugative and hyperconjugative interactions.

  12. Aerobic oxidation of aldehydes under ambient conditions using supported gold nanoparticle catalysts

    DEFF Research Database (Denmark)

    Marsden, Charlotte Clare; Taarning, Esben; Hansen, David

    2008-01-01

    A new, green protocol for producing simple esters by selectively oxidizing an aldehyde dissolved in a primary alcohol has been established, utilising air as the oxidant and supported gold nanoparticles as catalyst. The oxidative esterifications proceed with excellent selectivities at ambient cond...... conditions; the reactions can be performed in an open flask and at room temperature. Benzaldehyde is even oxidised at a reasonable rate below -70 degrees C. Acrolein is oxidised to methyl acrylate in high yield using the same protocol.......A new, green protocol for producing simple esters by selectively oxidizing an aldehyde dissolved in a primary alcohol has been established, utilising air as the oxidant and supported gold nanoparticles as catalyst. The oxidative esterifications proceed with excellent selectivities at ambient...

  13. Gut Microbial Glycerol Metabolism as an Endogenous Acrolein Source

    OpenAIRE

    Zhang, Jianbo; Sturla, Shana; Lacroix, Christophe; Schwab, Clarissa

    2018-01-01

    ABSTRACT Acrolein is a highly reactive electrophile causing toxic effects, such as DNA and protein adduction, oxidative stress, endoplasmic reticulum stress, immune dysfunction, and membrane damage. This Opinion/Hypothesis provides an overview of endogenous and exogenous acrolein sources, acrolein’s mode of action, and its metabolic fate. Recent reports underpin the finding that gut microbial glycerol metabolism leading to the formation of reuterin is an additional source of endogenous acrole...

  14. On detecting reference level of acrolein content in children's blood

    Directory of Open Access Journals (Sweden)

    T.S. Ulanova

    2017-03-01

    Full Text Available The article gives the results of complex chemical-analytical and clinical-laboratory research in course of which biological media of children living in Perm region were examined. To study impacts exerted by exogenous acrolein we examined 156 children in 2014–2016, aged 5–10, attending pre-school facilities and schools, and living in Perm region. As we conducted this research we detected average annual acrolein concentration in atmosphere on the examined territory; this concentration was equal to 0.000024 mg/m3, and it was 1.2 times higher than reference acrolein concentration in the air for chronic inhalation exposure. Average group acrolein concentration in children's blood was 1.2 times authentically higher (р3.96, p≤0.05. We used increased content of delta-aminolevulinic acid in urine as a limiting marker for effects occurring at chronic inhalation exposure to acrolein. Basing on the results of the performed examination we recommend concentration equal to 0.10 mgr/dm 3 as a reference level of acrolein content in blood at chronic inhalation exposure.

  15. First general methods toward aldehyde enolphosphates.

    Science.gov (United States)

    Barthes, Nicolas; Grison, Claude

    2012-02-01

    We herein report two innovative methods toward aldehyde enolphosphates and the first saccharidic aldehyde enolphosphates. Aldehyde enolphosphate function is worthwhile to be considered as a good phosphoenolpyruvate analogue. Copyright © 2011 Elsevier Inc. All rights reserved.

  16. Effects of maternal acrolein exposure during pregnancy on testicular testosterone production in fetal rats

    OpenAIRE

    Yang, Yuzhuo; Zhang, Zhe; Zhang, Hongliang; Hong, Kai; Tang, Wenhao; Zhao, Lianming; Lin, Haocheng; Liu, Defeng; Mao, Jiaming; Wu, Han; Jiang, Hui

    2017-01-01

    Acrolein has been reported to have diverse toxic effects on various organs, including the reproductive system. However, little is known regarding the effects of maternal acrolein exposure on testicular steroidogenesis in male offspring. The present study investigated the effects of acrolein on fetal testosterone production and associated genes. Pregnant Sprague-Dawley rats were intraperitoneally injected with vehicle (normal saline) or 1, 2 or 5 mg/kg acrolein from gestational day (GD) 14?20,...

  17. Acrolein cytotoxicity in hepatocytes involves endoplasmic reticulum stress, mitochondrial dysfunction and oxidative stress

    OpenAIRE

    Mohammad, Mohammad K; Avila, Diana; Zhang, Jingwen; Barve, Shirish; Arteel, Gavin; McClain, Craig; Joshi-Barve, Swati

    2012-01-01

    Acrolein is a common environmental, food and water pollutant and a major component of cigarette smoke. Also, it is produced endogenously via lipid peroxidation and cellular metabolism of certain amino acids and drugs. Acrolein is cytotoxic to many cell types including hepatocytes; however the mechanisms are not fully understood. We examined the molecular mechanisms underlying acrolein hepatotoxicity in primary human hepatocytes and hepatoma cells. Acrolein, at pathophysiological concentration...

  18. Organic acids and aldehydes in rainwater in a northwest region of Spain

    Energy Technology Data Exchange (ETDEWEB)

    Pena, R.M.; Garcia, S.; Herrero, C. [Universidad de Santiago de Compostela, Lugo (Spain). Departamento de Quimica Analitica, Nutricion y Bromatologia

    2002-11-01

    During a 1 year period, measurements of carboxylic acids and aldehydes were carried out in rainwater samples collected at nine different sites in NW Spain surrounding a thermal power plant in order to determine concentration levels and sources. In addition, certain major ions (Cl{sup -}, NO{sub 3}{sup -}, SO{sub 4}{sup 2-}, Na{sup +}, NH{sub 4}{sup +}, K{sup +}, Mg{sup 2+}, Ca{sup 2+}) were also determined. Aldehyde and carboxylic acid concentration patterns and their effects on rainwater composition concerning temporal, seasonal and spatial variations were evaluated. Among carboxylic acids, formic and acetic were predominant (VWA 7.0 and 8.3 {mu}M), while formaldehyde and acroleine were the dominant aldehydes (VWA 0.42 and 1.25 {mu}M). Carboxylic acids were estimated to account for 27.5% of the total free acidity (TFA), whereas sulphuric and nitric acid accounted for 46.2% and 26.2%, respectively. Oxalic acid was demonstrated to be an important contributing compound to the acidification in rainwater representing 7.1% of the TFA. The concentration of aldehydes and carboxylic acids, which originated mainly from biogenic emissions in the area studied, was strongly dependent on the season of the year (growing and non-growing). The ratios of formic to acetic acids are considerably different in the two seasons suggesting that there exist distinct sources in both growing and non-growing seasons. Principal component analysis was applied in order to elucidate the sources of aldehydes and organic acids in rainwater. The prevalence of natural vegetative origins for both of these compounds versus anthropogenic emissions was demonstrated and the importance of the oxidation of aldehydes as a relevant source of organic acids was also established. (author)

  19. Vocal fold ion transport and mucin expression following acrolein exposure.

    Science.gov (United States)

    Levendoski, Elizabeth Erickson; Sivasankar, M Preeti

    2014-05-01

    The vocal fold epithelium is exposed to inhaled particulates including pollutants during breathing in everyday environments. Yet, our understanding of the effects of pollutants on vocal fold epithelial function is extremely limited. The objective of this study was to investigate the effect of the pollutant acrolein on two vocal fold epithelial mechanisms: ion transport and mucin (MUC) synthesis. These mechanisms were chosen as each plays a critical role in vocal defense and in maintaining surface hydration which is necessary for optimal voice production. Healthy, native porcine vocal folds (N = 85) were excised and exposed to an acrolein or sham challenge. A 60-min acrolein, but not sham challenge significantly reduced ion transport and inhibited cyclic adenosine monophosphate-dependent, increases in ion transport. Decreases in ion transport were associated with reduced sodium absorption. Within the same timeline, no significant acrolein-induced changes in MUC gene or protein expression were observed. These results improve our understanding of the effects of acrolein on key vocal fold epithelial functions and inform the development of future investigations that seek to elucidate the impact of a wide range of pollutant exposures on vocal fold health.

  20. Levels of Crotonaldehyde and 4-hydroxy-(E-2-nonenal and Expression of Genes Encoding Carbonyl-Scavenging Enzyme at Critical Node During Rice Seed Aging

    Directory of Open Access Journals (Sweden)

    Fu Shenzao

    2018-05-01

    Full Text Available Abstract:: The critical node (CN is an important stage during seed aging, which is related to effective genebank conservation. Previous studies have demonstrated that proteins undergo carbonylated modification at the CN in rice, indicating oxidative damage. However, the levels of reactive carbonyl species (RCS and the associated scavenging system at the CN are largely unknown. In this study, we optimized methods for the extraction and analysis of RCS from dry rice embryos. In order to acquire seeds at the CN, rice seeds were subjected to natural conditions for 7, 9, 11 and 13 months, and the seed germination rates were reduced to 90%, 82%, 71% and 57%, respectively. We chose the stage with seed germination rate of 82% as the CN according to the rice seed vigor loss curve. The levels of crotonaldehyde and 4-hydroxy-(E-2-nonenal (HNE were significantly increased at the CN. In addition, genes encoding carbonyl-scavenging enzyme, including OsALDHs and OsAKRs, were significantly down-regulated at the CN, and reductions in the expression of OsALDH2-2, OsALDH2-5, OsALDH3-4, OsALDH7, OsAKR1 and OsAKR2 in particular could be responsible for RCS accumulation. Thus, the accumulations of crotonaldehyde and HNE and down-regulation of genes encoding carbonyl-scavenging enzyme might be related to an accelerating loss of seed viability at the CN. Key words: carbonyl-scavenging system, reactive carbonyl species, seed aging, crotonaldehyde, critical node, rice storage

  1. Determination of Urine 3-HPMA, a Stable Acrolein Metabolite in a Rat Model of Spinal Cord Injury

    OpenAIRE

    Zheng, Lingxing; Park, Jonghyuck; Walls, Michael; Tully, Melissa; Jannasch, Amber; Cooper, Bruce; Shi, Riyi

    2013-01-01

    Acrolein has been suggested to be involved in a variety of pathological conditions. The monitoring of acrolein is of significant importance in delineating the pathogenesis of various diseases. Aimed at overcoming the reactivity and volatility of acrolein, we describe a specific and stable metabolite of acrolein in urine, N-acetyl-S-3-hydroxypropylcysteine (3-HPMA), as a potential surrogate marker for acrolein quantification. Using the LC/MS/MS method, we demonstrated that 3-HPMA was significa...

  2. Studies on the polymerization of acrolein oxime, 6

    International Nuclear Information System (INIS)

    Masuda, Seizo; Tamai, Harumi; Ota, Tadatoshi; Torii, Munetomo; Tanaka, Masami.

    1979-01-01

    Radiation-induced polymerization and copolymerization of acrolein oxime are investigated in different solvents and at a wide range of temperature for obtaining information on the reaction mechanism. Acrolein oxime is polymerized ionically, irrespective of dryness of the sample. Arrhenius plots for the polymerization rate, which do not yield a linear relation, can be adequately approximated by two straight lines. An anionic mechanism is operative above the room temperature, while a cationic mechanism predominates below -23 0 C. The reaction in the intermediate temperature range proceeds by a competitive mechanism, and the rate of the anionic and cationic polymerizations becomes equal at the temperature near -5 0 C. The reaction rate is proportional to the square root of dose rate at room temperature and -23 0 C. On the basis of these data, it is proposed that the polymerization of acrolein oxime by γ-irradiation proceeds by free-ionic mechanisms. (author)

  3. Sirt3 confers protection against acrolein-induced oxidative stress in cochlear nucleus neurons.

    Science.gov (United States)

    Qu, Juan; Wu, Yong-Xiang; Zhang, Ting; Qiu, Yang; Ding, Zhong-Jia; Zha, Ding-Jun

    2018-03-01

    Acrolein is a ubiquitous dietary and environmental pollutant, which can also be generated endogenously during cellular stress. However, the molecular mechanisms underlying acrolein-induced neurotoxicity, especially in ototoxicity conditions, have not been fully determined. In this study, we investigated the mechanisms on acrolein-induced toxicity in primary cultured cochlear nucleus neurons with focus on Sirt3, a mitochondrial deacetylase. We found that acrolein treatment induced neuronal injury and programmed cell death (PCD) in a dose dependent manner in cochlear nucleus neurons, which was accompanied by increased intracellular reactive oxygen species (ROS) generation and lipid peroxidation. Acrolein exposure also significantly reduced the mitochondrial membrane potential (MMP) levels, promoted cytochrome c release and decreased mitochondrial ATP production. In addition, increased ER tracker fluorescence and activation of ER stress factors were observed after acrolein treatment, and the ER stress inhibitors were shown to attenuate acrolein-induced toxicity in cochlear nucleus neurons. The results of western blot and RT-PCR showed that acrolein markedly decreased the expression of Sirt3 at both mRNA and protein levels, and reduced the activity of downstream mitochondrial enzymes. Furthermore, overexpression of Sirt3 by lentivirus transfection partially prevented acrolein-induced neuronal injury in cochlear nucleus neurons. These results demonstrated that acrolein induces mitochondrial dysfunction and ER stress in cochlear nucleus neurons, and Sirt3 acts as an endogenous protective factor in acrolein-induced ototoxicity. Copyright © 2017. Published by Elsevier Ltd.

  4. The Uremic Toxin Acrolein Promotes Suicidal Erythrocyte Death

    Directory of Open Access Journals (Sweden)

    Mohamed Siyabeldin E. Ahmed

    2013-05-01

    Full Text Available Background: Anemia is a major complication of end stage renal disease. The anemia is mainly the result of impaired formation of erythrocytes due to lack of erythropoietin and iron deficiency. Compelling evidence, however, points to the contribution of accelerated erythrocyte death, which decreases the life span of circulating erythrocytes. Erythrocytes may enter suicidal death or eryptosis, which is characterized by cell shrinkage and by cell membrane scrambling with phosphatidylserine-exposure at the erythrocyte surface. Triggers of eryptosis include increase of cytosolic Ca2+-activity ([Ca2+]i. Erythrocytes could be sensitized to cytosolic Ca2+ by ceramide. In end stage renal disease, eryptosis may possibly be stimulated by uremic toxins. The present study explored, whether the uremic toxin acrolein could trigger eryptosis. Methods: Cell volume was estimated from forward scatter, phosphatidylserine-exposure from annexin-V-binding, hemolysis from hemoglobin release, [Ca2+]i from Fluo3-fluorescence, and ceramide from fluorescent antibodies. Results: A 48 h exposure to acrolein (30 - 50 µM did not significantly modify [Ca2+]i but significantly decreased forward scatter and increased annexin-V-binding. Acrolein further triggered slight, but significant hemolysis and increased ceramide formation in erythrocytes. Acrolein (50 µM induced annexin-V-binding was significantly blunted in the nominal absence of extracellular Ca2+. Acrolein augmented the annexin-V-binding following treatment with Ca2+ ionophore ionomycin (1 µM. Conclusion: Acrolein stimulates suicidal erythrocyte death or eryptosis, an effect at least in part due to stimulation of ceramide formation with subsequent sensitisation of the erythrocytes to cytosolic Ca2+.

  5. Metabolic shift in lung alveolar cell mitochondria following acrolein exposure.

    Science.gov (United States)

    Agarwal, Amit R; Yin, Fei; Cadenas, Enrique

    2013-11-15

    Acrolein, an α,β unsaturated electrophile, is an environmental pollutant released in ambient air from diesel exhausts and cooking oils. This study examines the role of acrolein in altering mitochondrial function and metabolism in lung-specific cells. RLE-6TN, H441, and primary alveolar type II (pAT2) cells were exposed to acrolein for 4 h, and its effect on mitochondrial oxygen consumption rates was studied by XF Extracellular Flux analysis. Low-dose acrolein exposure decreased mitochondrial respiration in a dose-dependent manner because of alteration in the metabolism of glucose in all the three cell types. Acrolein inhibited glyceraldehyde-3-phosphate dehydrogenase (GAPDH) activity, leading to decreased substrate availability for mitochondrial respiration in RLE-6TN, H441, and pAT2 cells; the reduced GAPDH activity was compensated in pAT2 cells by an increase in the activity of glucose-6-phosphate dehydrogenase, the regulatory control of the pentose phosphate pathway. The decrease in pyruvate from glucose metabolism resulted in utilization of alternative sources to support mitochondrial energy production: palmitate-BSA complex increased mitochondrial respiration in RLE-6TN and pAT2 cells. The presence of palmitate in alveolar cells for surfactant biosynthesis may prove to be the alternative fuel source for mitochondrial respiration. Accordingly, a decrease in phosphatidylcholine levels and an increase in phospholipase A2 activity were found in the alveolar cells after acrolein exposure. These findings have implications for understanding the decrease in surfactant levels frequently observed in pathophysiological situations with altered lung function following exposure to environmental toxicants.

  6. Effect of acrolein and glutathione depleting agents on thioredoxin

    International Nuclear Information System (INIS)

    Yang Xianmei; Wu Xuli; Choi, Young Eun; Kern, Julie C.; Kehrer, James P.

    2004-01-01

    Acrolein is a widespread environmental pollutant that reacts rapidly with nucleophiles, especially cellular thiols. In addition to glutathione (GSH), thioredoxin (Trx) and thioredoxin reductase (TR) contain thiol groups and may react with electrophiles. In the present study, A549 cells treated with 5-25 μM acrolein for 30 min lost cellular Trx activity in a dose-dependent fashion. Over 90% of Trx activity was lost at concentrations of 25 μM or greater. In contrast, Trx protein content, as assessed by western blotting, was not altered immediately after the 30 min acrolein treatment. Both Trx activity and protein levels increased 4 h after the acrolein treatment. However, Trx activity remained below control levels at 24 h. A similar dose-response relationship was seen with TR in A549 cells exposed to acrolein. There was, however, a rapid recovery of TR activity such that it attained normal levels by 4 h after doses ≤75 μM acrolein. Diethyl maleate (DEM), a common but not highly specific, agent used to deplete GSH, also inactivated Trx. A 2 h exposure of A549 cells to 1 mM DEM depleted cellular GSH by ∼50% and diminished Trx activity by over 67%. Lower DEM doses (0.125 mM and 0.25 mM) for 1 h had no significant effect on GSH but significantly decreased Trx activity 12 and 23%, respectively. Similar to immediately after acrolein exposure, DEM did not affect Trx protein levels. A Trx-1-GFP fusion protein was transfected into A549 cells. While the fusion protein was expressed, the Trx component was inactive by the insulin reducing assay. In summary, Trx and TR are inactivated by acrolein. In addition, the GSH depleting agent DEM inactivates Trx somewhat more effectively than it depletes GSH. The Trx-1-GFP fusion protein, while readily expressed, appears to have little or no activity, perhaps because the small size of Trx-1 (12 kDa) is affected by the larger GFP

  7. Acrolein exposure suppresses antigen-induced pulmonary inflammation

    Science.gov (United States)

    2013-01-01

    Background Adverse health effects of tobacco smoke arise partly from its influence on innate and adaptive immune responses, leading to impaired innate immunity and host defense. The impact of smoking on allergic asthma remains unclear, with various reports demonstrating that cigarette smoke enhances asthma development but can also suppress allergic airway inflammation. Based on our previous findings that immunosuppressive effects of smoking may be largely attributed to one of its main reactive electrophiles, acrolein, we explored the impact of acrolein exposure in a mouse model of ovalbumin (OVA)-induced allergic asthma. Methods C57BL/6 mice were sensitized to ovalbumin (OVA) by intraperitoneal injection with the adjuvant aluminum hydroxide on days 0 and 7, and challenged with aerosolized OVA on days 14–16. In some cases, mice were also exposed to 5 ppm acrolein vapor for 6 hrs/day on days 14–17. Lung tissues or brochoalveolar lavage fluids (BALF) were collected either 6 hrs after a single initial OVA challenge and/or acrolein exposure on day 14 or 48 hrs after the last OVA challenge, on day 18. Inflammatory cells and Th1/Th2 cytokine levels were measured in BALF, and lung tissue samples were collected for analysis of mucus and Th1/Th2 cytokine expression, determination of protein alkylation, cellular thiol status and transcription factor activity. Results Exposure to acrolein following OVA challenge of OVA-sensitized mice resulted in markedly attenuated allergic airway inflammation, demonstrated by decreased inflammatory cell infiltrates, mucus hyperplasia and Th2 cytokines. Acrolein exposure rapidly depleted lung tissue glutathione (GSH) levels, and induced activation of the Nrf2 pathway, indicated by accumulation of Nrf2, increased alkylation of Keap1, and induction of Nrf2-target genes such as HO-1. Additionally, analysis of inflammatory signaling pathways showed suppressed activation of NF-κB and marginally reduced activation of JNK in acrolein

  8. Protective Effect of Silymarin against Acrolein-Induced Cardiotoxicity in Mice

    Directory of Open Access Journals (Sweden)

    Elahe Taghiabadi

    2012-01-01

    Full Text Available Reactive α,β-unsaturated aldehydes such as acrolein (ACR are major components of environmental pollutants and have been implicated in the neurodegenerative and cardiac diseases. In this study, the protective effect of silymarin (SN against cardiotoxicity induced by ACR in mice was evaluated. Studies were performed on seven groups of six animals each, including vehicle-control (normal saline + 0.5% w/v methylcellulose, ACR (7.5 mg/kg/day, gavage for 3 weeks, SN (25, 50 and 100 mg/kg/day, i.p. plus ACR, vitamin E (Vit E, 100 IU/kg, i.p. plus ACR, and SN (100 mg/kg, i.p. groups. Mice received SN 7 days before ACR and daily thereafter throughout the study. Pretreatment with SN attenuated ACR-induced increased levels of malondialdehyde (MDA, serum cardiac troponin I (cTnI, and creatine kinase-MB (CK-MB, as well as histopathological changes in cardiac tissues. Moreover, SN improved glutathione (GSH content, superoxide dismutase (SOD, and catalase (CAT activities in heart of ACR-treated mice. Western blot analysis showed that SN pretreatment inhibited apoptosis provoked by ACR through decreasing Bax/Bcl-2 ratio, cytosolic cytochrome c content, and cleaved caspase-3 level in heart. In conclusion, SN may have protective effects against cardiotoxicity of ACR by reducing lipid peroxidation, renewing the activities of antioxidant enzymes, and preventing apoptosis.

  9. Evaluation of dementia by acrolein, amyloid-β and creatinine.

    Science.gov (United States)

    Igarashi, Kazuei; Yoshida, Madoka; Waragai, Masaaki; Kashiwagi, Keiko

    2015-10-23

    Plasma, urine and cerebrospinal fluid (CSF) were examined for biochemical markers of dementia. Protein-conjugated acrolein (PC-Acro) and the amyloid-β (Aβ)40/42 ratio in plasma can be used to detect mild cognitive impairment (MCI) and Alzheimer's disease (AD). In plasma, PC-Acro and the Aβ40/42 ratio in MCI and AD were significantly higher relative to non-demented subjects. Furthermore, urine acrolein metabolite, 3-hydroxypropyl mercapturic acid (3-HPMA)/creatinine (Cre) and amino acid-conjugated acrolein (AC-Acro)/Cre in AD were significantly lower than MCI. It was also shown that reduced urine 3-HPMA/Cre correlated with increased plasma Aβ40/42 ratio in dementia. The Aβ40/PC-Acro ratio in CSF, together with Aβ40 and Aβ40/42 ratio, was lower in AD than MCI. Increased plasma PC-Acro and Aβ40/42 ratio and decreased urine 3-HPMA/Cre correlated with cognitive ability (MMSE). These results indicate that the measurements of acrolein derivatives together with Aβ and Cre in biologic fluids is useful to estimate severity of dementia. Copyright © 2015 Elsevier B.V. All rights reserved.

  10. Effect of acrolein, a hazardous air pollutant in smoke, on human middle ear epithelial cells.

    Science.gov (United States)

    Song, Jae-Jun; Lee, Jong Dae; Lee, Byung Don; Chae, Sung Won; Park, Moo Kyun

    2013-10-01

    Acrolein is a hazardous air pollutant. Tobacco smoke and indoor air pollution are the main causes of human exposure. Acrolein has been shown to cause cytotoxicity in the airways and induce inflammation and mucin production in pulmonary cells. We investigated whether acrolein caused cytotoxicity, induced inflammation or increased expression of mucin in immortalized human middle ear epithelial cell lines (HMEECs). Cytotoxicity following acrolein treatment was investigated using the MTT assay, flow cytometry, and Hoechst 33342 staining of HMEECs. We measured expression of inflammatory cytokines tumor necrosis factor (TNF)-α and cyclo-oxygenase (COX)-2 and the mucin gene MUC5AC using semi-quantitative real-time reverse transcriptase polymerase chain reaction (RT-PCR) and Western blotting. Exposure to >50 μg/mL acrolein caused a decrease in cell viability. Acrolein induced apoptosis and necrosis at 50 μg/mL. Acrolein at 5-50 μg/mL increased expression of TNF-α and COX-2, as shown by RT-PCR and Western blotting. Acrolein exposure at 5-50 μg/mL for 2-24h increased MUC5AC expression, as determined by RT-PCR. Acrolein decreased cell viability, induced an inflammatory response, and increased mucin gene expression in HMEECs. These findings support the hypothesis that acrolein, a hazardous air pollutant in tobacco smoke and ambient air, is a risk factor for otitis media. Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.

  11. The tobacco smoke component acrolein induces glucocorticoid resistant gene expression via inhibition of histone deacetylase.

    Science.gov (United States)

    Randall, Matthew J; Haenen, Guido R M M; Bouwman, Freek G; van der Vliet, Albert; Bast, Aalt

    2016-01-05

    Chronic obstructive pulmonary disease (COPD) is the leading cause of cigarette smoke-related death worldwide. Acrolein, a crucial reactive electrophile found in cigarette smoke mimics many of the toxic effects of cigarette smoke-exposure in the lung. In macrophages, cigarette smoke is known to hinder histone deacetylases (HDACs), glucocorticoid-regulated enzymes that play an important role in the pathogenesis of glucocorticoid resistant inflammation, a common feature of COPD. Thus, we hypothesize that acrolein plays a role in COPD-associated glucocorticoid resistance. To examine the role of acrolein on glucocorticoid resistance, U937 monocytes, differentiated with PMA to macrophage-like cells were treated with acrolein for 0.5h followed by stimulation with hydrocortisone for 8h, or treated simultaneously with LPS and hydrocortisone for 8h without acrolein. GSH and nuclear HDAC activity were measured, or gene expression was analyzed by qPCR. Acrolein-mediated TNFα gene expression was not suppressed by hydrocortisone whereas LPS-induced TNFα expression was suppressed. Acrolein also significantly inhibited nuclear HDAC activity in macrophage-like cells. Incubation of recombinant HDAC2 with acrolein led to the formation of an HDAC2-acrolein adduct identified by mass spectrometry. Therefore, these results suggest that acrolein-induced inflammatory gene expression is resistant to suppression by the endogenous glucocorticoid, hydrocortisone. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.

  12. Determination of Urine 3-HPMA, a Stable Acrolein Metabolite in a Rat Model of Spinal Cord Injury

    Science.gov (United States)

    Zheng, Lingxing; Park, Jonghyuck; Walls, Michael; Tully, Melissa; Jannasch, Amber; Cooper, Bruce

    2013-01-01

    Abstract Acrolein has been suggested to be involved in a variety of pathological conditions. The monitoring of acrolein is of significant importance in delineating the pathogenesis of various diseases. Aimed at overcoming the reactivity and volatility of acrolein, we describe a specific and stable metabolite of acrolein in urine, N-acetyl-S-3-hydroxypropylcysteine (3-HPMA), as a potential surrogate marker for acrolein quantification. Using the LC/MS/MS method, we demonstrated that 3-HPMA was significantly elevated in a dose-dependent manner when acrolein was injected into rats IP or directly into the spinal cord, but not when acrolein scavengers were co-incubated with acrolein solution. A nonlinear mathematic relationship is established between acrolein injected directly into the spinal cord and a correlated dose-dependent increase of 3-HPMA, suggesting the increase of 3-HPMA becomes less apparent as the level of injected acrolein increases. The elevation of 3-HPMA was further detected in the rat spinal cord injury, a pathological condition known to be associated with elevated endogenous acrolein. This finding was further validated by concomitant confirmation of increased acrolein-lysine adducts using established dot immunoblotting techniques. The noninvasive nature of measuring 3-HPMA concentrations in urine allows for long-term monitoring of acrolein in the same animal and ultimately in human clinical studies. Due to wide spread involvement of acrolein in human health, the benefits of this study have the potential to enhance human health significantly. PMID:23697633

  13. Crude glycerol combustion: Particulate, acrolein, and other volatile organic emissions

    KAUST Repository

    Steinmetz, Scott

    2013-01-01

    Crude glycerol is an abundant by-product of biodiesel production. As volumes of this potential waste grow, there is increasing interest in developing new value added uses. One possible use, as a boiler fuel for process heating, offers added advantages of energy integration and fossil fuel substitution. However, challenges to the use of crude glycerol as a boiler fuel include its low energy density, high viscosity, and high autoignition temperature. We have previously shown that a refractory-lined, high swirl burner can overcome challenges related to flame ignition and stability. However, critical issues related to ash behavior and the possible formation of acrolein remained. The work presented here indicates that the presence of dissolved catalysts used during the esterification and transesterification processes results in extremely large amounts of inorganic species in the crude glycerol. For the fuels examined here, the result is a submicron fly ash comprised primarily of sodium carbonates, phosphates, and sulfates. These particles report to a well-developed accumulation mode (0.3-0.7 μm diameter), indicating extensive ash vaporization and particle formation via nucleation, condensation, and coagulation. Particle mass emissions were between 2 and 4 g/m3. These results indicate that glycerol containing soluble catalyst is not suitable as a boiler fuel. Fortunately, process improvements are currently addressing this issue. Additionally, acrolein is of concern due to its toxicity, and is known to be formed from the low temperature thermal decomposition of glycerol. Currently, there is no known reliable method for measuring acrolein in sources. Acrolein and emissions of other volatile organic compounds were characterized through the use of a SUMMA canister-based sampling method followed by GC-MS analysis designed for ambient measurements. Results indicate crude glycerol combustion produces relatively small amounts of acrolein (∼15 ppbv) and other volatile organic

  14. Acrolein contributes strongly to antimicrobial and heterocyclic amine transformation activities of reuterin.

    Science.gov (United States)

    Engels, Christina; Schwab, Clarissa; Zhang, Jianbo; Stevens, Marc J A; Bieri, Corinne; Ebert, Marc-Olivier; McNeill, Kristopher; Sturla, Shana J; Lacroix, Christophe

    2016-11-07

    Glycerol/diol dehydratases catalyze the conversion of glycerol to 3-hydroxypropionaldehyde (3-HPA), the basis of a multi-component system called reuterin. Reuterin has antimicrobial properties and undergoes chemical conjugation with dietary heterocyclic amines (HCAs). In aqueous solution reuterin is in dynamic equilibrium with the toxicant acrolein. It was the aim of this study to investigate the extent of acrolein formation at various physiological conditions and to determine its role in biological and chemical activities. The application of a combined novel analytical approach including IC-PAD, LC-MS and NMR together with specific acrolein scavengers suggested for the first time that acrolein, and not 3-HPA, is the active compound responsible for HCA conjugation and antimicrobial activity attributed to reuterin. As formation of the HCA conjugate was observed in vivo, our results imply that acrolein is formed in the human gut with implications on detoxification of HCAs. We propose to re-define the term reuterin to include acrolein.

  15. YqhD. A broad-substrate range aldehyde reductase with various applications in production of biorenewable fuels and chemicals

    Energy Technology Data Exchange (ETDEWEB)

    Jarboe, Laura R. [Iowa State Univ., Ames, IA (United States). Dept. of Chemical and Biological Engineering

    2011-01-15

    The Escherichia coli NADPH-dependent aldehyde reductase YqhD has contributed to a variety of metabolic engineering projects for production of biorenewable fuels and chemicals. As a scavenger of toxic aldehydes produced by lipid peroxidation, YqhD has reductase activity for a broad range of short-chain aldehydes, including butyraldehyde, glyceraldehyde, malondialdehyde, isobutyraldehyde, methylglyoxal, propanealdehyde, acrolein, furfural, glyoxal, 3-hydroxypropionaldehyde, glycolaldehyde, acetaldehyde, and acetol. This reductase activity has proven useful for the production of biorenewable fuels and chemicals, such as isobutanol and 1,3- and 1,2-propanediol; additional capability exists for production of 1-butanol, 1-propanol, and allyl alcohol. A drawback of this reductase activity is the diversion of valuable NADPH away from biosynthesis. This YqhD-mediated NADPH depletion provides sufficient burden to contribute to growth inhibition by furfural and 5-hydroxymethyl furfural, inhibitory contaminants of biomass hydrolysate. The structure of YqhD has been characterized, with identification of a Zn atom in the active site. Directed engineering efforts have improved utilization of 3-hydroxypropionaldehyde and NADPH. Most recently, two independent projects have demonstrated regulation of yqhD by YqhC, where YqhC appears to function as an aldehyde sensor. (orig.)

  16. Synthesis of Acrolein From Glycerol Using FePO4 Catalyst in Liquid Phase Dehydration

    OpenAIRE

    Abidin, Akhmad Zainal; Afandi, Rani Guslianti; Graha, Hafis Pratama Rendra

    2016-01-01

    Acrolein is currently produced using propylene from crude oil while its price and scarcity are increasing. A renewable material such as glycerol is an attractive alternative for acrolein production. It can be obtained from crude palm oil (CPO) and is a byproduct of biodiesel production. Besides being able to compete economically, glycerol is an environmentally friendly material. The purpose of this study is to synthesize acrolein from glycerol using FePO4 catalyst in liquid phase dehydration....

  17. Acrolein induces vasodilatation of rodent mesenteric bed via an EDHF-dependent mechanism

    International Nuclear Information System (INIS)

    Awe, S.O.; Adeagbo, A.S.O.; D'Souza, S.E.; Bhatnagar, A.; Conklin, D.J.

    2006-01-01

    Acrolein is generated endogenously during lipid peroxidation and inflammation and is an environmental pollutant. Protein adducts of acrolein are detected in atherosclerotic plaques and neurons of patients with Alzheimer's disease. To understand vascular effects of acrolein exposure, we studied acrolein vasoreactivity in perfused rodent mesenteric bed. Acrolein induced endothelium-dependent vasodilatation that was more robust and more sensitive than dilation induced by 4-hydroxy-trans-2-nonenal, trans-2-hexenal, or propionaldehyde. Acrolein-induced vasodilatation was mediated by K + -sensitive components, e.g., it was abolished in 0 [K + ] o buffer or in 3 mM tetrabutylammonium, inhibited 75% in 50 μM ouabain, and inhibited 64% in 20 mM K + buffer. Moreover, combined treatment with the Ca 2+ -activated K + channel inhibitors 1-[(2-chlorophenyl)diphenylmethyl]-1H-pyrazole (TRAM-34, 100 nM) and apamin (5 μM) significantly reduced vasodilatation without altering sensitivity to acrolein. However, acrolein-induced % dilation was unaffected by L-NAME or indomethacin pretreatment indicating mechanistic independence of NO and prostaglandins. Moreover, acrolein induced vasodilatation in cirazoline-precontracted mesenteric bed of eNOS-null mice confirming eNOS independence. Pretreatment with 6-(2-propargyloxyphenyl) hexanoic acid (PPOH 50 μM), an epoxygenase inhibitor, or the superoxide dismutase mimetic Tempol (100 μM) significantly attenuated acrolein-induced vasodilatation. Collectively, these data indicate that acrolein stimulates mesenteric bed vasodilatation due to endothelium-derived signal(s) that is K + -, ouabain-, PPOH-, and Tempol-sensitive, and thus, a likely endothelium-derived hyperpolarizing factor (EDHF). These data indicate that low level acrolein exposure associated with vascular oxidative stress or inflammation stimulates vasodilatation via EDHF release in medium-sized arteries - a novel function

  18. Cyclodextrin Aldehydes are Oxidase Mimics

    DEFF Research Database (Denmark)

    Fenger, Thomas Hauch; Bjerre, Jeannette; Bols, Mikael

    2009-01-01

    Cyclodextrins containing 6-aldehyde groups were found to catalyse oxidation of aminophenols in the presence of hydrogen peroxide. The catalysis followed Michaelis-Menten kinetics and is related to the catalysis previously observed with cyclodextrin ketones. A range of different cyclodextrin aldeh...

  19. Aldehyde levels in e-cigarette aerosol: Findings from a replication study and from use of a new-generation device.

    Science.gov (United States)

    Farsalinos, Konstantinos E; Kistler, Kurt A; Pennington, Alexander; Spyrou, Alketa; Kouretas, Dimitris; Gillman, Gene

    2018-01-01

    A recent study identified high aldehyde emissions from e-cigarettes (ECs), that when converted to reasonable daily human EC liquid consumption, 5 g/day, gave formaldehyde exposure equivalent to 604-3257 tobacco cigarettes. We replicated this study and also tested a new-generation atomizer under verified realistic (no dry puff) conditions. CE4v2 atomizers were tested at 3.8 V and 4.8 V, and a Nautilus Mini atomizer was tested at 9.0 W and 13.5 W. All measurements were performed in a laboratory ISO-accredited for EC aerosol collection and aldehyde measurements. CE4v2 generated dry puffs at both voltage settings. Formaldehyde levels were >10-fold lower, acetaldehyde 6-9-fold lower and acrolein 16-26-fold lower than reported in the previous study. Nautilus Mini did not generate dry puffs, and minimal aldehydes were emitted despite >100% higher aerosol production per puff compared to CE4v2 (formaldehyde: 16.7 and 16.5 μg/g; acetaldehyde: 9.6 and 10.3 μg/g; acrolein: 8.6 and 11.7 μg/g at 9.0 W and 13.5 W, respectively). EC liquid consumption of 5 g/day reduces aldehyde exposure by 94.4-99.8% compared to smoking 20 tobacco cigarettes. Checking for dry puffs is essential for EC emission testing. Under realistic conditions, new-generation ECs emit minimal aldehydes/g liquid at both low and high power. Validated methods should be used when analyzing EC aerosol. Copyright © 2017 Elsevier Ltd. All rights reserved.

  20. Idh2 Deficiency Exacerbates Acrolein-Induced Lung Injury through Mitochondrial Redox Environment Deterioration

    Directory of Open Access Journals (Sweden)

    Jung Hyun Park

    2017-01-01

    Full Text Available Acrolein is known to be involved in acute lung injury and other pulmonary diseases. A number of studies have suggested that acrolein-induced toxic effects are associated with depletion of antioxidants, such as reduced glutathione and protein thiols, and production of reactive oxygen species. Mitochondrial NADP+-dependent isocitrate dehydrogenase (idh2 regulates mitochondrial redox balance and reduces oxidative stress-induced cell injury via generation of NADPH. Therefore, we evaluated the role of idh2 in acrolein-induced lung injury using idh2 short hairpin RNA- (shRNA- transfected Lewis lung carcinoma (LLC cells and idh2-deficient (idh2−/− mice. Downregulation of idh2 expression increased susceptibility to acrolein via induction of apoptotic cell death due to elevated mitochondrial oxidative stress. Idh2 deficiency also promoted acrolein-induced lung injury in idh2 knockout mice through the disruption of mitochondrial redox status. In addition, acrolein-induced toxicity in idh2 shRNA-transfected LLC cells and in idh2 knockout mice was ameliorated by the antioxidant, N-acetylcysteine, through attenuation of oxidative stress resulting from idh2 deficiency. In conclusion, idh2 deficiency leads to mitochondrial redox environment deterioration, which causes acrolein-mediated apoptosis of LLC cells and acrolein-induced lung injury in idh2−/− mice. The present study supports the central role of idh2 deficiency in inducing oxidative stress resulting from acrolein-induced disruption of mitochondrial redox status in the lung.

  1. Acrolein increases 5-lipoxygenase expression in murine macrophages through activation of ERK pathway.

    Science.gov (United States)

    Kim, Chae E; Lee, Seung J; Seo, Kyo W; Park, Hye M; Yun, Jung W; Bae, Jin U; Bae, Sun S; Kim, Chi D

    2010-05-15

    Episodic exposure to acrolein-rich pollutants has been linked to acute myocardial infarction, and 5-lipoxygenase (5-LO) is involved in the production of matrix metalloproteinase-9 (MMP-9), which destabilizes atherosclerotic plaques. Thus, the present study determined the effect of acrolein on 5-LO/leukotriene B(4) (LTB(4)) production in murine macrophages. Stimulation of J774A.1 cells with acrolein led to increased LTB(4) production in association with increased 5-LO expression. Acrolein-evoked 5-LO expression was blocked by pharmacological inhibition of the ERK pathway, but not by inhibitors for JNK and p38 MAPK pathways. In line with these results, acrolein exclusively increased the phosphorylation of ERK among these MAPK, suggesting a role for the ERK pathway in acrolein-induced 5-LO expression with subsequent production of LTB(4). Among the receptor tyrosine kinases including epidermal growth factor receptor (EGFR) and platelet derived growth factor receptor (PDGFR), acrolein-evoked ERK phosphorylation was attenuated by AG1478, an EGFR inhibitor, but not by AG1295, a PDGFR inhibitor. In addition, acrolein-evoked 5-LO expression was also inhibited by inhibition of EGFR pathway, but not by inhibition of PDGFR pathway. These observations suggest that acrolein has a profound effect on the 5-LO pathway via an EGFR-mediated activation of ERK pathway, leading to acute ischemic syndromes through the generation of LTB(4), subsequent MMP-9 production and plaque rupture.

  2. Acrolein increases 5-lipoxygenase expression in murine macrophages through activation of ERK pathway

    International Nuclear Information System (INIS)

    Kim, Chae E.; Lee, Seung J.; Seo, Kyo W.; Park, Hye M.; Yun, Jung W.; Bae, Jin U.; Bae, Sun S.; Kim, Chi D.

    2010-01-01

    Episodic exposure to acrolein-rich pollutants has been linked to acute myocardial infarction, and 5-lipoxygenase (5-LO) is involved in the production of matrix metalloproteinase-9 (MMP-9), which destabilizes atherosclerotic plaques. Thus, the present study determined the effect of acrolein on 5-LO/leukotriene B 4 (LTB 4 ) production in murine macrophages. Stimulation of J774A.1 cells with acrolein led to increased LTB 4 production in association with increased 5-LO expression. Acrolein-evoked 5-LO expression was blocked by pharmacological inhibition of the ERK pathway, but not by inhibitors for JNK and p38 MAPK pathways. In line with these results, acrolein exclusively increased the phosphorylation of ERK among these MAPK, suggesting a role for the ERK pathway in acrolein-induced 5-LO expression with subsequent production of LTB 4 . Among the receptor tyrosine kinases including epidermal growth factor receptor (EGFR) and platelet derived growth factor receptor (PDGFR), acrolein-evoked ERK phosphorylation was attenuated by AG1478, an EGFR inhibitor, but not by AG1295, a PDGFR inhibitor. In addition, acrolein-evoked 5-LO expression was also inhibited by inhibition of EGFR pathway, but not by inhibition of PDGFR pathway. These observations suggest that acrolein has a profound effect on the 5-LO pathway via an EGFR-mediated activation of ERK pathway, leading to acute ischemic syndromes through the generation of LTB 4 , subsequent MMP-9 production and plaque rupture.

  3. Idh2 Deficiency Exacerbates Acrolein-Induced Lung Injury through Mitochondrial Redox Environment Deterioration.

    Science.gov (United States)

    Park, Jung Hyun; Ku, Hyeong Jun; Lee, Jin Hyup; Park, Jeen-Woo

    2017-01-01

    Acrolein is known to be involved in acute lung injury and other pulmonary diseases. A number of studies have suggested that acrolein-induced toxic effects are associated with depletion of antioxidants, such as reduced glutathione and protein thiols, and production of reactive oxygen species. Mitochondrial NADP + -dependent isocitrate dehydrogenase ( idh2 ) regulates mitochondrial redox balance and reduces oxidative stress-induced cell injury via generation of NADPH. Therefore, we evaluated the role of idh2 in acrolein-induced lung injury using idh2 short hairpin RNA- (shRNA-) transfected Lewis lung carcinoma (LLC) cells and idh2 -deficient ( idh2 -/- ) mice. Downregulation of idh2 expression increased susceptibility to acrolein via induction of apoptotic cell death due to elevated mitochondrial oxidative stress. Idh2 deficiency also promoted acrolein-induced lung injury in idh2 knockout mice through the disruption of mitochondrial redox status. In addition, acrolein-induced toxicity in idh2 shRNA-transfected LLC cells and in idh2 knockout mice was ameliorated by the antioxidant, N-acetylcysteine, through attenuation of oxidative stress resulting from idh2 deficiency. In conclusion, idh2 deficiency leads to mitochondrial redox environment deterioration, which causes acrolein-mediated apoptosis of LLC cells and acrolein-induced lung injury in idh2 -/- mice. The present study supports the central role of idh2 deficiency in inducing oxidative stress resulting from acrolein-induced disruption of mitochondrial redox status in the lung.

  4. Acrolein induced both pulmonary inflammation and the death of lung epithelial cells.

    Science.gov (United States)

    Sun, Yang; Ito, Sachiko; Nishio, Naomi; Tanaka, Yuriko; Chen, Nana; Isobe, Ken-Ichi

    2014-09-02

    Acrolein, a compound found in cigarette smoke, is a major risk factor for respiratory diseases. Previous research determined that both acrolein and cigarette smoke produced reactive oxygen species (ROS). As many types of pulmonary injuries are associated with inflammation, this study sought to ascertain the extent to which exposure to acrolein advanced inflammatory state in the lungs. Our results showed that intranasal exposure of mice to acrolein increased CD11c(+)F4/80(high) macrophages in the lungs and increased ROS formation via induction of NF-κB signaling. Treatment with acrolein activated macrophages and led to their increased production of ROS and expression of several key pro-inflammatory cytokines. In in vitro studies, acrolein treatment of bone marrow-derived GM-CSF-dependent immature macrophages (GM-IMs), activated the cells and led to their increased production of ROS and expression of several key pro-inflammatory cytokines. Acrolein treatment of macrophages induced apoptosis of lung epithelial cells. Inclusion of an inhibitor of ROS formation markedly decreased acrolein-mediated macrophage activation and reduced the extent of epithelial cell death. These results indicate that acrolein can cause lung damage, in great part by mediating the increased release of pro-inflammatory cytokines/factors by macrophages. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.

  5. Hydralazine inhibits compression and acrolein-mediated injuries in ex vivo spinal cord.

    Science.gov (United States)

    Hamann, Kristin; Nehrt, Genevieve; Ouyang, Hui; Duerstock, Brad; Shi, Riyi

    2008-02-01

    We have previously shown that acrolein, a lipid peroxidation byproduct, is significantly increased following spinal cord injury in vivo, and that exposure to neuronal cells results in oxidative stress, mitochondrial dysfunction, increased membrane permeability, impaired axonal conductivity, and eventually cell death. Acrolein thus may be a key player in the pathogenesis of spinal cord injury, where lipid peroxidation is known to be involved. The current study demonstrates that the acrolein scavenger hydralazine protects against not only acrolein-mediated injury, but also compression in guinea pig spinal cord ex vivo. Specifically, hydralazine (500 mumol/L to 1 mmol/L) can significantly alleviate acrolein (100-500 mumol/L)-induced superoxide production, glutathione depletion, mitochondrial dysfunction, loss of membrane integrity, and reduced compound action potential conduction. Additionally, 500 mumol/L hydralazine significantly attenuated compression-mediated membrane disruptions at 2 and 3 h following injury. This was consistent with our findings that acrolein-lys adducts were increased following compression injury ex vivo, an effect that was prevented by hydralazine treatment. These findings provide further evidence for the role of acrolein in spinal cord injury, and suggest that acrolein-scavenging drugs such as hydralazine may represent a novel therapy to effectively reduce oxidative stress in disorders such as spinal cord injury and neurodegenerative diseases, where oxidative stress is known to play a role.

  6. Acrolein inhalation prevents VEGF-induced mobilization of Flk-1+/Sca-1+ cells in mice

    Science.gov (United States)

    Wheat, Laura A.; Haberzettl, Petra; Hellmann, Jason; Baba, Shahid P.; Bertke, Matthew; Lee, Jongmin; McCracken, James; O’Toole, Timothy E.; Bhatnagar, Aruni; Conklin, Daniel J.

    2011-01-01

    Objectives Acrolein is a toxic chemical present in tobacco, wood and coal smoke as well as automobile exhaust. Because exposure to these pollutants is associated with an increase in cardiovascular disease risk, we studied the effects of acrolein on Flk-1+/Sca-1+ cells that are involved in vascular repair. Methods and Results In adult male C57BL/6 mice, inhalation of acrolein (1ppm, 6h/day, 4 days or 5ppm for 2 or 6h) led to the formation of protein-acrolein adducts in the bone marrow and diminished levels of plasma NOx and circulating Flk-1+/Sca-1+ but not Sca-1+ only cells. Acrolein exposure increased the number of apoptotic Flk-1+/Sca1+ cells in circulation, and increased bone marrow-derived cells with endothelial characteristics (Dil-acLDL/UE-lectin and Flk-1+/Sca-1+) in culture. Deficits in the circulating levels of Flk-1+/Sca-1+ cells were reversed after 7 days of recovery in acrolein-free air. Exposure to acrolein blocked VEGF/AMD3100-stimulated mobilization of Flk-1+/Sca-1+ but not Sca-1+ only cells and prevented VEGF-induced phosphorylation of Akt and eNOS in the aorta. Conclusions Inhalation of acrolein increases apoptosis and suppresses the circulating levels of Flk-1+/Sca-1+ cells, while increasing these cells in the bone marrow and preventing their mobilization by VEGF. Exposure to acrolein-rich pollutants could impair vascular repair capacity. PMID:21527748

  7. A single exposure to acrolein causes arrhythmogenesis, cardiac electrical dysfunction and decreased heart rate variability in hypertensive rats

    Science.gov (United States)

    Epidemiological studies demonstrate an association between cardiovascular morbidity, arrhythmias, and exposure to air toxicants such as acrolein. We hypothesized that a single exposure to acrolein would increase arrhythmias and cause changes in the electrocardiogram (ECG) of hype...

  8. An integrated QSAR-PBK/D modelling approach for predicting detoxification and DNA adduct formation of 18 acyclic food-borne α,β-unsaturated aldehydes

    Energy Technology Data Exchange (ETDEWEB)

    Kiwamoto, R., E-mail: reiko.kiwamoto@wur.nl; Spenkelink, A.; Rietjens, I.M.C.M.; Punt, A.

    2015-01-01

    Acyclic α,β-unsaturated aldehydes present in food raise a concern because the α,β-unsaturated aldehyde moiety is considered a structural alert for genotoxicity. However, controversy remains on whether in vivo at realistic dietary exposure DNA adduct formation is significant. The aim of the present study was to develop physiologically based kinetic/dynamic (PBK/D) models to examine dose-dependent detoxification and DNA adduct formation of a group of 18 food-borne acyclic α,β-unsaturated aldehydes without 2- or 3-alkylation, and with no more than one conjugated double bond. Parameters for the PBK/D models were obtained using quantitative structure–activity relationships (QSARs) defined with a training set of six selected aldehydes. Using the QSARs, PBK/D models for the other 12 aldehydes were defined. Results revealed that DNA adduct formation in the liver increases with decreasing bulkiness of the molecule especially due to less efficient detoxification. 2-Propenal (acrolein) was identified to induce the highest DNA adduct levels. At realistic dietary intake, the predicted DNA adduct levels for all aldehydes were two orders of magnitude lower than endogenous background levels observed in disease free human liver, suggesting that for all 18 aldehydes DNA adduct formation is negligible at the relevant levels of dietary intake. The present study provides a proof of principle for the use of QSAR-based PBK/D modelling to facilitate group evaluations and read-across in risk assessment. - Highlights: • Physiologically based in silico models were made for 18 α,β-unsaturated aldehydes. • Kinetic parameters were determined by in vitro incubations and a QSAR approach. • DNA adduct formation was negligible at levels relevant for dietary intake. • The use of QSAR-based PBK/D modelling facilitates group evaluations and read-across.

  9. Molecular Binding Contributes to Concentration Dependent Acrolein Deposition in Rat Upper Airways: CFD and Molecular Dynamics Analyses

    Directory of Open Access Journals (Sweden)

    Jinxiang Xi

    2018-03-01

    Full Text Available Existing in vivo experiments show significantly decreased acrolein uptake in rats with increasing inhaled acrolein concentrations. Considering that high-polarity chemicals are prone to bond with each other, it is hypothesized that molecular binding between acrolein and water will contribute to the experimentally observed deposition decrease by decreasing the effective diffusivity. The objective of this study is to quantify the probability of molecular binding for acrolein, as well as its effects on acrolein deposition, using multiscale simulations. An image-based rat airway geometry was used to predict the transport and deposition of acrolein using the chemical species model. The low Reynolds number turbulence model was used to simulate the airflows. Molecular dynamic (MD simulations were used to study the molecular binding of acrolein in different media and at different acrolein concentrations. MD results show that significant molecular binding can happen between acrolein and water molecules in human and rat airways. With 72 acrolein embedded in 800 water molecules, about 48% of acrolein compounds contain one hydrogen bond and 10% contain two hydrogen bonds, which agreed favorably with previous MD results. The percentage of hydrogen-bonded acrolein compounds is higher at higher acrolein concentrations or in a medium with higher polarity. Computational dosimetry results show that the size increase caused by the molecular binding reduces the effective diffusivity of acrolein and lowers the chemical deposition onto the airway surfaces. This result is consistent with the experimentally observed deposition decrease at higher concentrations. However, this size increase can only explain part of the concentration-dependent variation of the acrolein uptake and acts as a concurrent mechanism with the uptake-limiting tissue ration rate. Intermolecular interactions and associated variation in diffusivity should be considered in future dosimetry modeling of

  10. Molecular Binding Contributes to Concentration Dependent Acrolein Deposition in Rat Upper Airways: CFD and Molecular Dynamics Analyses.

    Science.gov (United States)

    Xi, Jinxiang; Hu, Qin; Zhao, Linlin; Si, Xiuhua April

    2018-03-27

    Existing in vivo experiments show significantly decreased acrolein uptake in rats with increasing inhaled acrolein concentrations. Considering that high-polarity chemicals are prone to bond with each other, it is hypothesized that molecular binding between acrolein and water will contribute to the experimentally observed deposition decrease by decreasing the effective diffusivity. The objective of this study is to quantify the probability of molecular binding for acrolein, as well as its effects on acrolein deposition, using multiscale simulations. An image-based rat airway geometry was used to predict the transport and deposition of acrolein using the chemical species model. The low Reynolds number turbulence model was used to simulate the airflows. Molecular dynamic (MD) simulations were used to study the molecular binding of acrolein in different media and at different acrolein concentrations. MD results show that significant molecular binding can happen between acrolein and water molecules in human and rat airways. With 72 acrolein embedded in 800 water molecules, about 48% of acrolein compounds contain one hydrogen bond and 10% contain two hydrogen bonds, which agreed favorably with previous MD results. The percentage of hydrogen-bonded acrolein compounds is higher at higher acrolein concentrations or in a medium with higher polarity. Computational dosimetry results show that the size increase caused by the molecular binding reduces the effective diffusivity of acrolein and lowers the chemical deposition onto the airway surfaces. This result is consistent with the experimentally observed deposition decrease at higher concentrations. However, this size increase can only explain part of the concentration-dependent variation of the acrolein uptake and acts as a concurrent mechanism with the uptake-limiting tissue ration rate. Intermolecular interactions and associated variation in diffusivity should be considered in future dosimetry modeling of high

  11. Spermine oxidase promotes bile canalicular lumen formation through acrolein production.

    Science.gov (United States)

    Uemura, Takeshi; Takasaka, Tomokazu; Igarashi, Kazuei; Ikegaya, Hiroshi

    2017-11-01

    Spermine oxidase (SMOX) catalyzes oxidation of spermine to generate spermidine, hydrogen peroxide (H 2 O 2 ) and 3-aminopropanal, which is spontaneously converted to acrolein. SMOX is induced by a variety of stimuli including bacterial infection, polyamine analogues and acetaldehyde exposure. However, the physiological functions of SMOX are not yet fully understood. We investigated the physiological role of SMOX in liver cells using human hepatocellular carcinoma cell line HepG2. SMOX localized to the bile canalicular lumen, as determined by F-actin staining. Knockdown of SMOX reduced the formation of bile canalicular lumen. We also found that phospho-Akt (phosphorylated protein kinase B) was localized to canalicular lumen. Treatment with Akt inhibitor significantly reduced the formation of bile canalicular lumen. Acrolein scavenger also inhibited the formation of bile canalicular lumen. PTEN, phosphatase and tensin homolog and an inhibitor of Akt, was alkylated in a SMOX-dependent manner. Our results suggest that SMOX plays a central role in the formation of bile canalicular lumen in liver cells by activating Akt pathway through acrolein production.

  12. Acrolein-exposed normal human lung fibroblasts in vitro: cellular senescence, enhanced telomere erosion, and degradation of Werner's syndrome protein.

    Science.gov (United States)

    Jang, Jun-Ho; Bruse, Shannon; Huneidi, Salam; Schrader, Ronald M; Monick, Martha M; Lin, Yong; Carter, A Brent; Klingelhutz, Aloysius J; Nyunoya, Toru

    2014-09-01

    Acrolein is a ubiquitous environmental hazard to human health. Acrolein has been reported to activate the DNA damage response and induce apoptosis. However, little is known about the effects of acrolein on cellular senescence. We examined whether acrolein induces cellular senescence in cultured normal human lung fibroblasts (NHLF). We cultured NHLF in the presence or absence of acrolein and determined the effects of acrolein on cell proliferative capacity, senescence-associated β-galactosidase activity, the known senescence-inducing pathways (e.g., p53, p21), and telomere length. We found that acrolein induced cellular senescence by increasing both p53 and p21. The knockdown of p53 mediated by small interfering RNA (siRNA) attenuated acrolein-induced cellular senescence. Acrolein decreased Werner's syndrome protein (WRN), a member of the RecQ helicase family involved in DNA repair and telomere maintenance. Acrolein-induced down-regulation of WRN protein was rescued by p53 knockdown or proteasome inhibition. Finally, we found that acrolein accelerated p53-mediated telomere shortening. These results suggest that acrolein induces p53-mediated cellular senescence accompanied by enhanced telomere attrition and WRN protein down-regulation.

  13. HPLC analysis of aldehydes in automobile exhaust gas: Comparison of exhaust odor and irritation in different types of gasoline and diesel engines

    International Nuclear Information System (INIS)

    Roy, Murari Mohon

    2008-01-01

    This study investigated high performance liquid chromatography (HPLC) to identify and measure aldehydes from automobile exhaust gas. Four aldehydes: formaldehyde (HCHO), acetaldehyde (CH 3 CHO), acrolein (H 2 C=CHCHO) and propionaldehyde (CH 3 CH 2 CHO) and one ketone, acetone (CH 3 ) 2 CO are separated. The other higher aldehydes in exhaust gas are very small and cannot be separated. A new method of gas sampling, hereafter called bag sampling in HPLC is introduced instead of the trapping gas sampling method. The superiority of the bag sampling method is its transient gas checking capability. In the second part of this study, HPLC results are applied to compare exhaust odor and irritation of exhaust gases in different types of gasoline and diesel engines. Exhaust odor, irritation and aldehydes are found worst in direct injection (DI) diesel engines and best in some good multi-point injection (MPI) gasoline and direct injection gasoline (DIG) engines. Indirect injection (IDI) diesel engines showed odor, irritation and aldehydes in between the levels of MPI gasoline, DIG and DI diesel engines

  14. Nanocarbons as catalyst for selective oxidation of acrolein to acrylic acid

    Energy Technology Data Exchange (ETDEWEB)

    Frank, B.; Blume, R.; Rinaldi, A.; Trunschke, A.; Schloegl, R. [Fritz Haber Institute of the Max Planck Society, Berlin (Germany). Dept. of Inorganic Chemistry

    2011-07-01

    Selective oxidations are key steps of industrial oil and gas processing for the synthesis of high-value chemicals. Mixed metal oxides based on redox active V or Mo are frequently used for oxidative C-H bond activation. However, multiple processes require precious metals or suffer from low product selectivity demanding an ongoing search for cost-effective alternatives. Recently, the nanostructured carbon was reported to catalyze the metal-free selective alkane activation by oxidative dehydrogenation (ODH). Electron-rich surface carbonyls coordinate this reaction and mimic the active oxygen species in metal oxide catalysts. Here we show that the graphitic carbon, beyond ODH, has the potential to selectively mediate the insertion of an oxygen atom into an organic molecule, i.e., acrolein. Multi-step atom rearrangements considerably exceed the mechanistic complexity of hydrogen abstraction and were so far believed to be the exclusive domain of metal (oxide) catalysis. In the carbon catalyzed process, the nucleophilic oxygen atoms terminating the graphite (0001) surface abstract the formyl hydrogen and the activated aldehyde gets oxidized by epoxide-type mobile oxygen, thus the sp{sup 2} carbon acts as a bifunctional catalyst. Substantial similarities between the metal oxide- and carbon-catalyzed reactions could be identified. Our results shed light on a rarely known facet of applications of nanostructured carbon materials being decorated with diverse oxygen functionalities to coordinate complex catalytic processes. We could successfully transfer the results obtained from the graphite model to carbon nanotubes (CNTs) providing a higher surface area, defect density, and intrinsic activity, to substantially increase the reactivity per catalyst volume. Indeed, low dimensional nanostructured carbon is a highly flexible and robust material which can be modified in a multiple manner to optimize its properties with respect to the intended application. The exploration of

  15. Brain infarction correlates more closely with acrolein than with reactive oxygen species.

    Science.gov (United States)

    Saiki, Ryotaro; Park, Hyerim; Ishii, Itsuko; Yoshida, Madoka; Nishimura, Kazuhiro; Toida, Toshihiko; Tatsukawa, Hideki; Kojima, Soichi; Ikeguchi, Yoshihiko; Pegg, Anthony E; Kashiwagi, Keiko; Igarashi, Kazuei

    2011-01-28

    Although it is thought that the major factor responsible for cell damage is reactive oxygen species (ROS), our recent studies have shown that acrolein is more toxic than ROS. Thus, the relative importance of acrolein and ROS in cell damage during brain infarction was compared using photochemically induced thrombosis model mice. The levels of acrolein-conjugated albumin, and of 4-hydroxynonenal (HNE)-conjugated albumin and 8-OHdG were evaluated as indicators of damage produced by acrolein and ROS, respectively. The increase in acrolein-conjugated albumin was much greater than the increase in HNE-conjugated albumin or 8-OHdG, suggesting that acrolein is more strongly involved in cell damage than ROS during brain infarction. It was also shown that infarction led more readily to RNA damage than to DNA or phospholipid damage. As a consequence, polyamines were released from RNA, and acrolein was produced from polyamines, especially from spermine by spermine oxidase. Production of acrolein from spermine by spermine oxidase was clarified using spermine synthase-deficient Gy mice and transglutaminase 2-knockout mice, in which spermine content is negligible or spermidine/spermine N(1)-acetyltransferase activity is elevated. Copyright © 2010 Elsevier Inc. All rights reserved.

  16. Indoor acrolein emission and decay rates resulting from domestic cooking events

    Science.gov (United States)

    Seaman, Vincent Y.; Bennett, Deborah H.; Cahill, Thomas M.

    2009-12-01

    Acrolein (2-propenal) is a common constituent of both indoor and outdoor air, can exacerbate asthma in children, and may contribute to other chronic lung diseases. Recent studies have found high indoor levels of acrolein and other carbonyls compared to outdoor ambient concentrations. Heated cooking oils produce considerable amounts of acrolein, thus cooking is likely an important source of indoor acrolein. A series of cooking experiments were conducted to determine the emission rates of acrolein and other volatile carbonyls for different types of cooking oils (canola, soybean, corn and olive oils) and deep-frying different food items. Similar concentrations and emission rates of carbonyls were found when different vegetable oils were used to deep-fry the same food product. The food item being deep-fried was generally not a significant source of carbonyls compared to the cooking oil. The oil cooking events resulted in high concentrations of acrolein that were in the range of 26.4-64.5 μg m -3. These concentrations exceed all the chronic regulatory exposure limits and many of the acute exposure limits. The air exchange rate and the decay rate of the carbonyls were monitored to estimate the half-life of the carbonyls. The half-life for acrolein was 14.4 ± 2.6 h, which indicates that indoor acrolein concentrations can persist for considerable time after cooking in poorly-ventilated homes.

  17. Acrolein activates matrix metalloproteinases by increasing reactive oxygen species in macrophages.

    Science.gov (United States)

    O'Toole, Timothy E; Zheng, Yu-Ting; Hellmann, Jason; Conklin, Daniel J; Barski, Oleg; Bhatnagar, Aruni

    2009-04-15

    Acrolein is a ubiquitous component of environmental pollutants such as automobile exhaust, cigarette, wood, and coal smoke. It is also a natural constituent of several foods and is generated endogenously during inflammation or oxidation of unsaturated lipids. Because increased inflammation and episodic exposure to acrolein-rich pollutants such as traffic emissions or cigarette smoke have been linked to acute myocardial infarction, we examined the effects of acrolein on matrix metalloproteinases (MMPs), which destabilize atherosclerotic plaques. Our studies show that exposure to acrolein resulted in the secretion of MMP-9 from differentiated THP-1 macrophages. Acrolein-treatment of macrophages also led to an increase in reactive oxygen species (ROS), free intracellular calcium ([Ca2+](i)), and xanthine oxidase (XO) activity. ROS production was prevented by allopurinol, but not by rotenone or apocynin and by buffering changes in [Ca2+](I) with BAPTA-AM. The increase in MMP production was abolished by pre-treatment with the antioxidants Tiron and N-acetyl cysteine (NAC) or with the xanthine oxidase inhibitors allopurinol or oxypurinol. Finally, MMP activity was significantly stimulated in aortic sections from apoE-null mice containing advanced atherosclerotic lesions after exposure to acrolein ex vivo. These observations suggest that acrolein exposure results in MMP secretion from macrophages via a mechanism that involves an increase in [Ca2+](I), leading to xanthine oxidase activation and an increase in ROS production. ROS-dependent activation of MMPs by acrolein could destabilize atherosclerotic lesions during brief episodes of inflammation or pollutant exposure.

  18. Acrolein-induced cell death in PC12 cells: role of mitochondria-mediated oxidative stress.

    Science.gov (United States)

    Luo, Jian; Robinson, J Paul; Shi, Riyi

    2005-12-01

    Oxidative stress has been implicated in acrolein cytotoxicity in various cell types, including mammalian spinal cord tissue. In this study we report that acrolein also decreases PC12 cell viability in a reactive oxygen species (ROS)-dependent manner. Specifically, acrolein-induced cell death, mainly necrosis, is accompanied by the accumulation of cellular ROS. Elevating ROS scavengers can alleviate acrolein-induced cell death. Furthermore, we show that exposure to acrolein leads to mitochondrial dysfunction, denoted by the loss of mitochondrial transmembrane potential, reduction of cellular oxygen consumption, and decrease of ATP level. This raises the possibility that the cellular accumulation of ROS could result from the increased production of ROS in the mitochondria of PC12 cells as a result of exposure to acrolein. The acrolein-induced significant decrease of ATP production in mitochondria may also explain why necrosis, not apoptosis, is the dominant type of cell death. In conclusion, our data suggest that one possible mechanism of acrolein-induced cell death could be through mitochondria as its initial target. The subsequent increase of ROS then inflicts cell death and further worsens mitochondria function. Such mechanism may play an important role in CNS trauma and neurodegenerative diseases.

  19. Acrolein activates matrix metalloproteinases by increasing reactive oxygen species in macrophages

    International Nuclear Information System (INIS)

    O'Toole, Timothy E.; Zheng Yuting; Hellmann, Jason; Conklin, Daniel J.; Barski, Oleg; Bhatnagar, Aruni

    2009-01-01

    Acrolein is a ubiquitous component of environmental pollutants such as automobile exhaust, cigarette, wood, and coal smoke. It is also a natural constituent of several foods and is generated endogenously during inflammation or oxidation of unsaturated lipids. Because increased inflammation and episodic exposure to acrolein-rich pollutants such as traffic emissions or cigarette smoke have been linked to acute myocardial infarction, we examined the effects of acrolein on matrix metalloproteinases (MMPs), which destabilize atherosclerotic plaques. Our studies show that exposure to acrolein resulted in the secretion of MMP-9 from differentiated THP-1 macrophages. Acrolein-treatment of macrophages also led to an increase in reactive oxygen species (ROS), free intracellular calcium ([Ca 2+ ] i ), and xanthine oxidase (XO) activity. ROS production was prevented by allopurinol, but not by rotenone or apocynin and by buffering changes in [Ca 2+ ] I with BAPTA-AM. The increase in MMP production was abolished by pre-treatment with the antioxidants Tiron and N-acetyl cysteine (NAC) or with the xanthine oxidase inhibitors allopurinol or oxypurinol. Finally, MMP activity was significantly stimulated in aortic sections from apoE-null mice containing advanced atherosclerotic lesions after exposure to acrolein ex vivo. These observations suggest that acrolein exposure results in MMP secretion from macrophages via a mechanism that involves an increase in [Ca 2+ ] I , leading to xanthine oxidase activation and an increase in ROS production. ROS-dependent activation of MMPs by acrolein could destabilize atherosclerotic lesions during brief episodes of inflammation or pollutant exposure.

  20. Acrolein and Human Disease: Untangling the Knotty Exposure Scenarios Accompanying Several Diverse Disorders.

    Science.gov (United States)

    Burcham, Philip C

    2017-01-17

    Acrolein is a highly toxic electrophile that participates in many diseases, yet efforts to delineate its precise mechanistic contributions to specific conditions are complicated by its wide distribution within human environments. This Perspective develops the proposal that due to its mixed status as environmental pollutant, metabolic byproduct, and endotoxicant which forms via ubiquitous pathophysiological processes, many diseases likely involve acrolein released from multiple sources. Although the category boundaries are indistinct, at least four identifiable exposure scenarios are identifiable. First, in some syndromes, such as those accompanying chronic or acute intoxication with smoke, whatever role acrolein plays in disease pathogenesis mainly traces to exogenous sources such as the combustion of tobacco or other organic matter. A second exposure category involves xenobiotics that undergo metabolism within the body to release acrolein. Still other health conditions, however, involve acrolein that forms via several endogenous pathways, some of which are activated upon intoxication with xenobiotics (i.e., Exposure Category 3), while still others accompany direct physical trauma to body tissues (Exposure Category 4). Further complicating efforts to clarify the role of endogenous acrolein in human disease is the likelihood that many such syndromes are complex phenomena that resemble "chemical mixture exposures" by involving multiple toxic substances simultaneously. This Perspective contends that while recent decades have witnessed much progress in describing the deleterious effects of acrolein at the cellular and molecular levels, more work is needed to define the contributions of different acrolein sources to "real-world" health conditions in human subjects.

  1. Protective effect of crocin on acrolein-induced tau phosphorylation in the rat brain.

    Science.gov (United States)

    Rashedinia, Marzieh; Lari, Parisa; Abnous, Khalil; Hosseinzadeh, Hossein

    2015-01-01

    Acrolein, as a by-product of lipid peroxidation, is implicated in brain aging and in the pathogenesis of oxidative stressmediated neurodegenerative disorders such as Alzheimer's disease (AD). Widespread human exposure to the toxic environmental pollutant that is acrolein renders it necessary to evaluate the effects of exogenous acrolein on the brain. This study investigated the toxic effects of oral administration of 3 mg/kg/day acrolein on the rat cerebral cortex. Moreover, the neuroprotective effects of crocin, the main constituent of saffron, against acrolein toxicity were evaluated. We showed that acrolein decreased concentration of glutathione (GSH) and increased levels of malondialdehyde (MDA), Amyloid-beta (Abeta) and phospho-tau in the brain. Simultaneously, acrolein activated Mitogen-Activated Protein Kinases (MAPKs) signalling pathways. Co-administration of crocin significantly attenuated MDA, Abeta and p-tau levels by modulating MAPKs signalling pathways. Our data demonstrated that environmental exposure to acrolein triggers some molecular events which contribute to brain aging and neurodisorders. Additionally, crocin as an antioxidant is a promising candidate for treatment of neurodegenerative disorders, such as brain aging and AD.

  2. SPATIAL AND TEMPORAL VARIABILITY IN ACROLEIN AND SELECT VOLATILE ORGANIC COMPOUNDS IN DETROIT, MICHIGAN

    Science.gov (United States)

    The variability in outdoor concentrations of acrolein, benzene, toluene, ethylbenzene and xylenes (BTEX), and 1,3-butadiene was examined for data measured during summer 2004 of the Detroit Exposure and Aerosol Research Study (DEARS). Results for acrolein indicated no significant...

  3. IRIS TOXICOLOGICAL REVIEW AND SUMMARY DOCUMENTS FOR ACROLEIN (EXTERNAL REVIEW DRAFT)

    Science.gov (United States)

    Acrolein is a colorless to yellowish flammable liquid with a disagreeable, choking odor. The principal use of acrolein is as an intermediate in the synthesis of acrylic acid, which is used to make acrylates, and of DL-methionine, an essential amino acid used as an animal feed su...

  4. Liposomal inhibition of acrolein-induced injury in rat cultured urothelial cells.

    Science.gov (United States)

    Nirmal, J; Wolf-Johnston, A S; Chancellor, M B; Tyagi, P; Anthony, M; Kaufman, J; Birder, L A

    2014-10-01

    To study the protection offered by empty liposomes (LPs) alone against acrolein-induced changes in urothelial cell viability and explored uptake of LPs by primary (rat) urothelial cells. Acrolein was used as a means to induce cellular damage and reduce urothelial cellular viability. The effect of acrolein or liposomal treatment on cellular proliferation was studied using 5-bromo-2'-deoxy-uridine assay. Cytokine release was measured after urothelial cells were exposed to acrolein. Temperature-dependent uptake study was carried out for fluorescent-labeled LPs using confocal microscopy. Liposome pretreatment protected against acrolein-induced decrease in urothelial cell proliferation. LPs also significantly affected the acrolein-induced cytokine (interferon-gamma) release offering protection to the urothelial cells against acrolein damage. We also observed a temperature-dependent urothelial uptake of fluorescent-labeled LPs occurred at 37 °C (but not at 4 °C). Empty LPs alone provide a therapeutic efficacy against acrolein-induced changes in urothelial cell viability and may be a promising local therapy for bladder diseases. Hence, our preliminary evidence provides support for liposome-therapy for urothelial protection and possible repair.

  5. Effect of variable power levels on the yield of total aerosol mass and formation of aldehydes in e-cigarette aerosols.

    Science.gov (United States)

    Gillman, I G; Kistler, K A; Stewart, E W; Paolantonio, A R

    2016-03-01

    The study objective was to determine the effect of variable power applied to the atomizer of refillable tank based e-cigarette (EC) devices. Five different devices were evaluated, each at four power levels. Aerosol yield results are reported for each set of 25 EC puffs, as mass/puff, and normalized for the power applied to the coil, in mass/watt. The range of aerosol produced on a per puff basis ranged from 1.5 to 28 mg, and, normalized for power applied to the coil, ranged from 0.27 to 1.1 mg/watt. Aerosol samples were also analyzed for the production of formaldehyde, acetaldehyde, and acrolein, as DNPH derivatives, at each power level. When reported on mass basis, three of the devices showed an increase in total aldehyde yield with increasing power applied to the coil, while two of the devices showed the opposite trend. The mass of formaldehyde, acetaldehyde, and acrolein produced per gram of total aerosol produced ranged from 0.01 to 7.3 mg/g, 0.006 to 5.8 mg/g, and acrolein from EC aerosols from specific devices, and were compared to estimated exposure from consumption of cigarettes, to occupational and workplace limits, and to previously reported results from other researchers. Copyright © 2015 The Authors. Published by Elsevier Inc. All rights reserved.

  6. Role of endoplasmic reticulum stress in acrolein-induced endothelial activation.

    Science.gov (United States)

    Haberzettl, Petra; Vladykovskaya, Elena; Srivastava, Sanjay; Bhatnagar, Aruni

    2009-01-01

    Acrolein is a ubiquitous environmental pollutant and an endogenous product of lipid peroxidation. It is also generated during the metabolism of several drugs and amino acids. In this study, we examined the effects of acrolein on endothelial cells. Treatment of human umbilical vein endothelial cells (HUVECs) with 2 to 10 microM acrolein led to an increase in the phosphorylation of eIF-2alpha within 10 to 30 min of exposure. This was followed by alternate splicing of XBP-1 mRNA and an increase in the expression of the endoplasmic reticulum (ER) chaperone genes Grp78 and Herp. Within 2-4 h of treatment, acrolein also increased the abundance and the nuclear transport of the transcription factors ATF3, AFT4, and CHOP. Acrolein-induced increase in ATF3 was prevented by treating the cells with the chemical chaperone - phenylbutyric acid (PBA). Treatment with acrolein increased phosphorylation of ERK1/2, p38, and JNK. The increase in JNK phosphorylation was prevented by PBA. Acrolein treatment led to activation and nuclear translocation of the transcription factor NF-kappaB and an increase in TNF-alpha, IL-6 and IL-8, but not MCP-1, mRNA. Increased expression of cytokine genes and NF-kappaB activation were not observed in cells treated with PBA. These findings suggest that exposure to acrolein induces ER stress and triggers the unfolded protein response and that NF-kappaB activation and stimulation of cytokine production by acrolein could be attributed, in part, to ER stress. Chemical chaperones of protein-folding may be useful in treating toxicological and pathological states associated with excessive acrolein exposure or production.

  7. Role of endoplasmic reticulum stress in acrolein-induced endothelial activation

    International Nuclear Information System (INIS)

    Haberzettl, Petra; Vladykovskaya, Elena; Srivastava, Sanjay; Bhatnagar, Aruni

    2009-01-01

    Acrolein is a ubiquitous environmental pollutant and an endogenous product of lipid peroxidation. It is also generated during the metabolism of several drugs and amino acids. In this study, we examined the effects of acrolein on endothelial cells. Treatment of human umbilical vein endothelial cells (HUVECs) with 2 to 10 μM acrolein led to an increase in the phosphorylation of eIF-2α within 10 to 30 min of exposure. This was followed by alternate splicing of XBP-1 mRNA and an increase in the expression of the endoplasmic reticulum (ER) chaperone genes Grp78 and Herp. Within 2-4 h of treatment, acrolein also increased the abundance and the nuclear transport of the transcription factors ATF3, AFT4, and CHOP. Acrolein-induced increase in ATF3 was prevented by treating the cells with the chemical chaperone - phenylbutyric acid (PBA). Treatment with acrolein increased phosphorylation of ERK1/2, p38, and JNK. The increase in JNK phosphorylation was prevented by PBA. Acrolein treatment led to activation and nuclear translocation of the transcription factor NF-κB and an increase in TNF-α, IL-6 and IL-8, but not MCP-1, mRNA. Increased expression of cytokine genes and NF-κB activation were not observed in cells treated with PBA. These findings suggest that exposure to acrolein induces ER stress and triggers the unfolded protein response and that NF-κB activation and stimulation of cytokine production by acrolein could be attributed, in part, to ER stress. Chemical chaperones of protein-folding may be useful in treating toxicological and pathological states associated with excessive acrolein exposure or production

  8. Acrolein relaxes mouse isolated tracheal smooth muscle via a TRPA1-dependent mechanism.

    Science.gov (United States)

    Cheah, Esther Y; Burcham, Philip C; Mann, Tracy S; Henry, Peter J

    2014-05-01

    Airway sensory C-fibres express TRPA1 channels which have recently been identified as a key chemosensory receptor for acrolein, a toxic and highly prevalent component of smoke. TRPA1 likely plays an intermediary role in eliciting a range of effects induced by acrolein including cough and neurogenic inflammation. Currently, it is not known whether acrolein-induced activation of TRPA1 produces other airway effects including relaxation of mouse airway smooth muscle. The aims of this study were to examine the effects of acrolein on airway smooth muscle tone in mouse isolated trachea, and to characterise the cellular and molecular mechanisms underpinning the effects of acrolein. Isometric tension recording studies were conducted on mouse isolated tracheal segments to characterise acrolein-induced relaxation responses. Release of the relaxant PGE₂ was measured by EIA to examine its role in the response. Use of selective antagonists/inhibitors permitted pharmacological characterisation of the molecular and cellular mechanisms underlying this relaxation response. Acrolein induced dose-dependent relaxation responses in mouse isolated tracheal segments. Importantly, these relaxation responses were significantly inhibited by the TRPA1 antagonists AP-18 and HC-030031, an NK₁ receptor antagonist RP-67580, and the EP₂ receptor antagonist PF-04418948, whilst completely abolished by the non-selective COX inhibitor indomethacin. Acrolein also caused rapid PGE₂ release which was suppressed by HC-030031. In summary, acrolein induced a novel bronchodilator response in mouse airways. Pharmacologic studies indicate that acrolein-induced relaxation likely involves interplay between TRPA1-expressing airway sensory C-fibres, NK₁ receptor-expressing epithelial cells, and EP₂-receptor expressing airway smooth muscle cells. Copyright © 2014 Elsevier Inc. All rights reserved.

  9. Process for producing furan from furfural aldehyde

    Science.gov (United States)

    Diebold, James P.; Evans, Robert J.

    1988-01-01

    A process of producing furan and derivatives thereof is disclosed. The process includes generating furfural aldehyde vapors and then passing those vapors over a zeolite catalyst at a temperature and for a residence time effective to decarbonylate the furfural aldehydes to form furans and derivatives thereof. The resultant furan vapors and derivatives are then separated. In a preferred form, the furfural aldehyde vapors are generated during the process of converting biomass materials to liquid and gaseous fuels.

  10. Process for producing furan from furfural aldehyde

    Science.gov (United States)

    Diebold, J.P.; Evans, R.J.

    1987-04-06

    A process of producing furan and derivatives thereof as disclosed. The process includes generating furfural aldehyde vapors and then passing those vapors over a zeolite catalyst at a temperature and for a residence time effective to decarbonylate the furfural aldehydes to form furans and derivatives thereof. The resultant furan vapors and derivatives are then separated. In a preferred form, the furfural aldehyde vapors are generated during the process of converting biomass materials to liquid and gaseous fuels.

  11. Contribution of PPARγ in modulation of acrolein-induced inflammatory signaling in gp91phox knock-out mice.

    Science.gov (United States)

    Yousefipour, Zivar; Chug, Neha; Marek, Katarzyna; Nesbary, Alicia; Mathew, Joseph; Ranganna, Kasturi; Newaz, Mohammad A

    2017-08-01

    Oxidative stress and inflammation are major contributors to acrolein toxicity. Peroxisome proliferator activated receptor gamma (PPARγ) has antioxidant and anti-inflammatory effects. We investigated the contribution of PPARγ ligand GW1929 to the attenuation of oxidative stress in acrolein-induced insult. Male gp91 phox knock-out (KO) mice were treated with acrolein (0.5 mg·(kg body mass) -1 by intraperitoneal injection for 7 days) with or without GW1929 (GW; 0.5 mg·(kg body mass) -1 ·day -1 , orally, for 10 days). The livers were processed for further analyses. Acrolein significantly increased 8-isoprostane and reduced PPARγ activity (P acrolein-treated WT mice, and was reduced by GW1929 (by 65%). KO mice exhibited higher xanthine oxidase (XO). Acrolein increased XO and COX in WT mice and XO in KO mice. GW1929 significantly reduced COX in WT and KO mice and reduced XO in KO mice. Acrolein significantly reduced the total antioxidant status in WT and KO mice (P acrolein-treated WT mice. GW1929 reduced NF-κB levels (by 51%) in KO mice. Acrolein increased CD36 in KO mice (by 43%), which was blunted with GW1929. Data confirms that the generation of free radicals by acrolein is mainly through NAD(P)H, but other oxygenates play a role too. GW1929 may alleviate the toxicity of acrolein by attenuating NF-κB, COX, and CD36.

  12. Studies on the polymerization of acrolein oxime, 13

    International Nuclear Information System (INIS)

    Ota, Tadatoshi; Mori, Yoshikazu; Tamai, Harumi; Masuda, Seizo; Tanaka, Masami.

    1980-01-01

    The radiation-induced polymerization of acrolein oxime was carried out at temperatures ranging from room temperature to -78 0 C, and the resulting low molecular products were analyzed by gas chromatography-mass spectrometry. Acetaldoxime, propionaldoxime, propenylhydroxylamines, dioximes etc. were obtained. Initial processes of the polymerization are discussed on the basis of these reaction products. The present work offers further corroborating evidence for the already-described postulation that an anionic mechanism is operative above room temperature, and a cationic mechanism is predominant below -23 0 C. (author)

  13. Critical role of acrolein in secondary injury following ex vivo spinal cord trauma.

    Science.gov (United States)

    Hamann, Kristin; Durkes, Abigail; Ouyang, Hui; Uchida, Koji; Pond, Amber; Shi, Riyi

    2008-11-01

    The pathophysiology of spinal cord injury (SCI) is characterized by the initial, primary injury followed by secondary injury processes in which oxidative stress is a critical component. Secondary injury processes not only exacerbate pathology at the site of primary injury, but also result in spreading of injuries to the adjacent, otherwise healthy tissue. The lipid peroxidation byproduct acrolein has been implicated as one potential mediator of secondary injury. To further and rigorously elucidate the role of acrolein in secondary injury, a unique ex vivo model is utilized to isolate the detrimental effects of mechanical injury from toxins such as acrolein that are produced endogenously following SCI. We demonstrate that (i) acrolein-Lys adducts are capable of diffusing from compressed tissue to adjacent, otherwise uninjured tissue; (ii) secondary injury by itself produces significant membrane damage and increased superoxide production; and (iii) these injuries are significantly attenuated by the acrolein scavenger hydralazine. Furthermore, hydralazine treatment results in significantly less membrane damage 2 h following compression injury, but not immediately after. These findings support our hypothesis that, following SCI, acrolein is increased to pathologic concentrations, contributes significantly to secondary injury, and thus represents a novel target for scavenging to promote improved recovery.

  14. Doxycycline attenuates acrolein-induced mucin production, in part by inhibiting MMP-9.

    Science.gov (United States)

    Ren, Shuang; Guo, Ling-Li; Yang, Jie; Liu, Dai-Shun; Wang, Tao; Chen, Lei; Chen, Ya-Juan; Xu, Dan; Feng, Yu-Lin; Wen, Fu-Qiang

    2011-01-10

    Matrix metalloproteinases (MMPs), especially MMP-9, have been found to increase the expression of epidermal growth factor (EGF) receptor, a possible regulator of acrolein-induced mucin expression in the airway epithelium. The aim of this study was to investigate whether doxycycline, a tetracycline antibiotic that inhibits MMPs, attenuates mucus production and synthesis of mucin MUC5AC in acrolein-exposed rats. Sprague-Dawley rats were exposed to acrolein aerosol [3.0parts/million (ppm), 6h/day, 12days] and they received 20mg/kg doxycycline daily by gavage, beginning two days before exposure to acrolein until the end of the experiment. The production of mucin glycoproteins and expression of the MMP-9 and MUC5AC genes were measured in rat trachea. The increase in levels of MMP-9 mRNA and protein in airway epithelium after acrolein exposure was accompanied by an increase in MUC5AC mRNA expression. Doxycycline significantly prevented these increases in acrolein-induced expression of MMP-9 and MUC5AC and attenuated mucus production in tracheal epithelium. These results indicate that doxycycline attenuated acrolein-induced mucin synthesis, in part by inhibiting expression of MMP-9. Thus doxycycline may have a prophylactic effect in the treatment of smoking-induced mucus hypersecretion. Crown Copyright © 2010. Published by Elsevier B.V. All rights reserved.

  15. Acute Acrolein Exposure Induces Impairment of Vocal Fold Epithelial Barrier Function.

    Science.gov (United States)

    Liu, Xinxin; Zheng, Wei; Sivasankar, M Preeti

    2016-01-01

    Acrolein is a ubiquitous pollutant abundant in cigarette smoke, mobile exhaust, and industrial waste. There is limited literature on the effects of acrolein on vocal fold tissue, although there are clinical reports of voice changes after pollutant exposures. Vocal folds are responsible for voice production. The overall objective of this study was to investigate the effects of acrolein exposure on viable, excised vocal fold epithelial tissue and to characterize the mechanism underlying acrolein toxicity. Vocal fold epithelia were studied because they form the outermost layer of the vocal folds and are a primary recipient of inhaled pollutants. Porcine vocal fold epithelia were exposed to 0, 50, 100, 500, 900 or 1300 μM of acrolein for 3 hours; the metabolic activity, epithelial resistance, epithelial permeability, tight junction protein (occludin and claudin 3) expression, cell membrane integrity and lipid peroxidation were investigated. The data demonstrated that acrolein exposure at 500 μM significantly reduced vocal fold epithelial metabolic activity by 27.2% (p≤0.001). Incubation with 100 μM acrolein caused a marked increase in epithelial permeability by 130.5% (pacrolein-treated samples, the cell membrane integrity was significantly damaged with a 45.6% increase of lipid peroxidation as compared to controls (pacrolein exposure impairs vocal fold epithelial barrier integrity. Lipid peroxidation-induced cell membrane damage may play an important role in reducing the barrier function of the epithelium.

  16. Ovicidal activity of acrolein vapors to Indian meal moth eggs of various ages.

    Science.gov (United States)

    Pourmirza, Ali Asghr

    2007-09-01

    The effect of acrolein vapors against carefully aged eggs of Indian meal moth at 27 +/- 1 and 17 +/- 1 degrees C at different dosage levels of acrolein over various exposure times was determined. Considerable variation in the susceptibility of different age groups of eggs was apparent in the fiducial limits of the LD50 values. At both temperatures and 24 h exposure period, eggs aged 1-2 day-old were more tolerant to acrolein than other age groups. In all bioassays, eggs exposed to higher dosages of acrolein developed at smaller rate. This was significant for the eggs, which were exposed to the highest dosage for 24 h. Increasing the temperature from 17 +/- 1 to 27 +/- 1 degrees C greatly increased the efficacy of acrolein. Overall, at 27 +/- 1 degrees C eggs of P. interpunctella were killed by less than one-fourth of the dosage required for control at 17 +/- 1 degrees C. Acrolein achieved 50% mortality with a dosage of 3.80 mg L(-1) in 1-2 day-old eggs at 27 +/- 1 degrees C. At this temperature hatching was retarded and greatly reduced when eggs aged 1-2 day-old were exposed to 32 mg L(-1) of acrolein for the 24 h exposure period. There was no evidence of a hatch delay longer than the time spent under vapors for eggs exposed at 17 +/- 1 or 27 +/- 1 degrees C, indicating that some development must have occurred under fumigation.

  17. Scavenging of Toxic Acrolein by Resveratrol and Hesperetin and Identification of Adducts.

    Science.gov (United States)

    Wang, Weixin; Qi, Yajing; Rocca, James R; Sarnoski, Paul J; Jia, Aiqun; Gu, Liwei

    2015-11-04

    The objective of this study was to investigate the ability of resveratrol and hesperetin to scavenge acrolein at pH 7.4 and 37 °C. About 6.4 or 5.2% of acrolein remained after reaction with resveratrol or hesperetin for 12 h at equimolar concentrations. An acrolein-resveratrol adduct and two acrolein-hesperetin adducts were isolated. Their structures were elucidated using mass and NMR spectroscopy. Acrolein reacted with resveratrol at the C-2 and C-3 positions through nucleophilic addition and formed an additional heterocyclic ring. Two similar monoacrolein-conjugated adducts were identified for hesperetin. Spectroscopic data suggested each acrolein-hesperetin adduct was a mixture of four stereoisomers due to the existence of two chiral carbon atoms. Yield of adducts was low at pH 5.4 but increased at pH 7.4 and 8.4. Higher pH also promoted the formation of diacrolein adducts. Results suggest that resveratrol and hesperetin exert health benefits in part through neutralizing toxic acrolein in vivo.

  18. Effects of maternal acrolein exposure during pregnancy on testicular testosterone production in fetal rats.

    Science.gov (United States)

    Yang, Yuzhuo; Zhang, Zhe; Zhang, Hongliang; Hong, Kai; Tang, Wenhao; Zhao, Lianming; Lin, Haocheng; Liu, Defeng; Mao, Jiaming; Wu, Han; Jiang, Hui

    2017-07-01

    Acrolein has been reported to have diverse toxic effects on various organs, including the reproductive system. However, little is known regarding the effects of maternal acrolein exposure on testicular steroidogenesis in male offspring. The present study investigated the effects of acrolein on fetal testosterone production and associated genes. Pregnant Sprague‑Dawley rats were intraperitoneally injected with vehicle (normal saline) or 1, 2 or 5 mg/kg acrolein from gestational day (GD) 14‑20, and fetal testes were examined on GD 21. Fetal body and testicular weights were markedly reduced in pups following exposure to high doses of acrolein (5 mg/kg) in late pregnancy. Notably, in utero exposure of 5 mg/kg acrolein significantly decreased the testicular testosterone level and downregulated the expression levels of steroidogenic acute regulatory protein (StAR) and 3β‑hydroxysteroid dehydrogenase (3β‑HSD), whereas the levels of other steroidogenic enzymes, including scavenger receptor class B, cholesterol side‑chain cleavage enzyme and steroid 17 alpha‑hydroxylase/17,20 lyase, were unaffected. Furthermore, the 3β‑HSD immunoreactive area in the interstitial region of the fetal testes was reduced at a 5 mg/kg dose, whereas the protein expression levels of 4‑hydroxynonenalwere dose‑dependently increased following maternal exposure to acrolein. mRNA expression levels of insulin‑like factor 3, a critical gene involved in testicular descent, were unaltered following maternal acrolein exposure. Taken together, the results of the present study suggested that maternal exposure to high doses of acrolein inhibited fetal testosterone synthesis, and abnormal expression of StAR and 3β‑HSD may be associated with impairment of the steroidogenic capacity.

  19. Acute Acrolein Exposure Induces Impairment of Vocal Fold Epithelial Barrier Function.

    Directory of Open Access Journals (Sweden)

    Xinxin Liu

    Full Text Available Acrolein is a ubiquitous pollutant abundant in cigarette smoke, mobile exhaust, and industrial waste. There is limited literature on the effects of acrolein on vocal fold tissue, although there are clinical reports of voice changes after pollutant exposures. Vocal folds are responsible for voice production. The overall objective of this study was to investigate the effects of acrolein exposure on viable, excised vocal fold epithelial tissue and to characterize the mechanism underlying acrolein toxicity. Vocal fold epithelia were studied because they form the outermost layer of the vocal folds and are a primary recipient of inhaled pollutants. Porcine vocal fold epithelia were exposed to 0, 50, 100, 500, 900 or 1300 μM of acrolein for 3 hours; the metabolic activity, epithelial resistance, epithelial permeability, tight junction protein (occludin and claudin 3 expression, cell membrane integrity and lipid peroxidation were investigated. The data demonstrated that acrolein exposure at 500 μM significantly reduced vocal fold epithelial metabolic activity by 27.2% (p≤0.001. Incubation with 100 μM acrolein caused a marked increase in epithelial permeability by 130.5% (p<0.05 and a reduction in transepithelial electrical resistance (TEER by 180.0% (p<0.001. While the expression of tight junctional protein did not change in acrolein-treated samples, the cell membrane integrity was significantly damaged with a 45.6% increase of lipid peroxidation as compared to controls (p<0.05. Taken together, these data provide evidence that acute acrolein exposure impairs vocal fold epithelial barrier integrity. Lipid peroxidation-induced cell membrane damage may play an important role in reducing the barrier function of the epithelium.

  20. Acrolein decreases endothelial cell migration and insulin sensitivity through induction of let-7a.

    Science.gov (United States)

    O'Toole, Timothy E; Abplanalp, Wesley; Li, Xiaohong; Cooper, Nigel; Conklin, Daniel J; Haberzettl, Petra; Bhatnagar, Aruni

    2014-08-01

    Acrolein is a major reactive component of vehicle exhaust, and cigarette and wood smoke. It is also present in several food substances and is generated endogenously during inflammation and lipid peroxidation. Although previous studies have shown that dietary or inhalation exposure to acrolein results in endothelial activation, platelet activation, and accelerated atherogenesis, the basis for these effects is unknown. Moreover, the effects of acrolein on microRNA (miRNA) have not been studied. Using AGILENT miRNA microarray high-throughput technology, we found that treatment of cultured human umbilical vein endothelial cells with acrolein led to a significant (>1.5-fold) upregulation of 12, and downregulation of 15, miRNAs. Among the miRNAs upregulated were members of the let-7 family and this upregulation was associated with decreased expression of their protein targets, β3 integrin, Cdc34, and K-Ras. Exposure to acrolein attenuated β3 integrin-dependent migration and reduced Akt phosphorylation in response to insulin. These effects of acrolein on endothelial cell migration and insulin signaling were reversed by expression of a let-7a inhibitor. Also, inhalation exposure of mice to acrolein (1 ppm x 6 h/day x 4 days) upregulated let-7a and led to a decrease in insulin-stimulated Akt phosphorylation in the aorta. These results suggest that acrolein exposure has broad effects on endothelial miRNA repertoire and that attenuation of endothelial cell migration and insulin signaling by acrolein is mediated in part by the upregulation of let-7a. This mechanism may be a significant feature of vascular injury caused by inflammation, oxidized lipids, and exposure to environmental pollutants. © The Author 2014. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For permissions, please email: journals.permissions@oup.com.

  1. ROLE OF ENDOPLASMIC RETICULUM STRESS IN ACROLEIN-INDUCED ENDOTHELIAL ACTIVATION

    OpenAIRE

    Haberzettl, Petra; Vladykovskaya, Elena; Srivastava, Sanjay; Bhatnagar, Aruni

    2008-01-01

    Acrolein is a ubiquitous environmental pollutant and an endogenous product of lipid peroxidation. It is also generated during the metabolism of several drugs and amino acids. In this study, we examined the effects of acrolein on endothelial cells. Treatment of human umbilical vein endothelial cells (HUVECs) with 2 to 10 μM acrolein led to an increase in the phosphorylation of eIF-2α within 10 to 30 min of exposure. This was followed by alternate splicing of XBP-1 mRNA and an increase in the e...

  2. Adaptation to acrolein through upregulating the protection by glutathione in human bronchial epithelial cells: the materialization of the hormesis concept.

    Science.gov (United States)

    Sthijns, Mireille M J P E; Randall, Matthew J; Bast, Aalt; Haenen, Guido R M M

    2014-04-18

    Acrolein is a thiol reactive compound present in cigarette smoke and plays a pivotal role in the deleterious effects of smoking. Acrolein causes toxicity in human bronchial epithelial cells in a dose dependent manner. GSH forms the first line of defense against acrolein-induced toxicity. At high doses of acrolein (⩾10 μM) the capacity of the cellular protection by GSH is overwhelmed and GSH is not able to quench all the acrolein, resulting in cytotoxicity. At a relatively low dose of acrolein (3 μM), no cytotoxicity is observed due to protection by GSH. Moreover we found that exposure to a low dose of acrolein protects cells against the toxic effect of a second higher dose of acrolein. The adaptation to acrolein is induced via Nrf2 mediated gene expression of γ-glutamylcysteine synthetase leading to elevated GSH levels. This upregulation of the protection by GSH demonstrates a hormetic response to acrolein. Hormesis is an adaptive or compensatory response induced by a relatively subtle challenge of homeostasis by a toxic compound. Insight into the mechanism of hormesis is mandatory for a more accurate societal regulation of toxic compounds. Copyright © 2014 Elsevier Inc. All rights reserved.

  3. Theoretical studies of acrolein hydrogenation on Au20 nanoparticle

    Science.gov (United States)

    Li, Zhe; Chen, Zhao-Xu; He, Xiang; Kang, Guo-Jun

    2010-05-01

    Gold nanoparticles play a key role in catalytic processes. We investigated the kinetics of stepwise hydrogenation of acrolein on Au20 cluster model and compared with that on Au(110) surface. The rate-limiting step barrier of CC reduction is about 0.5 eV higher than that of CO hydrogenation on Au(110) surface. On Au20 nanoparticle, however, the energy barrier of the rate-determining step for CC hydrogenation turns out to be slightly lower than the value for the CO reduction. The selectivity difference on the two substrate models are attributed to different adsorption modes of acrolein: via the CC on Au20, compared to through both CC and CO on Au(110). The preference switch implies that the predicted selectivity of competitive hydrogenation depends on substrate model sensitively, and particles with more low-coordinated Au atoms than flat surfaces are favorable for CC hydrogenation, which is in agreement with experimental result.

  4. Acrolein in wine: importance of 3-hydroxypropionaldehyde and derivatives in production and detection.

    Science.gov (United States)

    Bauer, Rolene; Cowan, Donald A; Crouch, Andrew

    2010-03-24

    Certain lactic acid bacteria strains belonging to the genus Lactobacillus have been implicated in the accumulation of 3-hydroxypropionaldehyde (3-HPA) during anaerobic glycerol fermentation. In aqueous solution 3-HPA undergoes reversible dimerization and hydration, resulting in an equilibrium state between different derivatives. Wine quality may be compromised by the presence of 3-HPA due to the potential for spontaneous conversion into acrolein under winemaking conditions. Acrolein is highly toxic and has been implicated in the development of bitterness in wine. Interconversion between 3-HPA derivatives and acrolein is a complex and highly dynamic process driven by hydration and dehydration reactions. Acrolein is furthermore highly reactive and its steady-state concentration in complex systems very low. As a result, analytical detection and quantification in solution is problematic. This paper reviews the biochemical and environmental conditions leading to accumulation of its precursor, 3-HPA. Recent advances in analytical detection are summarized, and the roles played by natural chemical derivatives are highlighted.

  5. Respiratory Effects and Systemic Stress Response Following Acute Acrolein Inhalation in Rats

    Data.gov (United States)

    U.S. Environmental Protection Agency — This data set is an Excel file pertaining to the study that examined nasal, pulmonary, and systemic effects of acrolein in rats acutely exposed to a range of...

  6. Protein conjugated with aldehydes derived from lipid peroxidation as an independent parameter of the carbonyl stress in the kidney damage

    Directory of Open Access Journals (Sweden)

    Medina-Navarro Rafael

    2011-11-01

    Full Text Available Abstract Background One of the well-defined and characterized protein modifications usually produced by oxidation is carbonylation, an irreversible non-enzymatic modification of proteins. However, carbonyl groups can be introduced into proteins by non-oxidative mechanisms. Reactive carbonyl compounds have been observed to have increased in patients with renal failure. In the present work we have described a procedure designed as aldehyde capture to calculate the protein carbonyl stress derived solely from lipid peroxidation. Methods Acrolein-albumin adduct was prepared as standard at alkaline pH. Rat liver microsomal membranes and serum samples from patients with diabetic nephropathy were subjected to the aldehyde capture procedure and aldol-protein formation. Before alkalinization and incubation, samples were precipitated and redisolved in 6M guanidine. The absorbances of the samples were read with a spectrophotometer at 266 nm against a blank of guanidine. Results Evidence showed abundance of unsaturated aldehydes derived from lipid peroxidation in rat liver microsomal membranes and in the serum of diabetic patients with advanced chronic kidney disease. Carbonyl protein and aldol-proteins resulted higher in the diabetic nephropathy patients (p Conclusion The aldehyde-protein adduct represents a non oxidative component of carbonyl stress, independent of the direct amino acid oxidation and could constitute a practical and novelty strategy to measure the carbonyl stress derived solely from lipid peroxidation and particularly in diabetic nephropathy patients. In addition, we are in a position to propose an alternative explanation of why alkalinization of urine attenuates rhabdomyolysis-induced renal dysfunction.

  7. Effects of acrolein on aldosterone release from zona glomerulosa cells in male rats.

    Science.gov (United States)

    Wang, Kai-Lee; Huang, Wen-Ching; Chou, Jou-Chun; Weng, Ting-Chun; Hu, Sindy; Lieu, Fu-Kong; Lai, Wei-Ho; Idova, Galina; Wang, Paulus S; Wang, Shyi-Wu

    2016-07-01

    A positive correlation between smoking and hypertension has been well established. Acrolein is a major toxic volatile compound found in cigarette smoke. Human exposure to low levels of acrolein is unavoidable due to its production in daily activities, such as smoke from industrial, hot oil cooking vapors, and exhaust fumes from vehicles. The toxicity and the action mechanism of acrolein to induce apoptosis have been extensively studied, but the effects of acrolein on hypertension are still unknown. The present study aimed to examine the effects of acrolein on aldosterone release both in vivo and in vitro. Male rats were divided into three groups, and intraperitoneally injected with normal saline, or acrolein (2mg/kg) for 1 (group A-1) or 3 (group A-3) days, respectively. After sacrificing, rat blood samples were obtained to measure plasma aldosterone and angiotensin II (Ang II) levels. Zona glomerulosa (ZG) cells were prepared from rat adrenal cortex, and were incubated with or without stimulants. We found that the serum aldosterone was increased by 1.2-fold (pacrolein enhanced the stimulatory effects of Ang II and 8-bromo-cyclic AMP on aldosterone secretion from ZG cells prepared in both A-1 and A-3 groups. Furthermore, the enzyme activity of P450scc, the rate-limiting step of aldosterone synthesis, was elevated after acrolein injection. Plasma level of Ang II was increased in both A-1 and A-3 groups. These results suggested that acrolein exposure increased aldosterone production, at least in part, through elevating the level of plasma Ang II and stimulating steroidogenesis pathways. Copyright © 2016 Elsevier Inc. All rights reserved.

  8. Idh2 Deficiency Exacerbates Acrolein-Induced Lung Injury through Mitochondrial Redox Environment Deterioration

    OpenAIRE

    Park, Jung Hyun; Ku, Hyeong Jun; Lee, Jin Hyup; Park, Jeen-Woo

    2017-01-01

    Acrolein is known to be involved in acute lung injury and other pulmonary diseases. A number of studies have suggested that acrolein-induced toxic effects are associated with depletion of antioxidants, such as reduced glutathione and protein thiols, and production of reactive oxygen species. Mitochondrial NADP+-dependent isocitrate dehydrogenase (idh2) regulates mitochondrial redox balance and reduces oxidative stress-induced cell injury via generation of NADPH. Therefore, we evaluated the ro...

  9. Synthesis of Acrolein from Glycerol Using FePO4 Catalyst in Liquid Phase Dehydration

    Directory of Open Access Journals (Sweden)

    Akhmad Zainal Abidin

    2016-02-01

    Full Text Available Acrolein is currently produced using propylene from crude oil while its price and scarcity are increasing. A renewable material such as glycerol is an attractive alternative for acrolein production. It can be obtained from crude palm oil (CPO and is a byproduct of biodiesel production. Besides being able to compete economically, glycerol is an environmentally friendly material. The purpose of this study is to synthesize acrolein from glycerol using FePO4 catalyst in liquid phase dehydration. The catalyst was prepared by three different methods: hydrothermal (catalyst A, deposition at Fe/P = 1.15 (catalyst B, and deposition at Fe/P = 1.20 (catalyst C. The experimental reaction temperature was varied at 220, 240 and 260 °C under constant atmospheric pressure. The results showed that catalyst C provided the best yield (91%, followed by catalyst A (90% and catalyst B (82%. The increasing reaction temperature showed a tendency to increase the yield of acrolein, while the presence of oxygen reduced the yield of acrolein and allowed the reaction to produce more side products such as glycerol propanal, acetaldehyde, and propionate. Catalyst reuse without any regeneration resulted in a yield profile of acrolein that continued to decline.

  10. A tailored catalyst for the sustainable conversion of glycerol to acrolein: mechanistic aspect of sequential dehydration.

    Science.gov (United States)

    Yun, Danim; Kim, Tae Yong; Park, Dae Sung; Yun, Yang Sik; Han, Jeong Woo; Yi, Jongheop

    2014-08-01

    Developing a catalyst to resolve deactivation caused from coke is a primary challenge in the dehydration of glycerol to acrolein. An open-macropore-structured and Brønsted-acidic catalyst (Marigold-like silica functionalized with sulfonic acid groups, MS-FS) was synthesized for the stable and selective production of acrolein from glycerol. A high acrolein yield of 73% was achieved and maintained for 50 h in the presence of the MS-FS catalyst. The hierarchical structure of the catalyst with macropores was found to have an important effect on the stability of the catalyst because coke polymerization and pore blocking caused by coke deposition were inhibited. In addition, the behavior of 3-hydroxypropionaldehyde (3-HPA) during the sequential dehydration was studied using density functional theory (DFT) calculations because 3-HPA conversion is one of the main causes for coke formation. We found that the easily reproducible Brønsted acid sites in MS-FS permit the selective and stable production of acrolein. This is because the reactive intermediate (3-HPA) is readily adsorbed on the regenerated acid sites, which is essential for the selective production of acrolein during the sequential dehydration. The regeneration ability of the acid sites is related not only to the selective production of acrolein but also to the retardation of catalyst deactivation by suppressing the formation of coke precursors originating from 3-HPA degradation. © 2014 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

  11. Selective Hydrogenation of Acrolein Over Pd Model Catalysts: Temperature and Particle-Size Effects.

    Science.gov (United States)

    O'Brien, Casey P; Dostert, Karl-Heinz; Schauermann, Swetlana; Freund, Hans-Joachim

    2016-10-24

    The selectivity in the hydrogenation of acrolein over Fe 3 O 4 -supported Pd nanoparticles has been investigated as a function of nanoparticle size in the 220-270 K temperature range. While Pd(111) shows nearly 100 % selectivity towards the desired hydrogenation of the C=O bond to produce propenol, Pd nanoparticles were found to be much less selective towards this product. In situ detection of surface species by using IR-reflection absorption spectroscopy shows that the selectivity towards propenol critically depends on the formation of an oxopropyl spectator species. While an overlayer of oxopropyl species is effectively formed on Pd(111) turning the surface highly selective for propenol formation, this process is strongly hindered on Pd nanoparticles by acrolein decomposition resulting in CO formation. We show that the extent of acrolein decomposition can be tuned by varying the particle size and the reaction temperature. As a result, significant production of propenol is observed over 12 nm Pd nanoparticles at 250 K, while smaller (4 and 7 nm) nanoparticles did not produce propenol at any of the temperatures investigated. The possible origin of particle-size dependence of propenol formation is discussed. This work demonstrates that the selectivity in the hydrogenation of acrolein is controlled by the relative rates of acrolein partial hydrogenation to oxopropyl surface species and of acrolein decomposition, which has significant implications for rational catalyst design. © 2016 Wiley-VCH Verlag GmbH & Co. KGaA, Weinheim.

  12. Acrolein inhibits NADH-linked mitochondrial enzyme activity: implications for Alzheimer's disease.

    Science.gov (United States)

    Pocernich, Chava B; Butterfield, D Allan

    2003-01-01

    In Alzheimer's disease (AD) brain increased lipid peroxidation and decreased energy utilization are found. Mitochondria membranes contain a significant amount of arachidonic and linoleic acids, precursors of lipid peroxidation products, 4-hydroxynonenal (HNE) and 2-propen-1-al (acrolein), that are extremely reactive. Both alkenals are increased in AD brain. In this study, we examined the effects of nanomolar levels of acrolein on the activities of pyruvate dehydrogenase (PDH) and Alpha-ketoglutarate dehydrogenase (KGDH), both reduced nicotinamide adenine dinucleotide (NADH)-linked mitochondrial enzymes. Acrolein decreased PDH and KGDH activities significantly in a dose-dependent manner. Using high performance liquid chromatography coupled to mass spectrometry (HPLC-MS), acrolein was found to bind lipoic acid, a component in both the PDH and KGDH complexes, most likely explaining the loss of enzyme activity. Acrolein also interacted with oxidized nicotinamide adenine dinucleotide (NAD(+)) in such a way as to decrease the production of NADH. Acrolein, which is increased in AD brain, may be partially responsible for the dysfunction of mitochondria and loss of energy found in AD brain by inhibition of PDH and KGDH activities, potentially contributing to the neurodegeneration in this disorder.

  13. Acrolein-activated matrix metalloproteinase 9 contributes to persistent mucin production.

    Science.gov (United States)

    Deshmukh, Hitesh S; Shaver, Colleen; Case, Lisa M; Dietsch, Maggie; Wesselkamper, Scott C; Hardie, William D; Korfhagen, Thomas R; Corradi, Massimo; Nadel, Jay A; Borchers, Michael T; Leikauf, George D

    2008-04-01

    Chronic obstructive pulmonary disease (COPD), a global public health problem, is characterized by progressive difficulty in breathing, with increased mucin production, especially in the small airways. Acrolein, a constituent of cigarette smoke and an endogenous mediator of oxidative stress, increases airway mucin 5, subtypes A and C (MUC5AC) production; however, the mechanism remains unclear. In this study, increased mMUC5AC transcripts and protein were associated with increased lung matrix metalloproteinase 9 (mMMP9) transcripts, protein, and activity in acrolein-exposed mice. Increased mMUC5AC transcripts and mucin protein were diminished in gene-targeted Mmp9 mice [Mmp9((-/-))] or in mice treated with an epidermal growth factor receptor (EGFR) inhibitor, erlotinib. Acrolein also decreased mTissue inhibitor of metalloproteinase protein 3 (an MMP9 inhibitor) transcript levels. In a cell-free system, acrolein increased pro-hMMP9 cleavage and activity in concentrations (100-300 nM) found in sputum from subjects with COPD. Acrolein increased hMMP9 transcripts in human airway cells, which was inhibited by an MMP inhibitor, EGFR-neutralizing antibody, or a mitogen-activated protein kinase (MAPK) 3/2 inhibitor. Together these findings indicate that acrolein can initiate cleavage of pro-hMMP9 and EGFR/MAPK signaling that leads to additional MMP9 formation. Augmentation of hMMP9 activity, in turn, could contribute to persistent excessive mucin production.

  14. [Changes of the Expression of Brain Derived Neurotrophic Factors in Rats Trachea Induced by Acrolein Exposure].

    Science.gov (United States)

    Yuan, Bing; Yang, Rui-an; Zhao, Wei; Xu, Yan-yan; Dan, Qi-qin; Zhang, Yun-hui

    2015-07-01

    To investigate expressional changes of brain derived neurotrophic factor (BDNF) in the trachea of rats with acrolein inhalation. Twenty two SD rats were divided into 2 groups: the rats in experimental group were subjected to acrolein inhalation for the induce of trachea inflammatory injury, while the rats with saline (NS) inhalation were as control. All the rats were sacrificed in 1,3,6 weeks after acrolein (n = 11 at each time point) or saline inhalation (n = 11 at each time point), the samples of trachea epithelium were harvested. The immunohistochemistry and in situ hybridization was performed to detect the location of BDNF protein and mRNA in trachea. The expression of BDNF mRNA in the trachea tissues were determined by RT-PCR. There are positive cells in epithelium of trachea for BDNF protein and mRNA, with cytoplasm staining. The expression of BDNF mRNA in the trachea was increased at 1 week after acrolein inhalation (P 0.05). The inflammatory injury in trachea induced by acrolein exposure could be associated with the increased expression of BDNF. BDNF may be one of the crucial inflammatory factors in the process of inflammatory reaction in trachea with acrolein stimulation.

  15. Enhancement of the Acrolein-Induced Production of Reactive Oxygen Species and Lung Injury by GADD34

    OpenAIRE

    Sun, Yang; Ito, Sachiko; Nishio, Naomi; Tanaka, Yuriko; Chen, Nana; Liu, Lintao; Isobe, Ken-ichi

    2015-01-01

    Chronic obstructive pulmonary disease (COPD) is characterized by lung destruction and inflammation. As a major compound of cigarette smoke, acrolein plays a critical role in the induction of respiratory diseases. GADD34 is known as a growth arrest and DNA damage-related gene, which can be overexpressed in adverse environmental conditions. Here we investigated the effects of GADD34 on acrolein-induced lung injury. The intranasal exposure of acrolein induced the expression of GADD34, developing...

  16. Acrolein stimulates the synthesis of IL-6 and C-reactive protein (CRP) in thrombosis model mice and cultured cells.

    Science.gov (United States)

    Saiki, Ryotaro; Hayashi, Daisuke; Ikuo, Yukiko; Nishimura, Kazuhiro; Ishii, Itsuko; Kobayashi, Kaoru; Chiba, Kan; Toida, Toshihiko; Kashiwagi, Keiko; Igarashi, Kazuei

    2013-12-01

    Measurements of protein-conjugated acrolein (PC-Acro), IL-6, and C-reactive protein (CRP) in plasma were useful for identifying silent brain infarction with high sensitivity and specificity. The aim of this study was to determine whether acrolein causes increased production of IL-6 and CRP in thrombosis model mice and cultured cells. In mice with photochemically induced thrombosis, acrolein produced at the locus of infarction increased the level of IL-6 and then CRP in plasma. This was confirmed in cell culture systems - acrolein stimulated the production of IL-6 in mouse neuroblastoma Neuro-2a cells, mouse macrophage-like J774.1 cells, and human umbilical vein endothelial cells (HUVEC), and IL-6 in turn stimulated the production of CRP in human hepatocarcinoma cells. The level of IL-6 mRNA was increased by acrolein through an increase in phosphorylation of the transcription factors, c-Jun, and NF-κB p65. Furthermore, CRP stimulated IL-6 production in mouse macrophage-like J774.1 cells and HUVEC. IL-6 functioned as a protective factor against acrolein toxicity in Neuro-2a cells and HUVEC. These results show that acrolein stimulates the synthesis of IL-6 and CRP, which function as protecting factors against acrolein toxicity, and that the combined measurement of PC-Acro, IL-6, and CRP is effective for identification of silent brain infarction. The combined measurements of protein-conjugated acrolein (PC-Acro), IL-6, and C-reactive protein (CRP) in plasma were useful for identifying silent brain infarction. The aim of this study was to determine whether acrolein causes increased production of IL-6 and CRP, and indeed acrolein increased IL-6 synthesis and IL-6 in turn increased CRP synthesis. Furthermore, IL-6 decreased acrolein toxicity in several cell lines. © 2013 International Society for Neurochemistry.

  17. Acrolein induces cyclooxygenase-2 and prostaglandin production in human umbilical vein endothelial cells: roles of p38 MAP kinase.

    Science.gov (United States)

    Park, Yong Seek; Kim, Jayoung; Misonou, Yoshiko; Takamiya, Rina; Takahashi, Motoko; Freeman, Michael R; Taniguchi, Naoyuki

    2007-06-01

    Acrolein, a known toxin in tobacco smoke, might be involved in atherogenesis. This study examined the effect of acrolein on expression of cyclooxygenase-2 (COX-2) and prostaglandin (PG) production in endothelial cells. Cyclooxygenase (COX)-2 induction by acrolein and signal pathways were measured using Western blots, Northern blots, immunofluorescence, ELISA, gene silencing, and promoter assay. Colocalization of COX2 and acrolein-adduct was determined by immunohistochemistry. Here we report that the levels of COX-2 mRNA and protein are increased in human umbilical vein endothelial cells (HUVECs) after acrolein exposure. COX-2 was found to colocalize with acrolein-lysine adducts in human atherosclerotic lesions. Inhibition of p38 MAPK activity abolished the induction of COX-2 protein and PGE2 accumulation by acrolein, while suppression of extracellular signal-regulated kinase (ERK) and JNK activity had no effect on the induction of COX-2 expression in experiments using inhibitors and siRNA. Furthermore, rottlerin, an inhibitor of protein kinase Cdelta (PKCdelta), abrogated the upregulation of COX-2 at both protein and mRNA levels. These results provide that acrolein may play a role in progression of atherosclerosis and new information on the signaling pathways involved in COX-2 upregulation in response to acrolein and provide evidence that PKCdelta and p38 MAPK are required for transcriptional activation of COX-2.

  18. Inhibition of acrolein-stimulated MUC5AC expression by Platycodon grandiflorum root-derived saponin in A549 cells.

    Science.gov (United States)

    Choi, Jae Ho; Hwang, Yong Pil; Han, Eun Hee; Kim, Hyung Gyun; Park, Bong Hwan; Lee, Hyun Sun; Park, Byung Keun; Lee, Young Chun; Chung, Young Chul; Jeong, Hye Gwang

    2011-09-01

    Mucin overproduction is a hallmark of chronic airway diseases such as chronic obstructive pulmonary disease. In this study, we investigated the inhibition of acrolein-induced expression of mucin 5, subtypes A and C (MUC5AC) by Changkil saponin (CKS) in A549 cells. Acrolein, a known toxin in tobacco smoke and an endogenous mediator of oxidative stress, increases the expression of airway MUC5AC, a major component of airway mucus. CKS, a Platycodon grandiflorum root-derived saponin, inhibited acrolein-induced MUC5AC expression and activity, through the suppression of NF-κB activation. CKS also repressed acrolein-induced phosphorylation of ERK1/2, JNK1/2, and p38MAPK, which are upstream signaling molecules that control MUC5AC expression. In addition, the MAPK inhibitors PD98059 (ERK1/2), SP600125 (JNK1/2), and SB203580 (p38 MAPK), and a PKC delta inhibitor (rottlerin; PKCδ) inhibited acrolein-induced MUC5AC expression and activity. CKS repressed acrolein-induced phosphorylation of PKCδ. Moreover, a reactive oxygen species (ROS) inhibitor, N-acetylcysteine, inhibited acrolein-induced MUC5AC expression and activity through the suppression of PKCδ and MAPK activation, and CKS repressed acrolein-induced ROS production. These results suggest that CKS suppresses acrolein-induced MUC5AC expression by inhibiting the activation of NF-κB via ROS-PKCδ-MAPK signaling. Copyright © 2011 Elsevier Ltd. All rights reserved.

  19. Acute systemic accumulation of acrolein in mice by inhalation at a concentration similar to that in cigarette smoke.

    Science.gov (United States)

    Tully, Melissa; Zheng, Lingxing; Acosta, Glen; Tian, Ran; Shi, Riyi

    2014-12-01

    Cigarette smoke is an important environmental factor associated with a wide array of public health concerns. Acrolein, a component of tobacco smoke and a known toxin to various cell types, may be a key pathological factor mediating the adverse effects linked with tobacco smoke. Although acrolein is known to accumulate in the respiratory system after acute nasal exposure, it is not clear if it accumulates systemically, and less is known in the nervous system. The aim of this study was to assess the degree of acrolein accumulation in the circulation and in the spinal cord following acute acrolein inhalation in mice. Using a laboratory-fabricated inhalation chamber, we found elevated urinary 3-HPMA, an acrolein metabolite, and increased acrolein adducts in the spinal cord after weeks of nasal exposure to acrolein at a concentration similar to that in tobacco smoke. The data indicated that acrolein is absorbed into the circulatory system and some enters the nervous system. It is expected that these findings may facilitate further studies to probe the pathological role of acrolein in the nervous system resulting from smoke and other external sources.

  20. Towards the sustainable production of acrolein by glycerol dehydration.

    Science.gov (United States)

    Katryniok, Benjamin; Paul, Sébastien; Capron, Mickaël; Dumeignil, Franck

    2009-01-01

    The massive increase in biodiesel production by transesterification of vegatable oils goes hand-in-hand with the availability of a large volume of glycerol, which must be valorized. Glycerol dehydration to acrolein over acid catalysts is one of the most promising ways of valorization, because this compound is an important chemical intermediate used in, for example, the DL-methionine synthesis. In this Minireview, we give a detailed critical view of the state-of-the-art of this dehydration reaction. The processes developed in both the liquid and the gas phases are detailed and the best catalytic results obtained so far are reported as a benchmark for future developments. The advances on the understanding of the reaction mechanism are also discussed and we further focus particularly on the main obstacles for an immediate industrial application of this technology, namely catalyst coking and crude glycerol direct-use issues.

  1. Myoglobin-Catalyzed Olefination of Aldehydes.

    Science.gov (United States)

    Tyagi, Vikas; Fasan, Rudi

    2016-02-12

    The olefination of aldehydes constitutes a most valuable and widely adopted strategy for constructing carbon-carbon double bonds in organic chemistry. While various synthetic methods have been made available for this purpose, no biocatalysts are known to mediate this transformation. Reported herein is that engineered myoglobin variants can catalyze the olefination of aldehydes in the presence of α-diazoesters with high catalytic efficiency (up to 4,900 turnovers) and excellent E diastereoselectivity (92-99.9 % de). This transformation could be applied to the olefination of a variety of substituted benzaldehydes and heteroaromatic aldehydes, also in combination with different alkyl α-diazoacetate reagents. This work provides a first example of biocatalytic aldehyde olefination and extends the spectrum of synthetically valuable chemical transformations accessible using metalloprotein-based catalysts. © 2016 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

  2. Efficient and Highly Aldehyde Selective Wacker Oxidation

    KAUST Repository

    Teo, Peili; Wickens, Zachary K.; Dong, Guangbin; Grubbs, Robert H.

    2012-01-01

    A method for efficient and aldehyde-selective Wacker oxidation of aryl-substituted olefins using PdCl 2(MeCN) 2, 1,4-benzoquinone, and t-BuOH in air is described. Up to a 96% yield of aldehyde can be obtained, and up to 99% selectivity can be achieved with styrene-related substrates. © 2012 American Chemical Society.

  3. Efficient and Highly Aldehyde Selective Wacker Oxidation

    KAUST Repository

    Teo, Peili

    2012-07-06

    A method for efficient and aldehyde-selective Wacker oxidation of aryl-substituted olefins using PdCl 2(MeCN) 2, 1,4-benzoquinone, and t-BuOH in air is described. Up to a 96% yield of aldehyde can be obtained, and up to 99% selectivity can be achieved with styrene-related substrates. © 2012 American Chemical Society.

  4. Acrolein Yields in Mainstream Smoke From Commercial Cigarette and Little Cigar Tobacco Products.

    Science.gov (United States)

    Cecil, Todd L; Brewer, Tim M; Young, Mimy; Holman, Matthew R

    2017-07-01

    Many carbonyls are produced from the combustion of tobacco products and many of these carbonyls are harmful or potentially harmful constituents of mainstream cigarette smoke. One carbonyl of particular interest is acrolein, which is formed from the incomplete combustion of organic matter and the most significant contributor to non-cancer respiratory effects from cigarette smoke. Sheet-wrapped cigars, also known as "little cigars," are a type of tobacco products that have not been extensively investigated in literature. This study uses standard cigarette testing protocols to determine the acrolein yields from sheet-wrapped cigars. Sheet-wrapped cigar and cigarette products were tested by derivatizing the mainstream smoke with 2,4-dinitrophenylhydrazine (DNPH) solution and then quantifying the derivatives using conventional analytical systems. The results demonstrate that sheet-wrapped cigars can be tested for acrolein yields in mainstream smoke using the same methods used for the evaluation of cigarettes. The variability in the sheet-wrapped cigars and cigarettes under the International Organization for Standardization smoking regimen is statistically similar at the 95% confidence interval; however, increased variability is observed for sheet-wrapped cigar products under the Health Canada Intense (CI) smoking regimen. The amount of acrolein released by smoking sheet-wrapped cigars can be measured using standard smoking regimen currently used for cigarettes. The sheet-wrapped cigars were determined to yield similar quantity of acrolein from commercial cigarette products using two standard smoking regimens. This article reports on the measured quantity of acrolein from 15 commercial sheet-wrapped cigars using a validated standard smoking test method that derivatizes acrolein in the mainstream smoke with DNPH solution, and uses Liquid Chromatography/Ultra-Violet Detection (LC/UV) for separation and detection. These acrolein yields were similar to the levels found in

  5. A comparative study of the adsorption and hydrogenation of acrolein on Pt(1 1 1), Ni(1 1 1) film and Pt Ni Pt(1 1 1) bimetallic surfaces

    Science.gov (United States)

    Murillo, Luis E.; Chen, Jingguang G.

    In this study we have investigated the reaction pathways for the decomposition and hydrogenation of acrolein (CH 2dbnd CH-CH dbnd O) on Ni/Pt(1 1 1) surfaces under ultra-high vacuum (UHV) conditions using temperature programmed desorption (TPD) and high-resolution electron energy loss spectroscopy (HREELS). While gas-phase hydrogenation products are not observed from clean Pt(1 1 1), the subsurface Pt-Ni-Pt(1 1 1), with Ni residing below the first layer of Pt, is active for the self-hydrogenation of the C dbnd O bond to produce unsaturated alcohol (2-propenol) and the C dbnd C bond to produce saturated aldehyde (propanal), with the latter being the main hydrogenation product without the consecutive hydrogenation to saturated alcohol. For a thick Ni(1 1 1) film prepared on Pt(1 1 1), the self-hydrogenation yields for both products are lower than that from the Pt-Ni-Pt(1 1 1) surface. The presence of pre-adsorbed hydrogen further enhances the selectivity toward C dbnd O bond hydrogenation on the Pt-Ni-Pt(1 1 1) surface. In addition, HREELS studies of the adsorption of the two hydrogenation products, 2-propenol and propanal, are performed on the Pt-Ni-Pt(1 1 1) surface to identify the possible surface intermediates during the reaction of acrolein. The results presented here indicate that the hydrogenation activity and selectivity of acrolein on Pt(1 1 1) can be significantly modified by the formation of the bimetallic surfaces.

  6. Toxic acrolein production due to Ca(2+) influx by the NMDA receptor during stroke.

    Science.gov (United States)

    Nakamura, Mizuho; Uemura, Takeshi; Saiki, Ryotaro; Sakamoto, Akihiko; Park, Hyerim; Nishimura, Kazuhiro; Terui, Yusuke; Toida, Toshihiko; Kashiwagi, Keiko; Igarashi, Kazuei

    2016-01-01

    N-Methyl-d-aspartate (NMDA) receptors have a high permeability to Ca(2+), contributing to neuronal cell death after stroke. We recently found that acrolein produced from polyamines is a major toxic compound during stroke. Thus, it was determined whether over-accumulation of Ca(2+) increases the production of acrolein from polyamines in a photochemically-induced thrombosis mouse model of stroke and in cell culture systems. A unilateral infarction was induced in mouse brain by photoinduction after injection of Rose Bengal. The volume of the infarction was analyzed using the public domain National Institutes of Health image program. Protein-conjugated acrolein levels at the locus of infarction and in cells were measured by Western blotting. Levels of polyamines were measured by high-performance liquid chromatography. When the size of brain infarction was decreased by N(1), N(4), N(8)-tribenzylspermidine, a channel blocker of the NMDA receptors, levels of Ca(2+) and protein-conjugated acrolein (PC-Acro) were reduced, while levels of polyamines were increased at the locus of infarction. When cell growth of mouse mammary carcinoma FM3A cells and neuroblastoma Neuro2a cells was inhibited by Ca(2+), the level of polyamines decreased, while that of PC-Acro increased. It was also shown that Ca(2+) toxicity was decreased in an acrolein toxicity decreasing FM3A mutant cells recently isolated. In addition, 20-40 μM Ca(2+) caused the release of polyamines from ribosomes. The results indicate that acrolein is produced from polyamines released from ribosomes through Ca(2+) increase. The results indicate that toxicity of Ca(2+) during brain infarction is correlated with the increase of acrolein. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.

  7. Nonredundant functions of alphabeta and gammadelta T cells in acrolein-induced pulmonary pathology.

    Science.gov (United States)

    Borchers, Michael T; Wesselkamper, Scott C; Eppert, Bryan L; Motz, Gregory T; Sartor, Maureen A; Tomlinson, Craig R; Medvedovic, Mario; Tichelaar, Jay W

    2008-09-01

    Acrolein exposure represents a significant human health hazard. Repeated acrolein exposure causes the accumulation of monocytes/macrophages and lymphocytes, mucous cell metaplasia, and epithelial injury. Currently, the mechanisms that control these events are unclear, and the relative contribution of T-cell subsets to pulmonary pathologies following repeated exposures to irritants is unknown. To examine whether lymphocyte subpopulations regulate inflammation and epithelial cell pathology, we utilized a mouse model of pulmonary pathology induced by repeated acrolein exposures. The role of lymphocyte subsets was examined by utilizing transgenic mice genetically deficient in either alphabeta T cells or gammadelta T cells, and changes in cellular, molecular, and pathologic outcomes associated with repeated inhalation exposure to 2.0 and 0.5 ppm acrolein were measured. To examine the potential functions of lymphocyte subsets, we purified these cells from the lungs of mice repeatedly exposed to 2.0 ppm acrolein, isolated and amplified messenger RNA, and performed microarray analysis. Our data demonstrate that alphabeta T cells are required for macrophage accumulation, whereas gammadelta T cells are critical regulators of epithelial cell homeostasis, as identified by epithelial cell injury and apoptosis, following repeated acrolein exposure. This is supported by microarray analyses that indicated the T-cell subsets are unique in their gene expression profiles following acrolein exposures. Microarray analyses identified several genes that may contribute to phenotypes mediated by T-cell subpopulations including those involved in cytokine receptor signaling, chemotaxis, growth factor production, lymphocyte activation, and apoptosis. These data provide strong evidence that T-cell subpopulations in the lung are major determinants of pulmonary pathology and highlight the advantages of dissecting their effector functions in response to toxicant exposures.

  8. Glu504Lys Single Nucleotide Polymorphism of Aldehyde Dehydrogenase 2 Gene and the Risk of Human Diseases

    Directory of Open Access Journals (Sweden)

    Yan Zhao

    2015-01-01

    Full Text Available Aldehyde dehydrogenase (ALDH 2 is a mitochondrial enzyme that is known for its important role in oxidation and detoxification of ethanol metabolite acetaldehyde. ALDH2 also metabolizes other reactive aldehydes such as 4-hydroxy-2-nonenal and acrolein. The Glu504Lys single nucleotide polymorphism (SNP of ALDH2 gene, which is found in approximately 40% of the East Asian populations, causes defect in the enzyme activity of ALDH2, leading to alterations in acetaldehyde metabolism and alcohol-induced “flushing” syndrome. Evidence suggests that ALDH2 Glu504Lys SNP is a potential candidate genetic risk factor for a variety of chronic diseases such as cardiovascular disease, cancer, and late-onset Alzheimer’s disease. In addition, the association between ALDH2 Glu504Lys SNP and the development of these chronic diseases appears to be affected by the interaction between the SNP and lifestyle factors such as alcohol consumption as well as by the presence of other genetic variations.

  9. Acrolein- and 4-Aminobiphenyl-DNA adducts in human bladder mucosa and tumor tissue and their mutagenicity in human urothelial cells.

    Science.gov (United States)

    Lee, Hyun-Wook; Wang, Hsiang-Tsui; Weng, Mao-wen; Hu, Yu; Chen, Wei-sheng; Chou, David; Liu, Yan; Donin, Nicholas; Huang, William C; Lepor, Herbert; Wu, Xue-Ru; Wang, Hailin; Beland, Frederick A; Tang, Moon-shong

    2014-06-15

    Tobacco smoke (TS) is a major cause of human bladder cancer (BC). Two components in TS, 4-aminobiphenyl (4-ABP) and acrolein, which also are environmental contaminants, can cause bladder tumor in rat models. Their role in TS related BC has not been forthcoming. To establish the relationship between acrolein and 4-ABP exposure and BC, we analyzed acrolein-deoxyguanosine (dG) and 4-ABP-DNA adducts in normal human urothelial mucosa (NHUM) and bladder tumor tissues (BTT), and measured their mutagenicity in human urothelial cells. We found that the acrolein-dG levels in NHUM and BTT are 10-30 fold higher than 4-ABP-DNA adduct levels and that the acrolein-dG levels in BTT are 2 fold higher than in NHUM. Both acrolein-dG and 4-ABP-DNA adducts are mutagenic; however, the former are 5 fold more mutagenic than the latter. These two types of DNA adducts induce different mutational signatures and spectra. We found that acrolein inhibits nucleotide excision and base excision repair and induces repair protein degradation in urothelial cells. Since acrolein is abundant in TS, inhaled acrolein is excreted into urine and accumulates in the bladder and because acrolein inhibits DNA repair and acrolein-dG DNA adducts are mutagenic, we propose that acrolein is a major bladder carcinogen in TS.

  10. Activation of the microsomal glutathione-S-transferase and reduction of the glutathione dependent protection against lipid peroxidation by acrolein

    NARCIS (Netherlands)

    Haenen, G R; Vermeulen, N P; Tai Tin Tsoi, J N; Ragetli, H M; Timmerman, H; Blast, A

    1988-01-01

    Allyl alcohol is hepatotoxic. It is generally believed that acrolein, generated out of allyl alcohol by cytosolic alcohol dehydrogenase, is responsible for this toxicity. The effect of acrolein in vitro and in vivo on the glutathione (GSH) dependent protection of liver microsomes against lipid

  11. POTENTIATION OF PULMONARY REFLEX RESPONSE TO CAPSAICIN 24 HOURS FOLLOWING WHOLE-BODY ACROLEIN EXPOSURE IS MEDIATED BY TRPV1

    Science.gov (United States)

    Pulmonary C-fibers are stimulated by irritant air pollutants producing apnea, bronchospasm, and decrease in HR. C-fiber chemoreflex activation is mediated by TRPV1 and release of substance P. While acrolein has been shown to stimulate C-fibers, the persistence of acrolein effect...

  12. Implications for the formation of abasic sites following modification of polydeoxycytidylic acid by acrolein in vitro

    International Nuclear Information System (INIS)

    Smith, R.A.; Sysel, I.A.; Tibbels, T.S.; Cohen, S.M.

    1988-01-01

    Polydeoxycytidylic acid (poly dC) was incubated with excess acrolein. A Nensorb 20 nucleic acid purification cartridge was used to bind the polymeric material in the poly dC/acrolein reaction mixture. The non-polymeric material eluted from this column had a UV absorbance four times higher than that of the control. The flourescence spectrum of the eluted material did not correspond to that of unmodified cytosine. Separate aliquots of the reaction mixture were digested to deoxynucleotide 3 ' -monophosphates by incubation with micrococcal nuclease and spleen phosphodiesterase. The products were converted to 3 2P-labelled deoxynucleotide 3 ' ,5-biphosphates by incubation with T4 polynucleotide kinase and excess [γ- 3 2P]ATP. The ' -monophosphate was selectively removed by incubation with nuclease P1. Two dimensional thin-layer chromatography (TLC) on polyethyleneimine cellulose (PEI)-cellulose and detection of 3 2P-labeled deoxynucleotide 5 ' -monophosphates by autoradiography failed to provide evidence for the formation of an acrolein adduct of deoxycytidine 5'-monophosphate. When acrolein-modified deoxycytidine 5 ' -monophosphate, was detected. These data show that acrolein-modified deoxycytidine 3 ' -monophosphates are substrates for 3 2P labeling by T4 polynucleotide kinase and are stable under the assay conditions employed

  13. SCGB3A2 Inhibits Acrolein-Induced Apoptosis through Decreased p53 Phosphorylation.

    Science.gov (United States)

    Kurotani, Reiko; Shima, Reika; Miyano, Yuki; Sakahara, Satoshi; Matsumoto, Yoshie; Shibata, Yoko; Abe, Hiroyuki; Kimura, Shioko

    2015-04-28

    Chronic obstructive pulmonary disease (COPD), a major global health problem with increasing morbidity and mortality rates, is anticipated to become the third leading cause of death worldwide by 2020. COPD arises from exposure to cigarette smoke. Acrolein, which is contained in cigarette smoke, is the most important risk factor for COPD. It causes lung injury through altering apoptosis and causes inflammation by augmenting p53 phosphorylation and producing reactive oxygen species (ROS). Secretoglobin (SCGB) 3A2, a secretory protein predominantly present in the epithelial cells of the lungs and trachea, is a cytokine-like small molecule having anti-inflammatory, antifibrotic, and growth factor activities. In this study, the effect of SCGB3A2 on acrolein-related apoptosis was investigated using the mouse fibroblast cell line MLg as the first step in determining the possible therapeutic value of SCGB3A2 in COPD. Acrolein increased the production of ROS and phosphorylation of p53 and induced apoptosis in MLg cells. While the extent of ROS production induced by acrolein was not affected by SCGB3A2, p53 phosphorylation was significantly decreased by SCGB3A2. These results demonstrate that SCGB3A2 inhibited acrolein-induced apoptosis through decreased p53 phosphorylation, not altered ROS levels.

  14. Effect of sildenafil on acrolein-induced airway inflammation and mucus production in rats.

    Science.gov (United States)

    Wang, T; Liu, Y; Chen, L; Wang, X; Hu, X-R; Feng, Y-L; Liu, D-S; Xu, D; Duan, Y-P; Lin, J; Ou, X-M; Wen, F-Q

    2009-05-01

    Airway inflammation with mucus overproduction is a distinguishing pathophysiological feature of many chronic respiratory diseases. Phosphodiesterase (PDE) inhibitors have shown anti-inflammatory properties. In the present study, the effect of sildenafil, a potent inhibitor of PDE5 that selectively degrades cyclic guanosine 3',5'-monophosphate (cGMP), on acrolein-induced inflammation and mucus production in rat airways was examined. Rats were exposed to acrolein for 14 and 28 days. Sildenafil or distilled saline was administered intragastrically prior to acrolein exposure. Bronchoalveolar lavage fluid (BALF) was acquired for cell count and the detection of pro-inflammatory cytokine levels. Lung tissue was examined for cGMP content, nitric oxide (NO)-metabolite levels, histopathological lesion scores, goblet cell metaplasia and mucin production. The results suggested that sildenafil pretreatment reversed the significant decline of cGMP content in rat lungs induced by acrolein exposure, and suppressed the increase of lung NO metabolites, the BALF leukocyte influx and pro-inflammatory cytokine release. Moreover, sildenafil pretreatment reduced acrolein-induced Muc5ac mucin synthesis at both mRNA and protein levels, and attenuated airway inflammation, as well as epithelial hyperplasia and metaplasia. In conclusion, sildenafil could attenuate airway inflammation and mucus production in the rat model, possibly through the nitric oxide/cyclic guanosine 3',5'-monophosphate pathway, and, thus, might have a therapeutic potential for chronic airway diseases.

  15. SCGB3A2 Inhibits Acrolein-Induced Apoptosis through Decreased p53 Phosphorylation

    International Nuclear Information System (INIS)

    Kurotani, Reiko; Shima, Reika; Miyano, Yuki; Sakahara, Satoshi; Matsumoto, Yoshie; Shibata, Yoko; Abe, Hiroyuki; Kimura, Shioko

    2015-01-01

    Chronic obstructive pulmonary disease (COPD), a major global health problem with increasing morbidity and mortality rates, is anticipated to become the third leading cause of death worldwide by 2020. COPD arises from exposure to cigarette smoke. Acrolein, which is contained in cigarette smoke, is the most important risk factor for COPD. It causes lung injury through altering apoptosis and causes inflammation by augmenting p53 phosphorylation and producing reactive oxygen species (ROS). Secretoglobin (SCGB) 3A2, a secretory protein predominantly present in the epithelial cells of the lungs and trachea, is a cytokine-like small molecule having anti-inflammatory, antifibrotic, and growth factor activities. In this study, the effect of SCGB3A2 on acrolein-related apoptosis was investigated using the mouse fibroblast cell line MLg as the first step in determining the possible therapeutic value of SCGB3A2 in COPD. Acrolein increased the production of ROS and phosphorylation of p53 and induced apoptosis in MLg cells. While the extent of ROS production induced by acrolein was not affected by SCGB3A2, p53 phosphorylation was significantly decreased by SCGB3A2. These results demonstrate that SCGB3A2 inhibited acrolein-induced apoptosis through decreased p53 phosphorylation, not altered ROS levels

  16. Enhancement of the Acrolein-Induced Production of Reactive Oxygen Species and Lung Injury by GADD34

    Directory of Open Access Journals (Sweden)

    Yang Sun

    2015-01-01

    Full Text Available Chronic obstructive pulmonary disease (COPD is characterized by lung destruction and inflammation. As a major compound of cigarette smoke, acrolein plays a critical role in the induction of respiratory diseases. GADD34 is known as a growth arrest and DNA damage-related gene, which can be overexpressed in adverse environmental conditions. Here we investigated the effects of GADD34 on acrolein-induced lung injury. The intranasal exposure of acrolein induced the expression of GADD34, developing the pulmonary damage with inflammation and increase of reactive oxygen species (ROS. Conversely, the integrality of pulmonary structure was preserved and the generation of ROS was reduced in GADD34-knockout mice. Acrolein-induced phosphorylation of eIF2α in GADD34-knockout epithelial cells by shRNA protected cell death by reducing misfolded protein-caused oxidative stress. These data indicate that GADD34 participates in the development of acrolein-induced lung injury.

  17. Enhancement of the acrolein-induced production of reactive oxygen species and lung injury by GADD34.

    Science.gov (United States)

    Sun, Yang; Ito, Sachiko; Nishio, Naomi; Tanaka, Yuriko; Chen, Nana; Liu, Lintao; Isobe, Ken-ichi

    2015-01-01

    Chronic obstructive pulmonary disease (COPD) is characterized by lung destruction and inflammation. As a major compound of cigarette smoke, acrolein plays a critical role in the induction of respiratory diseases. GADD34 is known as a growth arrest and DNA damage-related gene, which can be overexpressed in adverse environmental conditions. Here we investigated the effects of GADD34 on acrolein-induced lung injury. The intranasal exposure of acrolein induced the expression of GADD34, developing the pulmonary damage with inflammation and increase of reactive oxygen species (ROS). Conversely, the integrality of pulmonary structure was preserved and the generation of ROS was reduced in GADD34-knockout mice. Acrolein-induced phosphorylation of eIF2α in GADD34-knockout epithelial cells by shRNA protected cell death by reducing misfolded protein-caused oxidative stress. These data indicate that GADD34 participates in the development of acrolein-induced lung injury.

  18. Enhancement of the Acrolein-Induced Production of Reactive Oxygen Species and Lung Injury by GADD34

    Science.gov (United States)

    Sun, Yang; Ito, Sachiko; Nishio, Naomi; Tanaka, Yuriko; Chen, Nana; Isobe, Ken-ichi

    2015-01-01

    Chronic obstructive pulmonary disease (COPD) is characterized by lung destruction and inflammation. As a major compound of cigarette smoke, acrolein plays a critical role in the induction of respiratory diseases. GADD34 is known as a growth arrest and DNA damage-related gene, which can be overexpressed in adverse environmental conditions. Here we investigated the effects of GADD34 on acrolein-induced lung injury. The intranasal exposure of acrolein induced the expression of GADD34, developing the pulmonary damage with inflammation and increase of reactive oxygen species (ROS). Conversely, the integrality of pulmonary structure was preserved and the generation of ROS was reduced in GADD34-knockout mice. Acrolein-induced phosphorylation of eIF2α in GADD34-knockout epithelial cells by shRNA protected cell death by reducing misfolded protein-caused oxidative stress. These data indicate that GADD34 participates in the development of acrolein-induced lung injury. PMID:25821552

  19. Colorimetric Recognition of Aldehydes and Ketones.

    Science.gov (United States)

    Li, Zheng; Fang, Ming; LaGasse, Maria K; Askim, Jon R; Suslick, Kenneth S

    2017-08-07

    A colorimetric sensor array has been designed for the identification of and discrimination among aldehydes and ketones in vapor phase. Due to rapid chemical reactions between the solid-state sensor elements and gaseous analytes, distinct color difference patterns were produced and digitally imaged for chemometric analysis. The sensor array was developed from classical spot tests using aniline and phenylhydrazine dyes that enable molecular recognition of a wide variety of aliphatic or aromatic aldehydes and ketones, as demonstrated by hierarchical cluster, principal component, and support vector machine analyses. The aldehyde/ketone-specific sensors were further employed for differentiation among and identification of ten liquor samples (whiskies, brandy, vodka) and ethanol controls, showing its potential applications in the beverage industry. © 2017 Wiley-VCH Verlag GmbH & Co. KGaA, Weinheim.

  20. Thermotolerant cyclamen with reduced acrolein and methyl vinyl ketone.

    Science.gov (United States)

    Kai, Hiroomi; Hirashima, Keita; Matsuda, Osamu; Ikegami, Hidetoshi; Winkelmann, Traud; Nakahara, Takao; Iba, Koh

    2012-06-01

    Reduced levels of trienoic fatty acids (TAs) in chloroplast membranes induce thermotolerance in several plant species, but the underlying mechanisms remain unclear. TA peroxidation in plant cell membranes generates cytotoxic, TA-derived compounds containing α,β-unsaturated carbonyl groups. The relationship between low TA levels and the amounts of cytotoxic TA-derived compounds was examined using thermotolerant transgenic cyclamen (Cyclamen persicum Mill.) with low TA contents. Changes in the levels of the cytotoxic TA-derived acrolein (ACR), methyl vinyl ketone (MVK), (E)-2-hexenal, 4-hydroxy-2-nonenal, and malondialdehyde were analysed in the leaf tissues of wild-type (WT) and thermotolerant transgenic cyclamen under heat stress. Levels of ACR and MVK in the WT increased in parallel with the occurrence of heat-induced tissue damage, whereas no such changes were observed in the thermotolerant transgenic lines. Furthermore, exogenous ACR and MVK infiltrated into leaves to concentrations similar to those observed in heat-stressed WT leaves caused similar disease symptoms. These results suggest that thermotolerance in transgenic cyclamen depends on reduced production rates of ACR and MVK under heat stress, due to the low level of TAs in these plants.

  1. p38 MAPK and MMP-9 cooperatively regulate mucus overproduction in mice exposed to acrolein fog.

    Science.gov (United States)

    Liu, Dai-Shun; Wang, Tao; Han, Su-Xia; Dong, Jia-Jia; Liao, Zeng-Lin; He, Guang-Ming; Chen, Lei; Chen, Ya-Juan; Xu, Dan; Hou, Yan; Li, Yan-Ping; Wen, Fu-Qiang

    2009-09-01

    To evaluate the role of p38 mitogen-activated protein kinase (MAPK) on mice airway inflammation, mucus production and the possible cross-talk between p38 MAPK and matrix metalloproteinase-9 (MMP-9) in mucin protein synthesis. Mice were exposed to 4.0 ppm of acrolein for 21 days with daily intraperitoneal injection of SB203580, a specific inhibitor of p38 MAPK. In control mice, sterile saline was administered instead. On days 7 and 21, mice were sacrificed to examine airway inflammation and mucus production by BALF cell counts, cytokine ELISA, and H&E and AB-PAS staining. The mRNA and protein levels of Muc5ac, p38 MAPK and MMP-9 in the lung were determined by RT-PCR, immunohistochemistry and Western blotting analysis. MMP-9 activity was measured by gelatin zymography. Both the numbers of inflammatory cells and mucus-secreting goblet cells were significantly increased in the airways of mice exposed to acrolein as compared to the control mice. Acrolein-increased phosphorylation of p38 MAPK was significantly reduced by SB203580. The airway inflammation and goblet cell hyperplasia after acrolein challenge were also attenuated by SB203580 administration. Moreover, SB203580 treatment decreased the acrolein-induced increase of Muc5ac and MMP-9 expression and MMP-9 activity in airway epithelium. The results indicate an important role of p38 MAPK in acrolein-induced airway inflammation and mucus hypersecretion in mice. The cooperation of p38 and MMP-9 may contribute to the mucin overproduction after inflammatory challenge.

  2. Selective oxidation of propylene to acrolein by hydrothermally synthesized bismuth molybdates

    DEFF Research Database (Denmark)

    Schuh, Kirsten; Kleist, Wolfgang; Høj, Martin

    2014-01-01

    Hydrothermal synthesis has been used as a soft chemical method to prepare bismuth molybdate catalysts for the selective oxidation of propylene to acrolein. All obtained samples displayed a plate-like morphology, but their individual aspect ratios varied with the hydrothermal synthesis conditions...... of nitric acid during hydrothermal synthesis enhanced both propylene conversion and acrolein yield, possibly due to a change in morphology. Formation of β-Bi2Mo2O9 was not observed under the applied conditions. In general, the catalytic performance of all samples decreased notably after calcination at 550...

  3. Acrolein toxicity involves oxidative stress caused by glutathione depletion in the yeast Saccharomyces cerevisiae.

    Science.gov (United States)

    Kwolek-Mirek, M; Bednarska, S; Bartosz, G; Biliński, T

    2009-08-01

    Exposure of yeast cells to allyl alcohol results in intracellular production of acrolein. The toxicity of so formed acrolein involves oxidative stress, as (1) strains deficient in antioxidant defense are hypersensitive to allyl alcohol, (2) exposure to allyl alcohol increases the level of thiobarbituric-acid-reactive substances and decreases glutathione level in the cells, (3) hypoxic and anoxic atmosphere and antioxidants protect against allyl alcohol toxicity, and (4) allyl alcohol causes activation of Yap1p. No increased formation of reactive oxygen species was detected in cells exposed to allyl alcohol, so oxidative stress is due to depletion of cellular thiols and thus alteration in the redox state of yeast cells.

  4. 40 CFR 721.5762 - Aromatic aldehyde phenolic resin (generic).

    Science.gov (United States)

    2010-07-01

    ... 40 Protection of Environment 30 2010-07-01 2010-07-01 false Aromatic aldehyde phenolic resin... Specific Chemical Substances § 721.5762 Aromatic aldehyde phenolic resin (generic). (a) Chemical substance... aromatic aldehyde phenolic resin (PMN P-01-573) is subject to reporting under this section for the...

  5. In parkinsonian substantia nigra, alpha-synuclein is modified by acrolein, a lipid-peroxidation product, and accumulates in the dopamine neurons with inhibition of proteasome activity.

    Science.gov (United States)

    Shamoto-Nagai, M; Maruyama, W; Hashizume, Y; Yoshida, M; Osawa, T; Riederer, P; Naoi, M

    2007-01-01

    alpha-Synuclein (alphaSYN) plays a central role in the neural degeneration of Parkinson's disease (PD) through its conformational change. In PD, alphaSYN, released from the membrane, accumulates in the cytoplasm and forms Lewy body. However, the mechanism behind the translocation and conformational change of alphaSYN leading to the cell death has not been well elucidated. This paper reports that in the dopamine neurons of the substantia nigra containing neuromelanin from PD patients, alphaSYN was modified with acrolein (ACR), an aldehyde product of lipid peroxidation. Histopathological observation confirmed the co-localization of protein immunoreactive to anti-alphaSYN and ACR antibody. By Western blot analyses of samples precipitated with either anti-alphaSYN or anti-ACR antibody, increase in ACR-modified alphaSYN was confirmed in PD brain. Modification of recombinant alphaSYN by ACR enhanced its oligomerization, and at higher ACR concentrations alphaSYN was fragmented and polymerized forming a smear pattern in SDS-PAGE. ACR reduced 20S proteasome activity through the direct modification of the proteasome proteins and the production of polymerized ACR-modified proteins, which inhibited proteasome activity in vitro. These results suggest that ACR may initiate vicious cycle of modification and aggregation of proteins, including alphaSYN, and impaired proteolysis system, to cause neuronal death in PD.

  6. The Tobacco Smoke Component, Acrolein, Suppresses Innate Macrophage Responses by Direct Alkylation of c-Jun N-Terminal Kinase

    Science.gov (United States)

    Hristova, Milena; Spiess, Page C.; Kasahara, David I.; Randall, Matthew J.; Deng, Bin

    2012-01-01

    The respiratory innate immune system is often compromised by tobacco smoke exposure, and previous studies have indicated that acrolein, a reactive electrophile in tobacco smoke, may contribute to the immunosuppressive effects of smoking. Exposure of mice to acrolein at concentrations similar to those in cigarette smoke (5 ppm, 4 h) significantly suppressed alveolar macrophage responses to bacterial LPS, indicated by reduced induction of nitric oxide synthase 2, TNF-α, and IL-12p40. Mechanistic studies with bone marrow–derived macrophages or MH-S macrophages demonstrated that acrolein (1–30 μM) attenuated these LPS-mediated innate responses in association with depletion of cellular glutathione, although glutathione depletion itself was not fully responsible for these immunosuppressive effects. Inhibitory actions of acrolein were most prominent after acute exposure (acrolein with critical signaling pathways. Among the key signaling pathways involved in innate macrophage responses, acrolein marginally affected LPS-mediated activation of nuclear factor (NF)-κB, and significantly suppressed phosphorylation of c-Jun N-terminal kinase (JNK) and activation of c-Jun. Using biotin hydrazide labeling, NF-κB RelA and p50, as well as JNK2, a critical mediator of innate macrophage responses, were revealed as direct targets for alkylation by acrolein. Mass spectrometry analysis of acrolein-modified recombinant JNK2 indicated adduction to Cys41 and Cys177, putative important sites involved in mitogen-activated protein kinase (MAPK) kinase (MEK) binding and JNK2 phosphorylation. Our findings indicate that direct alkylation of JNK2 by electrophiles, such as acrolein, may be a prominent and hitherto unrecognized mechanism in their immunosuppressive effects, and may be a major factor in smoking-induced effects on the immune system. PMID:21778411

  7. Determination of acrolein, ethanol, volatile acidity, and copper in different samples of sugarcane spirits

    Directory of Open Access Journals (Sweden)

    José Masson

    2012-09-01

    Full Text Available Seventy-one samples of sugarcane spirits from small and average size stills produced in the northern and southern Minas Gerais (Brazil were analyzed for acrolein using HPLC (High Performance Liquid Chromatography. Ethanol and copper concentrations and volatile acidity were also determined according to methods established by the Ministry of Agriculture, Livestock and Supply (MAPA. A total of 9.85% of the samples tested showed levels of acrolein above the legal limits, while the copper concentrations of 21.00% of the samples and the volatile acidity of 8.85% of the samples were higher than the limits established by the Brazilian legislation. The concentration of acrolein varied from 0 to 21.97 mg.100 mL-1 of ethanol. However, no significant difference at 5% of significance was observed between the samples produced in the northern and southern Minas Gerais. The method used for determination of acrolein in sugarcane spirits involved the formation of a derivative with 2,4-dinitrophenylhydrazine (2,4-DNPH and subsequent analysis by HPLC.

  8. Electronic excitations in a dielectric continuum solvent with quantum Monte Carlo: Acrolein in water

    NARCIS (Netherlands)

    Floris, F.M.; Filippi, Claudia; Amovilli, C.

    2014-01-01

    We investigate here the vertical n → π* and π → π* transitions of s-trans-acrolein in aqueous solution by means of a polarizable continuum model (PCM) we have developed for the treatment of the solute at the quantum Monte Carlo (QMC) level of the theory. We employ the QMC approach which allows us to

  9. Glycerol valorization: dehydration to acrolein over silica-supported niobia catalysts

    NARCIS (Netherlands)

    Shiju, N.R.; Brown, D.R.; Wilson, K.; Rothenberg, G.

    2010-01-01

    The catalytic dehydration of glycerol to acrolein is investigated over silica-supported niobia catalysts in a continuous fixed-bed gas-phase reactor. Various supported niobia catalysts are prepared and characterized using surface analysis and spectroscopic methods (XRD, UV-Vis, XPS, N2 adsorption),

  10. Sensory irritation to mixtures of formaldehyde, acrolein, and acetaldehyde in rats

    NARCIS (Netherlands)

    Cassee, F.R.; Arts, J.H.E.; Groten, J.P.; Feron, V.J.

    1996-01-01

    Sensory irritation of formaldehyde (FRM), acrolein (ACR) and acetaldehyde (ACE) as measured by the decrease in breathing frequency (DBF) was studied in male Wistar rats using nose-only exposure. Groups of four rats were exposed to each of the single compounds separately or to mixtures of FRM, ACR

  11. Selective oxidation of propylene to acrolein by silica-supported bismuth molybdate catalysts

    DEFF Research Database (Denmark)

    Duc, Duc Truong; Ha, Hanh Nguyen; Fehrmann, Rasmus

    2011-01-01

    Silica-supported bismuth molybdate catalysts have been prepared by impregnation, structurally characterized and examined as improved catalysts for the selective oxidation of propylene to acrolein. Catalysts with a wide range of loadings (from 10 to 90 wt%) of beta bismuth molybdate (β-Bi2Mo2O9) w...

  12. Iron-tellurium-selenium mixed oxide catalysts for the selective oxidation of propylene to acrolein

    International Nuclear Information System (INIS)

    Patel, B.M.; Price, G.L.

    1990-01-01

    This paper reports on iron-tellurium-selenium mixed oxide catalysts prepared by coprecipitation from aqueous solution investigated for the propylene to acrolein reaction in the temperature range 543-773 K. Infrared spectroscopy, electron dispersive X-ray analysis, X-ray diffraction, and isotopic tracer techniques have also been employed to characterize this catalytic system. Properties of the Fe-Te-Se mixed oxide catalysts have been compared with Fe-Te mixed oxides in an effort to deduce the functionality of Se. The selenium in the Fe-Te-Se-O catalyst has been found to be the hydrocarbon activating site. The activation energies for the acrolein and carbon dioxide formation are 71 and 54 kJ/mol, respectively. Reactions carried out with 18 O 2 have shown lattice oxygen to be primarily responsible for the formation of both acrolein and carbon dioxide. The initial and rate-determining step for acrolein formation is hydrogen abstraction as determined by an isotope effect associated with the C 3 D 6 reaction. No isotope effect is observed for carbon dioxide formation from C 3 D 6 suggesting that CO 2 is formed by parallel, not consecutive, oxidation of propylene

  13. Acrolein-Exposed Normal Human Lung Fibroblasts in Vitro: Cellular Senescence, Enhanced Telomere Erosion, and Degradation of Werner’s Syndrome Protein

    Science.gov (United States)

    Jang, Jun-Ho; Bruse, Shannon; Huneidi, Salam; Schrader, Ronald M.; Monick, Martha M.; Lin, Yong; Carter, A. Brent; Klingelhutz, Aloysius J.

    2014-01-01

    Background: Acrolein is a ubiquitous environmental hazard to human health. Acrolein has been reported to activate the DNA damage response and induce apoptosis. However, little is known about the effects of acrolein on cellular senescence. Objectives: We examined whether acrolein induces cellular senescence in cultured normal human lung fibroblasts (NHLF). Methods: We cultured NHLF in the presence or absence of acrolein and determined the effects of acrolein on cell proliferative capacity, senescence-associated β-galactosidase activity, the known senescence-inducing pathways (e.g., p53, p21), and telomere length. Results: We found that acrolein induced cellular senescence by increasing both p53 and p21. The knockdown of p53 mediated by small interfering RNA (siRNA) attenuated acrolein-induced cellular senescence. Acrolein decreased Werner’s syndrome protein (WRN), a member of the RecQ helicase family involved in DNA repair and telomere maintenance. Acrolein-induced down-regulation of WRN protein was rescued by p53 knockdown or proteasome inhibition. Finally, we found that acrolein accelerated p53-mediated telomere shortening. Conclusions: These results suggest that acrolein induces p53-mediated cellular senescence accompanied by enhanced telomere attrition and WRN protein down-regulation. Citation: Jang JH, Bruse S, Huneidi S, Schrader RM, Monick MM, Lin Y, Carter AB, Klingelhutz AJ, Nyunoya T. 2014. Acrolein-exposed normal human lung fibroblasts in vitro: cellular senescence, enhanced telomere erosion, and degradation of Werner’s syndrome protein. Environ Health Perspect 122:955–962; http://dx.doi.org/10.1289/ehp.1306911 PMID:24747221

  14. Chlamydomonas reinhardtii responding to high light: a role for 2-propenal (acrolein).

    Science.gov (United States)

    Roach, Thomas; Baur, Theresa; Stöggl, Wolfgang; Krieger-Liszkay, Anja

    2017-09-01

    High light causes photosystem II to generate singlet oxygen ( 1 O 2 ), a reactive oxygen species (ROS) that can react with membrane lipids, releasing reactive electrophile species (RES), such as acrolein. To investigate how RES may contribute to light stress responses, Chlamydomonas reinhardtii was high light-treated in photoautotrophic and mixotrophic conditions and also in an oxygen-enriched atmosphere to elevate ROS production. The responses were compared to exogenous acrolein. Non-photochemical quenching (NPQ) was higher in photoautotrophic cells, as a consequence of a more de-epoxidized state of the xanthophyll cycle pool and more LHCSR3 protein, showing that photosynthesis was under more pressure than in mixotrophic cells. Photoautotrophic cells had lowered α-tocopherol and β-carotene contents and a higher level of protein carbonylation, indicators of elevated 1 O 2 production. Levels of glutathione, glutathione peroxidase (GPX5) and glutathione-S-transferase (GST1), important antioxidants against RES, were also increased in photoautotrophic cells. In parallel to the wild-type, the LHCSR3-deficient npq4 mutant was high light-treated, which in photoautotrophic conditions exhibited particular sensitivity under elevated oxygen, the treatment that induced the highest RES levels, including acrolein. The npq4 mutant had more GPX5 and GST1 alongside higher levels of carbonylated protein and a more oxidized glutathione redox state. In wild-type cells glutathione contents doubled after 4 h treatment, either with high light under elevated oxygen or with a non-critical dose (600 ppm) of acrolein. Exogenous acrolein also increased GST1 levels, but not GPX5. Overall, RES-associated oxidative damage and glutathione metabolism are prominently associated with light stress and potentially in signaling responses of C. reinhardtii. © 2017 Scandinavian Plant Physiology Society.

  15. Acute and long-term ocular effects of acrolein vapor on the eyes and potential therapies.

    Science.gov (United States)

    Dachir, Shlomit; Cohen, Maayan; Gutman, Hila; Cohen, Liat; Buch, Hillel; Kadar, Tamar

    2015-01-01

    Acrolein is a potent irritant and a vesicant that was used by the French during WWI as the warfare agent named: "papite". Nowadays, it is produced in large amounts all over the world in the industry for the production of acrylic acid and for agriculture use as herbicide. The aim of this study was to characterize the effects of acute eye exposure to acrolein vapor and to evaluate the efficacy of a topical post-exposure combination treatment with a local anesthetic and a steroid. Rabbit eyes were exposed to three doses of acrolein vapor (low, intermediate and high) and treated topically with either 0.4% benoxinate hydrochloride (localin, for 2 h) or dexamethasone (dexamycin, for 6 days) or a combination of both drugs. Clinical follow-up using slit lamp examinations and histological evaluation was performed 4 weeks post-exposure. Acrolein vapor caused immediate eye closure with excess tearing, corneal erosions and severe inflammation of the anterior chamber. This was followed by corneal neovascularization (NV) starting as early as 1 week post-exposure. The damage to the eyes was long lasting, and at 4 weeks following exposure, significant pathological changes were observed. Immediate post-exposure application of the local anesthetic, localin, prevented the eye closure, and the dexamycin treatment reduced significantly the initial inflammation as well as the extent and incidence of corneal NV. Short-term eye exposure to the irritant acrolein may result in immediate eye closure and long lasting pathologies that could lead to blindness. An anti-inflammatory treatment combined with short-term application of a local anesthetic prevents incapacitation and might minimize significantly the extent of eye injuries.

  16. Cyclophosphamide and acrolein induced oxidative stress leading to deterioration of metaphase II mouse oocyte quality.

    Science.gov (United States)

    Jeelani, Roohi; Khan, Sana N; Shaeib, Faten; Kohan-Ghadr, Hamid-Reza; Aldhaheri, Sarah R; Najafi, Tohid; Thakur, Mili; Morris, Robert; Abu-Soud, Husam M

    2017-09-01

    Cyclophosphamide (CTX) is a chemotherapeutic agent widely used to treat ovarian, breast, and hematological cancers as well as autoimmune disorders. Such chemotherapy is associated with reproductive failure and premature ovarian insufficiency. The mechanism by which CTX and/or its main metabolite, acrolein, affect female fertility remains unclear, but it is thought to be caused by an overproduction of reactive oxygen species (ROS). Here, we investigated the effect of CTX on metaphase II mouse oocytes obtained from treated animals (120mg/kg, 24h of single treatment), and oocytes directly exposed to increasing concentrations of CTX and acrolein (n=480; 0, 5, 10, 25, 50, and 100μM) with and without cumulus cells (CCs) for 45min which correlates to the time of maximum peak plasma concentrations after administration. Oocytes were fixed and subjected to indirect immunofluorescence and were scored based on microtubule spindle structure (MT) and chromosomal alignment (CH). Generation of ROS was evaluated using the Cellular Reactive Oxygen Species Detection Assay Kit. Deterioration of oocyte quality was noted when oocytes were obtained from CTX treated mice along with CTX and acrolein treated oocytes in a dose-dependent manner as shown by an increase in poor scores. Acrolein had an impact at a significantly lower level as compared to CTX, plateau at 10μM versus 50μM, respectively. These variation is are associated with the higher amount of ROS generated with acrolein exposure as compared to CTX (pacrolein scavengers may mitigate the damaging effects of these compounds and help women undergoing such treatment. Copyright © 2017. Published by Elsevier Inc.

  17. Identification of aldehyde oxidase 1 and aldehyde oxidase homologue 1 as dioxin-inducible genes

    International Nuclear Information System (INIS)

    Rivera, Steven P.; Choi, Hyun Ho; Chapman, Brett; Whitekus, Michael J.; Terao, Mineko; Garattini, Enrico; Hankinson, Oliver

    2005-01-01

    Aldehyde oxidases are a family of highly related molybdo-flavoenzymes acting upon a variety of compounds of industrial and medical importance. We have identified aldehyde oxidase 1 (AOX1) as a 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin) inducible gene in the mouse hepatoma cell line Hepa-1. AOX1 mRNA levels were not increased by dioxin in mutant derivatives of the Hepa-1 cell line lacking either functional aryl hydrocarbon receptor (AHR) or aryl hydrocarbon receptor nuclear translocator (ARNT) proteins, thus demonstrating that transcriptional induction of AOX1 in response to dioxin occurs through the AHR pathway. Dioxin induction of AOX1 mRNA was also observed in mouse liver. In addition, levels of AOX1 protein as well as those of aldehyde oxidase homologue 1 (AOH1), a recently identified homolog of AOX1, were elevated in mouse liver in response to dioxin. Employing an aldehyde oxidase specific substrate, AOX1/AOH1 activity was shown to be induced by dioxin in mouse liver. This activity was inhibited by a known inhibitor of aldehyde oxidases, and eliminated by including tungstate in the mouse diet, which is known to lead to inactivation of molybdoflavoenzymes, thus confirming that the enzymatic activity was attributable to AOX1/AOH1. Our observations thus identify two additional xenobiotic metabolizing enzymes induced by dioxin

  18. Passive Badge Assessment for Long-Term, Low-level Air Monitoring on Submarines: Acrolein Badge Validation

    National Research Council Canada - National Science Library

    Williams, Kimberly P; Rose-Pehrsson, Susan L; Kidwell, David A

    2006-01-01

    .... Passive badge monitors for acrolein detection were tested. Long-term sampling efficiency was evaluated for a 28-day period by comparing the response of the passive badge to an active tube sampling method...

  19. On the performance of quantum chemical methods to predict solvatochromic effects. The case of acrolein in aqueous solution

    DEFF Research Database (Denmark)

    Aidas, Kestutis; Møgelhøj, Andreas; Nilsson, Elna Johanna Kristina

    2008-01-01

    The performance of the Hartree–Fock method and the three density functionals B3LYP, PBE0, and CAM-B3LYP is compared to results based on the coupled cluster singles and doubles model in predictions of the solvatochromic effects on the vertical n¿* and ¿* electronic excitation energies of acrolein...... of acrolein in vapor phase and aqueous solution. The gas-to-aqueous solution shift of the n¿* excitation energy is well reproduced by using all density functional methods considered. However, the B3LYP and PBE0 functionals completely fail to describe the ¿* electronic transition in solution, whereas...... the recent CAM-B3LYP functional performs well also in this case. The ¿* excitation energy of acrolein in water solution is found to be very dependent on intermolecular induction and nonelectrostatic interactions. The computed excitation energies of acrolein in vacuum and solution compare well to experimental...

  20. Acrolein and asthma attack prevalence in a representative sample of the United States adult population 2000-2009.

    Science.gov (United States)

    deCastro, B Rey

    2014-01-01

    Acrolein is an air toxic and highly potent respiratory irritant. There is little epidemiology available, but US EPA estimates that outdoor acrolein is responsible for about 75 percent of non-cancer respiratory health effects attributable to air toxics in the United States, based on the Agency's 2005 NATA (National-Scale Air Toxics Assessment) and acrolein's comparatively potent inhalation reference concentration of 0.02 µg/m3. Assess the association between estimated outdoor acrolein exposure and asthma attack reported by a representative cross-sectional sample of the adult United States population. NATA 2005 chronic outdoor acrolein exposure estimates at the census tract were linked with residences oif adults (≥18 years old) in the NHIS (National Health Interview Survey) 2000-2009 (n = 271,348 subjects). A sample-weighted logistic regression model characterized the association between the prevalence of reporting at least one asthma attack in the 12 months prior to survey interview and quintiles of exposure to outdoor acrolein, controlling for potential confounders. In the highest quintile of outdoor acrolein exposure (0.05-0.46 µg/m3), there was a marginally significant increase in the asthma attack pOR (prevalence-odds ratio [95% CI]  = 1.08 [0.98∶1.19]) relative to the lowest quintile. The highest quintile was also associated with a marginally significant increase in prevalence-odds (1.13 [0.98∶1.29]) in a model limited to never smokers (n = 153,820). Chronic exposure to outdoor acrolein of 0.05-0.46 µg/m3 appears to increase the prevalence-odds of having at least one asthma attack in the previous year by 8 percent in a representative cross-sectional sample of the adult United States population.

  1. TRPA1 mediates changes in heart rate variability and cardiac mechanical function in mice exposed to acrolein

    Energy Technology Data Exchange (ETDEWEB)

    Kurhanewicz, Nicole [Curriculum in Toxicology, School of Medicine, University of North Carolina, Chapel Hill, NC 27599 (United States); McIntosh-Kastrinsky, Rachel [Department of Environmental Sciences and Engineering, Gillings School of Global Public Health, University of North Carolina, Chapel Hill, NC 27599 (United States); Tong, Haiyan; Ledbetter, Allen; Walsh, Leon; Farraj, Aimen [Environmental Public Health Division, National Health and Environmental Effects Research Laboratory, US Environmental Protection Agency, Research Triangle Park, NC 27711 (United States); Hazari, Mehdi, E-mail: hazari.mehdi@epa.gov [Environmental Public Health Division, National Health and Environmental Effects Research Laboratory, US Environmental Protection Agency, Research Triangle Park, NC 27711 (United States)

    2017-06-01

    Short-term exposure to ambient air pollution is linked with adverse cardiovascular effects. While previous research focused primarily on particulate matter-induced responses, gaseous air pollutants also contribute to cause short-term cardiovascular effects. Mechanisms underlying such effects have not been adequately described, however the immediate nature of the response suggests involvement of irritant neural activation and downstream autonomic dysfunction. Thus, this study examines the role of TRPA1, an irritant sensory receptor found in the airways, in the cardiac response of mice to acrolein and ozone. Conscious unrestrained wild-type C57BL/6 (WT) and TRPA1 knockout (KO) mice implanted with radiotelemeters were exposed once to 3 ppm acrolein, 0.3 ppm ozone, or filtered air. Heart rate (HR) and electrocardiogram (ECG) were recorded continuously before, during and after exposure. Analysis of ECG morphology, incidence of arrhythmia and heart rate variability (HRV) were performed. Cardiac mechanical function was assessed using a Langendorff perfusion preparation 24 h post-exposure. Acrolein exposure increased HRV independent of HR, as well as incidence of arrhythmia. Acrolein also increased left ventricular developed pressure in WT mice at 24 h post-exposure. Ozone did not produce any changes in cardiac function. Neither gas produced ECG effects, changes in HRV, arrhythmogenesis, or mechanical function in KO mice. These data demonstrate that a single exposure to acrolein causes cardiac dysfunction through TRPA1 activation and autonomic imbalance characterized by a shift toward parasympathetic modulation. Furthermore, it is clear from the lack of ozone effects that although gaseous irritants are capable of eliciting immediate cardiac changes, gas concentration and properties play important roles. - Highlights: • Acute acrolein exposure causes autonomic imbalance and altered CV function in mice. • TRPA1 mediates acrolein-induced autonomic nervous system cardiac

  2. TRPA1 mediates changes in heart rate variability and cardiac mechanical function in mice exposed to acrolein

    International Nuclear Information System (INIS)

    Kurhanewicz, Nicole; McIntosh-Kastrinsky, Rachel; Tong, Haiyan; Ledbetter, Allen; Walsh, Leon; Farraj, Aimen; Hazari, Mehdi

    2017-01-01

    Short-term exposure to ambient air pollution is linked with adverse cardiovascular effects. While previous research focused primarily on particulate matter-induced responses, gaseous air pollutants also contribute to cause short-term cardiovascular effects. Mechanisms underlying such effects have not been adequately described, however the immediate nature of the response suggests involvement of irritant neural activation and downstream autonomic dysfunction. Thus, this study examines the role of TRPA1, an irritant sensory receptor found in the airways, in the cardiac response of mice to acrolein and ozone. Conscious unrestrained wild-type C57BL/6 (WT) and TRPA1 knockout (KO) mice implanted with radiotelemeters were exposed once to 3 ppm acrolein, 0.3 ppm ozone, or filtered air. Heart rate (HR) and electrocardiogram (ECG) were recorded continuously before, during and after exposure. Analysis of ECG morphology, incidence of arrhythmia and heart rate variability (HRV) were performed. Cardiac mechanical function was assessed using a Langendorff perfusion preparation 24 h post-exposure. Acrolein exposure increased HRV independent of HR, as well as incidence of arrhythmia. Acrolein also increased left ventricular developed pressure in WT mice at 24 h post-exposure. Ozone did not produce any changes in cardiac function. Neither gas produced ECG effects, changes in HRV, arrhythmogenesis, or mechanical function in KO mice. These data demonstrate that a single exposure to acrolein causes cardiac dysfunction through TRPA1 activation and autonomic imbalance characterized by a shift toward parasympathetic modulation. Furthermore, it is clear from the lack of ozone effects that although gaseous irritants are capable of eliciting immediate cardiac changes, gas concentration and properties play important roles. - Highlights: • Acute acrolein exposure causes autonomic imbalance and altered CV function in mice. • TRPA1 mediates acrolein-induced autonomic nervous system cardiac

  3. Airborne acrolein induces keratin-8 (Ser-73) hyperphosphorylation and intermediate filament ubiquitination in bronchiolar lung cell monolayers.

    Science.gov (United States)

    Burcham, Philip C; Raso, Albert; Henry, Peter J

    2014-05-07

    The combustion product acrolein is a key mediator of pulmonary edema in victims of smoke inhalation injury. Since studying acrolein toxicity in conventional in vitro systems is complicated by reactivity with nucleophilic culture media constituents, we explored an exposure system which delivers airborne acrolein directly to lung cell monolayers at the air-liquid interface. Calu-3 lung adenocarcinoma cells were maintained on membrane inserts such that the basal surface was bathed in nucleophile-free media while the upper surface remained in contact with acrolein-containing air. Cells were exposed to airborne acrolein for 30 min before they were allowed to recover in fresh media, with cell sampling at defined time points to allow evaluation of toxicity and protein damage. After prior exposure to acrolein, cell ATP levels remained close to controls for 4h but decreased in an exposure-dependent manner by 24h. A loss of transepithelial electrical resistance and increased permeability to fluorescein isothiocyanate-labeled dextran preceded ATP loss. Use of antibody arrays to monitor protein expression in exposed monolayers identified strong upregulation of phospho-keratin-8 (Ser(73)) as an early consequence of acrolein exposure. These changes were accompanied by chemical damage to keratin-8 and other intermediate filament family members, while acrolein exposure also resulted in controlled ubiquitination of high mass proteins within the intermediate filament extracts. These findings confirm the usefulness of systems allowing delivery of airborne smoke constituents to lung cell monolayers during studies of the molecular basis for acute smoke intoxication injury. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.

  4. Acrolein and Asthma Attack Prevalence in a Representative Sample of the United States Adult Population 2000 – 2009

    Science.gov (United States)

    deCastro, B. Rey

    2014-01-01

    Background Acrolein is an air toxic and highly potent respiratory irritant. There is little epidemiology available, but US EPA estimates that outdoor acrolein is responsible for about 75 percent of non-cancer respiratory health effects attributable to air toxics in the United States, based on the Agency's 2005 NATA (National-Scale Air Toxics Assessment) and acrolein's comparatively potent inhalation reference concentration of 0.02 µg/m3. Objectives Assess the association between estimated outdoor acrolein exposure and asthma attack reported by a representative cross-sectional sample of the adult United States population. Methods NATA 2005 chronic outdoor acrolein exposure estimates at the census tract were linked with residences oif adults (≥18 years old) in the NHIS (National Health Interview Survey) 2000 – 2009 (n = 271,348 subjects). A sample-weighted logistic regression model characterized the association between the prevalence of reporting at least one asthma attack in the 12 months prior to survey interview and quintiles of exposure to outdoor acrolein, controlling for potential confounders. Results In the highest quintile of outdoor acrolein exposure (0.05 – 0.46 µg/m3), there was a marginally significant increase in the asthma attack pOR (prevalence-odds ratio [95% CI]  = 1.08 [0.98∶1.19]) relative to the lowest quintile. The highest quintile was also associated with a marginally significant increase in prevalence-odds (1.13 [0.98∶1.29]) in a model limited to never smokers (n = 153,820). Conclusions Chronic exposure to outdoor acrolein of 0.05 – 0.46 µg/m3 appears to increase the prevalence-odds of having at least one asthma attack in the previous year by 8 percent in a representative cross-sectional sample of the adult United States population. PMID:24816802

  5. Acrolein and asthma attack prevalence in a representative sample of the United States adult population 2000-2009.

    Directory of Open Access Journals (Sweden)

    B Rey deCastro

    Full Text Available BACKGROUND: Acrolein is an air toxic and highly potent respiratory irritant. There is little epidemiology available, but US EPA estimates that outdoor acrolein is responsible for about 75 percent of non-cancer respiratory health effects attributable to air toxics in the United States, based on the Agency's 2005 NATA (National-Scale Air Toxics Assessment and acrolein's comparatively potent inhalation reference concentration of 0.02 µg/m3. OBJECTIVES: Assess the association between estimated outdoor acrolein exposure and asthma attack reported by a representative cross-sectional sample of the adult United States population. METHODS: NATA 2005 chronic outdoor acrolein exposure estimates at the census tract were linked with residences oif adults (≥18 years old in the NHIS (National Health Interview Survey 2000-2009 (n = 271,348 subjects. A sample-weighted logistic regression model characterized the association between the prevalence of reporting at least one asthma attack in the 12 months prior to survey interview and quintiles of exposure to outdoor acrolein, controlling for potential confounders. RESULTS: In the highest quintile of outdoor acrolein exposure (0.05-0.46 µg/m3, there was a marginally significant increase in the asthma attack pOR (prevalence-odds ratio [95% CI]  = 1.08 [0.98∶1.19] relative to the lowest quintile. The highest quintile was also associated with a marginally significant increase in prevalence-odds (1.13 [0.98∶1.29] in a model limited to never smokers (n = 153,820. CONCLUSIONS: Chronic exposure to outdoor acrolein of 0.05-0.46 µg/m3 appears to increase the prevalence-odds of having at least one asthma attack in the previous year by 8 percent in a representative cross-sectional sample of the adult United States population.

  6. Polarographic study of acrolein and its determination by flow injection with amperometric detection at a mercury electrode.

    Science.gov (United States)

    Naranjo Rodríguez, I; Muñoz Leyva, J A; Hidalgo Hidalgo de Cisneros, J L

    1996-07-01

    A study of the electrochemical behavior of acrolein at a dropping mercury electrode using different polarographic techniques is described. Theoretical studies of the reversibility of the wave of acrolein were carried out using two different polarographic techniques: direct current tast and differential pulse. Differential pulse polarography may be used to determine acrolein concentration in a Britton-Robinson buffer solution of pH 10 in the ranges 2 x 10(-7)10(-8) and 5 x 10(-8)-10(-4) mol dm(-3) and a coefficient of variation of 1.7% for a concentration of 10(-5)mol dm(-3). A flow injection method with amperometric detection at a potential of -1.4V using a mercury electrode is also described. Before each injection, any drop hanging from the tip of the capillary needs to be dislodged and a new electrode drop dispensed; three different drop sizes were tested. A linear relationship between peak intensity and acrolein concentration was obtained in the range 10(-5)-10(-7) mol dm(-3), with a detection limit of 9.8 x 10(-8) mol dm(-) 3 and a coefficient of variation of 2.9% for a 2 x 10(-7) mol dm(-3) concentration. Several organic and inorganic species were tested in order to ascertain whether they interfered with the signal for acrolein. The proposed methods were applied to the determination of acrolein in seawater samples.

  7. Increase in acrolein-conjugated immunoglobulins in saliva from patients with primary Sjögren's syndrome.

    Science.gov (United States)

    Hirose, Tadao; Saiki, Ryotaro; Uemura, Takeshi; Suzuki, Takehiro; Dohmae, Naoshi; Ito, Satoshi; Takahashi, Hoyu; Ishii, Itsuko; Toida, Toshihiko; Kashiwagi, Keiko; Igarashi, Kazuei

    2015-10-23

    We previously reported that the level of protein-conjugated acrolein (PC-Acro), a marker of cell or tissue damage, was increased in saliva from patients with primary Sjögren's syndrome (pSS), and that the level of PC-Acro was well correlated with the severity of pSS. Acrolein-conjugated immunoglobulins were measured in saliva from pSS patients. The activities of autoantibodies recognizing Sjögren's syndrome SSA (Ro) and SSB (La) proteins in saliva from pSS patients were approximately 3- to 5-fold higher than those from control subjects. We also found that autoantibody activities recognizing SSA (Ro) and SSB (La) proteins increased after acrolein treatment of saliva from control subjects. When an antibody against human serum albumin was treated with acrolein, the ability to recognize albumin was reduced but the ability to recognize other proteins was increased. Twenty-four and eleven kinds of acrolein-conjugated amino acids were found at the variable and constant regions of peptides, respectively, obtained from the immunoglobulins in saliva from pSS patients. The altered recognition patterns of immunoglobulins due to acrolein conjugation are at least partially involved in autoimmune diseases. Copyright © 2015 Elsevier B.V. All rights reserved.

  8. Deodorants: An experimental provocation study with cinnamic aldehyde

    DEFF Research Database (Denmark)

    Bruze, M.; Johansen, J. D.; Andersen, K. E.

    2003-01-01

    BACKGROUND: Axillary dermatitis is common and overrepresented in individuals with contact allergy to fragrances. Many individuals suspect their deodorants to be the incriminating products. OBJECTIVE: Our aim was to investigate the significance of cinnamic aldehyde in deodorants for the development...... of axillary dermatitis when used by individuals with and without contact allergy to cinnamic aldehyde. METHODS: Patch tests with deodorants and ethanol solutions with cinnamic aldehyde, and repeated open application tests with roll-on deodorants without and with cinnamic aldehyde at different concentrations......, were performed in 37 patients with dermatitis, 20 without and 17 with contact allergy to cinnamic aldehyde. RESULTS: A repeated open application test with positive findings was noted only in patients hypersensitive to cinnamic aldehyde (P deodorants containing...

  9. Cellular fatty acids and aldehydes of oral Eubacterium.

    Science.gov (United States)

    Itoh, U; Sato, M; Tsuchiya, H; Namikawa, I

    1995-02-01

    The cellular fatty acids and aldehydes of oral Eubacterium species were determined by gas chromatography-mass spectrometry. E. brachy and E. lentum contained mainly branched-chain fatty acids, whereas the others contained straight-chain acids. E. brachy, E. lentum, E. yurii ssp. yurii, E. yurii spp. margaretiae, E. limosum, E. plauti and E. aerofaciens also contained aldehydes with even carbon numbers. In addition to species-specific components, the compositional ratios of fatty acids and aldehydes characterized each individual species. The 10 species tested were divided into 5 groups by the principal component analysis. Cellular fatty acids and aldehydes would be chemical markers for interspecies differentiation of oral Eubacterium.

  10. A comparative review of petroleum-based and bio-based acrolein production.

    Science.gov (United States)

    Liu, Lu; Ye, X Philip; Bozell, Joseph J

    2012-07-01

    Acrolein is an important chemical intermediate for many common industrial chemicals, leading to an array of useful end products. This paper reviews all the synthetic methods, including the former (aldol condensation) and contemporary (partial oxidation of propylene) manufacturing methods, the partial oxidation of propane, and most importantly, the bio-based glycerol-dehydration route. Emphasis is placed on the petroleum-based route from propylene and the bio-based route from glycerol, an abundantly available and relatively inexpensive raw material available from biodiesel production. This review provides technical details and incentives for industrial proyduction that justify a transition toward bio-based acrolein production. Copyright © 2012 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

  11. Detection of acrolein and acrylonitrile with a pulsed room temperature quantum cascade laser

    Science.gov (United States)

    Manne, J.; Jäger, W.; Tulip, J.

    2010-06-01

    We investigated the use of a pulsed, distributed feedback quantum cascade laser centered at 957 cm-1 in combination with an astigmatic Herriot cell with 250 m path length for the detection of acrolein and acrylonitrile. These molecules have been identified as hazardous air-pollutants because of their adverse health effects. The spectrometer utilizes the intra-pulse method, where a linear frequency down-chirp, that is induced when a top-hat current pulse is applied to the laser, is used for sweeping across the absorption line. Up to 450 ns long pulses were used for these measurements which resulted in a spectral window of ~2.2 cm-1. A room temperature mercury-cadmium-telluride detector was used, resulting in a completely cryogen free spectrometer. We demonstrated detection limits of ~3 ppb for acrylonitrile and ~6 ppb for acrolein with ~10 s averaging time. Laser characterization and optimization of the operational parameters for sensitivity improvement are discussed.

  12. A theoretical investigation of valence and Rydberg electronic states of acrolein

    International Nuclear Information System (INIS)

    Aquilante, Francesco; Barone, Vincenzo; Roos, Bjoern O.

    2003-01-01

    The main features of the ultraviolet spectrum of acrolein have been studied by a multireference perturbative treatment and by a time dependent density functional approach. The valence and Rydberg transition energies have been calculated and the assignment of the experimental bands has been clarified. The different relaxation trends of the three lowest singlet and triplet excited states have been analyzed by unconstrained geometry optimizations. This has allowed, in particular, the characterization of a twisted 3 (ππ*) state, which is crucial for the interesting photophysics and photochemistry of the acrolein molecule and, more generally, of the α,β-enones. Solvatochromic shifts in aqueous solution have been investigated using a combined discrete/continuum approach based on the so called polarizable continuum model. The experimental trends are well reproduced by this approach and a closer degeneracy in the triplet manifold has been detected in solution with respect to gas phase

  13. Environmental toxin acrolein alters levels of endogenous lipids, including TRP agonists: A potential mechanism for headache driven by TRPA1 activation

    Directory of Open Access Journals (Sweden)

    Emma Leishman

    2017-01-01

    Full Text Available Exposure to airborne toxins can trigger headaches, but the mechanisms are not well understood. Some environmental toxins, such as acrolein, activate transient receptor potential ankyrin 1 (TRPA1, a receptor involved in pain sensation that is highly expressed in the trigeminovascular system. It has been shown in rat models that repeated exposure to acrolein induces trigeminovascular sensitization to both TRPA1 and TRP vanilloid 1 (TRPV1 agonists, a phenomenon linked to headache. In this study, we test the hypothesis that the sensitization of trigeminovascular responses in rats after acrolein exposure via inhalation is associated with changes in levels of endogenous lipids, including TRPV1 agonists, in the trigeminal ganglia, trigeminal nucleus, and cerebellum. Lipidomics analysis of 80 lipids was performed on each tissue after acute acrolein, chronic acrolein, or room air control. Both acute and chronic acrolein exposure drove widespread alterations in lipid levels. After chronic acrolein exposure, levels of all 6 N-acyl ethanolamines in the screening library, including the endogenous cannabinoid and TRPV1 agonist, N-arachidonoyl ethanolamine, were elevated in trigeminal tissue and in the cerebellum. This increase in TRPV1 ligands by acrolein exposure may indicate further downstream signaling, in that we also show here that a combination of these TRPV1 endogenous agonists increases the potency of the individual ligands in TRPV1-HEK cells. In addition to these TRPV1 agonists, 3 TRPV3 antagonists, 4 TRPV4 agonists, and 25 orphan lipids were up and down regulated after acrolein exposure. These data support the hypothesis that lipid signaling may represent a mechanism by which repeated exposure to the TRPA1 agonist and environmental toxin, acrolein, drives trigeminovascular sensitization. Keywords: Lipidomics, Endogenous cannabinoid, TRPA1, TRPV1, Lipoamine, Acrolein, Migraine

  14. Activation of MMP-9 activity by acrolein in saliva from patients with primary Sjögren's syndrome and its mechanism.

    Science.gov (United States)

    Uemura, Takeshi; Suzuki, Takehiro; Saiki, Ryotaro; Dohmae, Naoshi; Ito, Satoshi; Takahashi, Hoyu; Toida, Toshihiko; Kashiwagi, Keiko; Igarashi, Kazuei

    2017-07-01

    We have recently reported that the altered recognition patterns of immunoglobulins due to acrolein conjugation are at least partially responsible for autoimmune diseases in patients with primary Sjögren's syndrome (pSS). In the current study, it was found that the specific activity (activity/ng protein) of metalloproteinase-9 (MMP-9) in saliva was elevated about 2.4-fold in pSS patients. Accordingly, it was examined whether MMP-9 is activated by acrolein. It was found that the MMP-9 with 92kDa molecular weight was activated by acrolein. Under the conditions studied, Cys99, located in the propeptide, was conjugated with acrolein together with Cys230, 244, 302, 314, 329, 347, 361, 373, 388 and 516, which are located in fibronectin repeats and glycosyl domains, but not on the active site of MMP-9. In addition, 82 and 68kDa constructs of MMP-9s, lacking the NH 2 -terminal domain that contains Cys99, were not activated by acrolein. The results suggest that acrolein conjugation at Cys99 caused the active site of MMP-9 to be exposed. Activation of MMP-9 by acrolein was inhibited by cysteine, and slightly by lysine, because these amino acids inhibited acrolein conjugation with MMP-9. Conversely, MMP-9 activity in the presence of 50μM acrolein was enhanced by 100μM histidine. This was due to the inhibition of acrolein conjugation with His405 and 411 located at the Zn 2+ binding site of MMP-9. These results suggest that activation of 92kDa MMP-9 by acrolein is involved in tissue damage in pSS patients and is regulated by cysteine and histidine, and slightly by lysine. Activated 82 and 68kDa MMP-9s were not detected in saliva of pSS patients by Western blotting. Copyright © 2017 Elsevier Ltd. All rights reserved.

  15. Peptide aldehyde inhibitors of bacterial peptide deformylases.

    Science.gov (United States)

    Durand, D J; Gordon Green, B; O'Connell, J F; Grant, S K

    1999-07-15

    Bacterial peptide deformylases (PDF, EC 3.5.1.27) are metalloenzymes that cleave the N-formyl groups from N-blocked methionine polypeptides. Peptide aldehydes containing a methional or norleucinal inhibited recombinant peptide deformylase from gram-negative Escherichia coli and gram-positive Bacillus subtilis. The most potent inhibitor was calpeptin, N-CBZ-Leu-norleucinal, which was a competitive inhibitor of the zinc-containing metalloenzymes, E. coli and B. subtilis PDF with Ki values of 26.0 and 55.6 microM, respectively. Cobalt-substituted E. coli and B. subtilis deformylases were also inhibited by these aldehydes with Ki values for calpeptin of 9.5 and 12.4 microM, respectively. Distinct spectral changes were observed upon binding of calpeptin to the Co(II)-deformylases, consistent with the noncovalent binding of the inhibitor rather than the formation of a covalent complex. In contrast, the chelator 1,10-phenanthroline caused the time-dependent inhibition of B. subtilis Co(II)-PDF activity with the loss of the active site metal. The fact that calpeptin was nearly equipotent against deformylases from both gram-negative and gram-positive bacterial sources lends further support to the idea that a single deformylase inhibitor might have broad-spectrum antibacterial activity. Copyright 1999 Academic Press.

  16. Vapour phase dehydration of glycerol to acrolein over tungstated zirconia catalysts

    Energy Technology Data Exchange (ETDEWEB)

    Rao Ginjupalli, Srinivasa; Mugawar, Sowmya; Rajan, Pethan N.; Kumar Balla, Putra; Chary Komandur, V.R., E-mail: kvrchary@iict.res.in

    2014-08-01

    Tetragonal (TZ) and monoclinic (MZ) polymorphs of zirconia supports were synthesised by sol–gel method followed by variation of the calcination temperature. Tungstated (10 wt% WO{sub 3}) supported on the zirconia polymorphs were prepared by impregnation method by using ammonium metatungstate precursor. The physico-chemical properties of the calcined catalysts were characterised by X-ray diffraction, UV–vis diffused reflectance spectroscopy, X-ray photoelectron spectroscopy (XPS), surface area and pore size distribution measurements to gain insight into the effect of morphology of the catalyst textural properties, and structure. The surface acidic properties have been determined by NH{sub 3} TPD method and also with FT-IR spectra of pyridine adsorption. Vapour phase dehydration of glycerol to acrolein was employed to investigate the catalytic functionalities. Glycerol conversion and acrolein selectivity was mainly dependent on the fraction of moderate acid sites with majority of them are due to Brønsted acidic sites. Monoclinic zirconia based catalysts have shown the highest activity and acrolein selectivity compared to the corresponding tetragonal zirconia catalysts.

  17. A cigarette component acrolein induces accelerated senescence in human diploid fibroblast IMR-90 cells.

    Science.gov (United States)

    Luo, Cheng; Li, Yan; Yang, Liang; Feng, Zhihui; Li, Yuan; Long, Jiangang; Liu, Jiankang

    2013-10-01

    Cigarette smoking causes various diseases, including lung cancer and cardiovascular disease, and reduces life span, though the mechanisms are not well understood. We hypothesize that smoking may cause cellular mitochondrial dysfunction and oxidative stress, leading to aging acceleration. In the present study, we tested the effects of acrolein, a major representative smoking toxicant, on human lung fibroblast IMR-90 cells with regard to cellular senescence, oxidative stress, and mitochondrial function. The results showed that subacute treatment with low dose of acrolein induces the following events compared to the control cells: cell senescence demonstrated by increases in the activity of β-galactosidase, the higher expression of p53 and p21, decreases in DNA synthesis, Sirt1 expression, and telomere length; oxidative stress occurred as the increases in the production of reactive oxygen species, DNA damage, and protein oxidation; and mitochondrial dysfunction shown as decreases in the mitochondrial membrane potential, mitochondrial biogenesis regulator PGC-1 alpha and mitochondria complex I, II, III, and V. These results suggest that acrolein may accelerate aging through the mechanism of increasing oxidative stress and mitochondrial dysfunction.

  18. The Reactions of Nitrogen Heterocycles with Acrolein: Scope and Prebiotic Significance

    Science.gov (United States)

    Cleaves, H. James

    2002-12-01

    It has been suggested that life began with a self-replicating RNA molecule. However, after much research into the prebiotic synthesis of RNA, the difficulties encountered have lead some to hypothesize that RNA was preceded by a simpler molecule, one more easily synthesized prebiotically. Many of the proposed alternative molecules are based on acrolein, since it reacts readily with nucleophiles, such as the nucleobases, via Michael addition and is readily synthesized from formaldehyde and acetaldehyde. Reports regarding the reactions of nucleobases with concentrated acrolein solutions suggest that this is a plausible reaction mechanism, though there are also reports that the "incorrect" isomers are obtained. The scope and kinetics of the reaction of acrolein with various nitrogen heterocycles are reported here. Reactions of pyrimidines often give N1 adducts as the major products. Reactions of purines often give N9 adducts in good yield. The reactions are rapid under neutral to slightly alkaline conditions, and proceed at low temperatures and dilutions. The implications of these findings for the origin of life are discussed.

  19. CO product energy distribution in the photodissociation of methylketene and acrolein at 193 nm

    Science.gov (United States)

    Fujimoto, G. T.; Umstead, M. E.; Lin, M. C.

    1985-04-01

    CO product vibrational energy distributions in the photodissociation of the two C3H4O isomers, methylketene (CH3CHCO) and acrolein (CH2CHCHO), at 193 nm have been measured by CO laser resonance absorption. The CO from methylketene was found to be vibrationally excited up to v=7, and from acrolein v=6, with average vibrational energies of 3.4±0.3 and 2.7±0.7 kcal/mol, respectively. The similarities observed in the appearance times and in the vibrational energy content of the CO formed in the two systems support our previous conclusion that in the case of acrolein isomerization to methylketene takes place prior to the dissociation process: CH2CHCHO+hν→CH3CHCO*†→CH3CH+CO†. The CO vibrational energy distributions observed in both systems agree closely with the statistical distribution predicted assuming that ethylidene rather than ethylene is formed in the photodissociation reaction.

  20. Vapour phase dehydration of glycerol to acrolein over tungstated zirconia catalysts

    Science.gov (United States)

    Rao Ginjupalli, Srinivasa; Mugawar, Sowmya; Rajan N., Pethan; Kumar Balla, Putra; Chary Komandur, V. R.

    2014-08-01

    Tetragonal (TZ) and monoclinic (MZ) polymorphs of zirconia supports were synthesised by sol-gel method followed by variation of the calcination temperature. Tungstated (10 wt% WO3) supported on the zirconia polymorphs were prepared by impregnation method by using ammonium metatungstate precursor. The physico-chemical properties of the calcined catalysts were characterised by X-ray diffraction, UV-vis diffused reflectance spectroscopy, X-ray photoelectron spectroscopy (XPS), surface area and pore size distribution measurements to gain insight into the effect of morphology of the catalyst textural properties, and structure. The surface acidic properties have been determined by NH3 TPD method and also with FT-IR spectra of pyridine adsorption. Vapour phase dehydration of glycerol to acrolein was employed to investigate the catalytic functionalities. Glycerol conversion and acrolein selectivity was mainly dependent on the fraction of moderate acid sites with majority of them are due to Brønsted acidic sites. Monoclinic zirconia based catalysts have shown the highest activity and acrolein selectivity compared to the corresponding tetragonal zirconia catalysts.

  1. Vapour phase dehydration of glycerol to acrolein over tungstated zirconia catalysts

    International Nuclear Information System (INIS)

    Rao Ginjupalli, Srinivasa; Mugawar, Sowmya; Rajan, Pethan N.; Kumar Balla, Putra; Chary Komandur, V.R.

    2014-01-01

    Tetragonal (TZ) and monoclinic (MZ) polymorphs of zirconia supports were synthesised by sol–gel method followed by variation of the calcination temperature. Tungstated (10 wt% WO 3 ) supported on the zirconia polymorphs were prepared by impregnation method by using ammonium metatungstate precursor. The physico-chemical properties of the calcined catalysts were characterised by X-ray diffraction, UV–vis diffused reflectance spectroscopy, X-ray photoelectron spectroscopy (XPS), surface area and pore size distribution measurements to gain insight into the effect of morphology of the catalyst textural properties, and structure. The surface acidic properties have been determined by NH 3 TPD method and also with FT-IR spectra of pyridine adsorption. Vapour phase dehydration of glycerol to acrolein was employed to investigate the catalytic functionalities. Glycerol conversion and acrolein selectivity was mainly dependent on the fraction of moderate acid sites with majority of them are due to Brønsted acidic sites. Monoclinic zirconia based catalysts have shown the highest activity and acrolein selectivity compared to the corresponding tetragonal zirconia catalysts.

  2. The oxidation of the aldehyde groups in dialdehyde starch

    NARCIS (Netherlands)

    Haaksman, I.K.; Besemer, A.C.; Jetten, J.M.; Timmermans, J.W.; Slaghek, T.M.

    2006-01-01

    This paper describes the difference in relative reactivity of the aldehyde groups present in dialdehyde starch towards different oxidising agents. The oxidation of dialdehyde starch with peracetic acid and sodium bromide leads to only partial oxidation to give mono-aldehyde-carboxy starch, while

  3. Threshold responses in cinnamic-aldehyde-sensitive subjects

    DEFF Research Database (Denmark)

    Johansen, J D; Andersen, K E; Rastogi, Suresh Chandra

    1996-01-01

    Cinnamic aldehyde is an important fragrance material and contact allergen. The present study was performed to provide quantitative data on the eliciting capacity of cinnamic aldehyde, to be considered in assessment of clinical relevance and health hazard. The skin response to serial dilution patch...

  4. 27 CFR 24.183 - Use of distillates containing aldehydes.

    Science.gov (United States)

    2010-04-01

    ... 27 Alcohol, Tobacco Products and Firearms 1 2010-04-01 2010-04-01 false Use of distillates... distillates containing aldehydes. Distillates containing aldehydes may be received on wine premises for use in the fermentation of wine and then returned to the distilled spirits plant from which distillates were...

  5. Reduction of Aldehydes and Ketones by Sodium Dithionite

    NARCIS (Netherlands)

    Vries, Johannes G. de; Kellogg, Richard M.

    1980-01-01

    Conditions have been developed for the effective reduction of aldehydes and ketones by sodium dithionite, Na2S2O4. Complete reduction of simple aldehydes and ketones can be achieved with excess Na2S2O4 in H2O/dioxane mixtures at reflux temperature. Some aliphatic ketones, for example, pentanone and

  6. Levels of oxylipins, endocannabinoids and related lipids in plasma before and after low-level exposure to acrolein in healthy individuals and individuals with chemical intolerance.

    Science.gov (United States)

    Claeson, Anna-Sara; Gouveia-Figueira, Sandra; Häggström, Jenny; Fowler, Christopher J; Nording, Malin L

    2017-06-01

    Oxylipins and endocannabinoids play important biological roles, including effects upon inflammation. It is not known whether the circulating levels of these lipids are affected by inhalation of the environmental pollutant acrolein. In the present study, we have investigated the consequences of low-level exposure to acrolein on oxylipin, endocannabinoid and related lipid levels in the plasma of healthy individuals and individuals with chemical intolerance (CI), an affliction with a suggested inflammatory origin. Participants were exposed twice (60min) to heptane and a mixture of heptane and acrolein. Blood samples were collected before exposure, after and 24h post-exposure. There were no overt effects of acrolein exposure on the oxylipin lipidome or endocannibinoids detectable in the bloodstream at the time points investigated. No relationship between basal levels or levels after exposure to acrolein and CI could be identified. This implicates a minor role of inflammatory mediators on the systemic level in CI. Copyright © 2017 Elsevier Ltd. All rights reserved.

  7. A possible role of acrolein in diabetic retinopathy: involvement of a VEGF/TGFβ signaling pathway of the retinal pigment epithelium in hyperglycemia.

    Science.gov (United States)

    Grigsby, Jeffery; Betts, Brandi; Vidro-Kotchan, Eileen; Culbert, Richard; Tsin, Andrew

    2012-11-01

    Acrolein has been implicated in retinal pigment epithelium (RPE) cell death, and has been associated with diabetic retinopathy. Our purpose was to investigate the potential effect of high glucose in influencing acrolein-mediated RPE cytokine production and cell death. We investigated the influence of the acrolein effect on ARPE-19 cells in high glucose conditions and quantified the release of transforming growth factor β (TGFβ1 and 2) and vascular endothelial growth factor (VEGF). We assessed the ability of N-benzylhydroxylamine(NBHA) as well as TGFβ pathway inhibitors SIS3 and SB431542 to prevent this effect of acrolein on ARPE-19 cells. Confluent ARPE-19 cells were treated with acrolein and/or NBHA in both 5.5 and 18.8 mM glucose conditions. Cells were also pretreated with SIS3, a specific inhibitor of the SMAD3 pathway, and SB431542, a specific inhibitor of TGFβ signaling pathway, before treating them with acrolein. Viable cells were counted and ELISAs were performed to measure the cytokines TGFβ1 and 2, and VEGF released into the conditioned media. In ARPE-19 cells exposed to acrolein and hyperglycemia there was reduced cell viability and an increase in the cell media of VEGF, TGFβ1, and TGFβ2, which was reversed by NBHA. Acrolein/hyperglycemia-induced cell viability reduction and cytokine overproduction was also reduced by TGFβ pathway blockade. We conclude that the effect of acrolein on the reduction of viability and VEGF increase by ARPE-19 cells in hyperglycemic media is conducted through the TGFβ signaling pathway. Our results suggest that benefits of sequestering acrolein by NBHA and the blockage of the TGFβ pathway by SB431542 and SIS3 offer suggestions as to potential useful pharmacological drug candidates for the prevention of diabetes-induced complications in the eye.

  8. A Possible Role of Acrolein in Diabetic Retinopathy: Involvement of a VEGF/TGFβ Signaling Pathway of the Retinal Pigment Epithelium in Hyperglycemia

    Science.gov (United States)

    Grigsby, Jeffery; Betts, Brandi; Vidro-Kotchan, Eileen; Culbert, Richard; Tsin, Andrew

    2015-01-01

    Purpose Acrolein has been implicated in retinal pigment epithelium (RPE) cell death, and has been associated with diabetic retinopathy. Our purpose was to investigate the potential effect of high glucose in influencing acrolein-mediated RPE cytokine production and cell death. We investigated the influence of the acrolein effect on ARPE-19 cells in high glucose conditions and quantified the release of transforming growth factor β (TGFβ1 and 2) and vascular endothelial growth factor (VEGF). We assessed the ability of N-benzylhydroxylamine(NBHA) as well as TGFβ pathway inhibitors SIS3 and SB431542 to prevent this effect of acrolein on ARPE-19 cells. Materials and methods Confluent ARPE-19 cells were treated with acrolein and/or NBHA in both 5.5 and 18.8 mM glucose conditions. Cells were also pretreated with SIS3, a specific inhibitor of the SMAD3 pathway, and SB431542, a specific inhibitor of TGFβ signaling pathway, before treating them with acrolein. Viable cells were counted and ELISAs were performed to measure the cytokines TGFβ1 and 2, and VEGF released into the conditioned media. Results In ARPE-19 cells exposed to acrolein and hyperglycemia there was reduced cell viability and an increase in the cell media of VEGF, TGFβ1, and TGFβ2, which was reversed by NBHA. Acrolein/hyperglycemia-induced cell viability reduction and cytokine overproduction was also reduced by TGFβ pathway blockade. Conclusions We conclude that the effect of acrolein on the reduction of viability and VEGF increase by ARPE-19 cells in hyperglycemic media is conducted through the TGFβ signaling pathway. Our results suggest that benefits of sequestering acrolein by NBHA and the blockage of the TGFβ pathway by SB431542 and SIS3 offer suggestions as to potential useful pharmacological drug candidates for the prevention of diabetes-induced complications in the eye. PMID:22906079

  9. Simvastatin attenuates acrolein-induced mucin production in rats: involvement of the Ras/extracellular signal-regulated kinase pathway.

    Science.gov (United States)

    Chen, Ya-Juan; Chen, Peng; Wang, Hai-Xia; Wang, Tao; Chen, Lei; Wang, Xun; Sun, Bei-Bei; Liu, Dai-Shun; Xu, Dan; An, Jing; Wen, Fu-Qiang

    2010-06-01

    Airway mucus overproduction is a cardinal feature of airway inflammatory diseases, such as chronic obstructive pulmonary disease and cystic fibrosis. Since the small G-protein Ras is known to modulate cellular functions in the lung, we sought to investigate whether the Ras inhibitor simvastatin could attenuate acrolein-induced mucin production in rat airways. Rats were exposed to acrolein for 12 days, after first being pretreated intragastrically for 24 h with either simvastatin alone or simvastatin in combination with mevalonate, which prevents the isoprenylation needed for Ras activation. Lung tissue was analyzed for extracellular signal-regulated kinase (ERK) activity, goblet cell metaplasia and mucin production. To analyze the effect of simvastatin on mucin production in more detail, acrolein-exposed human airway epithelial NCI-H292 cells were pretreated with simvastatin alone or together with mevalonate. Culture medium was collected to detect mucin secretion, and cell lysates were examined for Ras-GTPase activity and epidermal growth factor receptor (EGFR)/ERK phosphorylation. In vivo, simvastatin treatment dose-dependently suppressed acrolein-induced goblet cell hyperplasia and metaplasia in bronchial epithelium and inhibited ERK phosphorylation in rat lung homogenates. Moreover, simvastatin inhibited Muc5AC mucin synthesis at both the mRNA and protein levels in the lung. In vitro, simvastatin pretreatment attenuated the acrolein-induced significant increase in MUC5AC mucin expression, Ras-GTPase activity and EGFR/ERK phosphorylation. These inhibitory effects of simvastatin were neutralized by mevalonate administration both in vitro and in vivo. Our results suggest that simvastatin may attenuate acrolein-induced mucin protein synthesis in the airway and airway inflammation, possibly by blocking ERK activation mediated by Ras protein isoprenylation. Thus, the evidence from the experiment suggests that human trials are warranted to determine the potential

  10. Tissue sensitivity of the rat upper and lower extrapulmonary airways to the inhaled electrophilic air pollutants diacetyl and acrolein.

    Science.gov (United States)

    Cichocki, Joseph A; Smith, Gregory J; Morris, John B

    2014-11-01

    The target site for inhaled vapor-induced injury often differs in mouth-breathing humans compared with nose-breathing rats, thus complicating the use of rat inhalation toxicity data for assessment of human risk. We sought to examine sensitivity of respiratory/transitional nasal (RTM) and tracheobronchial (TBM) mucosa to two electrophilic irritant vapors: diacetyl and acrolein. Computational fluid dynamic physiologically based pharmacokinetic modeling was coupled with biomarker assessment to establish delivered dose-response relationships in RTM and TBM in male F344 rats following 6 h exposure to diacetyl or acrolein. Biomarkers included glutathione status, proinflammatory and antioxidant gene mRNA levels, and nuclear translocation of nuclear factor (erythroid-derived 2)-like 2 (Nrf2). Modeling revealed that 0.0094-0.1653 μg acrolein/min-cm(2) and 3.9-21.6 μg diacetyl/min-cm(2) were deposited into RTM/TBM. Results indicate RTM and TBM were generally of similar sensitivity to diacetyl and acrolein. For instance, both tissues displayed induction of antioxidant and proinflammatory genes, and nuclear accumulation of Nrf2 after electrophile exposure. Hierarchical cellular response patterns were similar in RTM and TBM but differed between vapors. Specifically, diacetyl exposure induced proinflammatory and antioxidant genes concomitantly at low exposure levels, whereas acrolein induced antioxidant genes at much lower exposure levels than that required to induce proinflammatory genes. Generally, diacetyl was less potent than acrolein, as measured by maximal induction of transcripts. In conclusion, the upper and lower extrapulmonary airways are of similar sensitivity to inhaled electrophilic vapors. Dosimetrically based extrapolation of nasal responses in nose-breathing rodents may provide an approach to predict risk to the lower airways of humans during mouth-breathing. © The Author 2014. Published by Oxford University Press on behalf of the Society of Toxicology. All

  11. Acrolein Is a Pathogenic Mediator of Alcoholic Liver Disease and the Scavenger Hydralazine Is Protective in MiceSummary

    Directory of Open Access Journals (Sweden)

    Wei-Yang Chen

    2016-09-01

    Full Text Available Background & Aims: Alcoholic liver disease (ALD remains a major cause of morbidity and mortality, with no Food and Drug Administration–approved therapy. Chronic alcohol consumption causes a pro-oxidant environment and increases hepatic lipid peroxidation, with acrolein being the most reactive/toxic by-product. This study investigated the pathogenic role of acrolein in hepatic endoplasmic reticulum (ER stress, steatosis, and injury in experimental ALD, and tested acrolein elimination/scavenging (using hydralazine as a potential therapy in ALD. Methods: In vitro (rat hepatoma H4IIEC cells and in vivo (chronic+binge alcohol feeding in C57Bl/6 mice models were used to examine alcohol-induced acrolein accumulation and consequent hepatic ER stress, apoptosis, and injury. In addition, the potential protective effects of the acrolein scavenger, hydralazine, were examined both in vitro and in vivo. Results: Alcohol consumption/metabolism resulted in hepatic accumulation of acrolein-protein adducts, by up-regulation of cytochrome P4502E1 and alcohol dehydrogenase, and down-regulation of glutathione-s-transferase-P, which metabolizes/detoxifies acrolein. Alcohol-induced acrolein adduct accumulation led to hepatic ER stress, proapoptotic signaling, steatosis, apoptosis, and liver injury; however, ER-protective/adaptive responses were not induced. Notably, direct exposure to acrolein in vitro mimicked the in vivo effects of alcohol, indicating that acrolein mediates the adverse effects of alcohol. Importantly, hydralazine, a known acrolein scavenger, protected against alcohol-induced ER stress and liver injury, both in vitro and in mice. Conclusions: Our study shows the following: (1 alcohol consumption triggers pathologic ER stress without ER adaptation/protection; (2 alcohol-induced acrolein is a potential therapeutic target and pathogenic mediator of hepatic ER stress, cell death, and injury; and (3 removal/clearance of acrolein

  12. Nanofilter platform based on functionalized carbon nanotubes for adsorption and elimination of Acrolein, a toxicant in cigarette smoke

    Science.gov (United States)

    Yoosefian, Mehdi; Pakpour, Atef; Etminan, Nazanin

    2018-06-01

    This paper discusses the use of carboxylated single-walled carbon nanotube as a general nanofilter platform for the removal of acrolein carcinogen from cigarette smoke. The analyses carried out in the detailed study of the electronic and structural effects of the adsorption of acrolein onto COOH loaded on single-walled carbon nanotube under the density functional theory framework. The results of Bader theory of atoms in molecules, natural bond orbital, molecular potential electron surface and density of state confirm the potential application of the suggested nanofilter platform.

  13. Analysis of reactive aldehydes formed from the irradiated skin lipid, triolein

    International Nuclear Information System (INIS)

    Niyati-Shirkhodaee, F.; Shibamoto. Y.

    1992-01-01

    One of the major skin lipids, triolein, was irradiated by 300 nm uv light under conditions approximately those at the skin surface exposed to sunlight for different periods of time. Irradiated samples were analyzed for acrolein, formaldehyde, and acetaldehyde by gas chromatography. Acrolein formed was derivatized to more stable 1-methyl-2-pyrazoline with N-methylhydrazine and analyzed by a nitrogen-phosphorus specific detector. Formaldehyde and acetaldehyde formed were reacted with cysteamine to give thiazolidine and 2-methylthiazolidine, respectively and analyzed by a flame photometric sulfur specific detector. The maximum amount of acrolein (1.05 nmol/mg triolein) was formed after 6 hr irradiation. The maximum quantities of formaldehyde (6 nmol/mg triolein) and acetaldehyde (2.71 nmol/mg triolein) were formed after 12 hr irradiation. Both formaldehyde and acrolein have been known to cause skin irritation in the levels of 1 ppM

  14. Acrolein-mediated conduction loss is partially restored by K+ channel blockers

    Science.gov (United States)

    Yan, Rui; Page, Jessica C.

    2015-01-01

    Acrolein-mediated myelin damage is thought to be a critical mechanism leading to conduction failure following neurotrauma and neurodegenerative diseases. The exposure and activation of juxtaparanodal voltage-gated K+ channels due to myelin damage leads to conduction block, and K+ channel blockers have long been studied as a means for restoring axonal conduction in spinal cord injury (SCI) and multiple sclerosis (MS). In this study, we have found that 100 μM K+ channel blockers 4-aminopyridine-3-methanol (4-AP-3-MeOH), and to a lesser degree 4-aminopyridine (4-AP), can significantly restore compound action potential (CAP) conduction in spinal cord tissue following acrolein-mediated myelin damage using a well-established ex vivo SCI model. In addition, 4-AP-3-MeOH can effectively restore CAP conduction in acrolein-damaged axons with a range of concentrations from 0.1 to 100 μM. We have also shown that while both compounds at 100 μM showed no preference of small- and large-caliber axons when restoring CAP conduction, 4-AP-3-MeOH, unlike 4-AP, is able to augment CAP amplitude while causing little change in axonal responsiveness measured in refractory periods and response to repetitive stimuli. In a prior study, we show that 4-AP-3-MeOH was able to functionally rescue mechanically injured axons. In this investigation, we conclude that 4-AP-3-MeOH is an effective K+ channel blocker in restoring axonal conduction following both primary (physical) and secondary (chemical) insults. These findings also suggest that 4-AP-3-MeOH is a viable alternative of 4-AP for treating myelin damage and improving function following central nervous system trauma and neurodegenerative diseases. PMID:26581866

  15. Metabolism and binding of cyclophosphamide and its metabolite acrolein to rat hepatic microsomal cytochrome P-450

    International Nuclear Information System (INIS)

    Marinello, A.J.; Bansal, S.K.; Paul, B.; Koser, P.L.; Love, J.; Struck, R.F.; Gurtoo, H.L.

    1984-01-01

    The hepatic cytochrome P-450-mediated metabolism and metabolic activation of [chloroethyl-3H]cyclophosphamide [( chloroethyl-3H]CP) and [4-14C]cyclophosphamide [( 4-14C]CP) were investigated in vitro in the reconstituted system containing cytochrome P-450 isolated from phenobarbital-treated rats. In addition, hepatic microsomal binding and the hepatic microsome-mediated metabolism of [14C]acrolein, a metabolite of [4-14C]CP, were also investigated. The metabolism of [chloroethyl-3H]CP and [4-14C]CP to polar metabolites was found to depend on the presence of NADPH and showed concentration dependence with respect to cytochrome P-450 and NADPH:cytochrome P-450 reductase. Km and Vmax values were essentially similar. The patterns of inhibition by microsomal mixed-function oxidase inhibitors, anti-cytochrome P-450 antibody, and heat denaturation of the cytochrome P-450 were essentially similar, with subtle differences between [4-14C]CP and [chloroethyl-3H]CP metabolism. The in vitro metabolic activation of CP in the reconstituted system demonstrated predominant binding of [chloroethyl-3H]CP to nucleic acids and almost exclusive binding of [4-14C]CP to proteins. Gel electrophoresis-fluorography of the proteins in the reconstituted system treated with [4-14C]CP demonstrated localization of the 14C label in the cytochrome P-450 region. To examine this association further, hepatic microsomes were modified with [14C]acrolein in the presence and the absence of NADPH. The results confirmed covalent association between [14C]acrolein and cytochrome P-450 in the microsomes and also demonstrated further metabolism of [14C]acrolein, apparently to an epoxide, which is capable of binding covalently to proteins. The results of these investigations not only confirm the significance of primary metabolism but also emphasize the potential role of the secondary metabolism of cyclophosphamide in some of its toxic manifestations

  16. The active component of vanadium-molybdenum catalysts for the oxidation of acrolein to acrylic acid

    International Nuclear Information System (INIS)

    Andrushkevich, T.V.; Kuznetsova, T.G.

    1986-01-01

    The catalytic properties of the vanadium-molybdenum oxide system were investigated in the oxidation of acrolein to acrylic acid. The active component of the catalyst is the compound VMo 3 O 11 , the maximum amount of which is observed at a content of 7-15 mole% V 2 O 4 . The compound VMo 3 O 11 is formed in the thermodecomposition of silicomolybdovanadium heteropoly acids or isopoly compounds, reduced with respect to vanadium, and contains V 4+ and Mo 6+ . The optimum treatment for the formation of this compound is treatment in the reaction mixture at 400 degrees C

  17. Cooperative properties of single phases of complex oxide catalyst for oxidation of propylene to acrolein

    International Nuclear Information System (INIS)

    Orel, L.I.; Udalova, O.V.; Korchak, V.N.; Isaev, O.V.; Krylov, O.V.; Gershenzon, Yu.M.; Aptekar', E.L.

    1992-01-01

    Synergetic effect of increase of acrolein yield during propylene oxidation on mechanical mixture of (α + β)CoMoO 4 and MoO 3 , as well as CO and CO 2 yield on mixture of CoMoO 4 and Bi 2 O 3 ·2MoO 3 was revealed. It is shown that CoMoO 4 generates allyl radicals, desorption of these radicals to gaseous phase is not practically observed with MoO 3 , bismuth molybdates and Fe 2 O 3 · Fe 2 O 3 ·3MoO 3

  18. A new method for the chemoselective reduction of aldehydes and ...

    Indian Academy of Sciences (India)

    Department of Chemistry, Akdeniz University, 07058, Antalya, Turkey e-mail: ... Kinetics of reduction of aldehydes and ketones to corresponding alcohols were also examined and .... hol and unreducted ketone remain in organic phase. The.

  19. The Reduction of Nitriles to Aldehydes: Applications of Raney Nickel ...

    African Journals Online (AJOL)

    NJD

    The selective reduction of a nitrile to an aldehyde, especially when the substrate ..... prelude to reductive amination chemistry was thwarted by a rapid aldol ... and allowed the direct incorporation of the α-methylbenzylamine chiral auxiliary.

  20. Silver-catalyzed synthesis of amides from amines and aldehydes

    Science.gov (United States)

    Madix, Robert J; Zhou, Ling; Xu, Bingjun; Friend, Cynthia M; Freyschlag, Cassandra G

    2014-11-18

    The invention provides a method for producing amides via the reaction of aldehydes and amines with oxygen adsorbed on a metallic silver or silver alloy catalyst. An exemplary reaction is shown in Scheme 1: (I), (II), (III). ##STR00001##

  1. Human liver aldehyde dehydrogenase: coenzyme binding

    International Nuclear Information System (INIS)

    Kosley, L.L.; Pietruszko, R.

    1987-01-01

    The binding of [U- 14 C] NAD to mitochondrial (E2) and cytoplasmin(E1) aldehyde dehydrogenase was measured by gel filtration and sedimentation techniques. The binding data for NAD and (E1) yielded linear Scatchard plots giving a dissociation constant of 25 (+/- 8) uM and the stoichiometry of 2 mol of NAD bound per mol of E1. The binding data for NAD and (E2) gave nonlinear Scatchard plots. The binding of NADH to E2 was measured via fluorescence enhancement; this could not be done with E1 because there was no signal. The dissociation constant for E2 by this technique was 0.7 (+/- 0.4) uM and stoichiometry of 1.0 was obtained. The binding of [U- 14 C] NADH to (E1) and (E2) was also measured by the sedimentation technique. The binding data for (E1) and NADH gave linear Scatchard plots giving a dissociation constant of 13 (+/- 6) uM and the stoichiometry of 2.0. The binding data for NADH to (E2) gave nonlinear Scatchard plots. With (E1), the dissociation constants for both NAD and NADH are similar to those determined kinetically, but the stoichiometry is only half of that found by stopped flow technique. With (E2) the dissociation constant by fluorometric procedure was 2 orders of magnitude less than that from catalytic reaction

  2. Acrolein and thiol-reactive electrophiles suppress allergen-induced innate airway epithelial responses by inhibition of DUOX1 and EGFR.

    Science.gov (United States)

    Danyal, Karamatullah; de Jong, Willem; O'Brien, Edmund; Bauer, Robert A; Heppner, David E; Little, Andrew C; Hristova, Milena; Habibovic, Aida; van der Vliet, Albert

    2016-11-01

    Acrolein is a major thiol-reactive component of cigarette smoke (CS) that is thought to contribute to increased asthma incidence associated with smoking. Here, we explored the effects of acute acrolein exposure on innate airway responses to two common airborne allergens, house dust mite and Alternaria alternata, and observed that acrolein exposure of C57BL/6 mice (5 ppm, 4 h) dramatically inhibited innate airway responses to subsequent allergen challenge, demonstrated by attenuated release of the epithelial-derived cytokines IL-33, IL-25, and IL-1α. Acrolein and other anti-inflammatory thiol-reactive electrophiles, cinnamaldehyde, curcumin, and sulforaphane, similarly inhibited allergen-induced production of these cytokines from human or murine airway epithelial cells in vitro. Based on our previous observations indicating the importance of Ca 2+ -dependent signaling, activation of the NADPH oxidase DUOX1, and Src/EGFR-dependent signaling in allergen-induced epithelial secretion of these cytokines, we explored the impact of acrolein on these pathways. Acrolein and other thiol-reactive electrophiles were found to dramatically prevent allergen-induced activation of DUOX1 as well as EGFR, and acrolein was capable of inhibiting EGFR tyrosine kinase activity via modification of C797. Biotin-labeling strategies indicated increased cysteine modification and carbonylation of Src, EGFR, as well as DUOX1, in response to acrolein exposure in vitro and in vivo, suggesting that direct alkylation of these proteins on accessible cysteine residues may be responsible for their inhibition. Collectively, our findings indicate a novel anti-inflammatory mechanism of CS-derived acrolein and other thiol-reactive electrophiles, by directly inhibiting DUOX1- and EGFR-mediated airway epithelial responses to airborne allergens. Copyright © 2016 the American Physiological Society.

  3. Unsuitability of using the DNPH-coated solid sorbent cartridge for determination of airborne unsaturated carbonyls

    Science.gov (United States)

    Ho, Steven Sai Hang; Ho, K. F.; Liu, W. D.; Lee, S. C.; Dai, W. T.; Cao, J. J.; Ip, H. S. S.

    2011-01-01

    Measurements of aldehydes and ketones are typically conducted by derivatization using sorbent cartridges coated with 2,4-dinitrophenylhydrazine (DNPH). The collected samples are eluted with acetonitrile and analyzed by high-pressure liquid chromatography coupled with an ultra-violet detector (HPLC/UV). This paper intends to examine artifacts about its suitability in identification of unsaturated carbonyls. Kinetic tests for acrolein, crotonaldehyde, methacrolein and methyl vinyl ketone (MVK) showed formations of carbonyl-DNP-hydrazone during sampling, which could further react with DNPH, resulting in undesired UV absorption products [e.g., carbonyl-DNP-hydrazone-DNPH (dimer) and 2(carbonyl-DNP-hydrazone)-DNPH (trimer)]. The dimerization and trimerization occurred for acrolein and MVK whereas only dimerization for crotonaldehyde and methacrolein. The polymerization products undoubtedly affect the integrity of the chromatogram, leading to misidentification and inaccurate quantification. Whether precautions taken during sampling and/or sample treatment could avoid or minimize this artifact has not been thoughtfully investigated. More often, such artifacts are usually overlooked by scientists when the data are reported.

  4. Infrared multiphoton dissociation of acrolein. Time-resolved observation of CO ( v = 1) IR emission at 4.7 μm

    Science.gov (United States)

    Chowdhury, P. K.; Rama Rao, K. V. S.; Mittal, J. P.

    1994-02-01

    In contrast to the photochemistry of electronically excited acrolein producing vinyl and formyl radicals via CC bond rupture, multiphoton vibrationally excited molecules undergo concerted dissociation generating CO and ethylene. Vibrational excitation in the CO product is detected immediately following the CO 2 laser pulse by observing IR emission at 4.7 μm. The decay of the IR emission was studied as a function of acrolein pressure. A vibrational-vibrational relaxation rate constant of CO ( v=1) by acrolein is found to be 1240 ± 200 Torr -1 s -1.

  5. Protective effect of Pycnogenol in human neuroblastoma SH-SY5Y cells following acrolein-induced cytotoxicity.

    Science.gov (United States)

    Ansari, Mubeen A; Keller, Jeffrey N; Scheff, Stephen W

    2008-12-01

    Oxidative stress is one of the hypotheses involved in the etiology of Alzheimer's disease (AD). Considerable attention has been focused on increasing the intracellular glutathione (GSH) levels in many neurodegenerative diseases, including AD. Pycnogenol (PYC) has antioxidant properties and stabilizes intracellular antioxidant defense systems including glutathione levels. The present study investigated the protective effects of PYC on acrolein-induced oxidative cell toxicity in cultured SH-SY5Y neuroblastoma cells. Decreased cell survival in SH-SY5Y cultures treated with acrolein correlated with oxidative stress, increased NADPH oxidase activity, free radical production, protein oxidation/nitration (protein carbonyl, 3-nitrotyrosine), and lipid peroxidation (4-hydroxy-2-nonenal). Pretreatment with PYC significantly attenuated acrolein-induced cytotoxicity, protein damage, lipid peroxidation, and cell death. A dose-response study suggested that PYC showed protective effects against acrolein toxicity by modulating oxidative stress and increasing GSH. These findings provide support that PYC may provide a promising approach for the treatment of oxidative stress-related neurodegenerative diseases such as AD.

  6. Influence of Catalyst Acid/Base Properties in Acrolein Production by Oxidative Coupling of Ethanol and Methanol.

    Science.gov (United States)

    Lilić, Aleksandra; Bennici, Simona; Devaux, Jean-François; Dubois, Jean-Luc; Auroux, Aline

    2017-05-09

    Oxidative coupling of methanol and ethanol represents a new route to produce acrolein. In this work, the overall reaction was decoupled in two steps, the oxidation and the aldolization, by using two consecutive reactors to investigate the role of the acid/base properties of silica-supported oxide catalysts. The oxidation of a mixture of methanol and ethanol to formaldehyde and acetaldehyde was performed over a FeMoO x catalyst, and then the product mixture was transferred without intermediate separation to a second reactor, in which the aldol condensation and dehydration to acrolein were performed over the supported oxides. The impact of the acid/base properties on the selectivity towards acrolein was investigated under oxidizing conditions for the first time. The acid/base properties of the catalysts were investigated by NH 3 -, SO 2 -, and methanol-adsorption microcalorimetry. A MgO/SiO 2 catalyst was the most active in acrolein production owing to an appropriate ratio of basic to acidic sites. © 2017 Wiley-VCH Verlag GmbH & Co. KGaA, Weinheim.

  7. Aggravation of brain infarction through an increase in acrolein production and a decrease in glutathione with aging.

    Science.gov (United States)

    Uemura, Takeshi; Watanabe, Kenta; Ishibashi, Misaki; Saiki, Ryotaro; Kuni, Kyoshiro; Nishimura, Kazuhiro; Toida, Toshihiko; Kashiwagi, Keiko; Igarashi, Kazuei

    2016-04-29

    We previously reported that tissue damage during brain infarction was mainly caused by inactivation of proteins by acrolein. This time, it was tested why brain infarction increases in parallel with aging. A mouse model of photochemically induced thrombosis (PIT) was studied using 2, 6, and 12 month-old female C57BL/6 mice. The size of brain infarction in the mouse PIT model increased with aging. The volume of brain infarction in 12 month-old mice was approximately 2-fold larger than that in 2 month-old mice. The larger brain infarction in 12 month-old mice was due to an increase in acrolein based on an increase in the activity of spermine oxidase, together with a decrease in glutathione (GSH), a major acrolein-detoxifying compound in cells, based on the decrease in one of the subunits of glutathione biosynthesizing enzymes, γ-glutamylcysteine ligase modifier subunit, with aging. The results indicate that aggravation of brain infarction with aging was mainly due to the increase in acrolein production and the decrease in GSH in brain. Copyright © 2016 Elsevier Inc. All rights reserved.

  8. Simultaneous exposure to concentrated ambient particles and acrolein causes cardiac effects mediated by parasympathetic modulation in mice

    Science.gov (United States)

    This study shows that exposure to CAPs and acrolein causes an increase in HRV that is mediated by the parasympathetic nervous system. Numerous studies show that short-term air pollution exposure modulates heart rate variability (HRV), which is an indicator of autonomic influence...

  9. Acrolein Causes TRPA1-Mediated Sensory Irritation and Indirect Potentiation of TRPV1-Mediated Pulmonary Chemoreflex Response

    Science.gov (United States)

    We previously demonstrated that acute exposure to acrolein causes immediate sensory irritation, with rapid decrease in heart rate (HR) and increase in inspiratory time (Ti), and potentiation of pulmonary chemoreflex response 24hrs later; of these effects only the latter is mediat...

  10. The adsorption of acrolein on a Pt (1 1 1): A study of chemical bonding and electronic structure

    Science.gov (United States)

    Pirillo, S.; López-Corral, I.; Germán, E.; Juan, A.

    2012-12-01

    The adsorption of acrolein on a Pt (1 1 1) surface was studied using ab-initio and semiempirical calculations. Geometry optimization and densities of states (DOS) curves were carried out using the Vienna Ab-initio Simulation Package (VASP) code. We started our study with the preferential geometries corresponding to the different acrolein/Pt (1 1 1) adsorption modes previously reported. Then, we examined the evolution of the chemical bonding in these geometries, using the crystal orbital overlap population (COOP) and overlap population (OP) analysis of selected pairs of atoms. We analyzed the acrolein intramolecular bonds, Pt (1 1 1) superficial bonds and new moleculesbnd surface formed bonds after adsorption. We found that Ptsbnd Pt bonds interacting with the molecule and acrolein Cdbnd O and Cdbnd C bonds are weakened after adsorption; this last bond is significantly linked to the surface. The obtained Csbnd Pt and Osbnd Pt OP values suggest that the most stable adsorption modes are η3-cis and η4-trans, while the η1-trans is the less favored configuration. We also found that C pz orbital and Pt pz and d orbitals participate strongly in the adsorption process.

  11. Influenza A infection attenuates relaxation responses of mouse tracheal smooth muscle evoked by acrolein.

    Science.gov (United States)

    Cheah, Esther Y; Mann, Tracy S; Burcham, Philip C; Henry, Peter J

    2015-02-15

    The airway epithelium is an important source of relaxant mediators, and damage to the epithelium caused by respiratory tract viruses may contribute to airway hyperreactivity. The aim of this study was to determine whether influenza A-induced epithelial damage would modulate relaxation responses evoked by acrolein, a toxic and prevalent component of smoke. Male BALB/c mice were inoculated intranasally with influenza A/PR-8/34 (VIRUS-infected) or allantoic fluid (SHAM-infected). On day 4 post-inoculation, isometric tension recording studies were conducted on carbachol pre-contracted tracheal segments isolated from VIRUS and SHAM mice. Relaxant responses to acrolein (30 μM) were markedly smaller in VIRUS segments compared to SHAM segments (2 ± 1% relaxation vs. 28 ± 5%, n=14, pacrolein and SP were reduced in VIRUS segments (>35% reduction, n=6, pacrolein were profoundly diminished in tracheal segments isolated from influenza A-infected mice. The mechanism through which influenza A infection attenuates this response appears to involve reduced production of PGE2 in response to SP due to epithelial cell loss, and may provide insight into the airway hyperreactivity observed with influenza A infection. Copyright © 2014 Elsevier Inc. All rights reserved.

  12. Decarbonylation and hydrogenation reactions of allyl alcohol and acrolein on Pd(110)

    Science.gov (United States)

    Shekhar, Ratna; Barteau, Mark A.

    1994-11-01

    Allyl alcohol and acrolein reactions on the Pd(110) surface were investigated using temperature programmed desorption. For both unsaturated oxygenates, three coverage-dependent reaction pathways were observed. At low coverages, allyl alcohol decomposed completely to CO, hydrogen and carbonaceous species on the surface. For θ > 0.15 monolayer, ethylene (and small amounts of ethane) desorbed at ca. 295 K. Near saturation coverages, desorption of propanal was detected at ca. 235 K. The parent molecule, allyl alcohol, desorbed only after exposures sufficient to saturate these channels. Acrolein decomposition spectra were similar to those observed for allyl alcohol decomposition on the clean surface. Additional experiments with allyl alcohol on hydrogen- and deuterium-precoveredPd(110) surfaces demonstrated increased hydrogenation of the C 2-hydrocarbon products along with hydrogenation of allyl alcohol to 1-propanol. However, in contrast to previous results for allyl alcohol on the Pd(111) surface, there was no evidence for C-O scission reactions of any C 3 oxygenate on Pd(110).

  13. Sensitive detection of acrolein and acrylonitrile with a pulsed quantum-cascade laser

    Science.gov (United States)

    Manne, J.; Lim, A.; Tulip, J.; Jäger, W.

    2012-05-01

    We report on spectroscopic measurements of acrolein and acrylonitrile at atmospheric pressure using a pulsed distributed feedback quantum-cascade laser in combination with intra- and inter-pulse techniques and compare the results. The measurements were done in the frequency region around 957 cm-1. In the inter-pulse technique, the laser is excited with short current pulses (5-10 ns), and the pulse amplitude is modulated with an external current ramp resulting in a ˜2.3 cm-1 frequency scan. In the intra-pulse technique, a linear frequency down-chirp during the pulse is used for sweeping across the absorption line. Long current pulses up to 500 ns were used for these measurements which resulted in a spectral window of ˜2.2 cm-1 during the down-chirp. These comparatively wide spectral windows facilitated the measurements of the relatively broad absorption lines (˜1 cm-1) of acrolein and acrylonitrile. The use of a room-temperature mercury-cadmium-telluride detector resulted in a completely cryogen-free spectrometer. We demonstrate ppb level detection limits within a data acquisition time of ˜10 s with these methodologies.

  14. [Changes of CD(4)(+) Foxp3+ regulatory T cells and CD(4)(+)IL-17+T cells in acrolein exposure rats].

    Science.gov (United States)

    Wei, Ming; Tu, Ling; Liang, Yinghong; Li, Jia; Gong, Yanjie; Zhang, Yihua; Yang, Lu

    2015-09-01

    To evaluate the changes of CD(4)(+) IL-17+T (Th17) and CD(4)(+)Foxp3+regulatory T (Treg) cells in peripheral blood and bronchoalveolar lavage fluid (BALF) , and therefore to explore the role of Th17 and Treg in acrolein exposure airway inflammation in rats. Forty male Wistar rats were randomly divided into 4 groups: a 2 wk acrolein exposure group, a 4 wk acrolein exposure group, a 2 wk control group and a 4 wk control group (n=10 each). Cells in BALF were collected and analyzed by absolute and differential cell counts.IL-17 and IL-6 levels in serum and BALF were tested by enzyme linked immunosorbent assay (ELISA). The proportion of CD(4)(+)IL-17+T and CD(4)(+) Foxp3+Treg in peripheral blood and BALF were determined by flow cytometry.The mRNA expressions of IL-17 and Foxp3 were measured by real-time PCR. Comparisons of the data between different groups were performed using one-way ANOVA, and SNK and Games-Howell test were used for comparison between 2 groups. Levels of IL-17 were remarkable increased in the 2 wk acrolein exposure group and the 4 wk acrolein exposure group in serum [(52.64 ± 1.89) ng/L, (76.73 ± 5.57) ng/L], and BALF [(79.07 ± 5.67) ng/L, (96.61 ± 6.44) ng/L] compared with the 2 wk control group [(40.05 ± 3.12) ng/L, (56.75 ± 4.37) ng/L] and the 4 wk control group [(38.75 ± 3.23) ng/L, (53.27 ± 4.48) ng/L], all Pcells and macrophages (r=0.5126, 0.5437, all Pcells and an vary of inflammatory cytokines were evident in airway inflammation of acrolein exposed rats, suggesting that Treg was involved in the immunological regulation and Th17 was associated with the persistent inflammation in acrolein induced airway inflammation in rats.

  15. Polyphenol extract from Phellinus igniarius protects against acrolein toxicity in vitro and provides protection in a mouse stroke model.

    Science.gov (United States)

    Suabjakyong, Papawee; Saiki, Ryotaro; Van Griensven, Leo J L D; Higashi, Kyohei; Nishimura, Kazuhiro; Igarashi, Kazuei; Toida, Toshihiko

    2015-01-01

    The basidiomycetous mushroom Phellinus igniarius (L.) Quel. has been used as traditional medicine in various Asian countries for many years. Although many reports exist on its anti-oxidative and anti-inflammatory activities and therapeutic effects against various diseases, our current knowledge of its effect on stroke is very limited. Stroke is a neurodegenerative disorder in which oxidative stress is a key hallmark. Following the 2005 discovery by Igarashi's group that acrolein produced from polyamines in vivo is a major cause of cell damage by oxidative stress, we now describe the effects of anti-oxidative extracts from P. igniarius on symptoms of experimentally induced stroke in mice. The toxicity of acrolein was compared with that of hydrogen peroxide in a mouse mammary carcinoma cell line (FM3A). We found that the complete inhibition of FM3A cell growth by 5 μM acrolein could be prevented by crude ethanol extract of P. igniarius at 0.5 μg/ml. Seven polyphenol compounds named 3,4-dihydroxybenzaldehyde, 4-(3,4-dihydroxyphenyl-3-buten-2one, inonoblin C, phelligridin D, inoscavin C, phelligridin C and interfungin B were identified from this ethanolic extract by LCMS and 1H NMR. Polyphenol-containing extracts of P. igniarius were then used to prevent acrolein toxicity in a mouse neuroblastoma (Neuro-2a) cell line. The results suggested that Neuro-2a cells were protected from acrolein toxicity at 2 and 5 μM by this polyphenol extract at 0.5 and 2 μg/ml, respectively. Furthermore, in mice with experimentally induced stroke, intraperitoneal treatment with P. igniarius polyphenol extract at 20 μg/kg caused a reduction of the infarction volume by 62.2% compared to untreated mice. These observations suggest that the polyphenol extract of P. igniarius could serve to prevent ischemic stroke.

  16. The adsorption of acrolein on a Pt (1 1 1): A study of chemical bonding and electronic structure

    International Nuclear Information System (INIS)

    Pirillo, S.; López-Corral, I.; Germán, E.; Juan, A.

    2012-01-01

    Highlights: ► Study of acrolein/Pt (1 1 1) adsorption using ab-initio and semiempirical methods. ► Geometry optimization and DOS curves were carried out using VASP code. ► Study of chemical bonding evolution using COOP and OP analysis. ► After adsorption Pt-Pt, C=O and C=C bonds are weakened. ► η 3 -cis and η 4 -trans most stable adsorption modes, η 1 -trans less favored one. - Abstract: The adsorption of acrolein on a Pt (1 1 1) surface was studied using ab-initio and semiempirical calculations. Geometry optimization and densities of states (DOS) curves were carried out using the Vienna Ab-initio Simulation Package (VASP) code. We started our study with the preferential geometries corresponding to the different acrolein/Pt (1 1 1) adsorption modes previously reported. Then, we examined the evolution of the chemical bonding in these geometries, using the crystal orbital overlap population (COOP) and overlap population (OP) analysis of selected pairs of atoms. We analyzed the acrolein intramolecular bonds, Pt (1 1 1) superficial bonds and new molecule-surface formed bonds after adsorption. We found that Pt-Pt bonds interacting with the molecule and acrolein C=O and C=C bonds are weakened after adsorption; this last bond is significantly linked to the surface. The obtained C-Pt and O-Pt OP values suggest that the most stable adsorption modes are η 3 -cis and η 4 -trans, while the η 1 -trans is the less favored configuration. We also found that C p z orbital and Pt p z and d z 2 orbitals participate strongly in the adsorption process.

  17. Cytotoxicity of Thirdhand Smoke and Identification of Acrolein as a Volatile Thirdhand Smoke Chemical That Inhibits Cell Proliferation.

    Science.gov (United States)

    Bahl, Vasundhra; Weng, Nikki J-H; Schick, Suzaynn F; Sleiman, Mohamad; Whitehead, Jacklyn; Ibarra, Allison; Talbot, Prue

    2016-03-01

    Thirdhand smoke (THS) is a mixture of chemicals that remain on indoor surfaces after smoking has ceased. These chemicals can be inhaled, ingested, or absorbed dermally, and thus could impact human health. We evaluated the cytotoxicity and mode of action of fresh and aged THS, the toxicity of volatile organic chemicals (VOCs) in THS, and the molecular targets of acrolein, a VOC in THS. Experiments were done using mouse neural stem cells (mNSC), human pulmonary fibroblasts (hPF), and lung A549 epithelial cells. THS-exposed cotton cloth was extracted in Dulbecco's Eagle Medium and caused cytotoxicity in the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. THS extracts induced blebbing, immotility, vacuolization, cell fragmentation, severing of microfilaments and depolymerization of microtubules in mNSC. Cytotoxicity was inversely related to headspace volume in the extraction container and was lost upon aging, suggesting that VOCs in THS were cytotoxic. Phenol, 2',5'-dimethyl furan and acrolein were identified as the most cytotoxic VOCs in THS, and in combination, their cytotoxicity increased. Acrolein inhibited proliferation of mNSC and hPF and altered expression of cell cycle regulatory genes. Twenty-four hours of treatment with acrolein decreased expression of transcription factor Dp-1, a factor needed for the G1 to S transition in the cell cycle. At 48 h, WEE1 expression increased, while ANACP1 expression decreased consistent with blocking entry into and completion of the M phase of the cell cycle. This study identified acrolein as a highly cytotoxic VOC in THS which killed cells at high doses and inhibited cell proliferation at low doses. © The Author 2015. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.

  18. Five Fatty Aldehyde Dehydrogenase Enzymes from Marinobacter and Acinetobacter spp. and Structural Insights into the Aldehyde Binding Pocket

    Energy Technology Data Exchange (ETDEWEB)

    Bertram, Jonathan H.; Mulliner, Kalene M.; Shi, Ke; Plunkett, Mary H.; Nixon, Peter; Serratore, Nicholas A.; Douglas, Christopher J.; Aihara, Hideki; Barney, Brett M.; Parales, Rebecca E.

    2017-04-07

    ABSTRACT

    Enzymes involved in lipid biosynthesis and metabolism play an important role in energy conversion and storage and in the function of structural components such as cell membranes. The fatty aldehyde dehydrogenase (FAldDH) plays a central function in the metabolism of lipid intermediates, oxidizing fatty aldehydes to the corresponding fatty acid and competing with pathways that would further reduce the fatty aldehydes to fatty alcohols or require the fatty aldehydes to produce alkanes. In this report, the genes for four putative FAldDH enzymes fromMarinobacter aquaeoleiVT8 and an additional enzyme fromAcinetobacter baylyiwere heterologously expressed inEscherichia coliand shown to display FAldDH activity. Five enzymes (Maqu_0438, Maqu_3316, Maqu_3410, Maqu_3572, and the enzyme reported under RefSeq accession no.WP_004927398) were found to act on aldehydes ranging from acetaldehyde to hexadecanal and also acted on the unsaturated long-chain palmitoleyl and oleyl aldehydes. A comparison of the specificities of these enzymes with various aldehydes is presented. Crystallization trials yielded diffraction-quality crystals of one particular FAldDH (Maqu_3316) fromM. aquaeoleiVT8. Crystals were independently treated with both the NAD+cofactor and the aldehyde substrate decanal, revealing specific details of the likely substrate binding pocket for this class of enzymes. A likely model for how catalysis by the enzyme is accomplished is also provided.

    IMPORTANCEThis study provides a comparison of multiple enzymes with the ability

  19. Transient receptor potential cation channel A1 (TRPA1) mediates changes in heart rate variability following a single exposure to acrolein in mice

    Science.gov (United States)

    The data show that a single exposure to acrolein causes autonomic imbalance in mice through the TRPA1 sensor and subsequent cardiac dysfunction. Human and animal studies have shown that short-term air pollution exposure causes...

  20. Contribution of ozone to airborne aldehyde formation in Paris homes.

    Science.gov (United States)

    Rancière, Fanny; Dassonville, Claire; Roda, Célina; Laurent, Anne-Marie; Le Moullec, Yvon; Momas, Isabelle

    2011-09-15

    Indoor aldehydes may result from ozone-initiated chemistry, mainly documented by experimental studies. As part of an environmental investigation included in the PARIS birth cohort, the aim of this study was to examine ozone contribution to airborne aldehyde formation in Paris homes. Formaldehyde, acetaldehyde and hexaldehyde levels, as well as styrene, nitrogen dioxide and nicotine concentrations, comfort parameters and carbon dioxide levels, were measured twice during the first year of life of the babies. Ambient ozone concentrations were collected from the closest background station of the regional air monitoring network. Traffic-related nitrogen oxide concentrations in front of the dwellings were estimated by an air pollution dispersion model. Home characteristics and families' way of life were described by questionnaires. Stepwise multiple linear regression models were used to link aldehyde levels with ambient ozone concentrations and a few aldehyde precursors involved in oxidation reactions, adjusting for other indoor aldehyde sources, comfort parameters and traffic-related nitrogen oxides. A 4 and 11% increase in formaldehyde and hexaldehyde levels was pointed out when 8-hour ozone concentrations increased by 20 μg/m(3). The influence of potential precursors such as indoor styrene level and frequent use of air fresheners, containing unsaturated volatile organic compounds as terpenes, was also found. Thus, our results suggest that ambient ozone can significantly impact indoor air quality, especially with regard to formaldehyde and hexaldehyde levels. Copyright © 2011 Elsevier B.V. All rights reserved.

  1. Carbonyl compound emissions from a heavy-duty diesel engine fueled with diesel fuel and ethanol-diesel blend.

    Science.gov (United States)

    Song, Chonglin; Zhao, Zhuang; Lv, Gang; Song, Jinou; Liu, Lidong; Zhao, Ruifen

    2010-05-01

    This paper presents an investigation of the carbonyl emissions from a direct injection heavy-duty diesel engine fueled with pure diesel fuel (DF) and blended fuel containing 15% by volume of ethanol (E/DF). The tests have been conducted under steady-state operating conditions at 1200, 1800, 2600 rpm and idle speed. The experimental results show that acetaldehyde is the most predominant carbonyl, followed by formaldehyde, acrolein, acetone, propionaldehyde and crotonaldehyde, produced from both fuels. The emission factors of total carbonyls vary in the range 13.8-295.9 mg(kWh)(-1) for DF and 17.8-380.2mg(kWh)(-1) for E/DF, respectively. The introduction of ethanol into diesel fuel results in a decrease in acrolein emissions, while the other carbonyls show general increases: at low engine speed (1200 rpm), 0-55% for formaldehyde, 4-44% for acetaldehyde, 38-224% for acetone, and 5-52% for crotonaldehyde; at medium engine speed (1800 rpm), 106-413% for formaldehyde, 4-143% for acetaldehyde, 74-113% for acetone, 114-1216% for propionaldehyde, and 15-163% for crotonaldehyde; at high engine speed (2600 rpm), 36-431% for formaldehyde, 18-61% for acetaldehyde, 22-241% for acetone, and 6-61% for propionaldehyde. A gradual reduction in the brake specific emissions of each carbonyl compound from both fuels is observed with increase in engine load. Among three levels of engine speed employed, both DF and E/DF emit most CBC emissions at high engine speed. On the whole, the presence of ethanol in diesel fuel leads to an increase in aldehyde emissions. Copyright (c) 2010 Elsevier Ltd. All rights reserved.

  2. Silver-Catalyzed Aldehyde Olefination Using Siloxy Alkynes.

    Science.gov (United States)

    Sun, Jianwei; Keller, Valerie A; Meyer, S Todd; Kozmin, Sergey A

    2010-03-20

    We describe the development of a silver-catalyzed carbonyl olefination employing electron rich siloxy alkynes. This process constitutes an efficient synthesis of trisubstituted unsaturated esters, and represents an alternative to the widely utilized Horner-Wadsworth-Emmons reaction. Excellent diastereoselectivities are observed for a range of aldehydes using either 1-siloxy-1-propyne or 1-siloxy-1-hexyne. This mild catalytic process also enables chemoselective olefination of aldehydes in the presence of either ester or ketone functionality. Furthermore, since no by-products are generated, this catalytic process is perfectly suited for development of sequential reactions that can be carried out in a single flask.

  3. Acrolein, A Reactive Product of Lipid Peroxidation, Induces Oxidative Modification of Cytochrome c

    Energy Technology Data Exchange (ETDEWEB)

    Kang, Jung Hoon [Cheongju Univ., Cheongju (Korea, Republic of)

    2013-11-15

    Acrolein (ACR) is a well-known carbonyl toxin produced by lipid peroxidation of polyunsaturated fatty acids, which is involved in the pathogenesis of neurodegenerative disorders such as Alzheimer's disease (AD). In Alzheimer's brain, ACR was found to be elevated in hippocampus and temporal cortex where oxidative stress is high. In this study, we evaluated oxidative modification of cytochrome c occurring after incubation with ACR. When cytochrome c was incubated with ACR, protein aggregation increased in a dose-dependent manner. The formation of carbonyl compounds and the release of iron were obtained in ACR-treated cytochrome c. Reactive oxygen species scavengers and iron specific chelator inhibited the ACR-mediated cytochrome c modification and carbonyl compound formation. Our data demonstrate that oxidative damage of cytochrome c by ACR might induce disruption of cyotochrome c structure and iron mishandling as a contributing factor to the pathology of AD.

  4. Acrolein, A Reactive Product of Lipid Peroxidation, Induces Oxidative Modification of Cytochrome c

    International Nuclear Information System (INIS)

    Kang, Jung Hoon

    2013-01-01

    Acrolein (ACR) is a well-known carbonyl toxin produced by lipid peroxidation of polyunsaturated fatty acids, which is involved in the pathogenesis of neurodegenerative disorders such as Alzheimer's disease (AD). In Alzheimer's brain, ACR was found to be elevated in hippocampus and temporal cortex where oxidative stress is high. In this study, we evaluated oxidative modification of cytochrome c occurring after incubation with ACR. When cytochrome c was incubated with ACR, protein aggregation increased in a dose-dependent manner. The formation of carbonyl compounds and the release of iron were obtained in ACR-treated cytochrome c. Reactive oxygen species scavengers and iron specific chelator inhibited the ACR-mediated cytochrome c modification and carbonyl compound formation. Our data demonstrate that oxidative damage of cytochrome c by ACR might induce disruption of cyotochrome c structure and iron mishandling as a contributing factor to the pathology of AD

  5. Electronic excitations in a dielectric continuum solvent with quantum Monte Carlo: Acrolein in water

    Energy Technology Data Exchange (ETDEWEB)

    Floris, Franca Maria, E-mail: floris@dcci.unipi.it; Amovilli, Claudio [Dipartimento di Chimica e Chimica Industriale, Università di Pisa, Via Risorgimento 35, 56126 Pisa (Italy); Filippi, Claudia [MESA Institute for Nanotechnology, University of Twente, P.O. Box 217, 7500 AE Enschede (Netherlands)

    2014-01-21

    We investigate here the vertical n → π{sup *} and π → π{sup *} transitions of s-trans-acrolein in aqueous solution by means of a polarizable continuum model (PCM) we have developed for the treatment of the solute at the quantum Monte Carlo (QMC) level of the theory. We employ the QMC approach which allows us to work with highly correlated electronic wave functions for both the solute ground and excited states and, to study the vertical transitions in the solvent, adopt the commonly used scheme of considering fast and slow dielectric polarization. To perform calculations in a non-equilibrium solvation regime for the solute excited state, we add a correction to the global dielectric polarization charge density, obtained self consistently with the solute ground-state wave function by assuming a linear-response scheme. For the solvent polarization in the field of the solute in the ground state, we use the static dielectric constant while, for the electronic dielectric polarization, we employ the solvent refractive index evaluated at the same frequency of the photon absorbed by the solute for the transition. This choice is shown to be better than adopting the most commonly used value of refractive index measured in the region of visible radiation. Our QMC calculations show that, for standard cavities, the solvatochromic shifts obtained with the PCM are underestimated, even though of the correct sign, for both transitions of acrolein in water. Only by reducing the size of the cavity to values where more than one electron is escaped to the solvent region, we regain the experimental shift for the n → π{sup *} case and also improve considerably the shift for the π → π{sup *} transition.

  6. Electronic excitations in a dielectric continuum solvent with quantum Monte Carlo: Acrolein in water

    International Nuclear Information System (INIS)

    Floris, Franca Maria; Amovilli, Claudio; Filippi, Claudia

    2014-01-01

    We investigate here the vertical n → π * and π → π * transitions of s-trans-acrolein in aqueous solution by means of a polarizable continuum model (PCM) we have developed for the treatment of the solute at the quantum Monte Carlo (QMC) level of the theory. We employ the QMC approach which allows us to work with highly correlated electronic wave functions for both the solute ground and excited states and, to study the vertical transitions in the solvent, adopt the commonly used scheme of considering fast and slow dielectric polarization. To perform calculations in a non-equilibrium solvation regime for the solute excited state, we add a correction to the global dielectric polarization charge density, obtained self consistently with the solute ground-state wave function by assuming a linear-response scheme. For the solvent polarization in the field of the solute in the ground state, we use the static dielectric constant while, for the electronic dielectric polarization, we employ the solvent refractive index evaluated at the same frequency of the photon absorbed by the solute for the transition. This choice is shown to be better than adopting the most commonly used value of refractive index measured in the region of visible radiation. Our QMC calculations show that, for standard cavities, the solvatochromic shifts obtained with the PCM are underestimated, even though of the correct sign, for both transitions of acrolein in water. Only by reducing the size of the cavity to values where more than one electron is escaped to the solvent region, we regain the experimental shift for the n → π * case and also improve considerably the shift for the π → π * transition

  7. Electronic excitations in a dielectric continuum solvent with quantum Monte Carlo: Acrolein in water

    Science.gov (United States)

    Floris, Franca Maria; Filippi, Claudia; Amovilli, Claudio

    2014-01-01

    We investigate here the vertical n → π* and π → π* transitions of s-trans-acrolein in aqueous solution by means of a polarizable continuum model (PCM) we have developed for the treatment of the solute at the quantum Monte Carlo (QMC) level of the theory. We employ the QMC approach which allows us to work with highly correlated electronic wave functions for both the solute ground and excited states and, to study the vertical transitions in the solvent, adopt the commonly used scheme of considering fast and slow dielectric polarization. To perform calculations in a non-equilibrium solvation regime for the solute excited state, we add a correction to the global dielectric polarization charge density, obtained self consistently with the solute ground-state wave function by assuming a linear-response scheme. For the solvent polarization in the field of the solute in the ground state, we use the static dielectric constant while, for the electronic dielectric polarization, we employ the solvent refractive index evaluated at the same frequency of the photon absorbed by the solute for the transition. This choice is shown to be better than adopting the most commonly used value of refractive index measured in the region of visible radiation. Our QMC calculations show that, for standard cavities, the solvatochromic shifts obtained with the PCM are underestimated, even though of the correct sign, for both transitions of acrolein in water. Only by reducing the size of the cavity to values where more than one electron is escaped to the solvent region, we regain the experimental shift for the n → π* case and also improve considerably the shift for the π → π* transition.

  8. Applicability of the theory of thermodynamic similarity to predict the enthalpies of vaporization of aliphatic aldehydes

    Science.gov (United States)

    Esina, Z. N.; Korchuganova, M. R.

    2015-06-01

    The theory of thermodynamic similarity is used to predict the enthalpies of vaporization of aliphatic aldehydes. The predicted data allow us to calculate the phase diagrams of liquid-vapor equilibrium in a binary water-aliphatic aldehyde system.

  9. Multitarget trehalose-carnosine conjugates inhibit Aβ aggregation, tune copper(II) activity and decrease acrolein toxicity.

    Science.gov (United States)

    Grasso, Giuseppa Ida; Bellia, Francesco; Arena, Giuseppe; Satriano, Cristina; Vecchio, Graziella; Rizzarelli, Enrico

    2017-07-28

    Increasing evidence is accumulating, showing that neurodegenerative disorders are somehow associated with the toxicity of amyloid aggregates, metal ion dyshomeostasis as well as with products generated by oxidative stress. Within the biological oxidation products, acrolein does have a prominent role. A promising strategy to deal with the above neurogenerative disorders is to use multi-functions bio-molecules. Herein, we show how a class of bio-conjugates takes advantage of the antiaggregating, antioxidant and antiglycating properties of trehalose and carnosine. Their ability to sequester acrolein and to inhibit both self- and metal-induced aggregation is here reported. The copper(II) coordination properties of a new trehalose-carnosine conjugate and the relative antioxidant effects have also been investigated. Copyright © 2017 Elsevier Masson SAS. All rights reserved.

  10. Changes in nonpolar aldehydes in bean cotyledons during ageing

    Czech Academy of Sciences Publication Activity Database

    Wilhelmová, Naděžda; Domingues, P.; Srbová, M.; Fuksová, H.; Wilhelm, J.

    2006-01-01

    Roč. 50, č. 4 (2006), s. 559-564 ISSN 0006-3134 R&D Projects: GA ČR GA522/03/0312 Institutional research plan: CEZ:AV0Z50380511 Keywords : Ageing * aldehydes * lipid peroxidation * lipofuscin-like pigments (LFP) Subject RIV: CE - Biochemistry Impact factor: 1.198, year: 2006

  11. Direct, enantioselective α-alkylation of aldehydes using simple olefins.

    Science.gov (United States)

    Capacci, Andrew G; Malinowski, Justin T; McAlpine, Neil J; Kuhne, Jerome; MacMillan, David W C

    2017-11-01

    Although the α-alkylation of ketones has already been established, the analogous reaction using aldehyde substrates has proven surprisingly elusive. Despite the structural similarities between the two classes of compounds, the sensitivity and unique reactivity of the aldehyde functionality has typically required activated substrates or specialized additives. Here, we show that the synergistic merger of three catalytic processes-photoredox, enamine and hydrogen-atom transfer (HAT) catalysis-enables an enantioselective α-aldehyde alkylation reaction that employs simple olefins as coupling partners. Chiral imidazolidinones or prolinols, in combination with a thiophenol, iridium photoredox catalyst and visible light, have been successfully used in a triple catalytic process that is temporally sequenced to deliver a new hydrogen and electron-borrowing mechanism. This multicatalytic process enables both intra- and intermolecular aldehyde α-methylene coupling with olefins to construct both cyclic and acyclic products, respectively. With respect to atom and step-economy ideals, this stereoselective process allows the production of high-value molecules from feedstock chemicals in one step while consuming only photons.

  12. Copepod reproduction is unaffected by diatom aldehydes or lipid composition

    DEFF Research Database (Denmark)

    Dutz, Jörg; Koski, Marja; Jonasdottir, Sigrun

    2008-01-01

    We investigated whether reduced reproductive success of copepods fed with diatoms was related to nutritional imbalances with regard to essential lipids or to the production of inhibitory aldehydes. In 10-d laboratory experiments, feeding, egg production, egg hatching success, and fecal pellet...

  13. Aldehydic acids in frying oils: formation, toxicological significance and analysis

    Directory of Open Access Journals (Sweden)

    Kamal-Eldin, Afaf

    1996-10-01

    Full Text Available Aldehydic acids are generated in oxidized lipids as a result of decomposition of hydroperoxides by (β-scission reactions. Aldehydes are known to interact with proteins and DNA and to impair enzymatic functions. Aldehydic esters from oxidized lipids were reabsorbed to a significant extent in rats. This paper reviews the mechanism of formation of esterified aldehydic acids in frying oils and their physiological/toxicological effects. The paper also gives an overview of relevant basic analytical techniques that needs to be improved to establish reliable quantitative method (s.

    Ácidos aldehídicos son producidos en lípidos oxidados como resultado de la descomposición de hidroperóxidos por reacciones de (β-escición. Es conocido que los aldehídos interaccionan con las proteínas y el ADN y debilitan las funciones enzimáticas. Los esteres aldehídicos de lípidos oxidados fueron reabsorbidos en una cantidad significativa en ratas. Este artículo revisa los mecanismos de formación de ácidos aldehídicos esterificados en aceites de fritura y sus efectos fisiológicos/toxicológicos. El artículo también ofrece una visión de conjunto de las técnicas analíticas básicas que necesitan ser mejoradas para establecer métodos cuantitativos fiables.

  14. Aldehyde Dehydrogenase 1 and Raf Kinase Inhibitor Protein ...

    African Journals Online (AJOL)

    Aldehyde Dehydrogenase 1 and Raf Kinase Inhibitor Protein Expression Defines the Proliferative Nature of Cervical Cancer Stem Cells. ... of cervical cancer stem cells and also to validate them in initial and advanced stages of cervical cancer. Keywords: Cervical cancer, ALDH1, BALB/c-nu/nu, HeLa cells, RKIP, Sox2 ...

  15. OXYGEN 18 EXCHANGE REACTIONS OF ALDEHYDES AND KETONES

    Energy Technology Data Exchange (ETDEWEB)

    Byrn, Marianne; Calvin, Melvin

    1965-12-01

    Using infra-red spectroscopy, the equilibrium exchange times have been determined for a series of ketones, aromatic aldehydes, and {beta}-ketoesters reacting with oxygen 18 enriched water. These exchange times have been evaluated in terms of steric and electronic considerations, and applied to a discussion of the exchange times of chlorophylls a and b and chlorophyll derivatives.

  16. Monitoring of fatty aldehyde dehydrogenase by formation of pyrenedecanoic acid from pyrenedecanal

    NARCIS (Netherlands)

    Keller, Markus A.; Watschinger, Katrin; Golderer, Georg; Maglione, Manuel; Sarg, Bettina; Lindner, Herbert H.; Werner-Felmayer, Gabriele; Terrinoni, Alessandro; Wanders, Ronald J. A.; Werner, Ernst R.

    2010-01-01

    Fatty aldehyde dehydrogenase (EC 1.2.1.48) converts long-chain fatty aldehydes to the corresponding acids. Deficiency in this enzyme causes the Sjogren Larsson Syndrome, a rare inherited disorder characterized by ichthyosis, spasticity, and mental retardation. Using a fluorescent aldehyde,

  17. Unsaturated aldehydes as alkene equivalents in the Diels-Alder reaction

    DEFF Research Database (Denmark)

    Taarning, Esben; Madsen, Robert

    2008-01-01

    A one-pot procedure is described for using alpha,beta-unsaturated aldehydes as olefin equivalents in the Diels-Alder reaction. The method combines the normal electron demand cycloaddition with aldehyde dienophiles and the rhodium-catalyzed decarbonylation of aldehydes to afford cyclohexenes...

  18. In-situ Studies of the Reactions of Bifunctional and Heterocyclic Molecules over Noble Metal Single Crystal and Nanoparticle Catalysts Studied with Kinetics and Sum-Frequency Generation Vibrational Spectroscopy

    Energy Technology Data Exchange (ETDEWEB)

    Kliewer, Christopher J. [Univ. of California, Berkeley, CA (United States)

    2009-06-30

    ,β-unsaturated aldehydes acrolein, crotonaldehyde, and prenal were investigated over Pt(111) and Pt(100). The selectivity for the hydrogenation of the C=C bond was found to depend on the number of methyl groups added to the bond. The adsorption modes of the three aldehydes were determined. The hydrogenation of crotonaldehyde was found to be nearly structure insensitive as the TOF and selectivity were very close to the same over Pt(111) and Pt(100). SFG-VS indicated identical surface intermediates over the two crystal faces during crotonaldehyde hydrogenation.

  19. Acrolein Disrupts Tight Junction Proteins and Causes Endoplasmic Reticulum Stress-Mediated Epithelial Cell Death Leading to Intestinal Barrier Dysfunction and Permeability.

    Science.gov (United States)

    Chen, Wei-Yang; Wang, Min; Zhang, Jingwen; Barve, Shirish S; McClain, Craig J; Joshi-Barve, Swati

    2017-12-01

    Increasing evidence suggests that environmental and dietary factors can affect intestinal epithelial integrity leading to gut permeability and bacterial translocation. Intestinal barrier dysfunction is a pathogenic process associated with many chronic disorders. Acrolein is an environmental and dietary pollutant and a lipid-derived endogenous metabolite. The impact of acrolein on the intestine has not been investigated before and is evaluated in this study, both in vitro and in vivo. Our data demonstrate that oral acrolein exposure in mice caused damage to the intestinal epithelial barrier, resulting in increased permeability and subsequently translocation of bacterial endotoxin-lipopolysaccharide into the blood. Similar results were seen in vitro using established Caco-2 cell monolayers wherein acrolein decreased barrier function and increased permeability. Acrolein also caused the down-regulation and/or redistribution of three representative tight junction proteins (ie, zonula occludens-1, Occludin, Claudin-1) that critically regulate epithelial paracellular permeability. In addition, acrolein induced endoplasmic reticulum stress-mediated death of epithelial cells, which is an important mechanism contributing to intestinal barrier damage/dysfunction, and gut permeability. Overall, we demonstrate that exposure to acrolein affects the intestinal epithelium by decrease/redistribution of tight junction proteins and endoplasmic reticulum stress-mediated epithelial cell death, thereby resulting in loss of barrier integrity and function. Our findings highlight the adverse consequences of environmental and dietary pollutants on intestinal barrier integrity/function with relevance to gut permeability and the development of disease. Copyright © 2017 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.

  20. Effects of the prescription of reinforcing kidney, nourishing blood, improving eyesight on ARPE-19 cells induced by acrolein

    Directory of Open Access Journals (Sweden)

    Man Li

    2015-05-01

    Full Text Available AIM: To explore the effects of the prescription of reinforcing kidney, nourishing blood, improving eyesight on the oxidative stress model of ARPE-19 cells induced by acrolein. METHODS: SD rats serum containing the prescription of reinforcing kidney, nourishing blood, improving eyesight and the content of distilled water in serum were prepared. The effects of the prescription and distilled water in serum at different concentration(2.5%, 5%, 10%, 20% and 40%on cell vitality was observed by cell counting kit(CCK-8assay. the logarithmic phase of ARPE-19 cells were pretreated by different concentrations(1.25%, 2.5% and 5%of the prescription serum and distilled water in serum for 24h. Then it was treated with 75μmol/L acrolein for 24h. Cell vitality was observed by CCK-8 assay. The change of cell nucleus was detected by DAPI staining.RESULTS: 2.5% and 5% serum had no effect on cell viability(P>0.05, while 10%, 20%, 40% serum could inhibit cell viability(PPCONCLUSION: The prescription of reinforcing kidney, nourishing blood, improving eyesight has the protective effect on ARPE-19 cell damage induced by acrolein.

  1. Evaluation of N-acetylcysteine and methylprednisolone as therapies for oxygen and acrolein-induced lung damage

    Energy Technology Data Exchange (ETDEWEB)

    Critchley, J.A.J.H. (Univ. of Edinburgh (England)); Beeley, J.M.; Clark, R.J.; Buchanan, J.D. (Royal Naval Hospital Hoslar, Gosport (England)); Summerfield, M.; Bell, S. (Admiralty Research Establishment, Alverstoke (England)); Spurlock, M.S.; Edginton, J.A.G. (Chemical Defence Establishment, Porton Down (England))

    1990-04-01

    Reactive oxidizing species are implicated in the etiology of a range of inhalational pulmonary injuries. Consequently, various free radical scavengers have been tested as potential prophylactic agents. The sulfydryl compound, N-acetylcysteine (NAC) is the only such compound clinically available for use in realistic dosages, and it is well established as an effective antidote for the hepatic and renal toxicity of paracetamol. Another approach in pulmonary injury prophylaxis is methylprednisolone therapy. The authors evaluated NAC and methylprednisolone in two rats models of inhalation injury: 40-hr exposure to >97% oxygen at 1.1 bar and 15-min exposure to acrolein vapor (210 ppm). The increases in lung wet/dry weight ratios, seen with both oxygen and acrolein toxicity were reduced with both treatments. However, with oxygen, NAC therapy was associated with considerably increased mortality and histological changes. Furthermore, IP NAC administration resulted in large volumes of ascitic fluid. With acrolein, IV, NAC had no significant effect on mortality or pulmonary histological damage. Methylprednisolone had no beneficial effects on either the mortality or histological damage observed in either toxicity model. They caution against the ad hoc use of NAC in the management of inhalational pulmonary injury.

  2. Catalytic Dehydration of Glycerol to Acrolein over a Catalyst of Pd/LaY Zeolite and Comparison with the Chemical Equilibrium

    Directory of Open Access Journals (Sweden)

    Israel Pala Rosas

    2017-02-01

    Full Text Available Glycerol dehydration to acrolein was studied with three catalysts using zeolite-Y. This zeolite in its protonic form (HY, with La (LaY and Pd with La (Pd/LaY, was characterized by X-ray diffraction (XRD, Fourier-transform-infrared spectroscopy (FTIR with pyridine, BET, Scanning Electron Microscope (SEM–Energy-Dispersive Spectroscopy X-ray (EDS and the catalytic activity tests were carried out under H2 atmosphere. It was found that La ions exchanged in the zeolite-Y resulted in the improvement of both glycerol conversion and yield to acrolein, also a relatively constant glycerol conversion was achieved up to three hours, due to the presence of Pd on the catalyst and H2 in the feed. The comparison of the calculated and experimental yields obtained from the catalytic tests of the Pd/LaY catalyst indicates a greater activity for the reaction to acrolein than for the reaction to acetol. The calculated equilibrium yields of the dehydration reaction from glycerol to acrolein, acetol, ethanal, methanol, and water and the experimental yields of a Pd/LaY catalyst were compared. Thermodynamically, a complete conversion of glycerol can be achieved since the general system remains exothermic and promotes the path to acetol below 480 K. Above this temperature the system consumes energy and favors the production of acrolein, reaching its maximum concentration at 600 K.

  3. Protein alkylation, transcriptional responses and cytochrome c release during acrolein toxicity in A549 cells: influence of nucleophilic culture media constituents.

    Science.gov (United States)

    Thompson, Colin A; Burcham, Philip C

    2008-06-01

    Acrolein is a toxic combustion product that elicits apoptotic and/or necrotic cell death depending on the conditions under which exposure occurs. As a strong electrophile, side-reactions with nucleophilic media constituents seem likely to accompany study of its toxicity in vitro, but these reactions are poorly characterized. We have thus examined the effect of media composition on the toxicity of acrolein in A549 cells. Cells were exposed to acrolein in either Dulbecco's buffered saline (DBS) or F12 supplemented with various concentrations of fetal bovine serum. Cell viability was assessed using the MTT assay, while heme oxygenase-1 (HO-1) and cytoplasmic cytochrome c were measured as respective markers of transcriptional response and apoptosis. Protein damage was evaluated using the protein carbonyl assay. Compared to F12 media (with or without serum), maximal cell death as evaluated using the MTT assay, as well as adduction of intracellular proteins, occurred when cells were exposed to acrolein in DBS. In contrast, cytochrome c release was maximal in cells exposed to acrolein in serum-containing F12, conditions which inhibited protein modification and overt cell death. These findings highlight the need for careful attention to experimental conditions when conducting in vitro toxicological studies of reactive substances.

  4. Methyltrioxorhenium as catalyst of a novel aldehyde olefination

    Energy Technology Data Exchange (ETDEWEB)

    Herrmann, W.A. (Technische Univ. Muenchen, Garching (Germany). Anorganisch-Chemisches Inst.); Wang Mei (Academia Sinica, Dalian Inst. of Chemical Physics (China))

    1991-12-01

    From aldehydes or cyclic ketones, diazoalkanes, and teritiary phosphanes, olefins may be prepared with MTO as catalyst. In particular, diazoacetates and -malonates (R{sup 2}, R{sup 3} = H, CO{sub 2}Et, or 2 x CO{sub 2}Me) can be transformed into olefins with aliphatic and aromatic aldehydes (R{sup 1} = iPr, trans-PhCH=CH, Ph, 4-NO{sub 2}C{sub 6}H{sub 4}, etc.). Readily accessible starting materials, easy handling, mild reaction conditions, and good yields characterize the new synthesis method. (R' = Ph, 3-C{sub 6}H{sub 4}SO{sub 3}Na, nBu.) (orig.).

  5. Maternal Aldehyde Elimination during Pregnancy Preserves the Fetal Genome

    Science.gov (United States)

    Oberbeck, Nina; Langevin, Frédéric; King, Gareth; de Wind, Niels; Crossan, Gerry P.; Patel, Ketan J.

    2014-01-01

    Summary Maternal metabolism provides essential nutrients to enable embryonic development. However, both mother and embryo produce reactive metabolites that can damage DNA. Here we discover how the embryo is protected from these genotoxins. Pregnant mice lacking Aldh2, a key enzyme that detoxifies reactive aldehydes, cannot support the development of embryos lacking the Fanconi anemia DNA repair pathway gene Fanca. Remarkably, transferring Aldh2−/−Fanca−/− embryos into wild-type mothers suppresses developmental defects and rescues embryonic lethality. These rescued neonates have severely depleted hematopoietic stem and progenitor cells, indicating that despite intact maternal aldehyde catabolism, fetal Aldh2 is essential for hematopoiesis. Hence, maternal and fetal aldehyde detoxification protects the developing embryo from DNA damage. Failure of this genome preservation mechanism might explain why birth defects and bone marrow failure occur in Fanconi anemia, and may have implications for fetal well-being in the many women in Southeast Asia that are genetically deficient in ALDH2. PMID:25155611

  6. Maternal aldehyde elimination during pregnancy preserves the fetal genome.

    Science.gov (United States)

    Oberbeck, Nina; Langevin, Frédéric; King, Gareth; de Wind, Niels; Crossan, Gerry P; Patel, Ketan J

    2014-09-18

    Maternal metabolism provides essential nutrients to enable embryonic development. However, both mother and embryo produce reactive metabolites that can damage DNA. Here we discover how the embryo is protected from these genotoxins. Pregnant mice lacking Aldh2, a key enzyme that detoxifies reactive aldehydes, cannot support the development of embryos lacking the Fanconi anemia DNA repair pathway gene Fanca. Remarkably, transferring Aldh2(-/-)Fanca(-/-) embryos into wild-type mothers suppresses developmental defects and rescues embryonic lethality. These rescued neonates have severely depleted hematopoietic stem and progenitor cells, indicating that despite intact maternal aldehyde catabolism, fetal Aldh2 is essential for hematopoiesis. Hence, maternal and fetal aldehyde detoxification protects the developing embryo from DNA damage. Failure of this genome preservation mechanism might explain why birth defects and bone marrow failure occur in Fanconi anemia, and may have implications for fetal well-being in the many women in Southeast Asia that are genetically deficient in ALDH2. Copyright © 2014 The Authors. Published by Elsevier Inc. All rights reserved.

  7. Vibrationally specific photoionization cross sections of acrolein leading to the Χ~A' ionic state

    International Nuclear Information System (INIS)

    López-Domínguez, Jesús A.; Lucchese, Robert R.; Fulfer, K. D.; Hardy, David; Poliakoff, E. D.; Aguilar, A. A.

    2014-01-01

    The vibrational branching ratios in the photoionization of acrolein for ionization leading to the Χ ~ A ' ion state were studied. Computed logarithmic derivatives of the cross section and the corresponding experimental data derived from measured vibrational branching ratios for several normal modes (ν 9 , ν 10 , ν 11 , and ν 12 ) were found to be in relatively good agreement, particularly for the lower half of the 11–100 eV photon energy range considered. Two shape resonances have been found near photon energies of 15.5 and 23 eV in the photoionization cross section and have been demonstrated to originate from the partial cross section of the A ′ scattering symmetry. The wave functions computed at the resonance complex energies are delocalized over the whole molecule. By looking at the dependence of the cross section on the different normal mode displacements together with the wave function at the resonant energy, a qualitative explanation is given for the change of the cross sections with respect to changing geometry

  8. A SUBCHRONIC INHALATION STUDY OF FISCHER 344 RATS EXPOSED TO 0, 0.4, 1.4 OR 4.0 PPM ACROLEIN

    International Nuclear Information System (INIS)

    KUTZMAN, R.S.

    1981-01-01

    Fischer 344 rats were exposed to 0.0, 0.4, 1.4, or 4.0 ppm acrolein for 62 days. The major objective of the study was to relate the results of a series of pulmonary function tests to biochemical and pathological alterations observed in the lung. Cytological and reproductive potential endpoints were also assessed after acrolein exposure. Rats were exposed to acrolein for 6 hours/day, 5 days/week for 62 days. Mortality was observed only in the 4.0 ppm chamber where 32 of 57 exposed males died; however, none of the 8 exposed females died. Most of the mortality occurred within the first 10 exposure days. Histologic examination indicated that the animals died of acute bronchopneumonia. The surviving males and females exposed to 4.0 ppm acrolein gained weight at a significantly slower rate than control animals. The growth of both sexes in the 0.4 and 1.4 ppm groups was similar to that of their respective controls. Histopathologic examination of animals after 62 days of exposure revealed bronchiolar epithelial necrosis and sloughing, bronchiolar edema with macrophages, and focal pulmonary edema in the 4.0 ppm group. These lesions were, in some cases, associated with edema of the trachea and peribronchial lymph nodes, and acute rhinitis which indicated an upper respiratory tract effect of acrolein. Of particular interest was the variability of response between rats in the 4.0 ppm group, some not affected at all while others were moderately affected. Intragroup variability in toxicity was also apparent in the 1.4 ppm exposure group where only 3 of 31 animals examined had lesions directly related to acrolein exposure. Extra respiratory organs appeared unaffected

  9. Structural and Kinetic Properties of the Aldehyde Dehydrogenase NahF, a Broad Substrate Specificity Enzyme for Aldehyde Oxidation.

    Science.gov (United States)

    Coitinho, Juliana B; Pereira, Mozart S; Costa, Débora M A; Guimarães, Samuel L; Araújo, Simara S; Hengge, Alvan C; Brandão, Tiago A S; Nagem, Ronaldo A P

    2016-09-27

    The salicylaldehyde dehydrogenase (NahF) catalyzes the oxidation of salicylaldehyde to salicylate using NAD(+) as a cofactor, the last reaction of the upper degradation pathway of naphthalene in Pseudomonas putida G7. The naphthalene is an abundant and toxic compound in oil and has been used as a model for bioremediation studies. The steady-state kinetic parameters for oxidation of aliphatic or aromatic aldehydes catalyzed by 6xHis-NahF are presented. The 6xHis-NahF catalyzes the oxidation of aromatic aldehydes with large kcat/Km values close to 10(6) M(-1) s(-1). The active site of NahF is highly hydrophobic, and the enzyme shows higher specificity for less polar substrates than for polar substrates, e.g., acetaldehyde. The enzyme shows α/β folding with three well-defined domains: the oligomerization domain, which is responsible for the interlacement between the two monomers; the Rossmann-like fold domain, essential for nucleotide binding; and the catalytic domain. A salicylaldehyde molecule was observed in a deep pocket in the crystal structure of NahF where the catalytic C284 and E250 are present. Moreover, the residues G150, R157, W96, F99, F274, F279, and Y446 were thought to be important for catalysis and specificity for aromatic aldehydes. Understanding the molecular features responsible for NahF activity allows for comparisons with other aldehyde dehydrogenases and, together with structural information, provides the information needed for future mutational studies aimed to enhance its stability and specificity and further its use in biotechnological processes.

  10. Theoretical Study on Regioselectivity of the Diels-Alder Reaction between 1,8-Dichloroanthracene and Acrolein.

    Science.gov (United States)

    Sultan, Mujeeb A; Karama, Usama; Almansour, Abdulrahman I; Soliman, Saied M

    2016-09-23

    A theoretical study of the regioselectivity of the Diels-Alder reaction between 1,8-dichloroanthracene and acrolein is performed using DFT at the B3LYP/6-31G(d,p) level of theory. The FMO analysis, global and local reactivity indices confirmed the reported experimental results. Potential energy surface analysis showed that the cycloadditions (CAs) favor the formation of the anti product. These results are in good agreement with the reported results obtained experimentally where the anti is the major product.

  11. Theoretical Study on Regioselectivity of the Diels-Alder Reaction between 1,8-Dichloroanthracene and Acrolein

    Directory of Open Access Journals (Sweden)

    Mujeeb A. Sultan

    2016-09-01

    Full Text Available A theoretical study of the regioselectivity of the Diels-Alder reaction between 1,8-dichloroanthracene and acrolein is performed using DFT at the B3LYP/6-31G(d,p level of theory. The FMO analysis, global and local reactivity indices confirmed the reported experimental results. Potential energy surface analysis showed that the cycloadditions (CAs favor the formation of the anti product. These results are in good agreement with the reported results obtained experimentally where the anti is the major product.

  12. The mild liquid-phase synthesis of 3-picoline from acrolein diethyl acetal and ammonia over heterogeneous catalysts

    Science.gov (United States)

    Luo, Cai-Wu; Chao, Zi-Sheng; Lei, Bo; Wang, Hong; Zhang, Jun; Wang, Zheng-Hao

    2017-11-01

    The liquid-phase synthesis of 3-picoline from the reaction of acrolein diethyl acetal and ammonia over ion-exchanged resins (D402 and D002) and HZSM-5 (Si/Al = 25) was carried out in a batch reactor. Various influencing parameters, including by the addition of water, ion-exchanged resins, reaction temperature and HZSM-5, were systematically investigated. The results showed that the reaction could be directly conducted, and organic acid wasn’t utilized. The highest yield of 3-picoline reached up to 24% using HZSM-5 as catalyst at 110 °C.

  13. Detoxification of aldehydes by histidine-containing dipeptides: from chemistry to clinical implications

    OpenAIRE

    Xie, Zhengzhi; Baba, Shahid P.; Sweeney, Brooke R.; Barski, Oleg A.

    2013-01-01

    Aldehydes are generated by oxidized lipids and carbohydrates at increased levels under conditions of metabolic imbalance and oxidative stress during atherosclerosis, myocardial and cerebral ischemia, diabetes, neurodegenerative diseases and trauma. In most tissues, aldehydes are detoxified by oxidoreductases that catalyze the oxidation or the reduction of aldehydes or enzymatic and nonenzymatic conjugation with low molecular weight thiols and amines, such as glutathione and histidine dipeptid...

  14. Application of heterocyclic aldehydes as components in Ugi–Smiles couplings

    Directory of Open Access Journals (Sweden)

    Katelynn M. Mason

    2016-09-01

    Full Text Available Efficient one-pot Ugi–Smiles couplings are reported for the use of furyl-substituted aldehyde components. In the presence of these heterocyclic aldehydes, reactions tolerated variations in amine components and led to either isolated N-arylamide Ugi–Smiles adducts or N-arylepoxyisoindolines, products of tandem Ugi–Smiles Diels–Alder cyclizations, in moderate yields. A thienyl-substituted aldehyde was also a competent component for Ugi–Smiles adduct formation.

  15. Ni-Catalyzed Dehydrogenative Cross-Coupling: Direct Transformation of Aldehydes to Esters and Amides

    Science.gov (United States)

    Whittaker, Aaron M.; Dong, Vy M.

    2015-01-01

    By exploring a new mode of Ni-catalyzed cross-coupling, we have developed a protocol to transform both aromatic and aliphatic aldehydes into either esters or amides directly. The success of this oxidative coupling depends on the appropriate choice of catalyst and organic oxidant, including the use of either α,α,α-trifluoroacetophenone or excess aldehyde. We present mechanistic data that supports a catalytic cycle involving oxidative addition into the aldehyde C–H bond. PMID:25424967

  16. On the nature of the olefination reaction involving ditungsten hexaalkoxides and aldehydes or ketones

    Energy Technology Data Exchange (ETDEWEB)

    Chisholm, M.H.; Huffman, J.C.; Lucas, E.A.; Sousa, A.; Streib, W.E. [Indiana Univ., Bloomington, IN (United States)

    1992-03-25

    Reductive coupling of aldehydes and ketones to olefins under the action of ditungsten hexaalkoxides was investigated. In these reactions, reductive cleavage of the aldehyde or ketone carbonyl is followed by formation of the olefinic C-C bond and breaking of the carbonyl C-O bond of the second aldehyde or ketone. Observations concerning the initial C-O bond cleavage and subsequent C-C bond formation are presented. 10 refs., 4 figs.

  17. [Pollution Characteristics of Aldehydes and Ketones Compounds in the Exhaust of Beijing Typical Restaurants].

    Science.gov (United States)

    Cheng, Jing-chen; Cui, Tong; He, Wan-qing; Nie, Lei; Wang, Jun-ling; Pan, Tao

    2015-08-01

    Aldehydes and ketones compounds, as one of the components in the exhaust of restaurants, are a class of volatile organic compounds (VOCs) with strong chemical reactivity. However, there is no systematic study on aldehydes and ketones compounds in the exhaust of restaurants. To further clarify the food source emission levels of aldehydes and ketones compounds and controlling measures, to access city group catering VOCs emissions control decision-making basis, this study selected 8 Beijing restaurants with different types. The aldehydes and ketones compounds were sampled using DNPH-silica tube, and then ultra performance liquid chromatography was used for quantitative measurement. The aldehydes and ketones concentrations of reference volume condition from 8 restaurants in descending order were Roasted Duck restaurant, Chinese Style Barbecue, Home Dishes, Western Fast-food, School Canteen, Chinese Style Fast-food, Sichuan Cuisine, Huaiyang Cuisine. The results showed that the range of aldehydes and ketones compounds (C1-C9) concentrations of reference volume condition in the exhaust of restaurants was 115.47-1035.99 microg x m(-3). The composition of aldehydes and ketones compounds in the exhaust of sampled restaurants was obviously different. The percentages of C1-C3 were above 40% in the exhaust from Chinese style restaurants. Fast food might emit more C4-C9 aldehydes and ketones compounds. From the current situation of existing aldehydes and ketones compounds control, the removal efficiency of high voltage electrostatic purifiers widely used in Beijing is limited.

  18. Acrolein preferentially damages nucleolus eliciting ribosomal stress and apoptosis in human cancer cells.

    Science.gov (United States)

    Wang, Hsiang-Tsui; Chen, Tzu-Ying; Weng, Ching-Wen; Yang, Chun-Hsiang; Tang, Moon-Shong

    2016-12-06

    Acrolein (Acr) is a potent cytotoxic and DNA damaging agent which is ubiquitous in the environment and abundant in tobacco smoke. Acr is also an active cytotoxic metabolite of the anti-cancer drugs cyclophosphamide and ifosfamide. The mechanisms via which Acr exerts its anti-cancer activity and cytotoxicity are not clear. In this study, we found that Acr induces cytotoxicity and cell death in human cancer cells with different activities of p53. Acr preferentially binds nucleolar ribosomal DNA (rDNA) to form Acr-deoxyguanosine adducts, and induces oxidative damage to both rDNA and ribosomal RNA (rRNA). Acr triggers ribosomal stress responses, inhibits rRNA synthesis, reduces RNA polymerase I binding to the promoter of rRNA gene, disrupts nucleolar integrity, and impairs ribosome biogenesis and polysome formation. Acr causes an increase in MDM2 levels and phosphorylation of MDM2 in A549 and HeLa cells which are p53 active and p53 inactive, respectively. It enhances the binding of ribosomal protein RPL11 to MDM2 and reduces the binding of p53 and E2F-1 to MDM2 resulting in stabilization/activation of p53 in A549 cells and degradation of E2F-1 in A549 and HeLa cells. We propose that Acr induces ribosomal stress which leads to activation of MDM2 and RPL11-MDM2 binding, consequently, activates p53 and enhances E2F-1 degradation, and that taken together these two processes induce apoptosis and cell death.

  19. Monolayer structures of alkyl aldehydes: Odd-membered homologues

    International Nuclear Information System (INIS)

    Phillips, T.K.; Clarke, S.M.; Bhinde, T.; Castro, M.A.; Millan, C.; Medina, S.

    2011-01-01

    Crystalline monolayers of three aldehydes with an odd number of carbon atoms in the alkyl chain (C 7 , C 9 and C 11 ) at low coverages are observed by a combination of X-ray and neutron diffraction. Analysis of the diffraction data is discussed and possible monolayer crystal structures are proposed; although unique structures could not be ascertained for all molecules. We conclude that the structures are flat on the surface, with the molecules lying in the plane of the layer. The C 11 homologue is determined to have a plane group of either p2, pgb or pgg, and for the C 7 homologue the p2 plane group is preferred.

  20. Untersuchungen zum atmosphärenchemischen Abbau langkettiger Aldehyde

    OpenAIRE

    Plagens, Heike

    2001-01-01

    In dieser Arbeit wurden die bimolekularen Geschwindigkeitskonstanten für die Reaktionen von Hexanal, Heptanal, Oktanal und Nonanal mit OH and Cl Radikalen bei (298 ± 2) K und (1000 ± 20) mbar experimentell bestimmt. Ebenso wurde die Chlorgeschwindigkeitskonstante für Butanal gemessen. Die Werte sind (in Einheiten von cm3 Molekül-1 s-1) in Tabelle 1 zusammengefaßt. Tabelle 1: Aldehyde kOH kCl Butanal - (2,21 ± 0,16) · 10-10 Hexan...

  1. Approximate inclusion of triple excitations in combined coupled cluster/molecular mechanics: Calculations of electronic excitation energies in solution for acrolein, water, formamide, and n-methylacetamide

    DEFF Research Database (Denmark)

    Sneskov, Kristian; Gras, Eduard Matito; Kongsted, Jacob

    2010-01-01

    as being applicable for averaging over many solvent configurations derived from, for example, molecular simulations. We test the proposed model using as a benchmark the two lowest-lying valence singlet excitations (n → π* and π → π*) of acrolein, formamide, and N-methylacetamide in aqueous solution as well...

  2. Immunogold electron microscopic localization of timothy grass (Phleum pratense) pollen major allergens Phl p I and Phl p V after anhydrous fixation in acrolein vapor

    NARCIS (Netherlands)

    Grote, M.; Dolecek, C.; van Ree, R.; Valenta, R.

    1994-01-01

    We used the vapor phase of acrolein as an anhydrous fixative for timothy grass pollen in an immunogold double-labeling localization study of two different major allergens, Phl p I and Phl p V. More than 48 hr of fixation were needed for the subcellular pollen structures to be satisfactorily

  3. Acrolein Exposure Blocks Down-Regulation of Cytokines and IgE Antibody in a Mucosal Tolerance Model but does not Alter Phenotypic Markers of Allergic Lung Disease

    Science.gov (United States)

    Acrolein (ACR) is a highly reactive upper airway toxicant that humans are exposed in a variety of environmental situations. Here we examined the effect of ACR exposure on development of immune tolerance in mice. To induce tolerance, female BALB/C mice were intranasally inoculate...

  4. Comparative analysis of the vibrational structure of the absorption spectra of acrolein in the excited ( S 1) electronic state

    Science.gov (United States)

    Koroleva, L. A.; Tyulin, V. I.; Matveev, V. K.; Pentin, Yu. A.

    2012-04-01

    The assignments of absorption bands of the vibrational structure of the UV spectrum are compared with the assignments of bands obtained by the CRDS method in a supersonic jet from the time of laser radiation damping for the trans isomer of acrolein in the excited ( S 1) electronic state. The ν00 trans = 25861 cm-1 values and fundamental frequencies, including torsional vibration frequency, obtained by the two methods were found to coincide in the excited electronic state ( S 1) for this isomer. The assignments of several absorption bands of the vibrational structure of the spectrum obtained by the CRDS method were changed. Changes in the assignment of (0-v') transition bands of the torsional vibration of the trans isomer in the Deslandres table from the ν00 trans trans origin allowed the table to be extended to high quantum numbers v'. The torsional vibration frequencies up to v' = 5 were found to be close to the frequencies found by analyzing the vibrational structure of the UV spectrum and calculated quantum-mechanically. The coincidence of the barrier to internal rotation (the cis-trans transition) in the one-dimensional model with that calculated quantum-mechanically using the two-dimensional model corresponds to a planar structure of the acrolein molecule in the excited ( S 1) electronic state.

  5. Increased salivary aldehyde dehydrogenase 1 in non-reticular oral lichen planus.

    Science.gov (United States)

    Mansourian, Arash; Shanbehzadeh, Najmeh; Kia, Seyed Javad; Moosavi, Mahdieh-Sadat

    2017-01-01

    Oral lichen planus is a potentially malignant disorder. One of the malignant transformation markers is cancer stem cells. One of the proposed marker for the detection of cancer stem cells's in head and neck cancer is aldehyde dehydrogenase. Recently it is shown that aldehyde dehydrogenase 1 expression in tissue samples is associated with oral lichen planus malignant transformation. This study evaluates salivary aldehyde dehydrogenase 1 in oral lichen planus. Thirty patients and 30 age and sex-matched healthy volunteers were recruited. Oral lichen planus was diagnosed based on the modified World Health Organization criteria. Subjects in the case group were divided into reticular and non-reticular forms. Unstimulated salivary samples were collected at 10-12 AM. Saliva concentrations of aldehyde dehydrogenase 1 were measured by ELISA. The differences between aldehyde dehydrogenase levels in the oral lichen planus group compared with the control group were not significant but aldehyde dehydrogenase in non-reticular oral lichen planus was significantly higher than that of the reticular form. This is a cross-sectional study, thus longitudinal studies in oral lichen planus may present similar or different results. The mechanism of malignant transformation in oral lichen planus is not defined. Previous analyses revealed that the aldehyde dehydrogenase 1 expression is significantly correlated with increased risk of transformation. This finding is consistent with our results because in the erosive and ulcerative forms of oral lichen planus, which have an increased risk of transformation, salivary aldehyde dehydrogenase 1 was overexpressed. A higher salivary aldehyde dehydrogenase level in non-reticular oral lichen planus can be a defensive mechanism against higher oxidative stress in these groups. Aldehyde dehydrogenase may be one of the malignant transformation markers in oral lichen planus. Further studies are needed for introducing aldehyde dehydrogenase as a prognostic

  6. Increased salivary aldehyde dehydrogenase 1 in non-reticular oral lichen planus*

    Science.gov (United States)

    Mansourian, Arash; Shanbehzadeh, Najmeh; Kia, Seyed Javad; Moosavi, Mahdieh-Sadat

    2017-01-01

    Background Oral lichen planus is a potentially malignant disorder. One of the malignant transformation markers is cancer stem cells. One of the proposed marker for the detection of cancer stem cells's in head and neck cancer is aldehyde dehydrogenase. Recently it is shown that aldehyde dehydrogenase 1 expression in tissue samples is associated with oral lichen planus malignant transformation. Objective This study evaluates salivary aldehyde dehydrogenase 1 in oral lichen planus. Method Thirty patients and 30 age and sex-matched healthy volunteers were recruited. Oral lichen planus was diagnosed based on the modified World Health Organization criteria. Subjects in the case group were divided into reticular and non-reticular forms. Unstimulated salivary samples were collected at 10-12 AM. Saliva concentrations of aldehyde dehydrogenase 1 were measured by ELISA. Results The differences between aldehyde dehydrogenase levels in the oral lichen planus group compared with the control group were not significant but aldehyde dehydrogenase in non-reticular oral lichen planus was significantly higher than that of the reticular form. Limitations of the study This is a cross-sectional study, thus longitudinal studies in oral lichen planus may present similar or different results. Conclusions The mechanism of malignant transformation in oral lichen planus is not defined. Previous analyses revealed that the aldehyde dehydrogenase 1 expression is significantly correlated with increased risk of transformation. This finding is consistent with our results because in the erosive and ulcerative forms of oral lichen planus, which have an increased risk of transformation, salivary aldehyde dehydrogenase 1 was overexpressed. A higher salivary aldehyde dehydrogenase level in non-reticular oral lichen planus can be a defensive mechanism against higher oxidative stress in these groups. Aldehyde dehydrogenase may be one of the malignant transformation markers in oral lichen planus. Further

  7. Toxic Diatom Aldehydes Affect Defence Gene Networks in Sea Urchins.

    Directory of Open Access Journals (Sweden)

    Stefano Varrella

    Full Text Available Marine organisms possess a series of cellular strategies to counteract the negative effects of toxic compounds, including the massive reorganization of gene expression networks. Here we report the modulated dose-dependent response of activated genes by diatom polyunsaturated aldehydes (PUAs in the sea urchin Paracentrotus lividus. PUAs are secondary metabolites deriving from the oxidation of fatty acids, inducing deleterious effects on the reproduction and development of planktonic and benthic organisms that feed on these unicellular algae and with anti-cancer activity. Our previous results showed that PUAs target several genes, implicated in different functional processes in this sea urchin. Using interactomic Ingenuity Pathway Analysis we now show that the genes targeted by PUAs are correlated with four HUB genes, NF-κB, p53, δ-2-catenin and HIF1A, which have not been previously reported for P. lividus. We propose a working model describing hypothetical pathways potentially involved in toxic aldehyde stress response in sea urchins. This represents the first report on gene networks affected by PUAs, opening new perspectives in understanding the cellular mechanisms underlying the response of benthic organisms to diatom exposure.

  8. Radon and aldehyde concentrations in the indoor environment. Final report

    International Nuclear Information System (INIS)

    Moschandreas, D.J.; Rector, H.E.

    1981-04-01

    Findings regarding indoor air contaminants in the energy-efficient residence (EER) in Mt. Airy, Maryland are reported. The objectives of the study were to collect and analyze relevant air quality samples (specifically radon and aldehydes), characterize the indoor air quality with respect to radon and aldehydes, and develop relationships between air infiltration rates and contaminant levels. One-fifth of the measured formaldehyde concentrations were in the range that may cause health concerns. Although indoor temperature and relative humidity affect indoor HCHO concentration, the elevated formaldehyde concentrations were measured under very low air infiltration rates. The data show that ventilation of the indoor air space is somewhat effective in reducing high HCHO concentrations. The operation of the heat exchanger led to an increase of the air infiltration rate which in turn resulted in substantial reduction of formaldehyde concentrations. A considerable number of the collected samples of indoor air displayed radon concentrations at levels higher than 1.0 to 4.0 nCim -3 (assuming an equilibrium factor of 0.5, these radon levels would correspond to working levels above the health guidelines suggested by the US EPA for homes in Florida built on land reclaimed from phosphate mining). As in the case of indoor formaldehyde concentrations, elevated indoor concentrations are substantially reduced when the infiltration rate is increased. The data base shows that the use of the air to air heat exchanger leads to reduction of indoor radon concentration by increasing the residential ventilation rate

  9. Volatile aldehydes are promising broad-spectrum postharvest insecticides.

    Science.gov (United States)

    Hammond, D G; Rangel, S; Kubo, I

    2000-09-01

    A variety of naturally occurring aldehydes common in plants have been evaluated for their insecticidal activity and for phytotoxicity to postharvest fruits, vegetables, and grains. Twenty-nine compounds were initially screened for their activity against aphids on fava bean leaf disks. Application under reduced pressure (partial vacuum) for the first quarter of fumigation increased insecticidal activity severalfold. The 11 best aldehydes were assayed against aphids placed under the third leaf of whole heads of iceberg lettuce using the same two-tier reduced-pressure regime, which caused no additional detriment to the commodity over fumigation at atmospheric pressure. Phytotoxicity to naked and wrapped iceburg lettuce, green and red table grapes, lemon, grapefruit, orange, broccoli, avocado, cabbage, pinto bean, and rice at doses that killed 100% of aphids was recorded for three promising fumigants: propanal, (E)-2-pentenal, and 2-methyl-(E)-2-butenal. These three compounds have excellent potential as affordable postharvest insect control agents, killing 100% of the aphids with little or no detectable harm to a majority of the commodities tested. Preliminary assays indicate that similar doses are also effective against mealybugs, thrips, and whitefly.

  10. Threshold responses in cinnamic-aldehyde-sensitive subjects: results and methodological aspects

    DEFF Research Database (Denmark)

    Johansen, J D; Andersen, Klaus Ejner; Rastogi, S C

    1996-01-01

    Cinnamic aldehyde is an important fragrance material and contact allergen. The present study was performed to provide quantitative data on the eliciting capacity of cinnamic aldehyde, to be considered in assessment of clinical relevance and health hazard. The skin response to serial dilution patch...

  11. Studying fatty aldehyde metabolism in living cells with pyrene-labeled compounds

    NARCIS (Netherlands)

    Keller, Markus A.; Watschinger, Katrin; Lange, Karsten; Golderer, Georg; Werner-Felmayer, Gabriele; Hermetter, Albin; Wanders, Ronald J. A.; Werner, Ernst R.

    2012-01-01

    The lack of fatty aldehyde dehydrogenase function in Sjogren Larsson Syndrome (SLS) patient cells not only impairs the conversion of fatty aldehydes into their corresponding fatty acid but also has an effect on connected pathways. Alteration of the lipid profile in these cells is thought to be

  12. Effect of whey protein on the In Vivo Release of Aldehydes.

    NARCIS (Netherlands)

    Weel, K.G.C.; Boelrijk, A.E.M.; Burger, J.J.; Claassen, N.E.; Gruppen, H.; Voragen, A.G.J.

    2003-01-01

    Retention of aldehydes by whey proteins in solutions buffered at a range of pH values was studied under static and dynamic headspace conditions and in vivo in exhaled air. Static headspace measurements showed a clear increase in retention in the presence of whey proteins for aldehydes with longer

  13. Role and structural characterization of plant aldehyde dehydrogenases from family 2 and family 7

    Czech Academy of Sciences Publication Activity Database

    Končitíková, R.; Vigouroux, A.; Kopečná, M.; Andree, T.; Bartoš, Jan; Šebela, M.; Moréra, S.; Kopečný, D.

    2015-01-01

    Roč. 468, Part: 1 (2015), s. 109-123 ISSN 0264-6021 R&D Projects: GA ČR GA15-22322S; GA MŠk(CZ) LO1204 Institutional support: RVO:61389030 Keywords : aldehyde dehydrogenase 2 (ALDH2) * aldehyde dehydrogenase 7 (ALDH7) * benzaldehyde Subject RIV: EB - Genetics ; Molecular Biology Impact factor: 3.562, year: 2015

  14. Direct chemoselective synthesis of glyconanoparticles from unprotected reducing glycans and glycopeptide aldehydes

    DEFF Research Database (Denmark)

    Thygesen, Mikkel Boas; Sørensen, Kasper Kildegaard; Cló, Emiliano

    2009-01-01

    Chemoselective oxime coupling was used for facile conjugation of unprotected, reducing glycans and glycopeptide aldehydes with core-shell gold nanoparticles carrying reactive aminooxy groups on the organic shell.......Chemoselective oxime coupling was used for facile conjugation of unprotected, reducing glycans and glycopeptide aldehydes with core-shell gold nanoparticles carrying reactive aminooxy groups on the organic shell....

  15. Effects of cooking method, cooking oil, and food type on aldehyde emissions in cooking oil fumes.

    Science.gov (United States)

    Peng, Chiung-Yu; Lan, Cheng-Hang; Lin, Pei-Chen; Kuo, Yi-Chun

    2017-02-15

    Cooking oil fumes (COFs) contain a mixture of chemicals. Of all chemicals, aldehydes draw a great attention since several of them are considered carcinogenic and formation of long-chain aldehydes is related to fatty acids in cooking oils. The objectives of this research were to compare aldehyde compositions and concentrations in COFs produced by different cooking oils, cooking methods, and food types and to suggest better cooking practices. This study compared aldehydes in COFs produced using four cooking oils (palm oil, rapeseed oil, sunflower oil, and soybean oil), three cooking methods (stir frying, pan frying, and deep frying), and two foods (potato and pork loin) in a typical kitchen. Results showed the highest total aldehyde emissions in cooking methods were produced by deep frying, followed by pan frying then by stir frying. Sunflower oil had the highest emissions of total aldehydes, regardless of cooking method and food type whereas rapeseed oil and palm oil had relatively lower emissions. This study suggests that using gentle cooking methods (e.g., stir frying) and using oils low in unsaturated fatty acids (e.g., palm oil or rapeseed oil) can reduce the production of aldehydes in COFs, especially long-chain aldehydes such as hexanal and t,t-2,4-DDE. Copyright © 2016 Elsevier B.V. All rights reserved.

  16. 'Real-world' compensatory behaviour with low nicotine concentration e-liquid: subjective effects and nicotine, acrolein and formaldehyde exposure.

    Science.gov (United States)

    Dawkins, Lynne; Cox, Sharon; Goniewicz, Maciej; McRobbie, Hayden; Kimber, Catherine; Doig, Mira; Kośmider, Leon

    2018-06-07

    To compare the effects of i) high versus low nicotine concentration e-liquid, ii) fixed versus adjustable power and iii) the interaction between the two on: a) vaping behaviour, b) subjective effects, c) nicotine intake, and d) exposure to acrolein and formaldehyde in e-cigarette users vaping in their everyday setting. Counterbalanced, repeated measures with four conditions: i) low nicotine (6 mg/mL)/fixed power; ii) low nicotine/adjustable power; iii) high nicotine (18 mg/mL)/fixed power; iv) high nicotine/adjustable power. London and the South East, England. Twenty experienced e-cigarette users (recruited between September 2016 and February 2017) vaped ad libitum using an eVic Supreme™ with a 'Nautilus Aspire' tank over four weeks (one week per condition). Puffing patterns (daily puff number [PN], puff duration [PD], inter-puff interval [IPI]), mL of e-liquid consumed, changes to power (where permitted), and subjective effects (urge to vape, nicotine withdrawal symptoms) were measured in each condition. Nicotine intake was measured via salivary cotinine. 3-hydroxypropylmercapturic acid (3-HPMA), a metabolite of the toxicant acrolein, and formate, a metabolite of the carcinogen formaldehyde, were measured in urine. There was a significant nicotine concentration x power interaction for PD (p<0.01). PD was longer with low nicotine/fixed power compared with i) high nicotine/fixed power (p< 0.001 and ii) low nicotine/adjustable power (p< 0.01). PN and liquid consumed were higher in the low versus high nicotine condition (main effect of nicotine, p<0.05). Urge to vape and withdrawal symptoms were lower, and nicotine intake was higher, in the high nicotine condition (main effects of nicotine: p<0.01). Whilst acrolein levels did not differ, there was a significant nicotine x power interaction for formaldehyde (p<0.05). Use of a lower nicotine concentration e-liquid may be associated with compensatory behaviour (e.g., higher number and duration of puffs) and increases

  17. Computational Approaches to the Determination of the Molecular Geometry of Acrolein in its T_1(n,π*) State

    Science.gov (United States)

    McAnally, Michael O.; Hlavacek, Nikolaus C.; Drucker, Stephen

    2012-06-01

    The spectroscopically derived inertial constants for acrolein (propenal) in its T_1(n,π*) state were used to test predictions from a variety of computational methods. One focus was on multiconfigurational methods, such as CASSCF and CASPT2, that are applicable to excited states. We also examined excited-state methods that utilize single reference configurations, including EOM-EE-CCSD and TD-PBE0. Finally, we applied unrestricted ground-state techniques, such as UCCSD(T) and the more economical UPBE0 method, to the T_1(n,π*) excited state under the constraint of C_s symmetry. The unrestricted ground-state methods are applicable because at a planar geometry, the T_1(n,π*) state of acrolein is the lowest-energy state of its spin multiplicity. Each of the above methods was used with a triple zeta quality basis set to optimize the T_1(n,π*) geometry. This procedure resulted in the following sets of inertial constants: Inertial constants (cm-1) of acrolein in its T_1(n,π*) state Method A B C Method A B C CASPT2(6,5) 1.667 0.1491 0.1368 UCCSD(T)^b 1.668 0.1480 0.1360 CASSCF(6,5) 1.667 0.1491 0.1369 UPBE0 1.699 0.1487 0.1367 EOM-EE-CCSD 1.675 0.1507 0.1383 TD-PBE0 1.719 0.1493 0.1374 Experiment^a 1.662 0.1485 0.1363 The two multiconfigurational methods produce the same inertial constants, and those constants agree closely with experiment. However the sets of computed bond lengths differ significantly for the two methods. In the CASSCF calculation, the lengthening of the C=O and C=C bonds and the shortening of the C--C bond are more pronounced than in CASPT2. O. S. Bokareva et al., Int. J. Quant. Chem. {108}, 2719 (2008).

  18. Electron impact ionization of cycloalkanes, aldehydes, and ketones

    Energy Technology Data Exchange (ETDEWEB)

    Gupta, Dhanoj; Antony, Bobby, E-mail: bka.ism@gmail.com [Department of Applied Physics, Indian School of Mines, Dhanbad, JH 826 004 (India)

    2014-08-07

    The theoretical calculations of electron impact total ionization cross section for cycloalkane, aldehyde, and ketone group molecules are undertaken from ionization threshold to 2 keV. The present calculations are based on the spherical complex optical potential formalism and complex scattering potential ionization contribution method. The results of most of the targets studied compare fairly well with the recent measurements, wherever available and the cross sections for many targets are predicted for the first time. The correlation between the peak of ionization cross sections with number of target electrons and target parameters is also reported. It was found that the cross sections at their maximum depend linearly with the number of target electrons and with other target parameters, confirming the consistency of the values reported here.

  19. The Arabidopsis aldehyde oxidase 3 (AA03) gene product catalyzes the final step in abscisic acid biosynthesis in leaves

    NARCIS (Netherlands)

    Seo, M.; Peeters, A.J.M.; Koiwai, H.; Oritani, T.; Marion-Poll, A.; Zeevaart, J.A.D.; Koornneef, M.; Kamiya, Y.; Koshiba, T.

    2000-01-01

    Abscisic acid (ABA) is a plant hormone involved in seed development and germination and in responses to various environmental stresses. The last step of ABA biosynthesis involves oxidation of abscisic aldehyde, and aldehyde oxidase (EC 1.2.3.1) is thought to catalyze this reaction. An aldehyde

  20. Development of analytical methods for the gas chromatographic determination of 1,2-epoxy-3-butene, 1,2:3,4-diepoxybutane, 3-butene-1,2-diol, 3,4-epoxybutane-1,2-diol and crotonaldehyde from perfusate samples of 1,3-butadiene exposed isolated mouse and rat livers

    Energy Technology Data Exchange (ETDEWEB)

    Bhowmik, S.; Schuster, A.; Filser, J.G.

    2003-07-01

    Mutagenicity and carcinogenicity of 1,3-butadiene (BD) highly probably results from epoxide metabolites as 1,2-epoxy-3-butene (EB), 1,2:3,4-diepoxybutane (DEB) and 3,4-epoxybutane-1,2-diol (EBD). A further metabolite crotonaldehyde (CA) has also been discussed to be relevant. So far, in BD exposed rodents only EB and DEB concentrations had been quantified. However, the methods used were either not very sensitive or instrumentally expensive. Therefore, the goal of the present work was to establish simple analytical methods selective and sensitive enough to determine all of these compounds and a further secondary BD intermediate, 3-butene-1,2-diol (B-diol), in BD exposed rodent livers. The once-through perfused liver system was chosen for testing the applicability of the methods to be developed, since it enables BD exposures of this quantitatively most relevant metabolising organ near to the in-vivo situation. All the metabolites were extracted from the aqueous perfusion medium and analysed using a gas chromatograph equipped with a mass selective detector (GC/MS) in the PCI mode. (orig.)

  1. Field experiences using acrolein (2-propenal) for control of SRB and MIC in an offshore production flowline and onshore production facility in Western Australia

    Energy Technology Data Exchange (ETDEWEB)

    Shield, M.; Charlesworth, M.; Paakkonen, S.

    2006-03-15

    Acrolein, 2-propenal, was evaluated as a microbiocide for control of sulphate-reducing bacteria (SRB) in a sub-sea pipeline and an onshore process plant operated by ChevronTexaco Australia Pty Ltd (CVX) in the North West Shelf (NWS) of Australia. An initial trial compared the efficacy of acrolein with that of a glutaraldehyde, quaternary amine blend (GQB) for control of SRB implicated in microbiologically induced corrosion (MIC) of the sub-sea pipeline. Based on improved performance, acrolein subsequently replaced the GQB for routine microbiocide treatment of the pipeline. In addition, a plant trial assessed the impact of acrolein supplementation of the existing tetrakishydroxy-methyl phosphonium sulphate (THPS) microbiocide programme for control of SRB in process plant operations. This paper overviews both the pipeline and plant trials as well as the programme implementation of acrolein microbiocide for routine pipeline treatment. In addition to an improved performance and safety profile, complete conversion of the microbiocide programme to acrolein is projected to result in direct savings of 40%, with further potential for secondary operational cost savings. on behalf of Ampol and Caltex; and, in 1964, the company discovered oil in commercial quantities on Barrow Island (BWI) off the North West Shelf of Australia. Today, CVX continues hydrocarbon production operations on BWI with over 300 million barrels produced since inception. BWI volumes have been augmented since 1989 through hydrocarbon recovery operations near Thevenard Island (TVI), a small island located 25 km north-north west of Onslow. To date, more than 146 million barrels have been processed through facilities on TVI. With the process plant covering only a small corner of the island, the majority of land mass on TVI is classified as a nature reserve for the protection of plants and animals. Important wildlife found on the island include green and flatback turtles that nest on the islands beaches. In

  2. Effect of thermal treatment conditions on properties of vanadium molybdenum oxide catalyst in acrolein oxidation reaction to acrylic acid

    International Nuclear Information System (INIS)

    Gorshkova, T.P.; Tarasova, D.V.; Olen'kova, I.P.; Andrushkevich, T.V.; Nikoro, T.A.

    1984-01-01

    The effect of thermal treatment conditions (temperature and gas medium) on properties of vanadium molybdenum oxide catalyst in acrolein oxidation reaction to acrylic acid is investigated. It is shown that active and selective catalysts are formed in the course of thermal decomposition of the drying product of ammonium metavanadate and paramolybdate under the conditions ensuring the vanadium ion reduction up to tetravalent state with conservation of molybdenum oxidation degree equal to 6. It is possible to realize it either by treatment of the catalyst calcinated in the air flow at 300 deg by the reaction mixture at the activation stage or by gas-reducer flow treatment at 280 deg. Thermal treatment in the reducing medium of the oxidized catalyst does not lead to complete regeneration of its properties

  3. Different specificities of two aldehyde dehydrogenases from Saccharomyces cerevisiae var. boulardii.

    Science.gov (United States)

    Datta, Suprama; Annapure, Uday S; Timson, David J

    2017-04-30

    Aldehyde dehydrogenases play crucial roles in the detoxification of exogenous and endogenous aldehydes by catalysing their oxidation to carboxylic acid counterparts. The present study reports characterization of two such isoenzymes from the yeast Saccharomyces cerevisiae var. boulardii (NCYC 3264), one mitochondrial (Ald4p) and one cytosolic (Ald6p). Both Ald4p and Ald6p were oligomeric in solution and demonstrated positive kinetic cooperativity towards aldehyde substrates. Wild-type Ald6p showed activity only with aliphatic aldehydes. Ald4p, on the contrary, showed activity with benzaldehyde along with a limited range of aliphatic aldehydes. Inspection of modelled structure of Ald6p revealed that a bulky amino acid residue (Met 177 , compared with the equivalent residue Leu 196 in Ald4p) might cause steric hindrance of cyclic substrates. Therefore, we hypothesized that specificities of the two isoenzymes towards aldehyde substrates were partly driven by steric hindrance in the active site. A variant of wild-type Ald6p with the Met 177 residue replaced by a valine was also characterized to address to the hypothesis. It showed an increased specificity range and a gain of activity towards cyclohexanecarboxaldehyde. It also demonstrated an increased thermal stability when compared with both the wild-types. These data suggest that steric bulk in the active site of yeast aldehyde dehydrogenases is partially responsible for controlling specificity. © 2017 The Author(s).

  4. Co-exposure to inhaled ambient particulate matter and acrolein alters myocardial synchrony in mice: evidence for TRPA1 involvement

    Science.gov (United States)

    Because air pollution is a complex mixture of constituents, often including particulates and aldehydes, attributing health effects to air pollutants in a given ambient air shed can be difficult when pollutants are studied in isolation. The purpose of this study was to examine the...

  5. Preparation of 3,5-disubstituted pyrazoles and isoxazoles from terminal alkynes, aldehydes, hydrazines, and hydroxylamine.

    Science.gov (United States)

    Harigae, Ryo; Moriyama, Katsuhiko; Togo, Hideo

    2014-03-07

    The reaction of terminal alkynes with n-BuLi, and then with aldehydes, followed by the treatment with molecular iodine, and subsequently hydrazines or hydroxylamine provided the corresponding 3,5-disubstituted pyrazoles or isoxazoles in good yields with high regioselectivity, through the formations of propargyl secondary alkoxides and α-alkynyl ketones. The present reactions are one-pot preparation of 3,5-disubstituted pyrazoles from terminal alkynes, aldehydes, molecular iodine, and hydrazines, and 3,5-disubstituted isoxazoles from terminal alkynes, aldehydes, molecular iodine, and hydroxylamine.

  6. An Efficient Synthesis of 2-Substituted Benzimidazoles via Photocatalytic Condensation of o-Phenylenediamines and Aldehydes.

    Science.gov (United States)

    Kovvuri, Jeshma; Nagaraju, Burri; Kamal, Ahmed; Srivastava, Ajay K

    2016-10-10

    A photocatalytic method has been developed for the efficient synthesis of functionalized benzimidazoles. This protocol involves photocatalytic condensation of o-phenylenediamines with various aldehydes using the Rose Bengal as photocatalyst. The method was found to be general and was successfully employed for accessing pharmaceutically important benzimidazoles by the condensation of aromatic, heteroaromatic and aliphatic aldehydes with o-phenylenediamines, in good-to-excellent yields. Notably, the method was found to be effective for the condensation of less reactive heterocyclic aldehydes with o-phenylenediamines.

  7. Structure and stability of acrolein and allyl alcohol networks on Ag(111) from density functional theory based calculations with dispersion corrections

    Science.gov (United States)

    Ferullo, Ricardo M.; Branda, Maria Marta; Illas, Francesc

    2013-11-01

    The interaction of acrolein and allyl alcohol with the Ag(111) surface has been studied by means of periodic density functional theory based calculations including explicitly dispersion terms. Different coverage values have been explored going from isolated adsorbed molecules to isolated dimers, interacting dimers or ordered overlayers. The inclusion of the dispersion terms largely affects the calculated values of the adsorption energy and also the distance between adsorbed molecule and the metallic surface but much less the adsorbate-adsorbate interactions. Owing to the large dipole moment of acrolein, the present calculations predict that at high coverage this molecule forms a stable extensive two-dimensional network on the surface, caused by the alignment of the adsorbate dipoles. For the case of allyl alcohol, dimers and complex networks exhibit similar stability.

  8. HPLC-MS Determination of Acrolein and Acetone Generated from 13C3 -Labeled Glycerol Added to Cigarette Tobacco Using Two Machine-Smoking Regimes

    Directory of Open Access Journals (Sweden)

    Yip SH

    2014-12-01

    Full Text Available The extent of blend glycerol degradation in a burning cigarette to form acrolein and acetone has been quantitatively determined by the addition of glycerol-13C3 to three styles of a leading commercial cigarette brand. Multiple Cambridge pads soaked with a solution of 2,4-dinitrophenylhydrazine (DNPH were employed to trap hydrazone derivatives of low molecular weight carbonyl compounds in both mainstream and sidestream smoke. High performance liquid chromatography coupled with negative ion mass spectrometry was used to isolate DNPH derivatives of the volatile carbonyl products of combustion and to ascertain their concentration. Acrolein, acetone, and propionaldehyde were the principal compounds of interest. The DNPH derivatives of acrolein-13C3 and acetone-13C3 were independently synthesized, and they served as external standards for absolute quantitation. The cost of fully labeled propionaldehyde precluded its use in this study. The brand styles selected for study represent the cigarette design features that are most prevalent in the U.S. market today and afford a representative range of standardized “tar” yields (14, 10, and 5 mg/cig, respectively by the Cambridge Filter Method. The brand styles studied are part of a commercial cigarette brand family that does not contain additives to the tobacco blend, including glycerol. Mainstream smoke was generated by an automated smoking machine employing the standard Cambridge Filter Smoking Regime and a more intense regime requiring larger, more frequent puffs and 100% vent blocking that is specified for regulatory purposes by the Canadian federal government. The research indicated that only a small fraction of added glycerol (~0.25%-0.30%, w/w was converted to the two compounds of interest, with the larger portion generally observed in sidestream smoke. Less than 0.1% of the added glycerol was converted to acrolein in mainstream smoke for all cigarette designs and smoking regimes studied.

  9. DFT-Based Explanation of the Effect of Simple Anionic Ligands on the Regioselectivity of the Heck Arylation of Acrolein Acetals

    DEFF Research Database (Denmark)

    Henriksen, Signe Teuber; Tanner, David Ackland; Cacchi, Sandro

    2009-01-01

    The Heck arylation of acrolein acetal has been studied computationally and compared to the corresponding reaction with allyl ethers. The reaction can be controlled to give either cinnamaldehydes or arylpropanoic esters by addition of different coordinating anions, acetate, or chloride. The comput...... reaction conditions. The difference between the two substrate classes could be rationalized in terms of relative hydride donating power of the two substrates....

  10. Oxidative Esterification of Aldehydes with Urea Hydrogen Peroxide Catalyzed by Aluminum Chloride Hexahydrate

    Energy Technology Data Exchange (ETDEWEB)

    Lee, Sin-Ae; Kim, Yoon Mi; Lee, Jong Chan [Chung-Ang University, Seoul (Korea, Republic of)

    2016-08-15

    We have developed a new, environmentally benign and highly efficient oxidative preparation of methyl esters by the reaction of various aldehydes with UHP in methanol catalyzed by readily accessible aluminum(III) chloride hexahydrate. This new greener and cost effective direct esterification method can serve as a useful alternative to existing protocols. Esters are some of the most important functional groups in organic chemistry and have been found in the sub-structure of a variety of natural products, industrial chemicals, and pharmaceuticals. Numerous methods have been reported for the preparation of various esters. In particular, this method gives low yields for both aldehydes containing electron donating substituents in aromatic rings and heterocyclic aldehydes. Therefore, development of a more general, efficient, and greener protocol for the esterification of aldehydes with readily available catalyst is still desirable.

  11. Microwave Assisted Solvent Free Synthesis of Azomethines from Aryl Aldehydes on Melamin Formaldehyde as Solid Support

    Directory of Open Access Journals (Sweden)

    Ramin Rezaei

    2011-01-01

    Full Text Available Various aryl aldehydes underwent prompt one pot conversion into the corresponding azomethines in high yields by reacting with hydroxylamine hydrochloride supported on melamine formaldehyde under microwave irradiation.

  12. ARA-aldehyde and ABA-trans-diol in apple fruits

    International Nuclear Information System (INIS)

    Rock, C.D.; Zeevaart, J.A.D.

    1989-01-01

    We have isolated ABA-aldehyde and ABA-t-diol from postharvest apple fruits, cv. Granny Smith and confirmed their structure by GC-MS. These putative ABA biosynthetic precursors incorporate 18 O to a similar degree as ABA during 48 hours under 18 O 2 atmospheres. The presence of significant amounts of ABA-aldehyde can explain the unique 18 O labeling pattern of ABA in this tissue, where a majority of ABA molecules containing 18 O is labeled in the 1'-hydroxyl group and not in the side chain carboxyl group, the primary site of incorporation for stressed leaves. Exchange of the carbonyl oxygen of ABA-aldehyde with water would decrease 18 O enrichment in the side chain. Results of 18 O 2 experiments and feeding studies using hexadeutero-ABA-aldehyde will be presented and the biosynthetic relationship of these compounds discussed

  13. A HIGHLY STEREOSELECTIVE, NOVEL COUPLING REACTION BETWEEN ALKYNES WITH ALDEHYDES. (R828129)

    Science.gov (United States)

    In the presence of indium triflate or gallium chloride, a novel coupling between internal alkynes and aldehydes occurred to give unsaturated ketones and [4+1] annulation products. Graphical Abstrac...

  14. ENVIRONMENTAL TECHNOLOGY PROTOCOL VERIFICATION REPORT, EMISSIONS OF VOCS AND ALDEHYDES FROM COMMERCIAL FURNITURE (WITH APPENDICES)

    Science.gov (United States)

    As part of a U.S. Environmental Protection Agency Environmental Technology Verification program, the Research Triangle Institute (RTI) developed a test protocol for measuring volatile organic compounds and aldehydes in a large chamber. RTI convened stakeholders for the commercial...

  15. Influence of environmental parameters on production of the acrolein precursor 3-hydroxypropionaldehyde by Lactobacillus reuteri DSMZ 20016 and its accumulation by wine lactobacilli.

    Science.gov (United States)

    Bauer, Rolene; du Toit, Maret; Kossmann, Jens

    2010-01-31

    Lactic acid bacteria belonging to the genus Lactobacillus are known to convert glycerol into 3-hydroxypropionaldehyde (3-HPA) during anaerobic glycerol fermentation. Wine quality can be gravely compromised by the accumulation of 3-HPA, due to its spontaneous conversion to acrolein under wine making conditions. Acrolein is not only a dangerous substance for the living cell, but has been implicated in the development of unpleasant bitterness in beverages. This study evaluates the effect of individual environmental parameters on 3-HPA production by Lactobacillus reuteri DSMZ 20016, which only proved possible under conditions that allow accumulation well below the threshold concentration affecting cell viability. 3-HPA production was optimal at pH 6 and in the presence of 300 mM glycerol. Production increased with an increase in cell concentration up to an OD(600) of 50, whereas higher cell concentrations inhibited accumulation. Data presented in this study suggest that 3-HPA plays a role in regulating its own production through quorum sensing. Glycerol dehydratase possessing bacterial strains isolated from South African red wine, L. pentosus and L. brevis, tested positive for 3-HPA accumulation. 3-HPA is normally intracellularly reduced to 1,3-propanediol. This is the first study demonstrating the ability of wine lactobacilli to accumulate 3-HPA in the fermentation media. Recommendations are made on preventing the formation of acrolein and its precursor 3-HPA in wine. Copyright 2009 Elsevier B.V. All rights reserved.

  16. Protective effects of the aqueous extract of Scutellaria baicalensis against acrolein-induced oxidative stress in cultured human umbilical vein endothelial cells.

    Science.gov (United States)

    Zhang, Xing-Wei; Li, Wei-Fen; Li, Wei-Wei; Ren, Kan-Han; Fan, Chao-Ming; Chen, Ying-Ying; Shen, Yue-Liang

    2011-03-01

     Scutellaria baicalensis Georgi (Labiatae) (SbG), one of the fifty fundamental herbs of Chinese herbology, has been reported to have anti-asthmatic, antifungal, antioxidative, and anti-inflammatory activities.  This study was designed to determine the protective effects of the extract of SbG against the acrolein-induced oxidative stress in cultured human umbilical vein endothelial cells (HUVEC).  The MTT reduction assay was employed to determine cell viability. The total cellular glutathione (GSH) level was detected using a colorimetric GSH assay kit. Cellular GSH production was conducted by detecting the mRNA expression levels of γ-glutamylcysteine ligase catalytic subunit and modifier subunit.  Concentration-dependent cytotoxic effects of acrolein were observed while SbG could effectively protect the acrolein-induced oxidative damage. The protective mechanism was investigated, showing that the increased GSH content in the SbG-incubated HUVE cells was associated with the protective effects of SbG-treated cells. Further RT-PCR data confirmed the elevated mRNA expressions of GSH synthesis enzymes.  The current study strongly indicated that SbG could be a potential antioxidant against oxidative stress in treating cardiovascular diseases.

  17. The Relationship Between Structural and Catalytic Activity of α and γ-Bismuth-Molybdate Catalysts for Partial Oxidation of Propylene to Acrolein

    Science.gov (United States)

    Fansuri, H.; Pham, G. H.; Wibawanta, S.; Zhang, D. K.; French, David

    Bismuth-molybdate catalysts are known to be effective for catalytic partial oxidation of propylene to acrolein. Their properties and the kinetics and reaction mechanisms for acrolein production have been extensively studied, especially in their basic forms, such as α, β, and γ-bismuth-molybdate. Although the reaction mechanisms have been reported widely in the literature, a general agreement has not been reached, especially from a catalyst-structure point of view. The present contribution reports an effort to understand the structural changes of α and γ-bismuth-molybdate catalysts at varying temperatures as examined using high temperature XRD and to relate the catalyst performance (activity and selectivity) for propylene partial oxidation to acrolein. The XRD analysis was performed at temperature between 250 and 450°C in ambient atmosphere and the Rietveld refinement method was used to extract unit cell parameters. The results showed a distinct similarity between the shapes of the thermal expansion of the catalysts and their activity and selectivity curves, indicating a significant role that the catalyst interatomic structure plays in the overall reaction mechanism.

  18. Kinetics, mechanism and thermodynamics of bisulfite-aldehyde adduct formation

    Energy Technology Data Exchange (ETDEWEB)

    Olson, T.M.; Boyce, S.D.; Hoffmann, M.R.

    1986-04-01

    The kinetics and mechanism of bisulfite addition to benzaldehyde were studied at low pH in order to assess the importance of this reaction in stabilizing S(IV) in fog-, cloud-, and rainwater. Previously, the authors established that appreciable concentrations of the formaldehyde-bisulfite adduct (HMSA) are often present in fogwater. Measured HMSA concentrations in fogwater often do not fully account for observed excess S(IV) concentrations, however, so that other S(IV)-aldehyde adducts may be present. Reaction rates were determined by monitoring the disappearance of benzaldehyde by U.V. spectrophotometry under pseudo-first order conditions, (S(IV))/sub T/ >>(phi-CHO)/sub T/, in the pH range 0 - 4.4 at 25/sup 0/C. The equilibrium constant was determined by dissolving the sodium salt of the addition compound in a solution adjusted to pH 3.9, and measuring the absorbance of the equilibrated solution at 250 nm. A literature value of the extinction coefficient for benzaldehyde was used to calculate the concentration of free benzaldehyde. All solutions were prepared under an N/sub 2/ atmosphere using deoxygenated, deionized water and ionic strength was maintained at 1.0 M with sodium chloride.

  19. Characterization of Aldehyde Crosslinked Kenaf Regenerated Cellulose Film

    Directory of Open Access Journals (Sweden)

    Hatika Kaco

    2015-08-01

    Full Text Available Regenerated cellulose film with better mechanical properties was successfully produced by introducing aldehyde crosslinker during the regeneration process. The cellulose source material was derived from kenaf core powder and dissolved in LiOH/urea solvent at −13 °C to form a cellulose solution. The cellulose solution was cast and coagulated in a crosslinker bath at different percentages of glutaraldehyde (GA and glyoxal (GX to form a regenerated cellulose film. According to Fourier transform infrared spectroscopy (FTIR spectra, the hydroxyl group of the cellulose was reduced, reducing the percentage of swelling as the percentage of crosslinker was increased. X-ray diffraction (XRD patterns showed that the crystallinity index of the crosslinked film was decreased. The pore size of the films decreased as the percentage of crosslinker was increased, resulting in decreased film transparency. The pore volume and percentage of swelling in water of the films also increased with decreases in the pore size as the percentage of crosslinker was increased. The tensile strengths of the GA- and GX-crosslinked films increased by 20 and 15% with the addition of 20% of each crosslinker, respectively.

  20. Oxidation of Group 8 transition-Metal Hydrides and Ionic Hydrogenation of Ketones and Aldehydes

    Energy Technology Data Exchange (ETDEWEB)

    Smith, Kjell-Tore

    1996-08-01

    Transition-metal hydrides have received considerable attention during the last decades because of their unusual reactivity and their potential as homogeneous catalysts for hydrogenation and other reactions of organic substrates. An important class of catalytic processes where transition-metal hydrides are involved is the homogeneous hydrogenation of alkenes, alkynes, ketones, aldehydes, arenes and nitro compounds. This thesis studies the oxidation of Group 8 transition-metal hydrides and the ionic hydrogenation of ketones and aldehydes.

  1. Detoxification of aldehydes by histidine-containing dipeptides: from chemistry to clinical implications

    Science.gov (United States)

    Xie, Zhengzhi; Baba, Shahid P.; Sweeney, Brooke R.; Barski, Oleg A.

    2015-01-01

    Aldehydes are generated by oxidized lipids and carbohydrates at increased levels under conditions of metabolic imbalance and oxidative stress during atherosclerosis, myocardial and cerebral ischemia, diabetes, neurodegenerative diseases and trauma. In most tissues, aldehydes are detoxified by oxidoreductases that catalyze the oxidation or the reduction of aldehydes or enzymatic and nonenzymatic conjugation with low molecular weight thiols and amines, such as glutathione and histidine dipeptides. Histidine dipeptides are present in micromolar to millimolar range in the tissues of vertebrates, where they are involved in a variety of physiological functions such as pH buffering, metal chelation, oxidant and aldehyde scavenging. Histidine dipeptides such as carnosine form Michael adducts with lipid-derived unsaturated aldehydes, and react with carbohydrate-derived oxo- and hydroxy- aldehydes forming products of unknown structure. Although these peptides react with electrophilic molecules at lower rate than glutathione, they can protect glutathione from modification by oxidant and they may be important for aldehyde quenching in glutathione-depleted cells or extracellular space where glutathione is scarce. Consistent with in vitro findings, treatment with carnosine has been shown to diminish ischemic injury, improve glucose control, ameliorate the development of complications in animal models of diabetes and obesity, promote wound healing and decrease atherosclerosis. The protective effects of carnosine have been linked to its anti-oxidant properties, it ability to promote glycolysis, detoxify reactive aldehydes and enhance histamine levels. Thus, treatment with carnosine and related histidine dipeptides may be a promising strategy for the prevention and treatment of diseases associated with high carbonyl load. PMID:23313711

  2. Copper(II)/amine synergistically catalyzed enantioselective alkylation of cyclic N-acyl hemiaminals with aldehydes.

    Science.gov (United States)

    Sun, Shutao; Mao, Ying; Lou, Hongxiang; Liu, Lei

    2015-07-07

    The first catalytic asymmetric alkylation of N-acyl quinoliniums with aldehydes has been described. A copper/amine synergistic catalytic system has been developed, allowing the addition of functionalized aldehydes to a wide range of electronically varied N-acyl quinoliniums in good yields with excellent enantiocontrol. The synergistic catalytic system was also effective for N-acyl dihydroisoquinoliniums and β-caboliniums, demonstrating the general applicability of the protocol in the enantioselective alkylation of diverse cyclic N-acyl hemiaminals.

  3. Effect of phenolic aldehydes and flavonoids on growth and inactivation of Oenococcus oeni and Lactobacillus hilgardii

    OpenAIRE

    Figueiredo, Ana Rita; Campos, Francisco; Freitas, Víctor de; Hogg, Tim; Couto, José António

    2008-01-01

    The aim of this work was to investigate the effect of wine phenolic aldehydes, flavonoids and tannins on growth and viability of strains of Oenococcus oeni and Lactobacillus hilgardii. Cultures were grown in ethanol-containing MRS/TJ medium supplemented with different concentrations of phenolic aldehydes or flavonoids and monitored spectrophotometrically. The effect of tannins was evaluated by monitoring the progressive inactivation of cells in ethanol-containing phosphate buffer supplemented...

  4. An Improved Protocol for the Aldehyde Olefination Reaction Using (bmim ( as Reaction Medium

    Directory of Open Access Journals (Sweden)

    Vivek Srivastava

    2013-01-01

    Full Text Available [Ru(CODCl2]/CuCl2·2H2O/LiCl catalytic system works efficiently in ionic liquid media for aldehyde olefination reaction. It offers good yield and selectivity with the added advantage of 5 times recyclability for [Ru(CODCl2] /CuCl2·2H2O/LiCl catalytic system. We also successfully reduced the reaction time from 12 hours to 9 hours for the aldehyde olefination reaction.

  5. The use of tomato aminoaldehyde dehydrogenase 1 for the detection of aldehydes in fruit distillates.

    Science.gov (United States)

    Frömmel, Jan; Tarkowski, Petr; Kopečný, David; Šebela, Marek

    2016-09-25

    Plant NAD(+)-dependent aminoaldehyde dehydrogenases (AMADHs, EC 1.2.1.19) belong to the family 10 of aldehyde dehydrogenases. They participate in the metabolism of polyamines or osmoprotectants. The enzymes are characterized by their broad substrate specificity covering ω-aminoaldehydes, aliphatic and aromatic aldehydes as well as nitrogen-containing heterocyclic aldehydes. The isoenzyme 1 from tomato (Solanum lycopersicum; SlAMADH1) oxidizes aliphatic aldehydes very efficiently and converts also furfural, its derivatives or benzaldehyde, which are present at low concentrations in alcoholic distillates such as fruit brandy. In this work, SlAMADH1 was examined as a bioanalytical tool for their detection. These aldehydes arise from fermentation processes or thermal degradation of sugars and their presence is related to health complications after consumption including nausea, emesis, sweating, decrease in blood pressure, hangover headache, among others. Sixteen samples of slivovitz (plum brandy) from local producers in Moravia, Czech Republic, were analyzed for their aldehyde content using a spectrophotometric activity assay with SlAMADH1. In all cases, there were oxidative responses observed when monitoring NADH production in the enzymatic reaction. Aldehydes in the distillate samples were also subjected to a standard determination using reversed-phase HPLC with spectrophotometric and tandem mass spectrometric detection after a derivatization with 2,4-dinitrophenylhydrazine. Results obtained by both methods were found to correlate well for a majority of the analyzed samples. The possible applicability of SlAMADH1 for the evaluation of aldehyde content in food and beverages has now been demonstrated. Copyright © 2015 Elsevier B.V. All rights reserved.

  6. The Intramolecular Diels–Alder Reaction of Tryptamine-Derived Zincke Aldehydes Is a Stepwise Process

    OpenAIRE

    Pham, Hung V.; Martin, David B. C.; Vanderwal, Christopher D.; Houk, K. N.

    2012-01-01

    Computational studies show that the base-mediated intramolecular Diels–Alder of tryptamine-derived Zincke aldehydes, used as a key step in the synthesis of the Strychnos alkaloids norfluorocurarine and strychnine, proceeds via a stepwise pathway. The experimentally determined importance of a potassium counterion in the base is explained by its ability to preorganize the Zincke aldehyde diene in an s-cis conformation suitable to bicyclization. Computation also supports the thermodynamic import...

  7. Reactions of the radical cations of aliphatic aldehydes in freon matrices

    International Nuclear Information System (INIS)

    Belevskij, V.N.; Belopushkin, S.I.; Feldman, V.I.

    1985-01-01

    ESR spectra of γ-irradiated solutions of acetic and propionic aldehydes in freon-11 and freon-113 affected by aldehyde concentration, temperature, and the action of light were studied. It is shown that the radical cations are converted into neutral radicals, and the cations CHsub(3)CHsub(2)CHOsup(+). are converted to RCO and CHsub(3)CHCHO due to ion-molecular reactions of proton transfer of hydrogen atom transfer. (author)

  8. Effect of selected aldehydes on the growth and fermentation of ethanologenic Escherichia coli

    Energy Technology Data Exchange (ETDEWEB)

    Zaldivar, J.; Ingram, L.O. [Univ. of Florida, Gainesville (United States). Dept. of Microbiology and Cell Science; Martinez, A. [Univ. of Florida, Gainesville (United States). Dept. of Microbiology and Cell Science]|[Univ. Nacional Autonoma de Mexico (Mexico). Inst. de Biotecnologia

    1999-10-05

    Bioethanol production from lignocellulosic raw-materials requires the hydrolysis of carbohydrate polymers into a fermentable syrup. During the hydrolysis of hemicellulose with dilute acid, a variety of toxic compounds are produced such as soluble aromatic aldehydes from lignin and furfural from pentose destruction. In this study, the authors have investigated the toxicity of representative aldehydes (furfural, 5-hydroxymethlyfurfural, 4-hydroxybenzaldehyde, syringaldehyde, and vanillin) as inhibitors of growth and ethanol production by ethanologenic derivatives of Escherichia coli B (strains K011 and LY01). Aromatic aldyhydes were at least twice as toxic as furfural of 5-hydroxymethylfurfural on a weight basis. The toxicities of all aldehydes (and ethanol) except furfural were additive when tested in binary combinations. In all cases, combinations with furfural were unexpectedly toxic. Although the potency of these aldehydes was directly related to hydrophobicity indicating a hydrophobic site of action, none caused sufficient membrane damage to allow the leakage of intracellular magnesium even when present at sixfold the concentrations required for growth inhibition. Of the aldehydes tested, only furfural strongly inhibited ethanol production in vitro. A comparison with published results for other microorganisms indicates that LY01 is equivalent or more resistant than other biocatalysts to the aldehydes examined in this study.

  9. Indoor aldehydes: measurement of contamination levels and identification of their determinants in Paris dwellings

    International Nuclear Information System (INIS)

    Clarisse, B.; Laurent, A.M.; Seta, N.; Le Moullec, Y.; El Hasnaoui, A.; Momas, I.

    2003-01-01

    The recent increased prevalence of childhood asthma and atopy has brought into question the impact of outdoor pollutants and indoor air quality. The contributory role of aldehydes to this problem and the fact that they are mainly derived from the domestic environment make them of particular interest. This study therefore measures six different aldehyde levels in Paris dwellings from potentially different sources and identifies their indoor determinants. The study was carried out in the three principal rooms of 61 flats with no previous history of complaint for olfactory nuisance or specific symptoms, two-thirds of the flats having been recently refurbished. Aldehydes were sampled in these rooms using passive samplers, and a questionnaire on potential aldehyde sources was filled out at the same time. A multiple linear regression model was used to investigate indoor aldehyde determinants. Our study revealed that propionaldehyde and benzaldehyde were of minor importance compared to formaldehyde, acetaldehyde, pentanal, and hexanal. We found that levels of these last four compounds depended on the age of wall or floor coverings (renovations less than 1 year old), smoking, and ambient parameters (carbon dioxide levels, temperature). These results could help in the assessment of indoor aldehyde emissions

  10. Acrolein Exposure in Hookah Smokers and Non-Smokers Exposed to Hookah Tobacco Secondhand Smoke: Implications for Regulating Hookah Tobacco Products.

    Science.gov (United States)

    Kassem, Nada O F; Kassem, Noura O; Liles, Sandy; Zarth, Adam T; Jackson, Sheila R; Daffa, Reem M; Chatfield, Dale A; Carmella, Steven G; Hecht, Stephen S; Hovell, Melbourne F

    2018-03-06

    Acrolein is a highly ciliatoxic agent, a toxic respiratory irritant, a cardiotoxicant, and a possible carcinogen present in tobacco smoke including hookah tobacco. 105 hookah smokers and 103 non-smokers attended exclusively hookah smoking social events at either a hookah lounge or private home, and provided urine samples the morning of and the morning after the event. Samples were analyzed for 3-hydroxypropylmercapturic acid (3-HPMA), a metabolite of acrolein. Geometric mean (GM) urinary 3-HPMA levels in hookah smokers and non-smokers exposed to secondhand smoke (SHS) increased significantly, 1.41 times, 95% CI = 1.15 to 1.74 and 1.39 times, 95% CI = 1.16 to 1.67, respectively, following a hookah social event. The highest increase (1.68 times, 95% CI = 1.15 to 2.45; p = 0.007) in 3-HPMA post a hookah social event was among daily hookah smokers (GM, from 1991 pmol/mg to 3348 pmol/mg). Pre-to-post event change in urinary 3-HPMA was significantly positively correlated with pre-to-post event change in urinary cotinine among hookah smokers at either location of hookah event, (ρ = 0.359, p = 0.001), and among non-smokers in hookah lounges (ρ = 0.369, p = 0.012). Hookah tobacco smoke is a source of acrolein exposure. Findings support regulating hookah tobacco products including reducing humectants and sugar additives, which are precursors of acrolein under certain pyrolysis conditions. We suggest posting health warning signs for indoor smoking in hookah lounges, and encouraging voluntary bans of smoking hookah tobacco in private homes. Our study is the first to quantify the increase in acrolein exposure in hookah smokers and non-smokers exposed to exclusively hookah tobacco SHS at hookah social events in homes or hookah lounges. Our findings provide additional support for regulating hookah tobacco product content, protecting non-smokers' health by posting health warning signs for indoor smoking in hookah lounges, and encouraging home bans on hookah tobacco smoking to

  11. Microenvironmental characteristics important for personal exposures to aldehydes in Sacramento, CA, and Milwaukee, WI

    Science.gov (United States)

    Raymer, J. H.; Akland, G.; Johnson, T. R.; Long, T.; Michael, L.; Cauble, L.; McCombs, M.

    Oxygenated additives in gasoline are designed to decrease the ozone-forming hydrocarbons and total air toxics, yet they can increase the emissions of aldehydes and thus increase human exposure to these toxic compounds. This paper describes a study conducted to characterize targeted aldehydes in microenvironments in Sacramento, CA, and Milwaukee, WI, and to improve our understanding of the impact of the urban environment on human exposure to air toxics. Data were obtained from microenvironmental concentration measurements, integrated, 24-h personal measurements, indoor and outdoor pollutant monitors at the participants' residences, from ambient pollutant monitors at fixed-site locations in each city, and from real-time diaries and questionnaires completed by the technicians and participants. As part of this study, a model to predict personal exposures based on individual time/activity data was developed for comparison to measured concentrations. Predicted concentrations were generally within 25% of the measured concentrations. The microenvironments that people encounter daily provide for widely varying exposures to aldehydes. The activities that occur in those microenvironments can modulate the aldehyde concentrations dramatically, especially for environments such as "indoor at home." By considering personal activity, location (microenvironment), duration in the microenvironment, and a knowledge of the general concentrations of aldehydes in the various microenvironments, a simple model can do a reasonably good job of predicting the time-averaged personal exposures to aldehydes, even in the absence of monitoring data. Although concentrations of aldehydes measured indoors at the participants' homes tracked well with personal exposure, there were instances where personal exposures and indoor concentrations differed significantly. Key to the ability to predict exposure based on time/activity data is the quality and completeness of the microenvironmental

  12. Influences of cinnamic aldehydes on H⁺ extrusion activity and ultrastructure of Candida.

    Science.gov (United States)

    Shreaz, Sheikh; Bhatia, Rimple; Khan, Neelofar; Muralidhar, Sumathi; Manzoor, Nikhat; Khan, Luqman Ahmad

    2013-02-01

    The antifungal effects of cinnamaldehyde, 4-hydroxy-3-methoxycinnamaldehyde (coniferyl aldehyde) and 3,5-dimethoxy-4-hydroxycinnamaldehyde (sinapaldehyde) were investigated against 65 strains of Candida (six standard, 39 fluconazole-sensitive and 20 fluconazole-resistant). MICs of cinnamaldehyde, coniferyl aldehyde and sinapaldehyde ranged from 100 to 500 µg ml(-1), 100 to 300 µg ml(-1) and 100 to 200 µg ml(-1), respectively. All tested isolates showed a marked sensitivity towards these aldehydes in spot and time-kill assays. Sinapaldehyde was found to be the most effective, followed by coniferyl aldehyde and cinnamaldehyde. At their respective MIC(90) values, the three compounds caused mean inhibition levels of glucose-stimulated H(+)-efflux of 36, 34 and 41 % (cinnamaldehyde), 41, 42 and 47 % (coniferyl aldehyde) and 43, 45 and 51 % (sinapaldehyde) for standard-sensitive, clinical-sensitive and clinical-resistant isolates, respectively. Inhibition levels of H(+)-efflux caused by plasma membrane ATPase inhibitors N,N'-dicyclohexylcarbodiimide (100 µM) and diethylstilbestrol (10 µM) were 34, 45 and 44 %, and 57, 39 and 35 %, for standard-sensitive, clinical-sensitive and clinical-resistant isolates, respectively. Intracellular pH (pHi) was found to decrease by 0.34, 0.42 and 0.50 units following incubation with three tested aldehydes from the control pHi of 6.70. Scanning electron microscopy and transmission electron microscopy analysis was performed on a representative strain, C. albicans 10261, showing alterations in morphology, cell wall, plasma membrane damage and lysis. Haemolytic activity of the three compounds varied from 10 to 15 % at their highest MIC compared to an activity level of 20 % shown by fluconazole at 30 µg ml(-1). In conclusion, this study shows significant activity of cinnamic aldehydes against Candida, including azole-resistant strains, suggesting that these molecules can be developed as antifungals.

  13. Quantitative analysis of aldehydes in canned vegetables using static headspace-gas chromatography-mass spectrometry.

    Science.gov (United States)

    Serrano, María; Gallego, Mercedes; Silva, Manuel

    2017-11-17

    Volatile aldehydes appear in canned vegetables as constituents and some of them can also be present as disinfection by-products (DBPs) because of the contact between vegetables and treated water. This paper describes two static headspace-gas chromatography-mass spectrometry (SHS-GC-MS) methods to determine 15 aldehydes in both the solid and the liquid phases of canned vegetables. The treatment for both phases of samples was carried out simultaneously into an SHS unit, including the leaching of the aldehydes (from the vegetable), their derivatization and volatilization of the oximes formed. Detection limits were obtained within the range of 15-400μg/kg and 3-40μg/L for aldehydes in the solid and the liquid phases of the food, respectively. The relative standard deviation was lower than 7% -for the whole array of the target analytes-, the trueness evaluated by recovery experiments provided %recoveries between 89 and 99% and short- and long-term stability studies indicated there was no significant variation in relative peak areas of all aldehydes in both phases of canned vegetables after their storing at 4°C for two weeks. The study of the origin of the 15 aldehydes detected between both phases of canned vegetables showed that: i) the presence of 13 aldehydes -at average concentrations of 2.2-39μg/kg and 0.25-71μg/L for the solid and the liquid phases, respectively- is because they are natural constituents of vegetables; and ii) the presence of glyoxal and methylglyoxal -which are mainly found in the liquid phase (average values, 1.4-4.1μg/L)- is ascribed to the use of treated water, thereby being DBPs. Copyright © 2017 Elsevier B.V. All rights reserved.

  14. Identification and characterization of an antennae-specific aldehyde oxidase from the navel orangeworm.

    Directory of Open Access Journals (Sweden)

    Young-Moo Choo

    Full Text Available Antennae-specific odorant-degrading enzymes (ODEs are postulated to inactivate odorant molecules after they convey their signal. Different classes of insect ODEs are specific to esters, alcohols, and aldehydes--the major functional groups of female-produced, hydrophobic sex pheromones from moth species. Esterases that rapidly inactive acetate and other esters have been well-studied, but less is known about aldehyde oxidases (AOXs. Here we report cloning of an aldehyde oxidase, AtraAOX2, from the antennae of the navel orangeworm (NOW, Amyelois transitella, and the first activity characterization of a recombinant insect AOX. AtraAOX2 gene spans 3,813 bp and encodes a protein with 1,270 amino acid residues. AtraAOX2 cDNA was expressed in baculovirus-infected insect Sf21 cells as a ≈280 kDa homodimer with 140 kDa subunits. Recombinant AtraAOX2 degraded Z11Z13-16Ald and plant volatile aldehydes as substrates. However, as expected for aldehyde oxidases, recombinant AtraAOX2 did not show specificity for Z11Z13-16Ald, the main constituent of the sex pheromone, but showed high activity for plant volatile aldehydes. Our data suggest AtraAOX2 might be involved in degradation of a diversity of aldehydes including sex pheromones, plant-derived semiochemicals, and chemical cues for oviposition sites. Additionally, AtraAOX2 could protect the insect's olfactory system from xenobiotics, including pesticides that might reach the sensillar lymph surrounding the olfactory receptor neurons.

  15. Assessment and predictor determination of indoor aldehyde levels in Paris newborn babies' homes.

    Science.gov (United States)

    Dassonville, C; Demattei, C; Laurent, A-M; Le Moullec, Y; Seta, N; Momas, I

    2009-08-01

    Exposure to indoor chemical air pollutants expected to be potentially involved in allergic respiratory diseases in infants is poorly documented. A specific environmental investigation included in a birth cohort study was carried out to first assess indoor airborne aldehyde levels, using passive devices and their variability within 1 year (1, 6, 9 and 12 months) in the bedroom of 196 Paris infants, and second, to identify predictors for aldehyde concentrations using interviewer administered questionnaires about housing factors. Comfort parameters and carbon dioxide levels were measured simultaneously. Aldehydes were detected in almost all dwellings and geometric mean levels (geometric standard deviation) at the first visit were respectively for formaldehyde, acetaldehyde, hexanal, and pentanal 19.4 (1.7) microg/m(3), 8.9 (1.8) microg/m(3), 25.3 (3.1) microg/m(3), 3.7 (2.3) microg/m(3), consistent with earlier published results. Generalized Estimating Equation multivariate analyses showed that, apart from comfort parameters, aeration and season, the main indoor aldehyde sources were either continuous (building materials and coverings especially when they were new) or discontinuous (smoking, use of air fresheners and cleaning products, DIY etc...). Finally, the data collected by questionnaires should be sufficient to enable us to classify each infant in our cohort study according to his/her degree of exposure to the main aldehydes. This analysis contributed to document indoor aldehyde levels in Parisian homes and to identify factors determining these levels. In the major part of newborn babies' homes, indoor formaldehyde levels were above the guideline value of 10 microg/m(3) proposed by the French Agency for Environmental and Occupational Health Safety for long-term exposure. Given this result, it is essential to study the health impact of exposure to aldehydes especially formaldehyde on the incidence of respiratory and allergic symptoms, particularly during the

  16. Vibrationally specific photoionization cross sections of acrolein leading to the Χ{sup ~}A{sup '} ionic state

    Energy Technology Data Exchange (ETDEWEB)

    López-Domínguez, Jesús A.; Lucchese, Robert R., E-mail: lucchese@mail.chem.tamu.edu [Department of Chemistry, Texas A and M University, College Station, Texas 77843-3255 (United States); Fulfer, K. D.; Hardy, David; Poliakoff, E. D. [Department of Chemistry, Louisiana State University, Baton Rouge, Louisiana 70803 (United States); Aguilar, A. A. [Advanced Light Source, Lawrence Berkeley National Laboratory, University of California, Berkeley, California 94720 (United States)

    2014-09-07

    The vibrational branching ratios in the photoionization of acrolein for ionization leading to the Χ{sup ~}A{sup '} ion state were studied. Computed logarithmic derivatives of the cross section and the corresponding experimental data derived from measured vibrational branching ratios for several normal modes (ν{sub 9}, ν{sub 10}, ν{sub 11}, and ν{sub 12}) were found to be in relatively good agreement, particularly for the lower half of the 11–100 eV photon energy range considered. Two shape resonances have been found near photon energies of 15.5 and 23 eV in the photoionization cross section and have been demonstrated to originate from the partial cross section of the A{sup ′} scattering symmetry. The wave functions computed at the resonance complex energies are delocalized over the whole molecule. By looking at the dependence of the cross section on the different normal mode displacements together with the wave function at the resonant energy, a qualitative explanation is given for the change of the cross sections with respect to changing geometry.

  17. Acrolein-stressed threshold adaptation alters the molecular and metabolic bases of an engineered Saccharomyces cerevisiae to improve glutathione production.

    Science.gov (United States)

    Zhou, Wenlong; Yang, Yan; Tang, Liang; Cheng, Kai; Li, Changkun; Wang, Huimin; Liu, Minzhi; Wang, Wei

    2018-03-14

    Acrolein (Acr) was used as a selection agent to improve the glutathione (GSH) overproduction of the prototrophic strain W303-1b/FGP PT . After two rounds of adaptive laboratory evolution (ALE), an unexpected result was obtained wherein identical GSH production was observed in the selected isolates. Then, a threshold selection mechanism of Acr-stressed adaption was clarified based on the formation of an Acr-GSH adduct, and a diffusion coefficient (0.36 ± 0.02 μmol·min -1 ·OD 600 -1 ) was calculated. Metabolomic analysis was carried out to reveal the molecular bases that triggered GSH overproduction. The results indicated that all three precursors (glutamic acid (Glu), glycine (Gly) and cysteine (Cys)) needed for GSH synthesis were at a relativity higher concentration in the evolved strain and that the accumulation of homocysteine (Hcy) and cystathionine might promote Cys synthesis and then improve GSH production. In addition to GSH and Cys, it was observed that other non-protein thiols and molecules related to ATP generation were at obviously different levels. To divert the accumulated thiols to GSH biosynthesis, combinatorial strategies, including deletion of cystathionine β-lyase (STR3), overexpression of cystathionine γ-lyase (CYS3) and cystathionine β-synthase (CYS4), and reduction of the unfolded protein response (UPR) through up-regulation of protein disulphide isomerase (PDI), were also investigated.

  18. Inhibition of acrolein-induced autophagy and apoptosis by a glycosaminoglycan from Sepia esculenta ink in mouse Leydig cells.

    Science.gov (United States)

    Gu, Yi-Peng; Yang, Xiao-Mei; Luo, Ping; Li, Yan-Qun; Tao, Ye-Xing; Duan, Zhen-Hua; Xiao, Wei; Zhang, Da-Yan; Liu, Hua-Zhong

    2017-05-01

    In our recent reports, a squid ink polysaccharide (SIP) was found having preventive activity against cyclophosphamide induced damage in mouse testis and ovary. Here we further reveal the regulative mechanism of SIP against chemical toxicity on testis. Leydig cells exposed to acrolein (ACR) underwent apoptosis at 12h and 24h. Before apoptosis, cells occurred autophagy that was confirmed by high autophagic rate and Beclin-1 protein content at 3h. PI3K/Akt and p38 MAPK signal pathways involved in the regulatory mechanisms. These outcomes of ACR were recovered completely by SIP, which was demonstrated by attenuated disruption of redox equilibrium and increased testosterone production, through suppressing ACR-caused autophagy and apoptosis regulated by PI3K/Akt and p38 MAPK signal pathways in Leydig cells. Summarily, autophagy occurred before apoptosis caused by ACR-activated p38 MAPK and PI3K/Akt pathways were blocked by SIP, resulting in survival and functional maintenance of Leydig cells. Copyright © 2017 Elsevier Ltd. All rights reserved.

  19. Study of ternary-component bismuth molybdate catalysts by 18O2 tracer in the oxidation of propylene to acrolein

    International Nuclear Information System (INIS)

    Ueda, W.; Moro-oka, Y.; Ikawa, T.

    1981-01-01

    Participation of lattice oxide ions of ternary-component bismuth molybdate catalysts M-Bi-Mo-O (M = Ni, Co, Mg, Mn, Ca, Sr, Ba, and Pb) was investigated using the 18 O 2 tracer in the selective oxidation of propylene to acrolein. The participation of the lattice oxide ions in the oxidation is prominent on every catalyst but the extent of the participation varies significantly depending on the structure of the catalyst. Only lattice oxide ions in the bismuth molybdate phase are incorporated into the oxidized products on the catalysts (M = Ni, Co, Mg, and Mn) where M have smaller ionic radius than Bi 3+ ; catalyst particles are composed of a shell of bismuth molybdates and a core of MMoO 4 . On the other hand, whole oxide ions in the active particles are involved in the oxidation on catalysts having a scheelite-type structure (M = Ca, Sr, Ba, and Pb) where M has a comparable ionic radius to Bi 3+

  20. Flavoring Compounds Dominate Toxic Aldehyde Production during E-Cigarette Vaping.

    Science.gov (United States)

    Khlystov, Andrey; Samburova, Vera

    2016-12-06

    The growing popularity of electronic cigarettes (e-cigarettes) raises concerns about the possibility of adverse health effects to primary users and people exposed to e-cigarette vapors. E-Cigarettes offer a very wide variety of flavors, which is one of the main factors that attract new, especially young, users. How flavoring compounds in e-cigarette liquids affect the chemical composition and toxicity of e-cigarette vapors is practically unknown. Although e-cigarettes are marketed as safer alternatives to traditional cigarettes, several studies have demonstrated formation of toxic aldehydes in e-cigarette vapors during vaping. So far, aldehyde formation has been attributed to thermal decomposition of the main components of e-cigarette e-liquids (propylene glycol and glycerol), while the role of flavoring compounds has been ignored. In this study, we have measured several toxic aldehydes produced by three popular brands of e-cigarettes with flavored and unflavored e-liquids. We show that, within the tested e-cigarette brands, thermal decomposition of flavoring compounds dominates formation of aldehydes during vaping, producing levels that exceed occupational safety standards. Production of aldehydes was found to be exponentially dependent on concentration of flavoring compounds. These findings stress the need for a further, thorough investigation of the effect of flavoring compounds on the toxicity of e-cigarettes.

  1. Nitrite promotes protein carbonylation and Strecker aldehyde formation in experimental fermented sausages: are both events connected?

    Science.gov (United States)

    Villaverde, A; Ventanas, J; Estévez, M

    2014-12-01

    The role played by curing agents (nitrite, ascorbate) on protein oxidation and Strecker aldehyde formation is studied. To fulfill this objective, increasing concentrations of nitrite (0, 75 and 150ppm) and ascorbate (0, 250 and 500ppm) were added to sausages subjected to a 54day drying process. The concurrence of intense proteolysis, protein carbonylation and formation of Strecker aldehydes during processing of sausages suggests that α-aminoadipic semialdehyde (AAS) and γ-glutamic semialdehyde (GGS) may be implicated in the formation of Strecker aldehydes. The fact that nitrite (150ppm, ingoing amount) significantly promoted the formation of protein carbonyls at early stages of processing and the subsequent formation of Strecker aldehydes provides strength to this hypothesis. Ascorbate (125 and 250ppm) controlled the overall extent of protein carbonylation in sausages without declining the formation of Strecker aldehydes. These results may contribute to understanding the chemistry fundamentals of the positive influence of nitrite on the flavor and overall acceptability of cured muscle foods. Copyright © 2014 Elsevier Ltd. All rights reserved.

  2. Toxicity of polyunsaturated aldehydes of diatoms to Indo-Pacific bioindicator organism Echinometra mathaei.

    Science.gov (United States)

    Sartori, Davide; Gaion, Andrea

    2016-01-01

    Although it is well known suitability of early developmental stages of sea urchin as recommended model for pollutant toxicity testing, little is known about the sensitivity of Indo-Pacific species Echinometra mathaei to polyunsaturated aldehydes. In this study, the effect of three short chain aldehydes, 2,4-decadienal (DD), 2,4-octadienal (OD) and 2,4-heptadienal (HD), normally found in many diatoms, such as Skeletonema costatum, Skeletonema marinoi and Thalassiosira rotula, was evaluated on larval development of E. mathaei embryos. Aldehydes affected larval development in a dose-dependent manner, in particular HD>OD>DD; the results of this study highlighted the higher sensitivity of this species toward aldehydes compared with data registered for other sea urchin species. In comparison with studies reported in the literature, contrasting results were observed during our tests; therefore, an increasing toxic effect was registered with decreasing the chain length of aldehydes. This work could provide new insights in the development of new toxicological assays toward most sensitive species.

  3. Aldehyde Dehydrogenases in Arabidopsis thaliana: Biochemical Requirements, Metabolic Pathways, and Functional Analysis.

    Science.gov (United States)

    Stiti, Naim; Missihoun, Tagnon D; Kotchoni, Simeon O; Kirch, Hans-Hubert; Bartels, Dorothea

    2011-01-01

    Aldehyde dehydrogenases (ALDHs) are a family of enzymes which catalyze the oxidation of reactive aldehydes to their corresponding carboxylic acids. Here we summarize molecular genetic and biochemical analyses of selected ArabidopsisALDH genes. Aldehyde molecules are very reactive and are involved in many metabolic processes but when they accumulate in excess they become toxic. Thus activity of aldehyde dehydrogenases is important in regulating the homeostasis of aldehydes. Overexpression of some ALDH genes demonstrated an improved abiotic stress tolerance. Despite the fact that several reports are available describing a role for specific ALDHs, their precise physiological roles are often still unclear. Therefore a number of genetic and biochemical tools have been generated to address the function with an emphasis on stress-related ALDHs. ALDHs exert their functions in different cellular compartments and often in a developmental and tissue specific manner. To investigate substrate specificity, catalytic efficiencies have been determined using a range of substrates varying in carbon chain length and degree of carbon oxidation. Mutational approaches identified amino acid residues critical for coenzyme usage and enzyme activities.

  4. Thermal, Catalytic Conversion of Alkanes to Linear Aldehydes and Linear Amines.

    Science.gov (United States)

    Tang, Xinxin; Jia, Xiangqing; Huang, Zheng

    2018-03-21

    Alkanes, the main constituents of petroleum, are attractive feedstocks for producing value-added chemicals. Linear aldehydes and amines are two of the most important building blocks in the chemical industry. To date, there have been no effective methods for directly converting n-alkanes to linear aldehydes and linear amines. Here, we report a molecular dual-catalyst system for production of linear aldehydes via regioselective carbonylation of n-alkanes. The system is comprised of a pincer iridium catalyst for transfer-dehydrogenation of the alkane using t-butylethylene or ethylene as a hydrogen acceptor working sequentially with a rhodium catalyst for olefin isomerization-hydroformylation with syngas. The system exhibits high regioselectivity for linear aldehydes and gives high catalytic turnover numbers when using ethylene as the acceptor. In addition, the direct conversion of light alkanes, n-pentane and n-hexane, to siloxy-terminated alkyl aldehydes through a sequence of Ir/Fe-catalyzed alkane silylation and Ir/Rh-catalyzed alkane carbonylation, is described. Finally, the Ir/Rh dual-catalyst strategy has been successfully applied to regioselective alkane aminomethylation to form linear alkyl amines.

  5. DNA damage by lipid peroxidation products: implications in cancer, inflammation and autoimmunity

    Directory of Open Access Journals (Sweden)

    Fabrizio Gentile

    2017-04-01

    Full Text Available Oxidative stress and lipid peroxidation (LPO induced by inflammation, excess metal storage and excess caloric intake cause generalized DNA damage, producing genotoxic and mutagenic effects. The consequent deregulation of cell homeostasis is implicated in the pathogenesis of a number of malignancies and degenerative diseases. Reactive aldehydes produced by LPO, such as malondialdehyde, acrolein, crotonaldehyde and 4-hydroxy-2-nonenal, react with DNA bases, generating promutagenic exocyclic DNA adducts, which likely contribute to the mutagenic and carcinogenic effects associated with oxidative stress-induced LPO. However, reactive aldehydes, when added to tumor cells, can exert an anticancerous effect. They act, analogously to other chemotherapeutic drugs, by forming DNA adducts and, in this way, they drive the tumor cells toward apoptosis. The aldehyde-DNA adducts, which can be observed during inflammation, play an important role by inducing epigenetic changes which, in turn, can modulate the inflammatory process. The pathogenic role of the adducts formed by the products of LPO with biological macromolecules in the breaking of immunological tolerance to self antigens and in the development of autoimmunity has been supported by a wealth of evidence. The instrumental role of the adducts of reactive LPO products with self protein antigens in the sensitization of autoreactive cells to the respective unmodified proteins and in the intermolecular spreading of the autoimmune responses to aldehyde-modified and native DNA is well documented. In contrast, further investigation is required in order to establish whether the formation of adducts of LPO products with DNA might incite substantial immune responsivity and might be instrumental for the spreading of the immunological responses from aldehyde-modified DNA to native DNA and similarly modified, unmodified and/or structurally analogous self protein antigens, thus leading to autoimmunity.

  6. Effects of light and copper ions on volatile aldehydes of milk and milk fractions

    Energy Technology Data Exchange (ETDEWEB)

    Jeno, W.; Bassette, R.; Crang, R.E.

    1988-09-01

    Raw, laboratory-pasteurized and plant-pasteurized homogenized milks were exposed to copper ions (5 ppm), to sunlight or fluorescent light and the effects determined on the composition of volatile aldehydes. The greatest change due to copper treatment was an increase in n-hexanal; acetaldehyde showed the least response in each of the sources of milk. The responses were similar from all three sources of milk with laboratory-pasteurized milk samples showing the greatest responses for each aldehyde analyzed. Similar milk samples exposed to sunlight also showed an increase in volatile aldehydes from all milk sources but with the greatest response being acetaldehyde and n-pentanal components. The milk fraction most susceptible to changes in the presence of light was neutralized whey, whereas resuspended cream was most susceptible to copper exposure. Overall, dialyzed whey appeared to be influenced more than other milk fractions by both light and copper ions.

  7. Oxidative desulfurization of diesel with TBHP/isobutyl aldehyde/air oxidation system

    Energy Technology Data Exchange (ETDEWEB)

    Guo, Wei; Wang, Chengyong; Lin, Peng; Lu, Xiaoping [Institute of Sonochemical Engineering, Nanjing University of Technology, Nanjing 210009, Jiangsu (China)

    2011-01-15

    Oxidative desulfurization of hydrogenation diesel (40 mL) was studied using air as oxidant, tert-butyl hydroperoxide (TBHP) as radical initiator at ambient pressure and moderate temperature in the presence of isobutyl aldehyde. TBHP could accelerate the production of carbonyl radical and its peroxidation. When the molar fraction of TBHP was 5 mmol, the conversion of DBT could reach 96.1% in the present of 20 mmol isobutyl aldehyde and air, which was more than that of 85.5% without initiator. The air was an effective oxidant and acetonitrile was an optimal solvent in this process. The sulfur content of the hydrogenation diesel could be reduced from 403 to 13 ppm (96.8% removed) under the synergistic effect of air, TBHP and isobutyl aldehyde. (author)

  8. Formation and Accumulation of Acetaldehyde and Strecker Aldehydes during Red Wine Oxidation

    Directory of Open Access Journals (Sweden)

    Mónica Bueno

    2018-02-01

    Full Text Available The main aim of the present work is to study the accumulation of acetaldehyde and Strecker aldehydes (isobutyraldehyde, 2-methylbutanal, isovaleraldehyde, methional, phenylacetaldehyde during the oxidation of red wines, and to relate the patterns of accumulation to the wine chemical composition. For that, eight different wines, extensively chemically characterized, were subjected at 25°C to three different controlled O2 exposure conditions: low (10 mg L−1 and medium or high (the stoichiometrically required amount to oxidize all wine total SO2 plus 18 or 32 mg L−1, respectively. Levels of volatile aldehydes and carbonyls were then determined and processed by different statistical techniques. Results showed that young wines (<2 years-old bottled wines hardly accumulate any acetaldehyde regardless of the O2 consumed. In contrast, aged wines (>3 years-old bottled wines accumulated acetaldehyde while their content in SO2 was not null, and the aged wine containing lowest polyphenols accumulated it throughout the whole process. Models suggest that the ability of a wine to accumulate acetaldehyde is positively related to its content in combined SO2, in epigallocatechin and to the mean degree of polymerization, and negatively to its content in Aldehyde Reactive Polyphenols (ARPs which, attending to our models, are anthocyanins and small tannins. The accumulation of Strecker aldehydes is directly proportional to the wine content in the amino acid precursor, being the proportionality factor much higher for aged wines, except for phenylacetaldehyde, for which the opposite pattern was observed. Models suggest that non-aromatic Strecker aldehydes share with acetaldehyde a strong affinity toward ARPs and that the specific pattern of phenylacetaldehyde is likely due to a much reduced reactivity toward ARPs, to the possibility that diacetyl induces Strecker degradation of phenyl alanine and to the potential higher reactivity of this amino acid to some

  9. Formation and accumulation of acetaldehyde and Strecker aldehydes during red wine oxidation

    Science.gov (United States)

    Bueno, Mónica; Marrufo-Curtido, Almudena; Carrascón, Vanesa; Fernández-Zurbano, Purificación; Escudero, Ana; Ferreira, Vicente

    2018-02-01

    The main aim of the present work is to study the accumulation of acetaldehyde and Strecker aldehydes (isobutyraldehyde, 2-methylbutanal, isovaleraldehyde, methional, phenylacetaldehyde) during the oxidation of red wines, and to relate the patterns of accumulation to the wine chemical composition. For that, eight different wines, extensively chemically characterized, were subjected at 25°C to three different controlled O2 exposure conditions: low (10 mg L-1) and medium or high (the stoichiometrically required amount to oxidize all wine total SO2 plus 18 or 32 mg L-1, respectively). Levels of volatile aldehydes and carbonyls were then determined and processed by different statistical techniques. Results showed that young wines (wines) hardly accumulate any acetaldehyde regardless of the O2 consumed. In contrast, aged wines (>3 years-old bottled wines) accumulated acetaldehyde while their content in SO2 was not null, and the aged wine containing lowest polyphenols accumulated it throughout the whole process. Models suggest that the ability of a wine to accumulate acetaldehyde is positively related to its content in combined SO2, in epigallocatechin and to the mean degree of polymerization, and negatively to its content in Aldehyde Reactive Polyphenols (ARPs) which, attending to our models, are anthocyanins and small tannins. The accumulation of Strecker aldehydes is directly proportional to the wine content in the amino acid precursor, being the proportionality factor much higher for aged wines, except for phenylacetaldehyde, for which the opposite pattern was observed. Models suggest that non-aromatic Strecker aldehydes share with acetaldehyde a strong affinity towards ARPs and that the specific pattern of phenylacetaldehyde is likely due to a much reduced reactivity towards ARPs, to the possibility that diacetyl induces Strecker degradation of phenyl alanine and to the potential higher reactivity of this amino acid to some quinones derived from catechin. All this

  10. Ubiquitin-aldehyde: a general inhibitor of ubiquitin-recycling processes

    International Nuclear Information System (INIS)

    Hershko, A.; Rose, I.A.

    1987-01-01

    The generation and characterization of ubiquitin (Ub)-aldehyde, a potent inhibitor of Ub-C-terminal hydrolase, has previously been reported. The authors examine the action of this compound on the Ub-mediated proteolytic pathway using the system derived from rabbit reticulocytes. Addition of Ub-aldehyde was found to strongly inhibit breakdown of added 125 I-labeled lysozyme, but inhibition was overcome by increasing concentrations of Ub. The following evidence shows the effect of Ub-aldehyde on protein breakdown to be indirectly caused by its interference with the recycling of Ub, leading to exhaustion of the supply of free Ub: (i) Ub-aldehyde markedly increased the accumulation of Ub-protein conjugates coincident with a much decreased rate of conjugate breakdown; (ii) release of Ub from isolated Ub-protein conjugates in the absence of ATP (and therefore not coupled to protein degradation) is markedly inhibited by Ub-aldehyde. On the other hand, the ATP-dependent degradation of the protein moiety of Ub conjugates, which is an integral part of the proteolytic process, is not inhibited by this agent; (iii) direct measurement of levels of free Ub showed a rapid disappearance caused by the inhibitor. The Ub is found to be distributed in derivatives of a wide range of molecular weight classes. It thus seems that Ub-aldehyde, previously demonstrated to inhibit the hydrolysis of Ub conjugates of small molecules, also inhibits the activity of a series of enzymes that regenerate free Ub from adducts with proteins and intermediates in protein breakdown

  11. Nephelauxetic and hypersensitive nature of neodymium(III) complexes with α-pyridyl-thiosemicarbazide and its furfural-2-aldehyde and thiophene-2-aldehyde derivatives

    International Nuclear Information System (INIS)

    Jain, C.L.; Mundley, P.N.; Khandelwal, B.E.

    1986-01-01

    A new series of octahedral Nd(III) complexes with recently synthesised α-pyridylthiosemicarbazide (C 6 H 8 N 4 S or 'PT'), N-(α-pyridyl)furfural-2-aldehyde-thiosemicarbazone (C 11 H 10 N 4 SO or 'PFT') and N-(α-pyridyl)thiophene-2-aldehyde-thiosemicarbazone (C 11 H 10 N 4 S 2 or 'PTT'), have been isolated and characterised on the basis of their elemental analysis, magnetic and reflectance and ir spectral data revealing 'PT' as bidentate (pyridinic-N and thioketo-S) and 'PFT' and 'PTT' as tetradentate with pyridinic-N, thioketo-S, imine-N and furfuryl-O/thiophenyl-S as donor sites. Isolation and characterisation of Nd(III) complexes with 'PT', 'PFT' and 'PTT' and their nephelauxetic and hypersensitive nature are studied in order to evaluate the stereochemistry of the ligands around Nd(III) ion. (author). 12 refs., 2 tables

  12. Lowest triplet (n, π*) electronic state of acrolein: Determination of structural parameters by cavity ringdown spectroscopy and quantum-chemical methods

    Science.gov (United States)

    Hlavacek, Nikolaus C.; McAnally, Michael O.; Drucker, Stephen

    2013-02-01

    The cavity ringdown absorption spectrum of acrolein (propenal, CH2=CH—CH=O) was recorded near 412 nm, under bulk-gas conditions at room temperature and in a free-jet expansion. The measured spectral region includes the 0^0_0 band of the T1(n, π*) ← S0 system. We analyzed the 0^0_0 rotational contour by using the STROTA computer program [R. H. Judge et al., J. Chem. Phys. 103, 5343 (1995)], 10.1063/1.470569, which incorporates an asymmetric rotor Hamiltonian for simulating and fitting singlet-triplet spectra. We used the program to fit T1(n, π*) inertial constants to the room-temperature contour. The determined values (cm-1), with 2σ confidence intervals, are A = 1.662 ± 0.003, B = 0.1485 ± 0.0006, C = 0.1363 ± 0.0004. Linewidth analysis of the jet-cooled spectrum yielded a value of 14 ± 2 ps for the lifetime of isolated acrolein molecules in the T1(n, π*), v = 0 state. We discuss the observed lifetime in the context of previous computational work on acrolein photochemistry. The spectroscopically derived inertial constants for the T1(n, π*) state were used to benchmark a variety of computational methods. One focus was on complete active space methods, such as complete active space self-consistent field (CASSCF) and second-order perturbation theory with a CASSCF reference function (CASPT2), which are applicable to excited states. We also examined the equation-of-motion coupled-cluster and time-dependent density function theory excited-state methods, and finally unrestricted ground-state techniques, including unrestricted density functional theory and unrestricted coupled-cluster theory with single and double and perturbative triple excitations. For each of the above methods, we or others [O. S. Bokareva et al., Int. J. Quantum Chem. 108, 2719 (2008)], 10.1002/qua.21803 used a triple zeta-quality basis set to optimize the T1(n, π*) geometry of acrolein. We find that the multiconfigurational methods provide the best agreement with fitted inertial

  13. Silica-Supported Catalyst for Enantioselective Arylation of Aldehydes under Batch and Continuous-Flow Conditions.

    Science.gov (United States)

    Watanabe, Satoshi; Nakaya, Naoyuki; Akai, Junichiro; Kanaori, Kenji; Harada, Toshiro

    2018-05-04

    A silica-supported 3-aryl H 8 -BINOL-derived titanium catalyst exhibited high performance in the enantioselective arylation of aromatic aldehydes using Grignard and organolithium reagents not only under batch conditions but also under continuous-flow conditions. Even with a simple pipet reactor packed with the heterogeneous catalyst, the enantioselective production of chiral diarylmethanols could be achieved through a continuous introduction of aldehydes and mixed titanium reagents generated from the organometallic precursors. The pipet reactor could be used repeatedly in different reactions without appreciable deterioration of the activity.

  14. Effects of the biodiesel blend fuel on aldehyde emissions from diesel engine exhaust

    Science.gov (United States)

    Peng, Chiung-Yu; Yang, Hsi-Hsien; Lan, Cheng-Hang; Chien, Shu-Mei

    Interest in use of biodiesel fuels derived from vegetable oils or animal fats as alternative fuels for petroleum-based diesels has increased due to biodiesels having similar properties of those of diesels, and characteristics of renewability, biodegradability and potential beneficial effects on exhaust emissions. Generally, exhaust emissions of regulated pollutants are widely studied and the results favor biodiesels on CO, HC and particulate emissions; however, limited and inconsistent data are showed for unregulated pollutants, such as carbonyl compounds, which are also important indicators for evaluating available vehicle fuels. For better understanding biodiesel, this study examines the effects of the biodiesel blend fuel on aldehyde chemical emissions from diesel engine exhausts in comparison with those from the diesel fuel. Test engines (Mitsubishi 4M40-2AT1) with four cylinders, a total displacement of 2.84 L, maximum horsepower of 80.9 kW at 3700 rpm, and maximum torque of 217.6 N m at 2000 rpm, were mounted and operated on a Schenck DyNAS 335 dynamometer. Exhaust emission tests were performed several times for each fuel under the US transient cycle protocol from mileages of 0-80,000 km with an interval of 20,000 km, and two additional measurements were carried out at 40,000 and 80,000 km after maintenance, respectively. Aldehyde samples were collected from diluted exhaust by using a constant volume sampling system. Samples were extracted and analyzed by the HPLC/UV system. Dominant aldehydes of both fuels' exhausts are formaldehyde and acetaldehyde. These compounds together account for over 75% of total aldehyde emissions. Total aldehyde emissions for B20 (20% waste cooking oil biodiesel and 80% diesel) and diesel fuels are in the ranges of 15.4-26.9 mg bhp-h -1 and 21.3-28.6 mg bhp-h -1, respectively. The effects of increasing mileages and maintenance practice on aldehyde emissions are insignificant for both fuels. B20 generates slightly less emission than

  15. Heat-stable, FE-dependent alcohol dehydrogenase for aldehyde detoxification

    Science.gov (United States)

    Elkins, James G.; Clarkson, Sonya

    2018-04-24

    The present invention relates to microorganisms and polypeptides for detoxifying aldehydes associated with industrial fermentations. In particular, a heat-stable, NADPH- and iron-dependent alcohol dehydrogenase was cloned from Thermoanaerobacter pseudethanolicus 39E and displayed activity against a number of aldehydes including inhibitory compounds that are produced during the dilute-acid pretreatment process of lignocellulosic biomass before fermentation to biofuels. Methods to use the microorganisms and polypeptides of the invention for improved conversion of bio mass to biofuel are provided as well as use of the enzyme in metabolic engineering strategies for producing longer-chain alcohols from sugars using thermophilic, fermentative microorganisms.

  16. Identification of glutathione adducts of α-chlorofatty aldehydes produced in activated neutrophils

    OpenAIRE

    Duerr, Mark A.; Aurora, Rajeev; Ford, David A.

    2015-01-01

    α-Chlorofatty aldehydes (α-ClFALDs) are produced by hypochlorous acid targeting plasmalogens during neutrophil activation. This study investigated the reaction of the α-chlorinated carbon of α-ClFALD with the nucleophile, GSH. Utilizing ESI/MS/MS, the reaction product of GSH and the 16-carbon α-ClFALD, 2-chlorohexadecanal (2-ClHDA), was characterized. The resulting conjugate of 2-ClHDA and GSH (HDA-GSH) has an intact free aldehyde, and the chlorine at the α-carbon is ejected. Stable isotope-l...

  17. Semi-catalytic reduction of secondary amides to imines and aldehydes.

    Science.gov (United States)

    Lee, Sun-Hwa; Nikonov, Georgii I

    2014-06-21

    Secondary amides can be reduced by silane HSiMe2Ph into imines and aldehydes by a two-stage process involving prior conversion of amides into iminoyl chlorides followed by catalytic reduction mediated by the ruthenium complex [Cp(i-Pr3P)Ru(NCCH3)2]PF6 (1). Alkyl and aryl amides bearing halogen, ketone, and ester groups were converted with moderate to good yields under mild reaction conditions to the corresponding imines and aldehydes. This procedure does not work for substrates bearing the nitro-group and fails for heteroaromatic amides. In the case of cyano substituted amides, the cyano group is reduced to imine.

  18. Aldehyde-Selective Wacker-Type Oxidation of Unbiased Alkenes Enabled by a Nitrite Co-Catalyst

    KAUST Repository

    Wickens, Zachary K.; Morandi, Bill; Grubbs, Robert H.

    2013-01-01

    Breaking the rules: Reversal of the high Markovnikov selectivity of Wacker-type oxidations was accomplished using a nitrite co-catalyst. Unbiased aliphatic alkenes can be oxidized with high yield and aldehyde selectivity, and several functional groups are tolerated. 18O-labeling experiments indicate that the aldehydic O atom is derived from the nitrite salt.

  19. Aldehyde-Selective Wacker-Type Oxidation of Unbiased Alkenes Enabled by a Nitrite Co-Catalyst

    KAUST Repository

    Wickens, Zachary K.

    2013-09-13

    Breaking the rules: Reversal of the high Markovnikov selectivity of Wacker-type oxidations was accomplished using a nitrite co-catalyst. Unbiased aliphatic alkenes can be oxidized with high yield and aldehyde selectivity, and several functional groups are tolerated. 18O-labeling experiments indicate that the aldehydic O atom is derived from the nitrite salt.

  20. Kinetic mechanism of an aldehyde reductase of Saccharomyces cerevisiae that relieves toxicity of furfural and 5-hydroxymethylfurfural

    Science.gov (United States)

    An effective means of relieving the toxicity of furan aldehydes, furfural (FFA) and 5-hydroxymethylfurfural (HMF), on fermenting organisms is essential for achieving efficient fermentation of lignocellulosic biomass to ethanol and other products. Ari1p, an aldehyde reductase from Saccharomyces cerev...

  1. Aldehyde Selective Wacker Oxidations of Phthalimide Protected Allylic Amines : A New Catalytic Route to beta(3)-Amino Acids

    NARCIS (Netherlands)

    Weiner, Barbara; Baeza Garcia, Alejandro; Jerphagnon, Thomas; Feringa, Ben L.

    2009-01-01

    A new method for the synthesis of B-3-amino acids is presented. Phthalimide protected allylic amines are oxidized under Wacker conditions selectively to aldehydes using PdCl2 and CuCl or Pd(MeCN)(2)Cl(NO2) and CuCl2 as complementary catalyst systems. The aldehydes are produced in excellent yields

  2. Elucidating the contributions of multiple aldehyde/alcohol dehydrogenases to butanol and ethanol production in Clostridium acetobutylicum

    OpenAIRE

    Dai, Zongjie; Dong, Hongjun; Zhang, Yanping; Li, Yin

    2016-01-01

    Ethanol and butanol biosynthesis in Clostridium acetobutylicum share common aldehyde/alcohol dehydrogenases. However, little is known about the relative contributions of these multiple dehydrogenases to ethanol and butanol production respectively. The contributions of six aldehyde/alcohol dehydrogenases of C. acetobutylicum on butanol and ethanol production were evaluated through inactivation of the corresponding genes respectively. For butanol production, the relative contributions from thes...

  3. Urban and rural ambient air aldehyde levels in Schenectady, New York and on Whiteface Mountain, New York

    Energy Technology Data Exchange (ETDEWEB)

    Schulam, P; Newbold, R; Hull, L A

    1985-01-01

    The air in the city of Schenectady, NY was sampled daily and analyzed for the presence of low molecular weight aldehydes during the months of June-August 1983. The diurnal variation of the aldehyde concentrations was also determined over a two day period during August. The dominant aldehyde was formaldehyde and its concentration varied from about 1-31 ppb. There was also observed a significant daily variation that appeared to correlate with traffic conditions. The technique was also used to monitor the aldehyde levels on the summit of Whiteface Mountain in Wilmington, NY at the SUNYA Atmospheric Sciences Research Center. The monitoring was done on a daily basis during the week of 14-20 August and, during that week, every 3 h for a 3-day period. The two dominant aldehydes were formaldehyde and acetaldehyde and they varied in concentration from about 0.8-2.6 and 0.2-0.8 ppb, respectively.

  4. Modelling of the partial oxidation of {alpha}, {beta}-unsaturated aldehydes on Mo-V-oxides based catalysts

    Energy Technology Data Exchange (ETDEWEB)

    Boehnke, H.; Petzoldt, J.C.; Stein, B.; Weimer, C.; Gaube, J.W. [Technische Univ. Darmstadt (Germany). Inst. fuer Chemische Technologie

    1998-12-31

    A kinetic model based on the Mars-van Krevelen mechanism that allows to describe the microkinetics of the heterogeneously catalysed partial oxidation of {alpha}, {beta}-unsaturated aldehydes is presented. This conversion is represented by a network, composed of the oxidation of the {alpha}, {beta}-unsaturated aldehyde towards the {alpha}, {beta}-unsaturated carboxylic acid and the consecutive oxidation of the acid as well as the parallel reaction of the aldehyde to products of deeper oxidation. The reaction steps of aldehyde respectively acid oxidation and catalyst reoxidation have been investigated separately in transient experiments. The combination of steady state and transient experiments has led to an improved understanding of the interaction of the catalyst with the aldehyde and the carboxylic acids as well as to a support of the kinetic model assumptions. (orig.)

  5. An Inter-Laboratory Comparison for the Urinary Acrolein Biomarker 3-Hydroxypropyl-Mercapturic Acid (3-HPMA

    Directory of Open Access Journals (Sweden)

    Scherer Gerhard

    2017-01-01

    Full Text Available An inter-laboratory comparison study on the acrolein biomarker of exposure 3-hydroxypropyl-mercapturic acid (3-HPMA with 12 laboratories from 7 globally distributed countries was performed. The laboratories received coded triplicates of 4 spiked and lyophilized urine samples (LU, 12 samples as well as 5 authentic urine pool samples (PU, 15 samples covering the 3-HPMA concentration range from background (non-smoking to heavy smoking levels for analysis by using their own (in-house analytical method. All laboratories applied liquid chromatography with tandem mass spectrometry (LC-MS/MS, with most of them (10 of 12 using solid phase extraction (SPE as sample work-up procedure. The intra-laboratory variation (indicating repeatability was determined by calculating the standard deviation (sr and the coefficient of variation (CVr of the triplicates, whereas the inter-laboratory variation (indicating reproducibility was determined by calculating the standard deviation between laboratories (sR and the corresponding coefficient of variation (CVR. After removal of outlier samples or laboratories, the mean CVr values for LU and PU test samples ranged from 2.1–3.6% (mean: 2.8% and 2.4–3.7% (mean: 3.3%, respectively, indicating good repeatability for the determination of 3-HPMA in both sample types. CVR for LU and PU test samples ranged from 9.1–31.9% (mean: 18.8% and 13.9–27.0% (mean: 18.5%, respectively, indicating limited reproducibility in 3-HPMA analysis for both sample types. Re-calculation of the PU results by applying an embedded calibration (EC, derived from the reported peak areas for the LU test samples, somewhat improved the CVR values (range: 9.6–28.8%, mean: 16.7%.

  6. Catalytic Oxidation of Lignins into the Aromatic Aldehydes: General Process Trends and Development Prospects

    Directory of Open Access Journals (Sweden)

    Valery E. Tarabanko

    2017-11-01

    Full Text Available This review discusses principal patterns that govern the processes of lignins’ catalytic oxidation into vanillin (3-methoxy-4-hydroxybenzaldehyde and syringaldehyde (3,5-dimethoxy-4-hydroxybenzaldehyde. It examines the influence of lignin and oxidant nature, temperature, mass transfer, and of other factors on the yield of the aldehydes and the process selectivity. The review reveals that properly organized processes of catalytic oxidation of various lignins are only insignificantly (10–15% inferior to oxidation by nitrobenzene in terms of yield and selectivity in vanillin and syringaldehyde. Very high consumption of oxygen (and consequentially, of alkali in the process—over 10 mol per mol of obtained vanillin—is highlighted as an unresolved and unexplored problem: scientific literature reveals almost no studies devoted to the possibilities of decreasing the consumption of oxygen and alkali. Different hypotheses about the mechanism of lignin oxidation into the aromatic aldehydes are discussed, and the mechanism comprising the steps of single-electron oxidation of phenolate anions, and ending with retroaldol reaction of a substituted coniferyl aldehyde was pointed out as the most convincing one. The possibility and development prospects of single-stage oxidative processing of wood into the aromatic aldehydes and cellulose are analyzed.

  7. Critical role of aldehydes in cigarette smoke-induced acute airway inflammation

    NARCIS (Netherlands)

    van der Toorn, Marco; Slebos, Dirk-Jan; de Bruin, Harold G.; Gras, Renee; Rezayat, Delaram; Jorge, Lucie; Sandra, Koen; van Oosterhout, Antoon J. M.

    2013-01-01

    Background: Cigarette smoking (CS) is the most important risk factor for COPD, which is associated with neutrophilic airway inflammation. We hypothesize, that highly reactive aldehydes are critical for CS-induced neutrophilic airway inflammation. Methods: BALB/c mice were exposed to CS, water

  8. Aldehyde-functionalized porous nanocellulose for effective removal of heavy metal ions from aqueous solutions

    Science.gov (United States)

    C. Yao; F. Wang; Z. Cai; X. Wang

    2016-01-01

    Nanoscale sorption is a promising strategy for catalyst and purification system design. In this paper, cellulose nanofibrils (CNFs) were densely attached with aldehyde functional groups on the surface via a mild periodate oxidation process, and then applied as mesoporous sorbents to remove Cu(II) and Pb(II) from aqueous solutions. In the studied concentration range (0....

  9. Analysis of aldehydes in human exhaled breath condensates by in-tube SPME-HPLC.

    Science.gov (United States)

    Wang, ShuLing; Hu, Sheng; Xu, Hui

    2015-11-05

    In this paper, polypyrrole/graphene (PPy/G) composite coating was prepared by a facile electrochemical polymerization strategy on the inner surface of a stainless steel (SS) tube. Based on the coating tube, a novel online in-tube solid-phase microextraction -high performance liquid chromatography (IT-SPME-HPLC) was developed and applied for the extraction of aldehydes in the human exhaled breath condensates (EBC). The hybrid PPy/G nanocomposite exhibits remarkable chemical and mechanical stability, high selectivity, and satisfactory extraction performance toward aldehyde compounds. Moreover, the proposed online IT-SPME-HPLC method possesses numerous superiorities, such as time and cost saving, process simplicity, high precision and sensitivity. Some parameters related to extraction efficiency were optimized systematically. Under the optimal conditions, the recoveries of the aldehyde compounds at three spiked concentration levels varied in the range of 85%-117%. Good linearity was obtained with excellent correlation coefficients (R(2)) being larger than 0.994. The relative standard deviations (n = 5) of the method ranged from 1.8% to 11.3% and the limits of detection were between 2.3 and 3.3 nmol L(-1). The successful application of the proposed method in human EBC indicated that it is a promising approach for the determination of trace aldehyde metabolites in complex EBC samples. Copyright © 2015 Elsevier B.V. All rights reserved.

  10. A Highly Efficient Solvent-Free Acetalization of Aldehydes to 1,1 ...

    African Journals Online (AJOL)

    1,1-Diacetates are prepared in excellent yields from aldehydes and acetic anhydride under solvent-free conditions at room temperature in short reaction times using catalytic amount of sulfonic acid functionalized silica (SiO2-Pr-SO3H) which could be easily handled and removed from the mixture of reaction. Keywords: 1 ...

  11. Efficient Method for Aromatic-Aldehyde Oxidation by Cleavage of Their Hydrazones Catalysed by Trimethylsilanolate

    Czech Academy of Sciences Publication Activity Database

    Bürglová, K.; Okorochenkov, S.; Buděšínský, Miloš; Hlaváč, J.

    2017-01-01

    Roč. 2017, č. 2 (2017), s. 389-396 ISSN 1434-193X R&D Projects: GA MŠk(CZ) LO1304 Institutional support: RVO:61388963 Keywords : aldehydes * oxidation * hydrazones * solid-phase synthesis * reaction mechanisms Subject RIV: CC - Organic Chemistry OBOR OECD: Organic chemistry Impact factor: 2.834, year: 2016

  12. Vapor pressures and enthalpies of vaporization of a series of the linear aliphatic aldehydes

    Czech Academy of Sciences Publication Activity Database

    Verevkin, S. P.; Krasnykh, E. L.; Vasiltsova, T. V.; Koutek, Bohumír; Doubský, Jan; Heintz, A.

    2003-01-01

    Roč. 206, - (2003), s. 331-339 ISSN 0378-3812 Institutional research plan: CEZ:AV0Z4055905 Keywords : aldehydes * vapor pressure * enthalpy of vaporization Subject RIV: CC - Organic Chemistry Impact factor: 1.165, year: 2003

  13. Substituent effect of phenolic aldehyde inhibition on alcoholic fermentation by Saccharomyces cerevisiae

    Science.gov (United States)

    Rui Xie; Maobing Tu; Thomas Elder

    2016-01-01

    Phenolic compounds significantly inhibit microbial fermentation of biomass hydrolysates. To understand thequantitative structure-inhibition relationship of phenolic aldehydes on alcoholic fermentation, the effect of 11 differentsubstituted benzaldehydes on the final ethanol yield was examined. The results showed that the degree of phenolic...

  14. Characterisation of recombinant human fatty aldehyde dehydrogenase: implications for Sjögren-Larsson syndrome

    NARCIS (Netherlands)

    Lloyd, Matthew D.; Boardman, Kieren D. E.; Smith, Andrew; van den Brink, Daan M.; Wanders, Ronald J. A.; Threadgill, Michael D.

    2007-01-01

    Fatty aldehyde dehydrogenase (FALDH) is an NAD+-dependent oxidoreductase involved in the metabolism of fatty alcohols. Enzyme activity has been implicated in the pathology of diabetes and cancer. Mutations in the human gene inactivate the enzyme and cause accumulation of fatty alcohols in

  15. Partial Reduction of Esters to Aldehydes Using a Novel Modified Red-Al Reducing Agent

    Energy Technology Data Exchange (ETDEWEB)

    Shin, Won Kyu; Kang, Daehoon; An, Duk Keun [Kangwon National Univ., Chunchon (Korea, Republic of)

    2014-07-15

    We have developed a convenient alternative method for the synthesis of aldehydes from both aromatic and aliphatic esters in very good to excellent yields in the absence of any additives using a modified Red-Al that was easily prepared by reacting commercially available Red-Al with cis-2,6-dimethyl morpholine. The advantages of the present methodology are as follows: simple preparation procedure of the reducing agent, improved product yields, convenient reaction temperature, and short reaction times. Therefore, the new reagent has great potential to be a useful alternative partial reducing agent for the synthesis of aldehydes from esters in organic synthesis. Aldehydes are valuable building blocks and reactive intermediates in organic synthesis. The general and classical syntheses of aldehydes from esters involve reduction-oxidation and partial reduction using efficient partial reducing agents. Obviously, one-step partial reduction methods are more useful than two-step reduction-oxidation methods owing to their simplicity, and generality in organic synthesis.

  16. Study on physico-chemical properties of dialdehyde yam starch with different aldehyde group contents

    International Nuclear Information System (INIS)

    Zhang, Liming; Liu, Peng; Wang, Yugao; Gao, Wenyuan

    2011-01-01

    Dialdehyde yam starches (DASs) are prepared and characterized. Compared with native starch, viscosity average molecular weight of DASs decreases, and the extent of degradation depends on content of the aldehyde groups. Fourier transform infrared (FT-IR) spectra confirm that the characteristic peak for C=O group at 1732 cm -1 is enhanced with the increasing of content of the aldehyde groups. Scanning electron microscopy (SEM) micrographs show that the surface of starch granules becomes wrinkled. X-ray diffraction (XRD) patterns clearly indicate that their crystallinity decreases with the increasing content of the aldehyde groups before they become amorphous at higher oxidation states. The experimental results of thermogravimetric analysis (TGA) show that DASs have poor stability as compared to native starch. With the increase in content of the aldehyde groups, the thermal stability of DAS declines gradually. According to the results of differential scanning calorimetry (DSC), gelatinization temperature (T o and T p ) of DASs are increased, whereas the gelatinization enthalpy decreased.

  17. Determination of Aldehyde Dehydrogenase (ALDH Isozymes in Human Cancer Samples - Comparison of Kinetic and Immunochemical Assays

    Directory of Open Access Journals (Sweden)

    Dorota Borecka

    2002-12-01

    Full Text Available A fluorimetric assay of aldehyde dehydrogenase isozymes, based on naphthaldehyde oxidation, is compared with Western Blotting analysis on several clinical samples obtained from surgery. The comparison reveals qualitatively good correlation of ALDH1A1 isozyme detection with two methods and somewhat worse on ALDH3A1 assay.

  18. Effect of phenolic aldehydes and flavonoids on growth and inactivation of Oenococcus oeni and Lactobacillus hilgardii.

    Science.gov (United States)

    Figueiredo, Ana Rita; Campos, Francisco; de Freitas, Víctor; Hogg, Tim; Couto, José António

    2008-02-01

    The aim of this work was to investigate the effect of wine phenolic aldehydes, flavonoids and tannins on growth and viability of strains of Oenococcus oeni and Lactobacillus hilgardii. Cultures were grown in ethanol-containing MRS/TJ medium supplemented with different concentrations of phenolic aldehydes or flavonoids and monitored spectrophotometrically. The effect of tannins was evaluated by monitoring the progressive inactivation of cells in ethanol-containing phosphate buffer supplemented with grape seed extracts with different molecular weight tannins. Of the phenolic aldehydes tested, sinapaldehyde, coniferaldehyde, p-hydroxybenzaldehyde, 3,4-dihydroxybenzaldehyde and 3,4,5-trihydroxybenzaldehyde significantly inhibited the growth of O. oeni VF, while vanillin and syringaldehyde had no effect at the concentrations tested. Lact. hilgardii 5 was only inhibited by sinapaldehyde and coniferaldehyde. Among the flavonoids, quercetin and kaempferol exerted an inhibitory effect especially on O. oeni VF. Myricetin and the flavan-3-ols studied (catechin and epicatechin) did not affect considerably the growth of both strains. Condensed tannins (particularly tetramers and pentamers) were found to strongly affect cell viability, especially in the case of O. oeni VF. In general, this strain was found to be more sensitive than Lact. hilgardii 5 to the phenolic compounds studied. This work contributes to the knowledge of the effect of different phenolic compounds on the activity of wine lactic acid bacteria, which, especially in the case of aldehydes and of different molecular weight fractions of tannins, is very scarce.

  19. The molecular cloning of dihydroartemisinic aldehyde reductase and its implication in artemisinin biosynthesis in Artemisia annua

    NARCIS (Netherlands)

    Ryden, A.M.; Ruyter-Spira, C.P.; Quax, W.J.; Hiroyuki, O.; Toshiya, M.; Kayser, O.; Bouwmeester, H.J.

    2010-01-01

    A key point in the biosynthesis of the antimalarial drug artemisinin is the formation of dihydroartemisinic aldehyde which represents the key difference between chemotype specific pathways. This key intermediate is the substrate for several competing enzymes, some of which increase the metabolic

  20. Supported Rh-phosphine complex catalysts for continuous gas-phase decarbonylation of aldehydes

    DEFF Research Database (Denmark)

    Malcho, Phillip; Garcia-Suarez, Eduardo J.; Mentzel, Uffe Vie

    2014-01-01

    Heterogeneous silica supported rhodium-phosphine complex catalysts are employed for the first time in the catalytic decarbonylation of aldehydes in continuous gas-phase. The reaction protocol is exemplified for the decarbonylation of p-tolualdehyde to toluene and further extended to other aromatic...

  1. A General and Convenient Method for the Rhodium-Catalyzed Decarbonylation of Aldehydes

    DEFF Research Database (Denmark)

    Kreis, Michael; Palmelund, Anders; Bunch, Lennart

    2006-01-01

    A practical protocol for the decarbonylation of a wide range of aldehydes has been developed by using commercially available RhCl3x3H2O and dppp in a diglyme solution. This method gives rise to decarbonylated products in good to high yield and is particularly useful because of its experimental si...

  2. Palladium-Catalyzed Anti-Markovnikov Oxidation of Allylic Amides to Protected beta-Amino Aldehydes

    NARCIS (Netherlands)

    Dong, Jiajia; Harvey, Emma C.; Fananas-Mastral, Martin; Browne, Wesley R.; Feringa, Bernard

    2014-01-01

    A general method for the preparation of N-protected beta-amino aldehydes from allylic amines or linear allylic alcohols is described. Here the Pd(II)-catalyzed oxidation of N-protected allylic amines with benzoquinone is achieved in tBuOH under ambient conditions with excellent selectivity toward

  3. Reduction of Aldehydes and Ketones to Corresponding Alcohols Using Diammonium Hydrogen Phosphite and Commercial Zinc Dust

    Directory of Open Access Journals (Sweden)

    K. Anil Kumar

    2011-01-01

    Full Text Available A mild and an efficient system has been developed for the reduction of aromatic aldehydes and ketones to their corresponding alcohols in good yield using inexpensive commercial zinc dust as catalyst and diammonium hydrogen phosphite as a hydrogen donor.

  4. Catalytic Oxidation of Lignins into the Aromatic Aldehydes: General Process Trends and Development Prospects

    Science.gov (United States)

    Tarabanko, Valery E.; Tarabanko, Nikolay

    2017-01-01

    This review discusses principal patterns that govern the processes of lignins’ catalytic oxidation into vanillin (3-methoxy-4-hydroxybenzaldehyde) and syringaldehyde (3,5-dimethoxy-4-hydroxybenzaldehyde). It examines the influence of lignin and oxidant nature, temperature, mass transfer, and of other factors on the yield of the aldehydes and the process selectivity. The review reveals that properly organized processes of catalytic oxidation of various lignins are only insignificantly (10–15%) inferior to oxidation by nitrobenzene in terms of yield and selectivity in vanillin and syringaldehyde. Very high consumption of oxygen (and consequentially, of alkali) in the process—over 10 mol per mol of obtained vanillin—is highlighted as an unresolved and unexplored problem: scientific literature reveals almost no studies devoted to the possibilities of decreasing the consumption of oxygen and alkali. Different hypotheses about the mechanism of lignin oxidation into the aromatic aldehydes are discussed, and the mechanism comprising the steps of single-electron oxidation of phenolate anions, and ending with retroaldol reaction of a substituted coniferyl aldehyde was pointed out as the most convincing one. The possibility and development prospects of single-stage oxidative processing of wood into the aromatic aldehydes and cellulose are analyzed. PMID:29140301

  5. Impulsive IR-multiphoton dissociation of acrolein: observation of non-statistical product vibrational excitation in CO ( v=1-12) by time resolved IR fluorescence spectroscopy

    Science.gov (United States)

    Chowdhury, P. K.

    2000-10-01

    On IR-multiphoton excitation, vibrationally highly excited acrolein molecules undergo concerted dissociation generating CO and ethylene. The vibrationally excited products, CO and ethylene, are detected immediately following the CO 2 laser pulse by observing IR fluorescence at 4.7 and 3.2 μm, respectively. The nascent CO is formed with significant vibrational excitation, with a Boltzmann population distribution for v=1-12 levels corresponding to T v=12 950±50 K. The average vibrational energy in the product CO is found to be 26 kcal mol -1, in contrast to its statistical share of 5 kcal mol -1, available from the product energy distribution. The nascent vibrationally excited ethylene either dissociates by absorbing further infrared laser photons from the tail of the CO 2 laser pulse or relaxes by collisional deactivation. Ethylene IR-fluorescence excitation spectrum showed a structure in the quasi-continuum, with a facile resonance at 10.53 μm corresponding to the 10P(14) CO 2 laser line, which explains the higher acetylene yield observed at a higher pressure. A hydrogen atom transfer mechanism followed by C-C impulsive break in the acrolein transition state may be responsible for such non-statistical product energy distribution.

  6. Occupational exposure of aldehydes resulting from the storage of wood pellets.

    Science.gov (United States)

    Rahman, Mohammad Arifur; Rossner, Alan; Hopke, Philip K

    2017-06-01

    An exposure assessment was conducted to investigate the potential for harmful concentrations of airborne short chain aldehydes emitted from recently stored wood pellets. Wood pellets can emit a number of airborne aldehydes include acetaldehyde, formaldehyde, propionaldehyde, butyraldehyde, valeraldehyde, and hexanal. Exposure limits have been set for these compounds since they can result in significant irritation of the upper respiratory system at elevated concentrations. Formaldehyde is a recognized human carcinogen and acetaldehyde is an animal carcinogen. Thus, air sampling was performed in a wood pellet warehouse at a pellet mill, two residential homes with bulk wood pellet storage bins, and in controlled laboratory experiments to evaluate the risk to occupants. Using NIOSH method 2539, sampling was conducted in five locations in the warehouse from April-June 2016 when it contained varying quantities of bagged pellets as well as two homes with ten ton bulk storage bins. The aldehyde concentrations were found to increase with the amount of stored pellets. Airborne concentrations of formaldehyde were as high as 0.45 ppm in the warehouse exceeding the NIOSH REL-C, and ACGIH TLV-C occupational exposure limits (OELs). The concentrations of aldehydes measured in the residential bins were also elevated indicating emissions may raise indoor air quality concerns for occupants. While individual exposures are of concern the combined irritant effect of all the aldehydes is a further raise the concerns for building occupants. To minimize exposure and the risk of adverse health effects to a building's occupants in storage areas with large quantities of pellets, adequate ventilation must be designed into storage areas.

  7. Role and structural characterization of plant aldehyde dehydrogenases from family 2 and family 7.

    Science.gov (United States)

    Končitíková, Radka; Vigouroux, Armelle; Kopečná, Martina; Andree, Tomáš; Bartoš, Jan; Šebela, Marek; Moréra, Solange; Kopečný, David

    2015-05-15

    Aldehyde dehydrogenases (ALDHs) are responsible for oxidation of biogenic aldehyde intermediates as well as for cell detoxification of aldehydes generated during lipid peroxidation. So far, 13 ALDH families have been described in plants. In the present study, we provide a detailed biochemical characterization of plant ALDH2 and ALDH7 families by analysing maize and pea ALDH7 (ZmALDH7 and PsALDH7) and four maize cytosolic ALDH(cALDH)2 isoforms RF2C, RF2D, RF2E and RF2F [the first maize ALDH2 was discovered as a fertility restorer (RF2A)]. We report the crystal structures of ZmALDH7, RF2C and RF2F at high resolution. The ZmALDH7 structure shows that the three conserved residues Glu(120), Arg(300) and Thr(302) in the ALDH7 family are located in the substrate-binding site and are specific to this family. Our kinetic analysis demonstrates that α-aminoadipic semialdehyde, a lysine catabolism intermediate, is the preferred substrate for plant ALDH7. In contrast, aromatic aldehydes including benzaldehyde, anisaldehyde, cinnamaldehyde, coniferaldehyde and sinapaldehyde are the best substrates for cALDH2. In line with these results, the crystal structures of RF2C and RF2F reveal that their substrate-binding sites are similar and are formed by an aromatic cluster mainly composed of phenylalanine residues and several nonpolar residues. Gene expression studies indicate that the RF2C gene, which is strongly expressed in all organs, appears essential, suggesting that the crucial role of the enzyme would certainly be linked to the cell wall formation using aldehydes from phenylpropanoid pathway as substrates. Finally, plant ALDH7 may significantly contribute to osmoprotection because it oxidizes several aminoaldehydes leading to products known as osmolytes.

  8. Cytochrome P450BM-3 reduces aldehydes to alcohols through a direct hydride transfer

    Energy Technology Data Exchange (ETDEWEB)

    Kaspera, Ruediger; Sahele, Tariku; Lakatos, Kyle [Department of Medicinal Chemistry, University of Washington, Box 357610, Seattle, WA 98195-7610 (United States); Totah, Rheem A., E-mail: rtotah@u.washington.edu [Department of Medicinal Chemistry, University of Washington, Box 357610, Seattle, WA 98195-7610 (United States)

    2012-02-17

    Highlights: Black-Right-Pointing-Pointer Cytochrome P450BM-3 reduced aldehydes to alcohols efficiently (k{sub cat} {approx} 25 min{sup -1}). Black-Right-Pointing-Pointer Reduction is a direct hydride transfer from R-NADP{sup 2}H to the carbonyl moiety. Black-Right-Pointing-Pointer P450 domain variants enhance reduction through potential allosteric/redox interactions. Black-Right-Pointing-Pointer Novel reaction will have implications for metabolism of xenobiotics. -- Abstract: Cytochrome P450BM-3 catalyzed the reduction of lipophilic aldehydes to alcohols efficiently. A k{sub cat} of {approx}25 min{sup -1} was obtained for the reduction of methoxy benzaldehyde with wild type P450BM-3 protein which was higher than in the isolated reductase domain (BMR) alone and increased in specific P450-domain variants. The reduction was caused by a direct hydride transfer from preferentially R-NADP{sup 2}H to the carbonyl moiety of the substrate. Weak substrate-P450-binding of the aldehyde, turnover with the reductase domain alone, a deuterium incorporation in the product from NADP{sup 2}H but not D{sub 2}O, and no inhibition by imidazole suggests the reductase domain of P450BM-3 as the potential catalytic site. However, increased aldehyde reduction by P450 domain variants (P450BM-3 F87A T268A) may involve allosteric or redox mechanistic interactions between heme and reductase domains. Th