Reversible Lithium Neurotoxicity: Review of the Literature

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Netto, Ivan

2012-01-01

Objective: Lithium neurotoxicity may be reversible or irreversible. Reversible lithium neurotoxicity has been defined as cases of lithium neurotoxicity in which patients recovered without any permanent neurologic sequelae, even after 2 months of an episode of lithium toxicity. Cases of reversible lithium neurotoxicity differ in clinical presentation from those of irreversible lithium neurotoxicity and have important implications in clinical practice. This review aims to study the clinical presentation of cases of reversible lithium neurotoxicity. Data Sources: A comprehensive electronic search was conducted in the following databases: MEDLINE (PubMed), 1950 to November 2010; PsycINFO, 1967 to November 2010; and SCOPUS (EMBASE), 1950 to November 2010. MEDLINE and PsycINFO were searched by using the OvidSP interface. Study Selection: A combination of the following search terms was used: lithium AND adverse effects AND central nervous system OR neurologic manifestation. Publications cited include articles concerned with reversible lithium neurotoxicity. Data Extraction: The age, sex, clinical features, diagnostic categories, lithium doses, serum lithium levels, precipitating factors, and preventive measures of 52 cases of reversible lithium neurotoxicity were extracted. Data Synthesis: Among the 52 cases of reversible lithium neurotoxicity, patients ranged in age from 10 to 80 years and a greater number were female (P = .008). Most patients had affective disorders, schizoaffective disorders, and/or depression (P lithium levels were less than or equal to 1.5 mEq/L (P lithium, underlying brain pathology, abnormal tissue levels, specific diagnostic categories, and elderly populations were some of the precipitating factors reported for reversible lithium neurotoxicity. The preventive measures were also described. Conclusions: Reversible lithium neurotoxicity presents with a certain clinical profile and precipitating factors for which there are appropriate

Reversible lithium neurotoxicity: review of the literatur.

Science.gov (United States)

Netto, Ivan; Phutane, Vivek H

2012-01-01

Lithium neurotoxicity may be reversible or irreversible. Reversible lithium neurotoxicity has been defined as cases of lithium neurotoxicity in which patients recovered without any permanent neurologic sequelae, even after 2 months of an episode of lithium toxicity. Cases of reversible lithium neurotoxicity differ in clinical presentation from those of irreversible lithium neurotoxicity and have important implications in clinical practice. This review aims to study the clinical presentation of cases of reversible lithium neurotoxicity. A comprehensive electronic search was conducted in the following databases: MEDLINE (PubMed), 1950 to November 2010; PsycINFO, 1967 to November 2010; and SCOPUS (EMBASE), 1950 to November 2010. MEDLINE and PsycINFO were searched by using the OvidSP interface. A combination of the following search terms was used: lithium AND adverse effects AND central nervous system OR neurologic manifestation. Publications cited include articles concerned with reversible lithium neurotoxicity. The age, sex, clinical features, diagnostic categories, lithium doses, serum lithium levels, precipitating factors, and preventive measures of 52 cases of reversible lithium neurotoxicity were extracted. Among the 52 cases of reversible lithium neurotoxicity, patients ranged in age from 10 to 80 years and a greater number were female (P = .008). Most patients had affective disorders, schizoaffective disorders, and/or depression (P lithium levels were less than or equal to 1.5 mEq/L (P lithium, underlying brain pathology, abnormal tissue levels, specific diagnostic categories, and elderly populations were some of the precipitating factors reported for reversible lithium neurotoxicity. The preventive measures were also described. Reversible lithium neurotoxicity presents with a certain clinical profile and precipitating factors for which there are appropriate preventive measures. This recognition will help in early diagnosis and prompt treatment of

Translocation and neurotoxicity of CdTe quantum dots in RMEs motor neurons in nematode Caenorhabditis elegans

International Nuclear Information System (INIS)

Zhao, Yunli; Wang, Xiong; Wu, Qiuli; Li, Yiping; Wang, Dayong

2015-01-01

Graphical abstract: - Highlights: • We investigated in vivo neurotoxicity of CdTe QDs on RMEs motor neurons in C. elegans. • CdTe QDs in the range of μg/L caused neurotoxicity on RMEs motor neurons. • Bioavailability of CdTe QDs may be the primary inducer for CdTe QDs neurotoxicity. • Both oxidative stress and cell identity regulate the CdTe QDs neurotoxicity. • CdTe QDs were translocated and deposited into RMEs motor neurons. - Abstract: We employed Caenorhabditis elegans assay system to investigate in vivo neurotoxicity of CdTe quantum dots (QDs) on RMEs motor neurons, which are involved in controlling foraging behavior, and the underlying mechanism of such neurotoxicity. After prolonged exposure to 0.1–1 μg/L of CdTe QDs, abnormal foraging behavior and deficits in development of RMEs motor neurons were observed. The observed neurotoxicity from CdTe QDs on RMEs motor neurons might be not due to released Cd 2+ . Overexpression of genes encoding Mn-SODs or unc-30 gene controlling cell identity of RMEs neurons prevented neurotoxic effects of CdTe QDs on RMEs motor neurons, suggesting the crucial roles of oxidative stress and cell identity in regulating CdTe QDs neurotoxicity. In nematodes, CdTe QDs could be translocated through intestinal barrier and be deposited in RMEs motor neurons. In contrast, CdTe@ZnS QDs could not be translocated into RMEs motor neurons and therefore, could only moderately accumulated in intestinal cells, suggesting that ZnS coating might reduce neurotoxicity of CdTe QDs on RMEs motor neurons. Therefore, the combinational effects of oxidative stress, cell identity, and bioavailability may contribute greatly to the mechanism of CdTe QDs neurotoxicity on RMEs motor neurons. Our results provide insights into understanding the potential risks of CdTe QDs on the development and function of nervous systems in animals

The neuronal nitric oxide synthase inhibitor, 7-nitroindazole, protects against methamphetamine-induced neurotoxicity in vivo.

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Itzhak, Y; Ali, S F

1996-10-01

The present study was undertaken to investigate whether the relatively selective neuronal nitric oxide synthase (NOS) inhibitor, 7-nitroindazole (7-NI), protects against methamphetamine (METH)-induced neurotoxicity. Male Swiss Webster mice received the following treatments (i.p.; q 3 h x 3): (a) vehicle/saline, (b) 7-NI (25 mg/kg)/saline, (c) vehicle/METH (5 mg/kg), and (d) 7-NI (25 mg/kg)/METH (5 mg/kg). On the second day, groups (a) and (b) received two vehicle injections, and groups (c) and (d) received two 7-NI injections (25 mg/kg, each). Administration of vehicle/METH resulted in 68, 44, and 55% decreases in the concentration of dopamine, 3,4-dihydroxyphenylacetic acid, and homovanillic acid, respectively, and a 48% decrease in the number of [3H]mazindol binding sites in the striatum compared with control values. Treatment with 7-NI (group d) provided full protection against the depletion of dopamine and its metabolites and the loss of dopamine transporter binding sites. Administration of 7-NI/saline (group b) affected neither the tissue concentration of dopamine and its metabolites nor the binding parameters of [3H] mazindol compared with control values. 7-NI had no significant effect on animals' body temperature, and it did not affect METH-induced hyperthermia. These findings indicate a role for nitric oxide in methamphetamine-induced neurotoxicity and also suggest that blockade of NOS may be beneficial for the management of Parkinson's disease.

Novel approach on the risk assessment of oxidized fats and oils for perspectives of food safety and quality. I. Oxidized fats and oils induces neurotoxicity relating pica behavior and hypoactivity.

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Gotoh, N; Watanabe, H; Osato, R; Inagaki, K; Iwasawa, A; Wada, S

2006-04-01

Food poisoning caused by deteriorated fat and oil in instant noodles was first reported in Japan approximately 40 years ago. In these cases, many people developed neurotoxic symptoms such as emesis and discomfort. The degree of oxidation of the fat and oil in the instant noodles that induced food poisoning was at least 100 meq/kg in peroxide value (PV). No general toxicity studies with animals, however, have examined the toxicity of fat and oil oxidized to that extent. In this study, pica behavior, a behavior characterized by eating a nonfood material such as kaolin and that relates to the degree of discomfort in animals, and alterations of locomotor activity of rats eating deteriorated fat and oil were measured. The groups fed fat and oil with at least 138.5 meq/kg PV consumed significantly more kaolin compared to the control group. Furthermore, rats that ate deteriorated fat and oil with at least 107.2 meq/kg PV had significantly decreased locomotor activity compared to control rats. These phenomena suggest that oxidized fat and oil with at least 100 meq/kg PV induce neurotoxicity. The toxicity of oxidized fat and oil has only been addressed using general toxicity tests, but the present results reveal the importance of evaluating toxicity by using other measures.

Translocation and neurotoxicity of CdTe quantum dots in RMEs motor neurons in nematode Caenorhabditis elegans

Energy Technology Data Exchange (ETDEWEB)

Zhao, Yunli; Wang, Xiong; Wu, Qiuli; Li, Yiping; Wang, Dayong, E-mail: dayongw@seu.edu.cn

2015-02-11

Graphical abstract: - Highlights: • We investigated in vivo neurotoxicity of CdTe QDs on RMEs motor neurons in C. elegans. • CdTe QDs in the range of μg/L caused neurotoxicity on RMEs motor neurons. • Bioavailability of CdTe QDs may be the primary inducer for CdTe QDs neurotoxicity. • Both oxidative stress and cell identity regulate the CdTe QDs neurotoxicity. • CdTe QDs were translocated and deposited into RMEs motor neurons. - Abstract: We employed Caenorhabditis elegans assay system to investigate in vivo neurotoxicity of CdTe quantum dots (QDs) on RMEs motor neurons, which are involved in controlling foraging behavior, and the underlying mechanism of such neurotoxicity. After prolonged exposure to 0.1–1 μg/L of CdTe QDs, abnormal foraging behavior and deficits in development of RMEs motor neurons were observed. The observed neurotoxicity from CdTe QDs on RMEs motor neurons might be not due to released Cd{sup 2+}. Overexpression of genes encoding Mn-SODs or unc-30 gene controlling cell identity of RMEs neurons prevented neurotoxic effects of CdTe QDs on RMEs motor neurons, suggesting the crucial roles of oxidative stress and cell identity in regulating CdTe QDs neurotoxicity. In nematodes, CdTe QDs could be translocated through intestinal barrier and be deposited in RMEs motor neurons. In contrast, CdTe@ZnS QDs could not be translocated into RMEs motor neurons and therefore, could only moderately accumulated in intestinal cells, suggesting that ZnS coating might reduce neurotoxicity of CdTe QDs on RMEs motor neurons. Therefore, the combinational effects of oxidative stress, cell identity, and bioavailability may contribute greatly to the mechanism of CdTe QDs neurotoxicity on RMEs motor neurons. Our results provide insights into understanding the potential risks of CdTe QDs on the development and function of nervous systems in animals.

Prophylactic Neuroprotection of Total Glucosides of Paeoniae Radix Alba against Semen Strychni-Induced Neurotoxicity in Rats: Suppressing Oxidative Stress and Reducing the Absorption of Toxic Components.

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Li, Shujuan; Chu, Yanjie; Zhang, Ruowen; Sun, Linjia; Chen, Xiaohui

2018-04-20

Strychnos alkaloids (SAs) are the main toxic constituents in Semen Strychni, a traditional Chinese medicine, which is known for its fatal neurotoxicity. Hence, the present study was carried out to evaluate the neurotoxicity induced by SAs and the pre-protective effects of the total glucosides of Paeoniae Radix Alba (TGP). An SA brain damage model was firstly established. The neurotoxicity induced by SAs and the pre-protective effects of TGP were confirmed by physical and behavioral testing, biochemical assay, and histological examination. Then, a liquid chromatography-tandem mass spectrometry method was developed and validated to investigate the time-course change and distribution of strychnine and brucine (two main SAs) in the brain after oral SA administration with or without TGP pretreatment. Biochemical analysis results indicated that TGP could ameliorate the oxidative stress status caused by SAs. Time-course change and distribution studies demonstrated that strychnine and brucine were rapidly absorbed into the brain, peaked early at 0.5 h, and were mainly located in the hippocampus and cerebellum. TGP showed a pre-protective effect against neurotoxicity by reducing the absorption of toxic alkaloids into the brain. These findings could provide beneficial information in facilitating future studies of Semen Strychni neurotoxicity and developing herbal medicines to alleviate neurotoxicity in the clinic.

Prophylactic Neuroprotection of Total Glucosides of Paeoniae Radix Alba against Semen Strychni-Induced Neurotoxicity in Rats: Suppressing Oxidative Stress and Reducing the Absorption of Toxic Components

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Shujuan Li

2018-04-01

Full Text Available Strychnos alkaloids (SAs are the main toxic constituents in Semen Strychni, a traditional Chinese medicine, which is known for its fatal neurotoxicity. Hence, the present study was carried out to evaluate the neurotoxicity induced by SAs and the pre-protective effects of the total glucosides of Paeoniae Radix Alba (TGP. An SA brain damage model was firstly established. The neurotoxicity induced by SAs and the pre-protective effects of TGP were confirmed by physical and behavioral testing, biochemical assay, and histological examination. Then, a liquid chromatography-tandem mass spectrometry method was developed and validated to investigate the time-course change and distribution of strychnine and brucine (two main SAs in the brain after oral SA administration with or without TGP pretreatment. Biochemical analysis results indicated that TGP could ameliorate the oxidative stress status caused by SAs. Time-course change and distribution studies demonstrated that strychnine and brucine were rapidly absorbed into the brain, peaked early at 0.5 h, and were mainly located in the hippocampus and cerebellum. TGP showed a pre-protective effect against neurotoxicity by reducing the absorption of toxic alkaloids into the brain. These findings could provide beneficial information in facilitating future studies of Semen Strychni neurotoxicity and developing herbal medicines to alleviate neurotoxicity in the clinic.

nNOS inhibitors attenuate methamphetamine-induced dopaminergic neurotoxicity but not hyperthermia in mice.

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Itzhak, Y; Martin, J L; Ail, S F

2000-09-11

Methamphetamine (METH)-induced dopaminergic neurotoxicity is associated with hyperthermia. We investigated the effect of several neuronal nitric oxide synthase (nNOS) inhibitors on METH-induced hyperthermia and striatal dopaminergic neurotoxicity. Administration of METH (5 mg/kg; q. 3 h x 3) to Swiss Webster mice produced marked hyperthermia and 50-60% depletion of striatal dopaminergic markers 72 h after METH administration. Pretreatment with the nNOS inhibitors S-methylthiocitrulline (SMTC; 10 mg/kg) or 3-bromo-7-nitroindazole (3-Br-7-NI; 20 mg/kg) before each METH injection did not affect the persistent hyperthermia produced by METH, but afforded protection against the depletion of dopaminergic markers. A low dose (25 mg/kg) of the nNOS inhibitor 7-nitroindazole (7-NI) did not affect METH-induced hyperthermia, but a high dose (50 mg/kg) produced significant hypothermia. These findings indicate that low dose of selective nNOS inhibitors protect against METH-induced neurotoxicity with no effect on body temperature and support the hypothesis that nitric oxide (NO) and peroxynitrite have a major role in METH-induced dopaminergic neurotoxicity.

Nitric oxide is a mediator of methamphetamine (METH)-induced neurotoxicity. In vitro evidence from primary cultures of mesencephalic cells.

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Sheng, P; Cerruti, C; Ali, S; Cadet, J L

1996-10-31

METH is a monoaminergic toxic that destroys dopamine terminals in vivo. Oxidative mechanisms associated with DA metabolism are thought to play an important role in its toxic effects. These ideas were supported by the demonstration that CuZn-superoxide dismutase (CuZnSOD) transgenic mice were protected against the toxic effects of the drug. In the present study, we sought to determine if nitric oxide (NO) production was also involved in METH-induced neurotoxicity using primary cultures obtained from fetal rat mesencephalon. METH caused dose- and time-dependent cell death in vitro. Blockade of nitric oxide (NO) formation with several nitric oxide (NO) synthase blockers attenuated METH-mediated toxicity. Moreover, inhibition of ADP-ribosylation with nicotinamide and benzamide also provided protection against the toxicity of the drug. These results, together with our previous results in transgenic mice, support a role for free radicals in METH-induced toxic effects.

Sex-, tissue-, and exposure duration-dependent effects of imidacloprid modulated by piperonyl butoxide and menadione in rats. Part I: oxidative and neurotoxic potentials.

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Yardimci, Mustafa; Sevgiler, Yusuf; Rencuzogullari, Eyyup; Arslan, Mehmet; Buyukleyla, Mehmet; Yilmaz, Mehmet

2014-12-01

Earlier research has evidenced the oxidative and neurotoxic potential of imidacloprid, a neonicotinoid insecticide, in different animal species. The primary aim of this study was to determine how metabolic modulators piperonyl butoxide and menadione affect imidacloprid's adverse action in the liver and kidney of Sprague-Dawley rats of both sexes. The animals were exposed to imidacloprid alone (170 mg kg⁻¹) or in combination with piperonyl butoxide (100 mg kg⁻¹) or menadione (25 mg kg⁻¹) for 12 and 24 h. Their liver and kidney homogenates were analysed spectrophotometrically for glutathione peroxidase, glutathione S-transferase, catalase, total cholinesterase specific activities, total glutathione, total protein content, and lipid peroxidation levels. Imidacloprid displayed its prooxidative and neurotoxic effects predominantly in the kidney of male rats after 24 h of exposure. Our findings suggest that the observed differences in prooxidative and neurotoxic potential of imidacloprid could be related to differences in its metabolism between the sexes. Co-exposure (90-min pre-treatment) with piperonyl butoxide or menadione revealed tissue-specific effect of imidacloprid on total cholinesterase activity. Increased cholinesterase activity in the kidney could be an adaptive response to imidacloprid-induced oxidative stress. In the male rat liver, co-exposure with piperonyl butoxide or menadione exacerbated imidacloprid toxicity. In female rats, imidacloprid+menadione co-exposure caused prooxidative effects, while no such effects were observed with imidacloprid alone or menadione alone. In conclusion, sex-, tissue-, and duration-specific effects of imidacloprid are remarkable points in its toxicity.

Pathophysiology of Manganese-Associated Neurotoxicity

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Racette, Brad A.; Aschner, Michael; Guilarte, Tomas R.; Dydak, Ulrike; Criswell, Susan R.; Zheng, Wei

2012-01-01

Conference Summary Manganese (Mn) is a well established neurotoxin associated with specific damage to the basal ganglia in humans. The phenotype associated with Mn neurotoxicity was first described in two workers with occupational exposure to Mn oxide.(Couper, 1837) Although the description did not use modern clinical terminology, a parkinsonian illness characterized by slowness of movement (bradykinesia), masked facies, and gait impairment (postural instability) appears to have predominated. Nearly 100 years later an outbreak of an atypical parkinsonian illness in a Chilean Mn mine provided a phenotypic description of a fulminant neurologic disorder with parkinsonism, dystonia, and neuropsychiatric symptoms.(Rodier J, 1955) Exposures associated with this syndrome were massive and an order of magnitude greater than modern exposures.(Rodier J, 1955; Hobson et al., 2011) The clinical syndrome associated with Mn neurotoxicity has been called manganism. Modern exposures to Mn occur primarily through occupations in the steel industry and welding. These exposures are often chronic and varied, occurring over decades in the healthy workforce. Although the severe neurologic disorder described by Rodier and Couper are no longer seen, several reports have suggested a possible increased risk of neurotoxicity in these workers.(Racette et al., 2005b; Bowler et al., 2007; Harris et al., 2011) Based upon limited prior imaging and pathologic investigations into the pathophysiology of neurotoxicity in Mn exposed workers,(Huang et al., 2003) many investigators have concluded that the syndrome spares the dopamine system distinguishing manganism from Parkinson disease (PD), the most common cause of parkinsonism in the general population, and a disease with characteristic degenerative changes in the dopaminergic system.(Jankovic, 2005) The purpose of this symposium was to highlight recent advances in the understanding of the pathophysiology of Mn associated neurotoxicity from C. elegans

Multiple neurotoxic effects of haloperidol resulting in neuronal death.

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Nasrallah, Henry A; Chen, Alexander T

2017-08-01

Several published studies have reported an association between antipsychotic medications, especially first-generation agents, and a decline in gray matter volume. This prompted us to review the possible neurotoxic mechanisms of first-generation antipsychotics (FGAs), especially haloperidol, which has been widely used over the past several decades. A PubMed search was conducted using the keywords haloperidol, antipsychotic, neurotoxicity, apoptosis, oxidative stress, and neuroplasticity. No restrictions were placed on the date of the articles or language. Studies with a clearly described methodology were included. Animal, cell culture, and human tissue studies were identified. Thirty reports met the criteria for the search. All studies included haloperidol; a few also included other FGAs (fluphenazine and perphenazine) and/or second-generation agents (SGAs) (aripiprazole, paliperidone, and risperidone). A neurotoxic effect of haloperidol and other FGAs was a common theme across all studies. Minimal (mainly at high doses) or no neurotoxic effects were noted in SGAs. A review of the literature suggests that haloperidol exerts measurable neurotoxic effects at all doses via many molecular mechanisms that lead to neuronal death. A similar effect was observed in 2 other FGAs, but the effect in SGAs was much smaller and occurred mainly at high doses. A stronger binding to serotonin 5HT-2A receptors than to dopamine D2 receptors may have a neuroprotective effect among SGAs. Further studies are warranted to confirm these findings.

Maneb and Paraquat-Mediated Neurotoxicity: Involvement of Peroxiredoxin/Thioredoxin System

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Roede, James R.; Hansen, Jason M.; Go, Young-Mi; Jones, Dean P.

2011-01-01

Epidemiological and in vivo studies have demonstrated that exposure to the pesticides paraquat (PQ) and maneb (MB) increase the risk of developing Parkinson’s disease (PD) and cause dopaminergic cell loss, respectively. PQ is a well-recognized cause of oxidative toxicity; therefore, the purpose of this study was to determine if MB potentiates oxidative stress caused by PQ, thus providing a mechanism for enhanced neurotoxicity by the combination. The results show that PQ alone at a moderately toxic dose (20–30% cell death in 24 h) caused increased reactive oxygen species (ROS) generation, oxidation of mitochondrial thioredoxin-2 and peroxiredoxin-3, lesser oxidation of cytoplasmic thioredoxin-1 and peroxiredoxin-1, and no oxidation of cellular GSH/GSSG. In contrast, MB alone at a similar toxic dose resulted in no ROS generation, no oxidation of thioredoxin and peroxiredoxin, and an increase in cellular GSH after 24 h. Together, MB increased GSH and inhibited ROS production and thioredoxin/peroxiredoxin oxidation observed with PQ alone, yet resulted in more extensive (> 50%) cell death. MB treatment resulted in increased abundance of nuclear Nrf2 and mRNA for phase II enzymes under the control of Nrf2, indicating activation of cell protective responses. The results show that MB potentiation of PQ neurotoxicity does not occur by enhancing oxidative stress and suggests that increased toxicity occurs by a combination of divergent mechanisms, perhaps involving alkylation by MB and oxidation by PQ. PMID:21402726

Oral supplements of inulin during gestation offsets rotenone-induced oxidative impairments and neurotoxicity in maternal and prenatal rat brain.

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Krishna, Gokul; Muralidhara

2018-05-25

Environmental insults including pesticide exposure and their entry into the immature brain are of increased concern due to their developmental neurotoxicity. Several lines of evidence suggest that maternal gut microbiota influences in utero fetal development via modulation of host's microbial composition with prebiotics. Hence we examined the hypothesis if inulin (IN) supplements during pregnancy in rats possess the potential to alleviate brain oxidative response and mitochondrial deficits employing a developmental model of rotenone (ROT) neurotoxicity. Initially, pregnant Sprague-Dawley rats were gavaged during gestational days (GDs) 6-19 with 0 (control), 10 (low), 30 (mid) or 50 (high) mg/kg bw/day of ROT to recapitulate developmental effects on general fetotoxicity (assessed by the number of fetuses, fetal body and placental weights), markers of oxidative stress and cholinergic activities in maternal brain regions and whole fetal-brain. Secondly, dams orally supplemented with inulin (2×/day, 2 g/kg/bw) on GD 0-21 were administered ROT (50 mg/kg, GD 6-19). IN supplements increased maternal cecal bacterial numbers that significantly corresponded with improved exploratory-related behavior among ROT administered rats. In addition, IN supplements improved fetal and placental weight on GD 19. IN diminished gestational ROT-induced increased reactive oxygen species levels, protein and lipid peroxidation biomarkers, and cholinesterase activity in maternal brain regions (cortex, cerebellum, and striatum) and fetal brain. Moreover, in the maternal cortex, mitochondrial assessment revealed IN protected against ROT-induced reduction in NADH cytochrome c oxidoreductase and ATPase activities. These data suggest a potential role for indigestible oligosaccharides in reducing oxidative stress-mediated developmental origins of neurodegenerative disorders. Copyright © 2018 Elsevier Masson SAS. All rights reserved.

Neuronal Nitric Oxide Synthase Induction in the Antitumorigenic and Neurotoxic Effects of 2-Methoxyestradiol

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Magdalena Gorska

2014-08-01

Full Text Available Objective: 2-Methoxyestradiol, one of the natural 17β-estradiol derivatives, is a novel, potent anticancer agent currently being evaluated in advanced phases of clinical trials. The main goal of the study was to investigate the anticancer activity of 2-methoxy-estradiol towards osteosarcoma cells and its possible neurodegenerative effects. We used an experimental model of neurotoxicity and anticancer activity of the physiological agent, 2-methoxyestradiol. Thus, we used highly metastatic osteosarcoma 143B and mouse immortalized hippocampal HT22 cell lines. The cells were treated with pharmacological (1 μM, 10 μM concentrations of 2-methoxyestradiol. Experimental: Neuronal nitric oxide synthase and 3-nitrotyrosine protein levels were determined by western blotting. Cell viability and induction of cell death were measured by MTT and PI/Annexin V staining and a DNA fragmentation ELISA kit, respectively. Intracellular levels of nitric oxide were determined by flow cytometry. Results: Here we demonstrated that the signaling pathways of neurodegenerative diseases and cancer may overlap. We presented evidence that 2-methoxyestradiol, in contrast to 17β-estradiol, specifically affects neuronal nitric oxide synthase and augments 3-nitrotyrosine level leading to osteosarcoma and immortalized hippocampal cell death. Conclusions: We report the dual facets of 2-methoxyestradiol, that causes cancer cell death, but on the other hand may play a key role as a neurotoxin.

Neurotoxicity of low-dose repeatedly intranasal instillation of nano- and submicron-sized ferric oxide particles in mice

Energy Technology Data Exchange (ETDEWEB)

Wang Bing; Feng Weiyue, E-mail: fengwy@mail.ihep.ac.cn; Zhu Motao; Wang Yun; Wang Meng [Chinese Academy of Sciences, Laboratory for Bio-Environmental Effects of Nanomaterials and Nanosafety and Key Laboratory of Nuclear Analytical Techniques, Institute of High Energy Physics (China); Gu Yiqun [Maternity Hospital of Haidian District (China); Ouyang Hong; Wang Huajian; Li Ming; Zhao Yuliang, E-mail: zhaoyuliang@mail.ihep.ac.cn; Chai Zhifang [Chinese Academy of Sciences, Laboratory for Bio-Environmental Effects of Nanomaterials and Nanosafety and Key Laboratory of Nuclear Analytical Techniques, Institute of High Energy Physics (China); Wang Haifang [Peking University, College of Chemistry and Molecular Engineering (China)

2009-01-15

Olfactory tract has been demonstrated to be an important portal for inhaled solid nanoparticle transportation into the central nervous system (CNS). We have previously demonstrated that intranasally instilled Fe{sub 2}O{sub 3} nanoparticles could transport into the CNS via olfactory pathway. In this study, we investigated the neurotoxicity and size effect of repeatedly low-dose (130 {mu}g) intranasal exposure of nano- and submicron-sized Fe{sub 2}O{sub 3} particles (21 nm and 280 nm) to mice. The biomarkers of oxidative stress, activity of nitric oxide synthases and release of monoamine neurotransmitter in the brain were studied. Our results showed that significant oxidative stress was induced by the two sizes of Fe{sub 2}O{sub 3} particles. The activities of GSH-Px, Cu,Zn-SOD, and cNOS significantly elevated and the total GSH and GSH/GSSG ratio significantly decreased in the olfactory bulb and hippocampus after the nano- and submicron-sized Fe{sub 2}O{sub 3} particle treatment (p < 0.05). The nano-sized Fe{sub 2}O{sub 3} generally induced greater alteration and more significant dose-effect response than the submicron-sized particle did. Some slight perturbation of monoamine neurotransmitters were found in the hippocampus after exposure to the two sizes of Fe{sub 2}O{sub 3} particle. The TEM image showed that some ultrastructural alterations in nerve cells, including neurodendron degeneration, membranous structure disruption and lysosome increase in the olfactory bulb, slight dilation in the rough endoplasmic reticulum and lysosome increase in the hippocampus were induced by the nano-sized Fe{sub 2}O{sub 3} treatment. In contrast, in the submicron-sized Fe{sub 2}O{sub 3} treated mice, slightly swollen mitochondria and some vacuoles were observed in the olfactory bulb and hippocampus, respectively. These results indicate that intranasal exposure of Fe{sub 2}O{sub 3} nanoparticles could induce more severe oxidative stress and nerve cell damage in the brain than the

Elucidating the neurotoxic effects of MDMA and its analogs.

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Karuppagounder, Senthilkumar S; Bhattacharya, Dwipayan; Ahuja, Manuj; Suppiramaniam, Vishnu; Deruiter, Jack; Clark, Randall; Dhanasekaran, Muralikrishnan

2014-04-17

There is a rapid increase in the use of methylenedioxymethamphetamine (MDMA) and its structural congeners/analogs globally. MDMA and MDMA-analogs have been synthesized illegally in furtive dwellings and are abused due to its addictive potential. Furthermore, MDMA and MDMA-analogs have shown to have induced several adverse effects. Hence, understanding the mechanisms mediating this neurotoxic insult of MDMA-analogs is of immense importance for the public health in the world. We synthesized and investigated the neurotoxic effects of MDMA and its analogs [4-methylenedioxyamphetamine (MDA), 2, 6-methylenedioxyamphetamine (MDMA), and N-ethyl-3, 4-methylenedioxyamphetamine (MDEA)]. The stimulatory or the dopaminergic agonist effects of MDMA and MDMA-analogs were elucidated using the established 6-hydroxydopamine lesioned animal model. Additionally, we also investigated the neurotoxic mechanisms of MDMA and MDMA-analogs on mitochondrial complex-I activity and reactive oxygen species generation. MDMA and MDMA-analogs exhibited stimulatory activity as compared to amphetamines and also induced several behavioral changes in the rodents. MDMA and MDMA-analogs enhanced the reactive oxygen generation and inhibited mitochondrial complex-I activity which can lead to neurodegeneration. Hence the mechanism of neurotoxicity, MDMA and MDMA-analogs can enhance the release of monoamines, alter the monoaminergic neurotransmission, and augment oxidative stress and mitochondrial abnormalities leading to neurotoxicity. Thus, our study will help in developing effective pharmacological and therapeutic approaches for the treatment of MDMA and MDMA-analog abuse. Copyright © 2014 Elsevier Inc. All rights reserved.

THC Prevents MDMA Neurotoxicity in Mice.

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Clara Touriño

2010-02-01

Full Text Available The majority of MDMA (ecstasy recreational users also consume cannabis. Despite the rewarding effects that both drugs have, they induce several opposite pharmacological responses. MDMA causes hyperthermia, oxidative stress and neuronal damage, especially at warm ambient temperature. However, THC, the main psychoactive compound of cannabis, produces hypothermic, anti-inflammatory and antioxidant effects. Therefore, THC may have a neuroprotective effect against MDMA-induced neurotoxicity. Mice receiving a neurotoxic regimen of MDMA (20 mg/kg x 4 were pretreated with THC (3 mg/kg x 4 at room (21 degrees C and at warm (26 degrees C temperature, and body temperature, striatal glial activation and DA terminal loss were assessed. To find out the mechanisms by which THC may prevent MDMA hyperthermia and neurotoxicity, the same procedure was carried out in animals pretreated with the CB(1 receptor antagonist AM251 and the CB(2 receptor antagonist AM630, as well as in CB(1, CB(2 and CB(1/CB(2 deficient mice. THC prevented MDMA-induced-hyperthermia and glial activation in animals housed at both room and warm temperature. Surprisingly, MDMA-induced DA terminal loss was only observed in animals housed at warm but not at room temperature, and this neurotoxic effect was reversed by THC administration. However, THC did not prevent MDMA-induced hyperthermia, glial activation, and DA terminal loss in animals treated with the CB(1 receptor antagonist AM251, neither in CB(1 and CB(1/CB(2 knockout mice. On the other hand, THC prevented MDMA-induced hyperthermia and DA terminal loss, but only partially suppressed glial activation in animals treated with the CB(2 cannabinoid antagonist and in CB(2 knockout animals. Our results indicate that THC protects against MDMA neurotoxicity, and suggest that these neuroprotective actions are primarily mediated by the reduction of hyperthermia through the activation of CB(1 receptor, although CB(2 receptors may also contribute to

Mitochondrial dysfunction contribute to diabetic neurotoxicity induced by streptozocin in mice: protective effect of Urtica dioica and pioglitazone.

Science.gov (United States)

Shokrzadeh, Mohammad; Mirshafa, Atefeh; Yekta Moghaddam, Niusha; Birjandian, Behnoosh; Shaki, Fatemeh

2018-04-18

Uncontrolled chronic hyperglycemia in diabetic patients could result in various complications, including neurotoxicity. Urtica dioica L. (UD) is known for its hypoglycemic and antioxidant effects. In this study, we evaluated the efficacy of UD and pioglitazone (PIO) in reduction of neurotoxicity and oxidative stress in streptozocin-induced diabetic mice. Male mice were divided into seven groups: control, diabetic, dimethyl sulfoxide-treated control, PIO-treated, UD-treated, UD-PIO-treated, and vitamin E-treated. For induction of diabetes, streptozocin was injected in a single dose (65 mg/kg, i.p.). All treatments were performed for 5 weeks. Neurotoxicity was evaluated through hot plate and formalin test. Then, animals were killed, brain tissue was separated and the mitochondrial fraction was isolated with different centrifuge technique. Also, oxidative stress markers (reactive oxygen species, lipid peroxidation, protein carbonyl, glutathione) were measured in brain. Mitochondrial function was evaluated by MTT test in brain isolated mitochondria. Elevation of oxidative stress markers and mitochondrial damage were observed in diabetic mice compared to control group. Administration of PIO and UD ameliorated the oxidative stress and mitochondrial damage (p < 0.05) in diabetic mice. Also increase in pain score was shown in diabetic mice that treatment with UD and PIO diminished elevation of pain score in diabetic mice. Interestingly, simultaneous administration of PIO and UD showed synergism effect in attenuation of oxidative stress and hyperglycemia. UD showed a therapeutic potential for the attenuation of oxidative stress and diabetes-induced hyperglycemia that can be considered as co-treatment in treatment of diabetic neurotoxicity.

Getting to NO Alzheimer’s Disease: Neuroprotection versus Neurotoxicity Mediated by Nitric Oxide

Directory of Open Access Journals (Sweden)

Rachelle Balez

2016-01-01

Full Text Available Alzheimer’s disease (AD is a neurodegenerative disorder involving the loss of neurons in the brain which leads to progressive memory loss and behavioral changes. To date, there are only limited medications for AD and no known cure. Nitric oxide (NO has long been considered part of the neurotoxic insult caused by neuroinflammation in the Alzheimer’s brain. However, focusing on early developments, prior to the appearance of cognitive symptoms, is changing that perception. This has highlighted a compensatory, neuroprotective role for NO that protects synapses by increasing neuronal excitability. A potential mechanism for augmentation of excitability by NO is via modulation of voltage-gated potassium channel activity (Kv7 and Kv2. Identification of the ionic mechanisms and signaling pathways that mediate this protection is an important next step for the field. Harnessing the protective role of NO and related signaling pathways could provide a therapeutic avenue that prevents synapse loss early in disease.

L-Ascorbate Protects Against Methamphetamine-Induced Neurotoxicity of Cortical Cells via Inhibiting Oxidative Stress, Autophagy, and Apoptosis.

Science.gov (United States)

Huang, Ya-Ni; Yang, Ling-Yu; Wang, Jing-Ya; Lai, Chien-Cheng; Chiu, Chien-Tsai; Wang, Jia-Yi

2017-01-01

Methamphetamine (METH)-induced cell death contributes to the pathogenesis of neurotoxicity; however, the relative roles of oxidative stress, apoptosis, and autophagy remain unclear. L-Ascorbate, also called vitamin (Vit.) C, confers partial protection against METH neurotoxicity via induction of heme oxygenase-1. We further investigated the role of Vit. C in METH-induced oxidative stress, apoptosis, and autophagy in cortical cells. Exposure to lower concentrations (0.1, 0.5, 1 mM) of METH had insignificant effects on ROS production, whereas cells exposed to 5 mM METH exhibited ROS production in a time-dependent manner. We confirmed METH-induced apoptosis (by nuclear morphology revealed by Hoechst 33258 staining and Western blot showing the protein levels of pro-caspase 3 and cleaved caspase 3) and autophagy (by Western blot showing the protein levels of Belin-1 and conversion of microtubule-associated light chain (LC)3-I to LC3-II and autophagosome staining by monodansylcadaverine). The apoptosis as revealed by cleaved caspase-3 expression marked an increase at 18 h after METH exposure while both autophagic markers, Beclin 1 and LC3-II, marked an increase in cells exposed to METH for 6 and 24 h, respectively. Treating cells with Vit. C 30 min before METH exposure time-dependently attenuated the production of ROS. Vitamin C also attenuated METH-induced Beclin 1 and LC3-II expression and METH toxicity. Treatment of cells with Vit. C before METH exposure attenuated the expression of cleaved caspase-3 and reduced the number of METH-induced apoptotic cells. We suggest that the protective effect of Vit. C against METH toxicity might be through attenuation of ROS production, autophagy, and apoptosis.

Antioxidant and neuroprotective effects of Scrophularia striata extract against oxidative stress-induced neurotoxicity.

Science.gov (United States)

Azadmehr, Abbas; Oghyanous, Keyvan Alizadeh; Hajiaghaee, Reza; Amirghofran, Zahra; Azadbakht, Mohammad

2013-11-01

In this study, the neuroprotective effect of Scrophularia striata Boiss (Scrophulariaceae) extract, a plant growing in northeastern of Iran, against oxidative stress-induced neurocytotoxicity in PC12 was evaluated. The PC12 cell line pretreated with different concentrations (10, 50, 100, and 200 μg/ml) of the extract and then treated with H2O2 to induce oxidative stress and neurotoxicity. Survival of the cells, reactive oxygen species (ROS) generation, and apoptosis were measured using MTT assay, fluorescent probe 2',7'-dichlorofluorescein diacetate, and annexin V/propidium iodide, respectively. Moreover, the 2,2-diphenyl-1-picryl-hydrazyl (DPPH) was used to evaluate the antioxidant capacity of the plant extract. Phytochemical assay by thin layer chromatography showed that the main components, including phenolic compounds, phenyl propanoids and flavonoids, were presented in the S. striata extract. The extract in concentrations of 50-200 μg/ml protected PC12 cells from H2O2-induced toxicity. The survival of the cells at concentration of 200 μg/ml was 64 % compared to that of H2O2 alone-treated cells (48 %) (p extract also dose-dependently reduced intracellular ROS production (p extract showed antioxidative effects and decreased apoptotic cells. Collectively, these findings indicated the ability of S. striata to decrease ROS generation and cell apoptosis and also suggest the presence of the neuroprotective agents in this plant.

Evidence for hydroxyl radical scavenging action of nitric oxide donors in the protection against 1-methyl-4-phenylpyridinium-induced neurotoxicity in rats.

Science.gov (United States)

Banerjee, Rebecca; Saravanan, Karuppagounder S; Thomas, Bobby; Sindhu, Kizhake M; Mohanakumar, Kochupurackal P

2008-06-01

In the present study we provide evidence for hydroxyl radical (*OH) scavenging action of nitric oxide (NO*), and subsequent dopaminergic neuroprotection in a hemiparkinsonian rat model. Reactive oxygen species are strongly implicated in the nigrostriatal dopaminergic neurotoxicity caused by the parkinsonian neurotoxin, 1-methyl-4-phenylpyridinium (MPP+). Since the role of this free radical as a neurotoxicant or neuroprotectant is debatable, we investigated the effects of some of the NO* donors such as S-nitroso-N-acetylpenicillamine (SNAP), 3-morpholinosydnonimine hydrochloride (SIN-1), sodium nitroprusside (SNP) and nitroglycerin (NG) on in vitro *OH generation in a Fenton-like reaction involving ferrous citrate, as well as in MPP+-induced *OH production in the mitochondria. We also tested whether co-administration of NO* donor and MPP+ could protect against MPP+-induced dopaminergic neurotoxicity in rats. While NG, SNAP and SIN-1 attenuated MPP+-induced *OH generation in the mitochondria, and in a Fenton-like reaction, SNP caused up to 18-fold increase in *OH production in the latter reaction. Striatal dopaminergic depletion following intranigral infusion of MPP+ in rats was significantly attenuated by NG, SNAP and SIN-1, but not by SNP. Solutions of NG, SNAP and SIN-1, exposed to air for 48 h to remove NO*, when administered similarly failed to attenuate MPP+-induced neurotoxicity in vivo. Conversely, long-time air-exposed SNP solution when administered in rats intranigrally, caused a dose-dependent depletion of the striatal dopamine. These results confirm the involvement of *OH in the nigrostriatal degeneration caused by MPP+, indicate the *OH scavenging ability of NO*, and demonstrate protection by NO* donors against MPP+-induced dopaminergic neurotoxicity in rats.

Mechanisms underlying the neurotoxicity induced by glyphosate-based herbicide in immature rat hippocampus: Involvement of glutamate excitotoxicity

International Nuclear Information System (INIS)

Cattani, Daiane; Oliveira Cavalli, Liz Vera Lúcia de; Heinz Rieg, Carla Elise; Domingues, Juliana Tonietto; Dal-Cim, Tharine; Tasca, Carla Inês; Mena Barreto Silva, Fátima Regina; Zamoner, Ariane

2014-01-01

Graphical abstract: - Highlights: • Roundup ® induces Ca 2+ influx through L-VDCC and NMDA receptor activation. • The mechanisms underlying Roundup ® neurotoxicity involve glutamatergic excitotoxicity. • Kinase pathways participate in Roundup ® -induced neural toxicity. • Roundup ® alters glutamate uptake, release and metabolism in hippocampal cells. - Abstract: Previous studies demonstrate that glyphosate exposure is associated with oxidative damage and neurotoxicity. Therefore, the mechanism of glyphosate-induced neurotoxic effects needs to be determined. The aim of this study was to investigate whether Roundup ® (a glyphosate-based herbicide) leads to neurotoxicity in hippocampus of immature rats following acute (30 min) and chronic (pregnancy and lactation) pesticide exposure. Maternal exposure to pesticide was undertaken by treating dams orally with 1% Roundup ® (0.38% glyphosate) during pregnancy and lactation (till 15-day-old). Hippocampal slices from 15 day old rats were acutely exposed to Roundup ® (0.00005–0.1%) during 30 min and experiments were carried out to determine whether glyphosate affects 45 Ca 2+ influx and cell viability. Moreover, we investigated the pesticide effects on oxidative stress parameters, 14 C-α-methyl-amino-isobutyric acid ( 14 C-MeAIB) accumulation, as well as glutamate uptake, release and metabolism. Results showed that acute exposure to Roundup ® (30 min) increases 45 Ca 2+ influx by activating NMDA receptors and voltage-dependent Ca 2+ channels, leading to oxidative stress and neural cell death. The mechanisms underlying Roundup ® -induced neurotoxicity also involve the activation of CaMKII and ERK. Moreover, acute exposure to Roundup ® increased 3 H-glutamate released into the synaptic cleft, decreased GSH content and increased the lipoperoxidation, characterizing excitotoxicity and oxidative damage. We also observed that both acute and chronic exposure to Roundup ® decreased 3 H-glutamate uptake and

Electron uptake by iron-oxidizing phototrophic bacteria

Energy Technology Data Exchange (ETDEWEB)

Bose, A; Gardel, EJ; Vidoudez, C; Parra, EA; Girguis, PR

2014-02-26

Oxidation-reduction reactions underlie energy generation in nearly all life forms. Although most organisms use soluble oxidants and reductants, some microbes can access solid-phase materials as electron-acceptors or -donors via extracellular electron transfer. Many studies have focused on the reduction of solid-phase oxidants. Far less is known about electron uptake via microbial extracellular electron transfer, and almost nothing is known about the associated mechanisms. Here we show that the iron-oxidizing photoautotroph Rhodopseudomonas palustris TIE-1 accepts electrons from a poised electrode, with carbon dioxide as the sole carbon source/electron acceptor. Both electron uptake and ruBisCo form I expression are stimulated by light. Electron uptake also occurs in the dark, uncoupled from photosynthesis. Notably, the pioABC operon, which encodes a protein system essential for photoautotrophic growth by ferrous iron oxidation, influences electron uptake. These data reveal a previously unknown metabolic versatility of photoferrotrophs to use extracellular electron transfer for electron uptake.

Adaptive oxide electronics: A review

Science.gov (United States)

Ha, Sieu D.; Ramanathan, Shriram

2011-10-01

Novel information processing techniques are being actively explored to overcome fundamental limitations associated with CMOS scaling. A new paradigm of adaptive electronic devices is emerging that may reshape the frontiers of electronics and enable new modalities. Creating systems that can learn and adapt to various inputs has generally been a complex algorithm problem in information science, albeit with wide-ranging and powerful applications from medical diagnosis to control systems. Recent work in oxide electronics suggests that it may be plausible to implement such systems at the device level, thereby drastically increasing computational density and power efficiency and expanding the potential for electronics beyond Boolean computation. Intriguing possibilities of adaptive electronics include fabrication of devices that mimic human brain functionality: the strengthening and weakening of synapses emulated by electrically, magnetically, thermally, or optically tunable properties of materials.In this review, we detail materials and device physics studies on functional metal oxides that may be utilized for adaptive electronics. It has been shown that properties, such as resistivity, polarization, and magnetization, of many oxides can be modified electrically in a non-volatile manner, suggesting that these materials respond to electrical stimulus similarly as a neural synapse. We discuss what device characteristics will likely be relevant for integration into adaptive platforms and then survey a variety of oxides with respect to these properties, such as, but not limited to, TaOx, SrTiO3, and Bi4-xLaxTi3O12. The physical mechanisms in each case are detailed and analyzed within the framework of adaptive electronics. We then review theoretically formulated and current experimentally realized adaptive devices with functional oxides, such as self-programmable logic and neuromorphic circuits. Finally, we speculate on what advances in materials physics and engineering may

Comprehensive neurotoxicity assessment

NARCIS (Netherlands)

Kulig, B.M.

1996-01-01

Significant progress has been made in recent years in terms of both the conceptualization of neurotoxicity assessment strategies as well as in the development of behavioral techniques for evaluating neurotoxic exposures. A tiered approach, for example, has been advocated as an assessment strategy in

Oral intake of hydrogen-rich water ameliorated chlorpyrifos-induced neurotoxicity in rats

Energy Technology Data Exchange (ETDEWEB)

Wang, Tingting; Zhao, Ling; Liu, Mengyu; Xie, Fei; Ma, Xuemei, E-mail: xmma@bjut.edu.cn; Zhao, Pengxiang; Liu, Yunqi; Li, Jiala; Wang, Minglian; Yang, Zhaona; Zhang, Yutong

2014-10-01

Chronic exposure to low-levels of organophosphate (OP) compounds, such as chlorpyrifos (CPF), induces oxidative stress and could be related to neurological disorders. Hydrogen has been identified as a novel antioxidant which could selectively scavenge hydroxyl radicals. We explore whether intake of hydrogen-rich water (HRW) can protect Wistar rats from CPF-induced neurotoxicity. Rats were gavaged daily with 6.75 mg/kg body weight (1/20 LD{sub 50}) of CPF and given HRW by oral intake. Nissl staining and electron microscopy results indicated that HRW intake had protective effects on the CPF-induced damage of hippocampal neurons and neuronal mitochondria. Immunostaining results showed that the increased glial fibrillary acidic protein (GFAP) expression in astrocytes induced by CPF exposure can be ameliorated by HRW intake. Moreover, HRW intake also attenuated CPF-induced oxidative stress as evidenced by enhanced level of MDA, accompanied by an increase in GSH level and SOD and CAT activity. Acetylcholinesterase (AChE) activity tests showed significant decrease in brain AChE activity after CPF exposure, and this effect can be ameliorated by HRW intake. An in vitro study demonstrated that AChE activity was more intense in HRW than in normal water with or without chlorpyrifos-oxon (CPO), the metabolically-activated form of CPF. These observations suggest that HRW intake can protect rats from CPF-induced neurotoxicity, and the protective effects of hydrogen may be mediated by regulating the oxidant and antioxidant status of rats. Furthermore, this work defines a novel mechanism of biological activity of hydrogen by directly increasing the AChE activity. - Highlights: • Hydrogen molecules protect rats from CPF-induced damage of hippocampal neurons. • The increased GFAP expression induced by CPF can also be ameliorated by hydrogen. • Hydrogen molecules attenuated the increase in CPF-induced oxidative stress. • Hydrogen molecules attenuated AChE inhibition in vivo

Oral intake of hydrogen-rich water ameliorated chlorpyrifos-induced neurotoxicity in rats

International Nuclear Information System (INIS)

Wang, Tingting; Zhao, Ling; Liu, Mengyu; Xie, Fei; Ma, Xuemei; Zhao, Pengxiang; Liu, Yunqi; Li, Jiala; Wang, Minglian; Yang, Zhaona; Zhang, Yutong

2014-01-01

Chronic exposure to low-levels of organophosphate (OP) compounds, such as chlorpyrifos (CPF), induces oxidative stress and could be related to neurological disorders. Hydrogen has been identified as a novel antioxidant which could selectively scavenge hydroxyl radicals. We explore whether intake of hydrogen-rich water (HRW) can protect Wistar rats from CPF-induced neurotoxicity. Rats were gavaged daily with 6.75 mg/kg body weight (1/20 LD 50 ) of CPF and given HRW by oral intake. Nissl staining and electron microscopy results indicated that HRW intake had protective effects on the CPF-induced damage of hippocampal neurons and neuronal mitochondria. Immunostaining results showed that the increased glial fibrillary acidic protein (GFAP) expression in astrocytes induced by CPF exposure can be ameliorated by HRW intake. Moreover, HRW intake also attenuated CPF-induced oxidative stress as evidenced by enhanced level of MDA, accompanied by an increase in GSH level and SOD and CAT activity. Acetylcholinesterase (AChE) activity tests showed significant decrease in brain AChE activity after CPF exposure, and this effect can be ameliorated by HRW intake. An in vitro study demonstrated that AChE activity was more intense in HRW than in normal water with or without chlorpyrifos-oxon (CPO), the metabolically-activated form of CPF. These observations suggest that HRW intake can protect rats from CPF-induced neurotoxicity, and the protective effects of hydrogen may be mediated by regulating the oxidant and antioxidant status of rats. Furthermore, this work defines a novel mechanism of biological activity of hydrogen by directly increasing the AChE activity. - Highlights: • Hydrogen molecules protect rats from CPF-induced damage of hippocampal neurons. • The increased GFAP expression induced by CPF can also be ameliorated by hydrogen. • Hydrogen molecules attenuated the increase in CPF-induced oxidative stress. • Hydrogen molecules attenuated AChE inhibition in vivo and in

The 2016 oxide electronic materials and oxide interfaces roadmap

DEFF Research Database (Denmark)

Lorenz, M.; Rao, M. S. Ramachandra; Venkatesan, T.

2016-01-01

of these materials to understand the tunability of their properties and the novel properties that evolve due to their nanostructured nature is another facet of the challenge. The research related to the oxide electronic field is at an impressionable stage, and this has motivated us to contribute with a roadmap......, Pentcheva, and Gegenwart. Finally, Miletto Granozio presents the European action ‘towards oxide-based electronics’ which develops an oxide electronics roadmap with emphasis on future nonvolatile memories and the required technologies.In summary, we do hope that this oxide roadmap appears as an interesting...

Prenatal exposure to nanosized zinc oxide in rats: neurotoxicity and postnatal impaired learning and memory ability.

Science.gov (United States)

Xiaoli, Feng; Junrong, Wu; Xuan, Lai; Yanli, Zhang; Limin, Wei; Jia, Liu; Longquan, Shao

2017-04-01

To examine the neurotoxicity of prenatal exposure to ZnO nanoparticles on rat offspring. Pregnant Sprague-Dawley rats were exposed to ZnO nanoparticles (NPs) by gavage. Toxicity was assessed including zinc biodistribution, cerebral histopathology, antioxidant status and learning and memory capability. A significantly elevated concentration of zinc was detected in offspring brains. Transmission electron microscope observations showed abnormal neuron ultrastructures. Histopathologic changes such as decreased proliferation and higher apoptotic death were observed. An obvious imbalanced antioxidant status occurred in brains. Adult experimental offspring exhibited impaired learning and memory behavior in the Morris water maze test compared with control groups. These adverse effects on offspring brain may cause impaired learning and memory capabilities in adulthood, particularly in female rats.

Optical properties and electronic transitions of zinc oxide, ferric oxide, cerium oxide, and samarium oxide in the ultraviolet and extreme ultraviolet

DEFF Research Database (Denmark)

Pauly, N; Yubero, F; Espinós, J P

2017-01-01

Optical properties and electronic transitions of four oxides, namely zinc oxide, ferric oxide, cerium oxide, and samarium oxide, are determined in the ultraviolet and extreme ultraviolet by reflection electron energy loss spectroscopy using primary electron energies in the range 0.3-2.0 ke...

Transparent Oxide Semiconductors for Emerging Electronics

KAUST Repository

Caraveo-Frescas, Jesus Alfonso

2013-01-01

Transparent oxide electronics have emerged as promising materials to shape the future of electronics. While several n-type oxides have been already studied and demonstrated feasibility to be used as active materials in thin film transistors, high

Unraveling the neurotoxicity of titanium dioxide nanoparticles: focusing on molecular mechanisms

Directory of Open Access Journals (Sweden)

Bin Song

2016-04-01

Full Text Available Titanium dioxide nanoparticles (TiO2 NPs possess unique characteristics and are widely used in many fields. Numerous in vivo studies, exposing experimental animals to these NPs through systematic administration, have suggested that TiO2 NPs can accumulate in the brain and induce brain dysfunction. Nevertheless, the exact mechanisms underlying the neurotoxicity of TiO2 NPs remain unclear. However, we have concluded from previous studies that these mechanisms mainly consist of oxidative stress (OS, apoptosis, inflammatory response, genotoxicity, and direct impairment of cell components. Meanwhile, other factors such as disturbed distributions of trace elements, disrupted signaling pathways, dysregulated neurotransmitters and synaptic plasticity have also been shown to contribute to neurotoxicity of TiO2 NPs. Recently, studies on autophagy and DNA methylation have shed some light on possible mechanisms of nanotoxicity. Therefore, we offer a new perspective that autophagy and DNA methylation could contribute to neurotoxicity of TiO2 NPs. Undoubtedly, more studies are needed to test this idea in the future. In short, to fully understand the health threats posed by TiO2 NPs and to improve the bio-safety of TiO2 NPs-based products, the neurotoxicity of TiO2 NPs must be investigated comprehensively through studying every possible molecular mechanism.

Antioxidant potential properties of mushroom extract (Agaricus bisporus) against aluminum-induced neurotoxicity in rat brain.

Science.gov (United States)

Waly, Mostafa I; Guizani, Nejib

2014-09-01

Aluminum (Al) is an environmental toxin that induces oxidative stress in neuronal cells. Mushroom cultivar extract (MCE) acted as a potent antioxidant agent and protects against cellular oxidative stress in human cultured neuronal cells. This study aimed to investigate the neuroprotective effect of MCE against Al-induced neurotoxicity in rat brain. Forty Sprague-Dawley rats were divided into 4 groups (10 rats per group), control group, MCE-fed group, Al-administered group and MCE/Al-treated group. Animals were continuously fed ad-libitum their specific diets for 4 weeks. At the end of the experiment, all rats were sacrificed and the brain tissues were homogenized and examined for biochemical measurements of neurocellular oxidative stress indices [glutathione (GSH), Total Antioxidant Capacity (TAC), antioxidant enzymes and oxidized dichlorofluorescein (DCF)]. Al-administration caused inhibition of antioxidant enzymes and a significant decrease in GSH and TAC levels, meanwhile it positively increased cellular oxidized DCF level, as well as Al concentration in brain tissues. Feeding animals with MCE had completely offset the Al-induced oxidative stress and significantly restrict the Al accumulation in brain tissues of Al-administered rats. The results obtained suggest that MCE acted as a potent dietary antioxidant and protects against Al-mediated neurotoxicity, by abrogating neuronal oxidative stress.

Biomarkers of adult and developmental neurotoxicity

International Nuclear Information System (INIS)

Slikker, William; Bowyer, John F.

2005-01-01

Neurotoxicity may be defined as any adverse effect on the structure or function of the central and/or peripheral nervous system by a biological, chemical, or physical agent. A multidisciplinary approach is necessary to assess adult and developmental neurotoxicity due to the complex and diverse functions of the nervous system. The overall strategy for understanding developmental neurotoxicity is based on two assumptions: (1) significant differences in the adult versus the developing nervous system susceptibility to neurotoxicity exist and they are often developmental stage dependent; (2) a multidisciplinary approach using neurobiological, including gene expression assays, neurophysiological, neuropathological, and behavioral function is necessary for a precise assessment of neurotoxicity. Application of genomic approaches to developmental studies must use the same criteria for evaluating microarray studies as those in adults including consideration of reproducibility, statistical analysis, homogenous cell populations, and confirmation with non-array methods. A study using amphetamine to induce neurotoxicity supports the following: (1) gene expression data can help define neurotoxic mechanism(s) (2) gene expression changes can be useful biomarkers of effect, and (3) the site-selective nature of gene expression in the nervous system may mandate assessment of selective cell populations

Electron donating and acid-base properties of cerium oxide and its mixed oxides with alumina

International Nuclear Information System (INIS)

Sugunan, S.; Jalaja, J.M.

1994-01-01

The electron donating properties of cerium oxide activated at 300, 500 and 800 degC and of its mixed oxides with alumina were examined based on the adsorption of electron acceptors exhibiting different electron affinities. The surface acidity/basicity of the oxides was determined by titrimetry; the H 0,max values are given. The limit of electron transfer from the oxide surface lies within the region of 1.77 and 2.40 eV in terms of the electron affinity of the electron acceptor. Cerium oxide promotes the electron donor nature of alumina while leaving the limit of electron transfer unchanged. 2 tabs., 4 figs., 13 refs

Neuronal Nicotinic Receptors as New Targets for Amphetamine-Induced Oxidative Damage and Neurotoxicity

Directory of Open Access Journals (Sweden)

Elena Escubedo

2011-06-01

Full Text Available Amphetamine derivatives such as methamphetamine (METH and 3,4-methylenedioxymethamphetamine (MDMA, “ecstasy” are widely abused drugs in a recreational context. This has led to concern because of the evidence that they are neurotoxic in animal models and cognitive impairments have been described in heavy abusers. The main targets of these drugs are plasmalemmal and vesicular monoamine transporters, leading to reverse transport and increased monoamine efflux to the synapse. As far as neurotoxicity is concerned, increased reactive oxygen species (ROS production seems to be one of the main causes. Recent research has demonstrated that blockade of a7 nicotinic acetylcholine receptors (nAChR inhibits METH- and MDMA-induced ROS production in striatal synaptosomes which is dependent on calcium and on NO-synthase activation. Moreover, a7 nAChR antagonists (methyllycaconitine and memantine attenuated in vivo the neurotoxicity induced by METH and MDMA, and memantine prevented the cognitive impairment induced by these drugs. Radioligand binding experiments demonstrated that both drugs have affinity to a7 and heteromeric nAChR, with MDMA showing lower Ki values, while fluorescence calcium experiments indicated that MDMA behaves as a partial agonist on a7 and as an antagonist on heteromeric nAChR. Sustained Ca increase led to calpain and caspase-3 activation. In addition, modulatory effects of MDMA on a7 and heteromeric nAChR populations have been found.

Effects of interfacial Fe electronic structures on magnetic and electronic transport properties in oxide/NiFe/oxide heterostructures

International Nuclear Information System (INIS)

Liu, Qianqian; Chen, Xi; Zhang, Jing-Yan; Yang, Meiyin; Li, Xu-Jing; Jiang, Shao-Long; Liu, Yi-Wei; Cao, Yi; Wu, Zheng-Long; Feng, Chun; Ding, Lei; Yu, Guang-Hua

2015-01-01

Highlights: • The magnetic and transport properties of oxide/NiFe/oxide films were studied. • The oxide (SiO 2 , MgO and HfO 2 ) has different elemental electronegativity. • Redox reaction at different NiFe/oxide interface is dependent on the oxide layer. • Different interfacial electronic structures shown by XPS influence the properties. - Abstract: We report that the magnetic and electronic transport properties in oxide/NiFe(2 nm)/oxide film (oxide = SiO 2 , MgO or HfO 2 ) are strongly influenced by the electronic structure of NiFe/oxide interface. Magnetic measurements show that there exist magnetic dead layers in the SiO 2 sandwiched film and MgO sandwiched film, whereas there is no magnetic dead layer in the HfO 2 sandwiched film. Furthermore, in the ultrathin SiO 2 sandwiched film no magnetoresistance (MR) is detected, while in the ultrathin MgO sandwiched film and HfO 2 sandwiched film the MR ratios reach 0.35% and 0.88%, respectively. The investigation by X-ray photoelectron spectroscopy reveals that the distinct interfacial redox reactions, which are dependent on the oxide layers, lead to the variation of magnetic and transport properties in different oxide/NiFe/oxide heterostructures

Electron trapping during irradiation in reoxidized nitrided oxide

International Nuclear Information System (INIS)

Mallik, A.; Vasi, J.; Chandorkar, A.N.

1993-01-01

Isochronal detrapping experiments have been performed following irradiation under different gate biases in reoxidized nitrided oxide (RNO) MOS capacitors. These show electron trapping by the nitridation-induced electron traps at low oxide fields during irradiation. A difference in the detrapping behavior of trapped holes and electrons is observed, with trapped holes being detrapped at relatively lower temperatures compared to trapped electrons. Electron trapping shows a strong dependence on tile magnitude of the applied gate bias during irradiation but is independent of its polarity. Conventional oxide devices, as expected, do not show any electron trapping during irradiation by the native electron traps. Finally, a comparison of the isochronal detrapping behavior following irradiation and following avalanche injection of electrons has been made to estimate the extent of electron trapping. The results show that electron trapping by the nitridation-induced electron traps does not play the dominant role in improving radiation performance of RNO, though its contribution cannot be completely neglected for low oxide field irradiations

Botanical Polyphenols Mitigate Microglial Activation and Microglia-Induced Neurotoxicity: Role of Cytosolic Phospholipase A2.

Science.gov (United States)

Chuang, Dennis Y; Simonyi, Agnes; Cui, Jiankun; Lubahn, Dennis B; Gu, Zezong; Sun, Grace Y

2016-09-01

Microglia play a significant role in the generation and propagation of oxidative/nitrosative stress, and are the basis of neuroinflammatory responses in the central nervous system. Upon stimulation by endotoxins such as lipopolysaccharides (LPS), these cells release pro-inflammatory factors which can exert harmful effects on surrounding neurons, leading to secondary neuronal damage and cell death. Our previous studies demonstrated the effects of botanical polyphenols to mitigate inflammatory responses induced by LPS, and highlighted an important role for cytosolic phospholipase A2 (cPLA2) upstream of the pro-inflammatory pathways (Chuang et al. in J Neuroinflammation 12(1):199, 2015. doi: 10.1186/s12974-015-0419-0 ). In this study, we investigate the action of botanical compounds and assess whether suppression of cPLA2 in microglia is involved in the neurotoxic effects on neurons. Differentiated SH-SY5Y neuroblastoma cells were used to test the neurotoxicity of conditioned medium from stimulated microglial cells, and WST-1 assay was used to assess for the cell viability of SH-SY5Y cells. Botanicals such as quercetin and honokiol (but not cyanidin-3-O-glucoside, 3CG) were effective in inhibiting LPS-induced nitric oxide (NO) production and phosphorylation of cPLA2. Conditioned medium from BV-2 cells stimulated with LPS or IFNγ caused neurotoxicity to SH-SY5Y cells. Decrease in cell viability could be ameliorated by pharmacological inhibitors for cPLA2 as well as by down-regulating cPLA2 with siRNA. Botanicals effective in inhibition of LPS-induced NO and cPLA2 phosphorylation were also effective in ameliorating microglial-induced neurotoxicity. Results demonstrated cytotoxic factors from activated microglial cells to cause damaging effects to neurons and potential use of botanical polyphenols to ameliorate the neurotoxic effects.

A dopamine receptor contributes to paraquat-induced neurotoxicity in Drosophila

Science.gov (United States)

Cassar, Marlène; Issa, Abdul-Raouf; Riemensperger, Thomas; Petitgas, Céline; Rival, Thomas; Coulom, Hélène; Iché-Torres, Magali; Han, Kyung-An; Birman, Serge

2015-01-01

Long-term exposure to environmental oxidative stressors, like the herbicide paraquat (PQ), has been linked to the development of Parkinson's disease (PD), the most frequent neurodegenerative movement disorder. Paraquat is thus frequently used in the fruit fly Drosophila melanogaster and other animal models to study PD and the degeneration of dopaminergic neurons (DNs) that characterizes this disease. Here, we show that a D1-like dopamine (DA) receptor, DAMB, actively contributes to the fast central nervous system (CNS) failure induced by PQ in the fly. First, we found that a long-term increase in neuronal DA synthesis reduced DAMB expression and protected against PQ neurotoxicity. Secondly, a striking age-related decrease in PQ resistance in young adult flies correlated with an augmentation of DAMB expression. This aging-associated increase in oxidative stress vulnerability was not observed in a DAMB-deficient mutant. Thirdly, targeted inactivation of this receptor in glutamatergic neurons (GNs) markedly enhanced the survival of Drosophila exposed to either PQ or neurotoxic levels of DA, whereas, conversely, DAMB overexpression in these cells made the flies more vulnerable to both compounds. Fourthly, a mutation in the Drosophila ryanodine receptor (RyR), which inhibits activity-induced increase in cytosolic Ca2+, also strongly enhanced PQ resistance. Finally, we found that DAMB overexpression in specific neuronal populations arrested development of the fly and that in vivo stimulation of either DNs or GNs increased PQ susceptibility. This suggests a model for DA receptor-mediated potentiation of PQ-induced neurotoxicity. Further studies of DAMB signaling in Drosophila could have implications for better understanding DA-related neurodegenerative disorders in humans. PMID:25158689

Protective effects of ebselen (Ebs) and para-aminosalicylic acid (PAS) against manganese (Mn)-induced neurotoxicity

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Marreilha dos Santos, A.P., E-mail: apsantos@ff.ul.pt [I-Med.UL, Department of Toxicology and Food Sciences, Faculty of Pharmacy, University of Lisbon, Lisbon (Portugal); Lucas, Rui L.; Andrade, Vanda; Mateus, M. Luísa [I-Med.UL, Department of Toxicology and Food Sciences, Faculty of Pharmacy, University of Lisbon, Lisbon (Portugal); Milatovic, Dejan; Aschner, Michael [Department of Pediatrics, Vanderbilt University Medical Center, Nashville, TN 37232 (United States); Batoreu, M. Camila [I-Med.UL, Department of Toxicology and Food Sciences, Faculty of Pharmacy, University of Lisbon, Lisbon (Portugal)

2012-02-01

Chronic, excessive exposure to manganese (Mn) may induce neurotoxicity and cause an irreversible brain disease, referred to as manganism. Efficacious therapies for the treatment of Mn are lacking, mandating the development of new interventions. The purpose of the present study was to investigate the efficacy of ebselen (Ebs) and para-aminosalicylic acid (PAS) in attenuating the neurotoxic effects of Mn in an in vivo rat model. Exposure biomarkers, inflammatory and oxidative stress biomarkers, as well as behavioral parameters were evaluated. Co-treatment with Mn plus Ebs or Mn plus PAS caused a significant decrease in blood and brain Mn concentrations (compared to rats treated with Mn alone), concomitant with reduced brain E{sub 2} prostaglandin (PGE{sub 2}) and enhanced brain glutathione (GSH) levels, decreased serum prolactin (PRL) levels, and increased ambulation and rearing activities. Taken together, these results establish that both PAS and Ebs are efficacious in reducing Mn body burden, neuroinflammation, oxidative stress and locomotor activity impairments in a rat model of Mn-induced toxicity. -- Highlights: ► The manuscript is unique in its approach to the neurotoxicity of Mn. ► The manuscript incorporates molecular, cellular and functional (behavioral) analyses. ► Both PAS and Ebs are effective in restoring Mn behavioral function. ► Both PAS and Ebs are effective in reducing Mn-induced oxidative stress. ► Both PAS and Ebs led to a decrease in Mn-induced neuro-inflammation.

Protective effects of ebselen (Ebs) and para-aminosalicylic acid (PAS) against manganese (Mn)-induced neurotoxicity

International Nuclear Information System (INIS)

Marreilha dos Santos, A.P.; Lucas, Rui L.; Andrade, Vanda; Mateus, M. Luísa; Milatovic, Dejan; Aschner, Michael; Batoreu, M. Camila

2012-01-01

Chronic, excessive exposure to manganese (Mn) may induce neurotoxicity and cause an irreversible brain disease, referred to as manganism. Efficacious therapies for the treatment of Mn are lacking, mandating the development of new interventions. The purpose of the present study was to investigate the efficacy of ebselen (Ebs) and para-aminosalicylic acid (PAS) in attenuating the neurotoxic effects of Mn in an in vivo rat model. Exposure biomarkers, inflammatory and oxidative stress biomarkers, as well as behavioral parameters were evaluated. Co-treatment with Mn plus Ebs or Mn plus PAS caused a significant decrease in blood and brain Mn concentrations (compared to rats treated with Mn alone), concomitant with reduced brain E 2 prostaglandin (PGE 2 ) and enhanced brain glutathione (GSH) levels, decreased serum prolactin (PRL) levels, and increased ambulation and rearing activities. Taken together, these results establish that both PAS and Ebs are efficacious in reducing Mn body burden, neuroinflammation, oxidative stress and locomotor activity impairments in a rat model of Mn-induced toxicity. -- Highlights: ► The manuscript is unique in its approach to the neurotoxicity of Mn. ► The manuscript incorporates molecular, cellular and functional (behavioral) analyses. ► Both PAS and Ebs are effective in restoring Mn behavioral function. ► Both PAS and Ebs are effective in reducing Mn-induced oxidative stress. ► Both PAS and Ebs led to a decrease in Mn-induced neuro-inflammation.

Protection against MDMA-induced dopaminergic neurotoxicity in mice by methyllycaconitine: involvement of nicotinic receptors.

Science.gov (United States)

Chipana, C; Camarasa, J; Pubill, D; Escubedo, E

2006-09-01

Methylenedioxymethamphetamine (MDMA) is a relatively selective dopaminergic neurotoxin in mice. Previous studies demonstrated the participation of alpha-7 nicotinic receptors (nAChR) in the neurotoxic effect of methamphetamine. The aim of this paper was to study the role of this receptor type in the acute effects and neurotoxicity of MDMA in mice. In vivo, methyllycaconitine (MLA), a specific alpha-7 nAChR antagonist, significantly prevented MDMA-induced neurotoxicity at dopaminergic but not at serotonergic level, without affecting MDMA-induced hyperthermia. Glial activation was also fully prevented by MLA. In vitro, MDMA induced intrasynaptosomal reactive oxygen species (ROS) generation, which was calcium-, nitric-oxide synthase-, and protein kinase C-dependent. Also, the increase in ROS was prevented by MLA and alpha-bungarotoxin. Experiments with reserpine point to endogenous dopamine (DA) as the main source of MDMA-induced ROS. MLA also brought the MDMA-induced inhibition of [3H]DA uptake down, from 73% to 11%. We demonstrate that a coordinated activation of alpha-7 nAChR, blockade of DA transporter function and displacement of DA from intracellular stores induced by MDMA produces a neurotoxic effect that can be prevented by MLA, suggesting that alpha-7 nAChR have a key role in the MDMA neurotoxicity in mice; however, the involvement of nicotinic receptors containing the beta2 subunit cannot be conclusively ruled out.

Spirulina maxima Extract Prevents Neurotoxicity via Promoting Activation of BDNF/CREB Signaling Pathways in Neuronal Cells and Mice.

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Koh, Eun-Jeong; Seo, Young-Jin; Choi, Jia; Lee, Hyeon Yong; Kang, Do-Hyung; Kim, Kui-Jin; Lee, Boo-Yong

2017-08-17

Spirulina maxima is a microalgae which contains flavonoids and other polyphenols. Although Spirulina maxima 70% ethanol extract (SM70EE) has diverse beneficial effects, its effects on neurotoxicity have not been fully understood. In this study, we investigated the neuroprotective effects of SM70EE against trimethyltin (TMT)-induced neurotoxicity in HT-22 cells. SM70EE inhibited the cleavage of poly-ADP ribose polymerase (PARP). Besides, ROS production was decreased by down-regulating oxidative stress-associated enzymes. SM70EE increased the factors of brain-derived neurotrophic factor (BDNF)/cyclic AMPresponsive elementbinding protein (CREB) signalling pathways. Additionally, acetylcholinesterase (AChE) was suppressed by SM70EE. Furthermore, we investigated whether SM70EE prevents cognitive deficits against scopolamine-induced neurotoxicity in mice by applying behavioral tests. SM70EE increased step-through latency time and decreased the escape latency time. Therefore, our data suggest that SM70EE may prevent TMT neurotoxicity through promoting activation of BDNF/CREB neuroprotective signaling pathways in neuronal cells. In vivo study, SM70EE would prevent cognitive deficits against scopolamine-induced neurotoxicity in mice.

Thallium Toxicity: General Issues, Neurological Symptoms, and Neurotoxic Mechanisms.

Science.gov (United States)

Osorio-Rico, Laura; Santamaria, Abel; Galván-Arzate, Sonia

2017-01-01

Thallium (Tl + ) is a ubiquitous natural trace metal considered as the most toxic among heavy metals. The ionic ratio of Tl + is similar to that of potassium (K + ), therefore accounting for the replacement of the latter during enzymatic reactions. The principal organelle damaged after Tl + exposure is mitochondria. Studies on the mechanisms of Tl + include intrinsic pathways altered and changes in antiapoptotic and proapoptotic proteins, cytochrome c, and caspases. Oxidative damage pathways increase after Tl + exposure to produce reactive oxygen species (ROS), changes in physical properties of the cell membrane caused by lipid peroxidation, and concomitant activation of antioxidant mechanisms. These processes are likely to account for the neurotoxic effects of the metal. In humans, Tl + is absorbed through the skin and mucous membranes and then is widely distributed throughout the body to be accumulated in bones, renal medulla, liver, and the Central Nervous System. Given the growing relevance of Tl + intoxication, in recent years there is a notorious increase in the number of reports attending Tl + pollution in different countries. In this sense, the neurological symptoms produced by Tl + and its neurotoxic effects are gaining attention as they represent a serious health problem all over the world. Through this review, we present an update to general information about Tl + toxicity, making emphasis on some recent data about Tl + neurotoxicity, as a field requiring attention at the clinical and preclinical levels.

The protective effect of Physalis peruviana L. against cadmium-induced neurotoxicity in rats.

Science.gov (United States)

Abdel Moneim, Ahmed E; Bauomy, Amira A; Diab, Marwa M S; Shata, Mohamed Tarek M; Al-Olayan, Ebtesam M; El-Khadragy, Manal F

2014-09-01

The present study was carried out to investigate the protective effect of Physalis peruviana L. (family Solanaceae) against cadmium-induced neurotoxicity in rats. Adult male Wistar rats were randomly divided into four groups. Group 1 was used as control. Group 2 was intraperitoneally injected with 6.5 mg/kg bwt of cadmium chloride for 5 days. Group 3 was treated with 200 mg/kg bwt of methanolic extract of Physalis (MEPh). Group 4 was pretreated with MEPh 1 h before cadmium for 5 days. Cadmium treatment induced marked disturbances in neurochemical parameters as indicating by significant (p Physalis has a beneficial effect in ameliorating the cadmium-induced oxidative neurotoxicity in the brain of rats.

Bilirubin-Induced Neurotoxicity in the Preterm Neonate.

Science.gov (United States)

Watchko, Jon F

2016-06-01

Bilirubin-induced neurotoxicity in preterm neonates remains a clinical concern. Multiple cellular and molecular cascades likely underlie bilirubin-induced neuronal injury, including plasma membrane perturbations, excitotoxicity, neuroinflammation, oxidative stress, and cell cycle arrest. Preterm newborns are particularly vulnerable secondary to central nervous system immaturity and concurrent adverse clinical conditions that may potentiate bilirubin toxicity. Acute bilirubin encephalopathy in preterm neonates may be subtle and manifest primarily as recurrent symptomatic apneic events. Low-bilirubin kernicterus continues to be reported in preterm neonates, and although multifactorial in nature, is often associated with marked hypoalbuminemia. Copyright © 2016 Elsevier Inc. All rights reserved.

The role of system Xc- in methamphetamine-induced dopaminergic neurotoxicity in mice.

Science.gov (United States)

Dang, Duy-Khanh; Shin, Eun-Joo; Tran, Hai-Quyen; Kim, Dae-Joong; Jeong, Ji Hoon; Jang, Choon-Gon; Nah, Seung-Yeol; Sato, Hideyo; Nabeshima, Toshitaka; Yoneda, Yukio; Kim, Hyoung-Chun

2017-09-01

The cystine/glutamate antiporter (system Xc - , Sxc) transports cystine into cell in exchange for glutamate. Since xCT is a specific subunit of Sxc, we employed xCT knockout mice and investigated whether this antiporter affected methamphetamine (MA)-induced dopaminergic neurotoxicity. MA treatment significantly increased striatal oxidative burdens in wild type mice. xCT inhibitor [i.e., S-4-carboxy-phenylglycine (CPG), sulfasalazine] or an xCT knockout significantly protected against these oxidative burdens. MA-induced increases in Iba-1 expression and Iba-1-labeled microglial immunoreactivity (Iba-1-IR) were significantly attenuated by CPG or sulfasalazine administration or xCT knockout. CPG or sulfasalazine significantly attenuated MA-induced TUNEL-positive cell populations in the striatum of Taconic ICR mice. The decrease in excitatory amino acid transporter-2 (or glutamate transporter-1) expression and increase in glutamate release were attenuated by CPG, sulfasalazine or xCT knockout. In addition, CPG, sulfasalazine or xCT knockout significantly protected against dopaminergic loss (i.e., decreases in tyrosine hydroxylase expression and immunoreactivity, and an increase in dopamine turnover rate) induced by MA. However, CPG, sulfasalazine or xCT knockout did not significantly affect the impaired glutathione system [i.e., decrease in reduced glutathione (GSH) and increase in oxidized glutathione (GSSG)] induced by MA. Our results suggest that Sxc mediates MA-induced neurotoxicity via facilitating oxidative stress, microgliosis, proapoptosis, and glutamate-related toxicity. Copyright © 2017 Elsevier Ltd. All rights reserved.

Elevated environmental temperature and methamphetamine neurotoxicity

International Nuclear Information System (INIS)

Miller, Diane B.; O'Callaghan, James P.

2003-01-01

Amphetamines have been of considerable research interest for the last several decades. More recent work has renewed interest in the role of ambient temperature in both the toxicity and neurotoxicity of these drugs. We have determined that the striatal dopaminergic neurotoxicity observed in the mouse is linked in some fashion to both body and environmental temperature. Most studies of d-methamphetamine (d-METH) neurotoxicity are conducted at standard laboratory ambient temperatures (e.g., ∼21-22 deg. C) and utilizing a repeated dosage regimen (e.g., three to four injections spaced 2 h apart). A lowering of the ambient temperature provides neuro protection, while an elevation increases neurotoxicity. d-METH causes long-term depletions of triatal dopamine (DA) that are accompanied by other changes that are indicative of nerve terminal degeneration. These include argyrophilia, as detected by silver degeneration stains, and an elevation in glial fibrillary acidic protein (GFAP), a marker of reactive gliosis in response to injury, as well as a long-term decrease in tyrosine hydroxylase (TH) protein levels. here we show that increasing the ambient temperature during and for some time following dosing increases the neurotoxicity of d-METH. Mice (female 57BL6/J) given a single dosage of d-METH (20 mg/kg s.c.) and maintained at the usual laboratory ambient temperature show minimal striatal damage (an ∼15% depletion of DA and an ∼ 86% increase in GFAP). substantial striatal damage (e.g., an ∼70% depletion of DA and an ∼200% elevation in GFAP) was induced by this regimen if mice were maintained at 27 deg. C for 24 or 72 h following dosing. An increase in neurotoxicity was also apparent in mice kept at an elevated temperature for only 5 or 9 h, but keeping animals at 27 deg. C for 24 or 72 h was the most effective in increasing the neurotoxicity of d-METH. Our data show how a relatively minor change in ambient temperature can have a major impact on the degree of

Different Molecular Mechanisms Mediate Direct or Glia-Dependent Prion Protein Fragment 90-231 Neurotoxic Effects in Cerebellar Granule Neurons.

Science.gov (United States)

Thellung, Stefano; Gatta, Elena; Pellistri, Francesca; Villa, Valentina; Corsaro, Alessandro; Nizzari, Mario; Robello, Mauro; Florio, Tullio

2017-10-01

Glia over-stimulation associates with amyloid deposition contributing to the progression of central nervous system neurodegenerative disorders. Here we analyze the molecular mechanisms mediating microglia-dependent neurotoxicity induced by prion protein (PrP)90-231, an amyloidogenic polypeptide corresponding to the protease-resistant portion of the pathological prion protein scrapie (PrP Sc ). PrP90-231 neurotoxicity is enhanced by the presence of microglia within neuronal culture, and associated to a rapid neuronal [Ca ++ ] i increase. Indeed, while in "pure" cerebellar granule neuron cultures, PrP90-231 causes a delayed intracellular Ca ++ entry mediated by the activation of NMDA receptors; when neuron and glia are co-cultured, a transient increase of [Ca ++ ] i occurs within seconds after treatment in both granule neurons and glial cells, then followed by a delayed and sustained [Ca ++ ] i raise, associated with the induction of the expression of inducible nitric oxide synthase and phagocytic NADPH oxidase. [Ca ++ ] i fast increase in neurons is dependent on the activation of multiple pathways since it is not only inhibited by the blockade of voltage-gated channel activity and NMDA receptors but also prevented by the inhibition of nitric oxide and PGE 2 release from glial cells. Thus, Ca ++ homeostasis alteration, directly induced by PrP90-231 in cerebellar granule cells, requires the activation of NMDA receptors, but is greatly enhanced by soluble molecules released by activated glia. In glia-enriched cerebellar granule cultures, the activation of inducible nitric oxide (iNOS) and NADPH oxidase represents the main mechanism of toxicity since their pharmacological inhibition prevented PrP90-231 neurotoxicity, whereas NMDA blockade by D(-)-2-amino-5-phosphonopentanoic acid is ineffective; conversely, in pure cerebellar granule cultures, NMDA blockade but not iNOS inhibition strongly reduced PrP90-231 neurotoxicity. These data indicate that amyloidogenic peptides

Transparent oxide electronics from materials to devices

CERN Document Server

Martins, Rodrigo; Barquinha, Pedro; Pereira, Luis

2012-01-01

Transparent electronics is emerging as one of the most promising technologies for the next generation of electronic products, away from the traditional silicon technology. It is essential for touch display panels, solar cells, LEDs and antistatic coatings. The book describes the concept of transparent electronics, passive and active oxide semiconductors, multicomponent dielectrics and their importance for a new era of novel electronic materials and products. This is followed by a short history of transistors, and how oxides have revolutionized this field. It concludes with a glance at lo

Hirsutine, an indole alkaloid of Uncaria rhynchophylla, inhibits inflammation-mediated neurotoxicity and microglial activation.

Science.gov (United States)

Jung, Hwan Yong; Nam, Kyong Nyon; Woo, Byung-Choel; Kim, Kyoo-Pil; Kim, Sung-Ok; Lee, Eunjoo H

2013-01-01

Chronic microglial activation endangers neuronal survival through the release of various pro-inflammatory and neurotoxic factors. As such, negative regulators of microglial activation have been considered as potential therapeutic candidates to reduce the risk of neurodegeneration associated with inflammation. Uncaria rhynchophylla (U. rhynchophylla) is a traditional oriental herb that has been used for treatment of disorders of the cardiovascular and central nervous systems. Hirsutine (HS), one of the major indole alkaloids of U. rhynchophylla, has demonstrated neuroprotective potential. The aim of the present study was to examine the efficacy of HS in the repression of inflammation-induced neurotoxicity and microglial cell activation. In organotypic hippocampal slice cultures, HS blocked lipopolysaccharide (LPS)-related hippocampal cell death and production of nitric oxide (NO), prostaglandin (PG) E2 and interleukin-1β. HS was demonstrated to effectively inhibit LPS-induced NO release from cultured rat brain microglia. The compound reduced the LPS-stimulated production of PGE2 and intracellular reactive oxygen species. HS significantly decreased LPS-induced phosphorylation of the mitogen-activated protein kinases and Akt signaling proteins. In conclusion, HS reduces the production of various neurotoxic factors in activated microglial cells and possesses neuroprotective activity in a model of inflammation-induced neurotoxicity.

Immunosuppressant-Associated Neurotoxicity Responding to Olanzapine

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James A. Bourgeois

2014-01-01

Full Text Available Immunosuppressants, particularly tacrolimus, can induce neurotoxicity in solid organ transplantation cases. A lower clinical threshold to switch from tacrolimus to another immunosuppressant agent has been a common approach to reverse this neurotoxicity. However, immunosuppressant switch may place the graft at risk, and, in some cases, continuation of the same treatment protocol may be necessary. We report a case of immunosuppressant-associated neurotoxicity with prominent neuropsychiatric manifestation and describe psychiatric intervention with olanzapine that led to clinical improvement while continuing tacrolimus maintenance.

Engineering complex oxide interfaces for oxide electronics

NARCIS (Netherlands)

Roy, Saurabh

2015-01-01

A complex interplay of physics and chemistry in transition metal oxides determines their electronic, magnetic, and ferroic properties enabling a wide range of applications of these materials. BiFeO_3, a canonical multiferroic system exhibits the interesting feature of enhanced conductivity on

Electron transport properties of indium oxide - indium nitride metal-oxide-semiconductor heterostructures

International Nuclear Information System (INIS)

Wang, C.Y.; Hauguth, S.; Polyakov, V.; Schwierz, F.; Cimalla, V.; Kups, T.; Himmerlich, M.; Schaefer, J.A.; Krischok, S.; Ambacher, O.; Morales, F.M.; Lozano, J.G.; Gonzalez, D.; Lebedev, V.

2008-01-01

The structural, chemical and electron transport properties of In 2 O 3 /InN heterostructures and oxidized InN epilayers are reported. It is shown that the accumulation of electrons at the InN surface can be manipulated by the formation of a thin surface oxide layer. The epitaxial In 2 O 3 /InN heterojunctions show an increase in the electron concentration due to the increasing band banding at the heterointerface. The oxidation of InN results in improved transport properties and in a reduction of the sheet carrier concentration of the InN epilayer very likely caused by a passivation of surface donors. (copyright 2008 WILEY-VCH Verlag GmbH and Co. KGaA, Weinheim) (orig.)

Naringenin protects against 6-OHDA-induced neurotoxicity via activation of the Nrf2/ARE signaling pathway.

Science.gov (United States)

Lou, Haiyan; Jing, Xu; Wei, Xinbing; Shi, Huanying; Ren, Dongmei; Zhang, Xiumei

2014-04-01

There is increasing evidence that oxidative stress is critically involved in the pathogenesis of Parkinson's disease (PD), suggesting that pharmacological targeting of the antioxidant machinery may have therapeutic value. Naringenin, a natural flavonoid compound, has been reported to possess neuroprotective effect against PD related pathology; however the mechanisms underlying its beneficial effects are poorly defined. Thus, the purpose of the present study was to investigate the potential neuroprotective role of naringenin and to delineate its mechanism of action against 6-hydroxydopamine (6-OHDA)-induced neurotoxicity in models of PD both in vitro and in vivo. Naringenin treatment resulted in an increase in nuclear factor E2-related factor 2 (Nrf2) protein levels and subsequent activation of antioxidant response element (ARE) pathway genes in SH-SY5Y cells and in mice. Exposure of SH-SY5Y cells to naringenin provided protection against 6-OHDA-induced oxidative insults that was dependent on Nrf2, since treatment with Nrf2 siRNA failed to block against 6-OHDA neurotoxicity or induce Nrf2-dependent cytoprotective genes in SH-SY5Y cells. In mice, oral administration of naringenin resulted in significant protection against 6-OHDA-induced nigrostriatal dopaminergic neurodegeneration and oxidative damage. Our results indicate that activation of Nrf2/ARE signaling by naringenin is strongly associated with its neuroprotective effects against 6-OHDA neurotoxicity and suggest that targeting the Nrf2/ARE pathway may be a promising approach for therapeutic intervention in PD. Copyright © 2013 Elsevier Ltd. All rights reserved.

Biochemical Factors Modulating Cellular Neurotoxicity of Methylmercury

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Parvinder Kaur

2011-01-01

Full Text Available Methylmercury (MeHg, an environmental toxicant primarily found in fish and seafood, poses a dilemma to both consumers and regulatory authorities, given the nutritional benefits of fish consumption versus the possible adverse neurological damage. Several studies have shown that MeHg toxicity is influenced by a number of biochemical factors, such as glutathione (GSH, fatty acids, vitamins, and essential elements, but the cellular mechanisms underlying these complex interactions have not yet been fully elucidated. The objective of this paper is to outline the cellular response to dietary nutrients, as well as to describe the neurotoxic exposures to MeHg. In order to determine the cellular mechanism(s of toxicity, the effect of pretreatment with biochemical factors (e.g., N-acetyl cysteine, (NAC; diethyl maleate, (DEM; docosahexaenoic acid, (DHA; selenomethionine, SeM; Trolox and MeHg treatment on intercellular antioxidant status, MeHg content, and other endpoints was evaluated. This paper emphasizes that the protection against oxidative stress offered by these biochemical factors is among one of the major mechanisms responsible for conferring neuroprotection. It is therefore critical to ascertain the cellular mechanisms associated with various dietary nutrients as well as to determine the potential effects of neurotoxic exposures for accurately assessing the risks and benefits associated with fish consumption.

Astragalus Polysaccharide Suppresses 6-Hydroxydopamine-Induced Neurotoxicity in Caenorhabditis elegans

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Haifeng Li

2016-01-01

Full Text Available Astragalus membranaceus is a medicinal plant traditionally used in China for a variety of conditions, including inflammatory and neural diseases. Astragalus polysaccharides are shown to reduce the adverse effect of levodopa which is used to treat Parkinson’s disease (PD. However, the neuroprotective effect of Astragalus polysaccharides per se in PD is lacking. Using Caenorhabditis elegans models, we investigated the protective effect of astragalan, an acidic polysaccharide isolated from A. membranaceus, against the neurotoxicity of 6-hydroxydopamine (6-OHDA, a neurotoxin that can induce parkinsonism. We show that 6-OHDA is able to degenerate dopaminergic neurons and lead to the deficiency of food-sensing behavior and a shorter lifespan in C. elegans. Interestingly, these degenerative symptoms can be attenuated by astragalan treatment. Astragalan is also shown to alleviate oxidative stress through reducing reactive oxygen species level and malondialdehyde content and increasing superoxide dismutase and glutathione peroxidase activities and reduce the expression of proapoptotic gene egl-1 in 6-OHDA-intoxicated nematodes. Further studies reveal that astragalan is capable of elevating the decreased acetylcholinesterase activity induced by 6-OHDA. Together, our results demonstrate that the protective effect of astragalan against 6-OHDA neurotoxicity is likely due to the alleviation of oxidative stress and regulation of apoptosis pathway and cholinergic system and thus provide an important insight into the therapeutic potential of Astragalus polysaccharide in neurodegeneration.

General anesthetics in children: neurotoxic or neuroprotective?

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Jéssica Farias Rebouças

2017-02-01

Full Text Available Introduction: general anesthetics are involved in neuroprotection in adults after ischemic events and cognitive impairment, thus, they also may be associated with learning disorders in children exposed to them before three years of age. Objective: Describe about the neurotoxic effects of general anesthetics in experimental animals and children. Method: This is a systematic review, performed from search in databases and on PubMed using the keywords "neurotoxicity" and "general anesthetics," and "general anesthetics," "neurotoxicity", "children", "young child "and" pediatric ". Results: The search resulted in 185 articles. Out of these, 78 met our inclusion criteria. We found that there was a significant evidence of neurotoxicity induced by general anesthetics in experimental animals that were just born, resulting in late and permanent cognitive deficits. This effect was associated with multiple exposures, exposure length of time and combination of drugs. However, some studies found cognitive impairment after a single exposure to anesthetic. Conclusion: There is insufficient evidence to state that general anesthetics are neurotoxic and have the potential to trigger learning and behavior disabilities in children. However, we suggest caution in indicating surgery in children under three years old, analyzing risk-benefit and inserting the family in the decision process.   Keywords: Neurotoxicity; Neuroprotection; Cognitive Impairment; Children; General Anesthesics

Non-Serotonergic Neurotoxicity by MDMA (Ecstasy in Neurons Derived from Mouse P19 Embryonal Carcinoma Cells.

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Dina Popova

Full Text Available 3,4-methylenedioxymethamphetamine (MDMA; ecstasy is a commonly abused recreational drug that causes neurotoxic effects in both humans and animals. The mechanism behind MDMA-induced neurotoxicity is suggested to be species-dependent and needs to be further investigated on the cellular level. In this study, the effects of MDMA in neuronally differentiated P19 mouse embryonal carcinoma cells have been examined. MDMA produces a concentration-, time- and temperature-dependent toxicity in differentiated P19 neurons, as measured by intracellular MTT reduction and extracellular LDH activity assays. The P19-derived neurons express both the serotonin reuptake transporter (SERT, that is functionally active, and the serotonin metabolizing enzyme monoamine oxidase A (MAO-A. The involvement of these proteins in the MDMA-induced toxicity was investigated by a pharmacological approach. The MAO inhibitors clorgyline and deprenyl, and the SERT inhibitor fluoxetine, per se or in combination, were not able to mimic the toxic effects of MDMA in the P19-derived neurons or block the MDMA-induced cell toxicity. Oxidative stress has been implicated in MDMA-induced neurotoxicity, but pre-treatment with the antioxidants α-tocopherol or N-acetylcysteine did not reveal any protective effects in the P19 neurons. Involvement of mitochondria in the MDMA-induced cytotoxicity was also examined, but MDMA did not alter the mitochondrial membrane potential (ΔΨm in the P19 neurons. We conclude that MDMA produce a concentration-, time- and temperature-dependent neurotoxicity and our results suggest that the mechanism behind MDMA-induced toxicity in mouse-derived neurons do not involve the serotonergic system, oxidative stress or mitochondrial dysfunction.

Non-Serotonergic Neurotoxicity by MDMA (Ecstasy) in Neurons Derived from Mouse P19 Embryonal Carcinoma Cells.

Science.gov (United States)

Popova, Dina; Forsblad, Andréas; Hashemian, Sanaz; Jacobsson, Stig O P

2016-01-01

3,4-methylenedioxymethamphetamine (MDMA; ecstasy) is a commonly abused recreational drug that causes neurotoxic effects in both humans and animals. The mechanism behind MDMA-induced neurotoxicity is suggested to be species-dependent and needs to be further investigated on the cellular level. In this study, the effects of MDMA in neuronally differentiated P19 mouse embryonal carcinoma cells have been examined. MDMA produces a concentration-, time- and temperature-dependent toxicity in differentiated P19 neurons, as measured by intracellular MTT reduction and extracellular LDH activity assays. The P19-derived neurons express both the serotonin reuptake transporter (SERT), that is functionally active, and the serotonin metabolizing enzyme monoamine oxidase A (MAO-A). The involvement of these proteins in the MDMA-induced toxicity was investigated by a pharmacological approach. The MAO inhibitors clorgyline and deprenyl, and the SERT inhibitor fluoxetine, per se or in combination, were not able to mimic the toxic effects of MDMA in the P19-derived neurons or block the MDMA-induced cell toxicity. Oxidative stress has been implicated in MDMA-induced neurotoxicity, but pre-treatment with the antioxidants α-tocopherol or N-acetylcysteine did not reveal any protective effects in the P19 neurons. Involvement of mitochondria in the MDMA-induced cytotoxicity was also examined, but MDMA did not alter the mitochondrial membrane potential (ΔΨm) in the P19 neurons. We conclude that MDMA produce a concentration-, time- and temperature-dependent neurotoxicity and our results suggest that the mechanism behind MDMA-induced toxicity in mouse-derived neurons do not involve the serotonergic system, oxidative stress or mitochondrial dysfunction.

Liu Jun Zi Tang—A Potential, Multi-Herbal Complementary Therapy for Chemotherapy-Induced Neurotoxicity

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Chun-Tang Chiou

2018-04-01

Full Text Available Liu Jun Zi Tang (LJZT has been used to treat functional dyspepsia and depression, suggesting its effects on gastrointestinal and neurological functions. LJZT is currently used as a complementary therapy to attenuate cisplatin-induced side effects, such as dyspepsia. However, its effect on chemotherapy-induced neuropathic pain or neurotoxicity has rarely been studied. Thus, we explored potential mechanisms underlying LJZT protection against cisplatin-induced neurotoxicity. We observed that LJZT attenuated cisplatin-induced thermal hyperalgesia in mice and apoptosis in human neuroblastoma SH-SY5Y cells. Furthermore, it also attenuated cisplatin-induced cytosolic and mitochondrial free radical formation, reversed the cisplatin-induced decrease in mitochondrial membrane potential, and increased the release of mitochondrial pro-apoptotic factors. LJZT not only activated the peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α promoter region, but also attenuated the cisplatin-induced reduction of PGC-1α expression. Silencing of the PGC-1α gene counteracted the protection of LJZT. Taken together, LJZT mediated, through anti-oxidative effect and mitochondrial function regulation, to prevent cisplatin-induced neurotoxicity.

Central neurotoxicity of immunomodulatory drugs in multiple myeloma

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Urmeel H. Patel

2015-03-01

Full Text Available Immunomodulatory drugs (IMiDs currently used in the treatment of multiple myeloma, are thalidomide, lenalidomide and pomalidomide. One of the most common side effects of thalidomide is neurotoxicity, predominantly in the form of peripheral neuropathy. We report 6 cases of significant central neurotoxicity associated with IMiD therapy. Treatment with thalidomide (1 patient, lenalidomide (4 patients, and pomalidomide (1 patient was associated with various clinical manifestations of central neurotoxicity, including reversible coma, amnesia, expressive aphasia, and dysarthria. Central neurotoxicity should be recognized as an important side effect of IMiD therapy.

Central neurotoxicity of immunomodulatory drugs in multiple myeloma.

Science.gov (United States)

Patel, Urmeel H; Mir, Muhammad A; Sivik, Jeffrey K; Raheja, Divisha; Pandey, Manoj K; Talamo, Giampaolo

2015-02-24

Immunomodulatory drugs (IMiDs) currently used in the treatment of multiple myeloma, are thalidomide, lenalidomide and pomalidomide. One of the most common side effects of thalidomide is neurotoxicity, predominantly in the form of peripheral neuropathy. We report 6 cases of significant central neurotoxicity associated with IMiD therapy. Treatment with thalidomide (1 patient), lenalidomide (4 patients), and pomalidomide (1 patient) was associated with various clinical manifestations of central neurotoxicity, including reversible coma, amnesia, expressive aphasia, and dysarthria. Central neurotoxicity should be recognized as an important side effect of IMiD therapy.

Corneal Neurotoxicity Due to Topical Benzalkonium Chloride

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Sarkar, Joy; Chaudhary, Shweta; Namavari, Abed; Ozturk, Okan; Chang, Jin-Hong; Yco, Lisette; Sonawane, Snehal; Khanolkar, Vishakha; Hallak, Joelle; Jain, Sandeep

2012-01-01

Topical application of benzalkonium chloride (BAK) to the eye causes dose-related corneal neurotoxicity. Corneal inflammation and reduction in aqueous tear production accompany neurotoxicity. Cessation of BAK treatment leads to recovery of corneal nerve density.

The neurotoxicity of pyridinium metabolites of haloperidol

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Agnieszka Górska

2015-10-01

Full Text Available Haloperydol is a butyrophenone, typical neuroleptic agent characterized as a high antipsychotics effects in the treatment of schizophrenia and in palliative care to alleviation many syndromes, such as naursea, vomiting and delirium. Clinical problems occurs during and after administration of the drug are side effects, particularly extrapyrramidal symptoms (EPS. The neurotoxicity of haloperydol may be initiated by the cationic metabolites of haloperydol, HPP+, RHPP+, formed by oxidation and reduction pathways. These metabolites are transported by human organic cation transporters (hOCT to several brain structures for exapmle, in substantia nigra, striatum, caudate nucleus, hippocampus. After reaching the dopaminergic neurons inhibits mitochondrial complex I, evidence for free radical involvement, thus leading to neurodegeneration.

Endocytic pathways mediating oligomeric Aβ42 neurotoxicity

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Laxton Kevin

2010-05-01

Full Text Available Abstract Background One pathological hallmark of Alzheimer's disease (AD is amyloid plaques, composed primarily of amyloid-β peptide (Aβ. Over-production or diminished clearance of the 42 amino acid form of Aβ (Aβ42 in the brain leads to accumulation of soluble Aβ and plaque formation. Soluble oligomeric Aβ (oAβ has recently emerged to be as a likely proximal cause of AD. Results Here we demonstrate that endocytosis is critical in mediating oAβ42-induced neurotoxicity and intraneuronal accumulation of Aβ. Inhibition of clathrin function either with a pharmacological inhibitor, knock-down of clathrin heavy chain expression, or expression of the dominant-negative mutant of clathrin-assembly protein AP180 did not block oAβ42-induced neurotoxicity or intraneuronal accumulation of Aβ. However, inhibition of dynamin and RhoA by expression of dominant negative mutants reduced neurotoxicity and intraneuronal Aβ accumulation. Pharmacologic inhibition of the dynamin-mediated endocytic pathway by genistein also reduced neurotoxicity. Conclusions These data suggest that dynamin-mediated and RhoA-regulated endocytosis are integral steps for oligomeric Aβ42-induced neurotoxicity and intraneuronal Aβ accumulation.

Neuroprotective effect of curcumin-loaded lactoferrin nano particles against rotenone induced neurotoxicity.

Science.gov (United States)

Bollimpelli, V Satish; Kumar, Prashant; Kumari, Sonali; Kondapi, Anand K

2016-05-01

Curcumin is known to have neuroprotective role and possess antioxidant, anti-inflammatory activities. Rotenone, a flavonoid induced neurotoxicity in dopaminergic cells is being widely studied in Parkinson's Disease (PD) research. In the present study, curcumin loaded lactoferrin nano particles prepared by sol-oil chemistry were used to protect dopaminergic cell line SK-N-SH against rotenone induced neurotoxicity. These curcumin loaded nano particles were of 43-60 nm diameter size and around 100 nm hydrodynamic size as assessed by transmission electron microscopy, atomic force microscopy and dynamic light scattering analysis respectively. The encapsulation efficiency was 61.3% ± 2.4%. Cellular uptake of curcumin through these nano particles was confirmed by confocal imaging and spectrofluorimetric analysis. The curcumin loaded lactoferrin nanoparticles showed greater intracellular drug uptake, sustained retention and greater neuroprotection than soluble counterpart. Neuroprotective activity was characterized through viability assays and by estimating ROS levels. Furthermore rotenone induced PD like features were characterized by decrease in tyrosine hydroxylase expression and increase in α-synuclein expression. Taken together curcumin loaded lactoferrin nanoparticles could be a promising drug delivery strategy against neurotoxicity in dopaminergic neurons. Copyright © 2016 Elsevier Ltd. All rights reserved.

Soybean-derived Bowman-Birk inhibitor inhibits neurotoxicity of LPS-activated macrophages

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Persidsky Yuri

2011-02-01

Full Text Available Abstract Background Lipopolysaccharide (LPS, the major component of the outer membrane of gram-negative bacteria, can activate immune cells including macrophages. Activation of macrophages in the central nervous system (CNS contributes to neuronal injury. Bowman-Birk inhibitor (BBI, a soybean-derived protease inhibitor, has anti-inflammatory properties. In this study, we examined whether BBI has the ability to inhibit LPS-mediated macrophage activation, reducing the release of pro-inflammatory cytokines and subsequent neurotoxicity in primary cortical neural cultures. Methods Mixed cortical neural cultures from rat were used as target cells for testing neurotoxicity induced by LPS-treated macrophage supernatant. Neuronal survival was measured using a cell-based ELISA method for expression of the neuronal marker MAP-2. Intracellular reactive oxygen species (ROS production in macrophages was measured via 2', 7'-dichlorofluorescin diacetate (DCFH2DA oxidation. Cytokine expression was determined by quantitative real-time PCR. Results LPS treatment of macrophages induced expression of proinflammatory cytokines (IL-1β, IL-6 and TNF-α and of ROS. In contrast, BBI pretreatment (1-100 μg/ml of macrophages significantly inhibited LPS-mediated induction of these cytokines and ROS. Further, supernatant from BBI-pretreated and LPS-activated macrophage cultures was found to be less cytotoxic to neurons than that from non-BBI-pretreated and LPS-activated macrophage cultures. BBI, when directly added to the neuronal cultures (1-100 μg/ml, had no protective effect on neurons with or without LPS-activated macrophage supernatant treatment. In addition, BBI (100 μg/ml had no effect on N-methyl-D-aspartic acid (NMDA-mediated neurotoxicity. Conclusions These findings demonstrate that BBI, through its anti-inflammatory properties, protects neurons from neurotoxicity mediated by activated macrophages.

L-Ascorbate attenuates methamphetamine neurotoxicity through enhancing the induction of endogenous heme oxygenase-1

Energy Technology Data Exchange (ETDEWEB)

Huang, Ya-Ni [Department of Nursing, Hsin Sheng College of Medical Care and Management, Taoyuan, Taiwan (China); Wang, Jiz-Yuh [Department of Neurology, Faculty of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan (China); Lee, Ching-Tien [Department of Nursing, Hsin Sheng College of Medical Care and Management, Taoyuan, Taiwan (China); Lin, Chih-Hung [Graduate Institute of Medical Sciences and Department of Physiology, College of Medicine, Taipei Medical University, Taipei, Taiwan (China); Lai, Chien-Cheng [Far Eastern Memorial Hospital, Department of Surgery, Taipei, Taiwan (China); Wang, Jia-Yi, E-mail: jywang2010@tmu.edu.tw [Graduate Institute of Medical Sciences and Department of Physiology, College of Medicine, Taipei Medical University, Taipei, Taiwan (China)

2012-12-01

Methamphetamine (METH) is a drug of abuse which causes neurotoxicity and increased risk of developing neurodegenerative diseases. We previously found that METH induces heme oxygenase (HO)-1 expression in neurons and glial cells, and this offers partial protection against METH toxicity. In this study, we investigated the effects of L-ascorbate (vitamin C, Vit. C) on METH toxicity and HO-1 expression in neuronal/glial cocultures. Cell viability and damage were evaluated by 3-(4,5-dimethylthianol-2-yl)-2,5 diphenyl tetrazolium bromide (MTT) reduction and lactate dehydrogenase (LDH) release, respectively. Neuronal and glial localization of HO-1 were identified by double immunofluorescence staining. Reactive oxygen species (ROS) production was measured using the fluorochrome 2′,7′-dichlorofluorescin diacetate. HO-1 mRNA and protein expression were examined by RT-qPCR and Western blotting, respectively. Results show that Vit. C induced HO-1 mRNA and protein expressions in time- and concentration-dependent manners. Inhibition of p38 mitogen-activated protein kinase (MAPK) but not extracellular signal-regulated kinase (ERK) significantly blocked induction of HO-1 by Vit. C. HO-1 mRNA and protein expressions were significantly elevated by a combination of Vit. C and METH, compared to either Vit. C or METH alone. Pretreatment with Vit. C enhanced METH-induced HO-1 expression and attenuated METH-induced ROS production and neurotoxicity. Pharmacological inhibition of HO activity abolished suppressive effects of Vit. C on METH-induced ROS production and attenuated neurotoxicity. We conclude that induction of HO-1 expression contributes to the attenuation of METH-induced ROS production and neurotoxicity by Vit. C. We suggest that HO-1 induction by Vit. C may serve as a strategy to alleviate METH neurotoxicity. -- Highlights: ► Besides the anti-oxidant effect, Vit. C also induces HO-1 expression in brain cells. ► Vit. C reduces METH neurotoxicity and ROS production by

L-Ascorbate attenuates methamphetamine neurotoxicity through enhancing the induction of endogenous heme oxygenase-1

International Nuclear Information System (INIS)

Huang, Ya-Ni; Wang, Jiz-Yuh; Lee, Ching-Tien; Lin, Chih-Hung; Lai, Chien-Cheng; Wang, Jia-Yi

2012-01-01

Methamphetamine (METH) is a drug of abuse which causes neurotoxicity and increased risk of developing neurodegenerative diseases. We previously found that METH induces heme oxygenase (HO)-1 expression in neurons and glial cells, and this offers partial protection against METH toxicity. In this study, we investigated the effects of L-ascorbate (vitamin C, Vit. C) on METH toxicity and HO-1 expression in neuronal/glial cocultures. Cell viability and damage were evaluated by 3-(4,5-dimethylthianol-2-yl)-2,5 diphenyl tetrazolium bromide (MTT) reduction and lactate dehydrogenase (LDH) release, respectively. Neuronal and glial localization of HO-1 were identified by double immunofluorescence staining. Reactive oxygen species (ROS) production was measured using the fluorochrome 2′,7′-dichlorofluorescin diacetate. HO-1 mRNA and protein expression were examined by RT-qPCR and Western blotting, respectively. Results show that Vit. C induced HO-1 mRNA and protein expressions in time- and concentration-dependent manners. Inhibition of p38 mitogen-activated protein kinase (MAPK) but not extracellular signal-regulated kinase (ERK) significantly blocked induction of HO-1 by Vit. C. HO-1 mRNA and protein expressions were significantly elevated by a combination of Vit. C and METH, compared to either Vit. C or METH alone. Pretreatment with Vit. C enhanced METH-induced HO-1 expression and attenuated METH-induced ROS production and neurotoxicity. Pharmacological inhibition of HO activity abolished suppressive effects of Vit. C on METH-induced ROS production and attenuated neurotoxicity. We conclude that induction of HO-1 expression contributes to the attenuation of METH-induced ROS production and neurotoxicity by Vit. C. We suggest that HO-1 induction by Vit. C may serve as a strategy to alleviate METH neurotoxicity. -- Highlights: ► Besides the anti-oxidant effect, Vit. C also induces HO-1 expression in brain cells. ► Vit. C reduces METH neurotoxicity and ROS production by

Patterning of high mobility electron gases at complex oxide interfaces

DEFF Research Database (Denmark)

Trier, Felix; Prawiroatmodjo, G. E. D. K.; von Soosten, Merlin

2015-01-01

Oxide interfaces provide an opportunity for electronics. However, patterning of electron gases at complex oxide interfaces is challenging. In particular, patterning of complex oxides while preserving a high electron mobility remains underexplored and inhibits the study of quantum mechanical effects...... of amorphous-LSM (a-LSM) thin films, which acts as a hard mask during subsequent depositions. Strikingly, the patterned modulation-doped interface shows electron mobilities up to ∼8 700 cm2/V s at 2 K, which is among the highest reported values for patterned conducting complex oxide interfaces that usually...... where extended electron mean free paths are paramount. This letter presents an effective patterning strategy of both the amorphous-LaAlO3/SrTiO3 (a-LAO/STO) and modulation-doped amorphous-LaAlO3/La7/8Sr1/8MnO3/SrTiO3 (a-LAO/LSM/STO) oxide interfaces. Our patterning is based on selective wet etching...

17β-estradiol and tamoxifen protect mice from manganese-induced dopaminergic neurotoxicity.

Science.gov (United States)

Pajarillo, Edward; Johnson, James; Kim, Judong; Karki, Pratap; Son, Deok-Soo; Aschner, Michael; Lee, Eunsook

2018-03-01

Chronic exposure to manganese (Mn) causes neurotoxicity, referred to as manganism, with common clinical features of parkinsonism. 17β-estradiol (E2) and tamoxifen (TX), a selective estrogen receptor modulator (SERM), afford neuroprotection in several neurological disorders, including Parkinson's disease (PD). In the present study, we tested if E2 and TX attenuate Mn-induced neurotoxicity in mice, assessing motor deficit and dopaminergic neurodegeneration. We implanted E2 and TX pellets in the back of the neck of ovariectomized C57BL/6 mice two weeks prior to a single injection of Mn into the striatum. One week later, we assessed locomotor activity and molecular mechanisms by immunohistochemistry, real-time quantitative PCR, western blot and enzymatic biochemical analyses. The results showed that both E2 and TX attenuated Mn-induced motor deficits and reversed the Mn-induced loss of dopaminergic neurons in the substantia nigra. At the molecular level, E2 and TX reversed the Mn-induced decrease of (1) glutamate aspartate transporter (GLAST) and glutamate transporter 1 (GLT-1) mRNA and protein levels; (2) transforming growth factor-α (TGF-α) and estrogen receptor-α (ER-α) protein levels; and (3) catalase (CAT) activity and glutathione (GSH) levels, and Mn-increased (1) malondialdehyde (MDA) levels and (2) the Bax/Bcl-2 ratio. These results indicate that E2 and TX afford protection against Mn-induced neurotoxicity by reversing Mn-reduced GLT1/GLAST as well as Mn-induced oxidative stress. Our findings may offer estrogenic agents as potential candidates for the development of therapeutics to treat Mn-induced neurotoxicity. Copyright © 2017 Elsevier B.V. All rights reserved.

Neurotoxic effects of ecstasy on the thalamus

NARCIS (Netherlands)

de Win, Maartje M. L.; Jager, Gerry; Booij, Jan; Reneman, Liesbeth; Schilt, Thelma; Lavini, Cristina; Olabarriaga, Sílvia D.; Ramsey, Nick F.; den Heeten, Gerard J.; van den Brink, Wim

2008-01-01

Background Neurotoxic effects of ecstasy have been reported, although it remains unclear whether effects can be attributed to ecstasy, other recreational drugs or a combination of these. Aims To assess specific/independent neurotoxic effects of heavy ecstasy use and contributions of amphetamine,

Management of paclitaxel-induced neurotoxicity

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Manisha Bhutani

2011-12-01

Full Text Available Paclitaxel exerts its antitumor activity by promoting microtubule assembly and stabilizing microtubules. Microtubules are important for the development and maintenance of neurons. As a consequence, neurotoxicity is one of the drug’s major side effects. The risk of neurotoxicity depends on dose, duration and schedule of paclitaxel. Risk increases for patients with pre-existing conditions that may cause neuropathy (such as alcohol consumption, diabetes, or renal disease or with simultaneous or prior exposure to other neurotoxic chemotherapy such as platinum-based drugs, vinca alkaloids, immunomodulators, proteasome inhibitors, and epothilones. Patients with paclitaxel-induced neurotoxicity (PINT experience a constellation of symptoms over the course of treatment and beyond, ranging from mild to severe. Typically, the clinical presentation reflects an axonal peripheral neuropathy with glove-and-stocking distribution sensory loss, combined with features suggestive of nerve hyperexcitability including paresthesia, dysesthesia, and pain. Proprioceptive and motor effects become apparent as neuropathy becomes more advanced. These symptoms may be prolonged, severe, disabling, relatively resistant to intervention and adversely affect activities of daily living and thereby quality of life. Management is mainly symptomatic and supportive. Despite attempts to minimize PINT with changes in dose, vehicle, delivery systems, infusion schedule and premedication or co-treatment with neuroprotective agents, PINT remains dose-limiting in many instances and is a barrier to achieving the desired clinical response.

Cetuximab-induced hypomagnesaemia aggravates peripheral sensory neurotoxicity caused by oxaliplatin

Science.gov (United States)

Satomi, Machiko; Asama, Toshiyuki; Ebisawa, Yoshiaki; Chisato, Naoyuki; Suno, Manabu; Karasaki, Hidenori; Furukawa, Hiroyuki; Matsubara, Kazuo

2010-01-01

Calcium and magnesium replacement is effective in reducing oxaliplatin-induced neurotoxicity. However, cetuximab treatment has been associated with severe hypomagnesaemia. Therefore, we retrospectively investigated whether cetuximab-induced hypomagnesaemia exacerbated oxaliplatin-induced neurotoxicity. Six patients with metastatic colorectal cancer who were previously treated with oxaliplatin-fluorouracil combination therapy were administered cetuximab in combination with irinotecan alone or irinotecan and fluorouracil as a second-line treatment. All patients had normal magnesium levels before receiving cetuximab. The Common Terminology Criteria for Adverse Events version 3.0 was used to evaluate the grade of neurotoxicity, hypomagnesaemia, hypocalcaemia, and hypokalemia every week. All six patients had grade 1 or higher hypomagnesaemia after starting cetuximab therapy. The serum calcium and potassium levels were within the normal range at the onset of hypomagnesaemia. Oxaliplatin-induced neurotoxicity occurred in all patients at the beginning of cetuximab therapy, with grade 1 neurotoxicity in five patients and grade 2 in one patient. After cetuximab administration, the neurotoxicity worsened in all six patients, and three progressed to grade 3. Among the three patients with grade 3 neurotoxicity, two required a dose reduction and one had to discontinue cetuximab therapy. A discontinuation or dose reduction in cetuximab therapy was associated with exacerbated oxaliplatin-induced neurotoxicity due to cetuximab-induced hypomagnesaemia in half of patients who had previously received oxaliplatin. Therefore, when administering cetuximab after oxaliplatin therapy, we suggest serially evaluating serum magnesium levels and neurotoxicity. PMID:22811813

Biotransformation and neurotoxicity of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and its two-electron oxidation product, and 1-methyl-4-phenyl-2,3-dihydropyridinium (MPDP+) species

International Nuclear Information System (INIS)

Wu, E.Y.

1989-01-01

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) specifically destroys the nitrostriatal tract in humans and certain laboratory animals, and produces a Parkinsonian syndrome. The mechanism of cellular toxicity induced by the metabolites, however, has not been elucidated. The in vitro and in vivo metabolic behavior of MPTP and MPDP + and the possible role of factors other than MAO in determining the fate of these species was examined. Neuromelanin, which enhanced the rate of oxidation of MPDP + to MPP + , may also act as a reservoir in the substantia nigra to trap MPP + and prolong its exposure to susceptible brain neurons. Diethyldithiocarbamate (DDC), reported to increase the neurotoxic effect of MPTP in mice potentiated the formation of MPDP + from the MAO B catalyzed biotransformation of MPTP and significantly lowered brain dopamine levels in animals pretreated with DDC before MPTP administration. The ability of the dihydropyridinium species to gain access to susceptible neurons via the dopamine uptake system was assessed using the stable, 3,4-dihydro-2-methyl-9-H-indeno [2,1-c]pryidinium (DMIP + ) species. DMIP + , however, proved to be a poor inhibitor of both [ 3 H]dopamine and [ 3 H]MPP + uptake

Ellagic acid promotes A{beta}42 fibrillization and inhibits A{beta}42-induced neurotoxicity

Energy Technology Data Exchange (ETDEWEB)

Feng, Ying [Department of Histology and Embryology, College of Basic Medical Science, China Medical University, Shenyang 110001 (China); Tsinghua University School of Medicine, Haidian District, Beijing 100084 (China); Yang, Shi-gao; Du, Xue-ting; Zhang, Xi; Sun, Xiao-xia; Zhao, Min [Tsinghua University School of Medicine, Haidian District, Beijing 100084 (China); Sun, Gui-yuan, E-mail: sungy2004@sohu.com [Department of Histology and Embryology, College of Basic Medical Science, China Medical University, Shenyang 110001 (China); Liu, Rui-tian, E-mail: rtliu@tsinghua.edu.cn [Tsinghua University School of Medicine, Haidian District, Beijing 100084 (China)

2009-12-25

Smaller, soluble oligomers of {beta}-amyloid (A{beta}) play a critical role in the pathogenesis of Alzheimer's disease (AD). Selective inhibition of A{beta} oligomer formation provides an optimum target for AD therapy. Some polyphenols have potent anti-amyloidogenic activities and protect against A{beta} neurotoxicity. Here, we tested the effects of ellagic acid (EA), a polyphenolic compound, on A{beta}42 aggregation and neurotoxicity in vitro. EA promoted A{beta} fibril formation and significant oligomer loss, contrary to previous results that polyphenols inhibited A{beta} aggregation. The results of transmission electron microscopy (TEM) and Western blot displayed more fibrils in A{beta}42 samples co-incubated with EA in earlier phases of aggregation. Consistent with the hypothesis that plaque formation may represent a protective mechanism in which the body sequesters toxic A{beta} aggregates to render them harmless, our MTT results showed that EA could significantly reduce A{beta}42-induced neurotoxicity toward SH-SY5Y cells. Taken together, our results suggest that EA, an active ingredient in many fruits and nuts, may have therapeutic potential in AD.

Secondary electron emission characteristics of oxide electrodes in flat electron emission lamp

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Chang-Lin Chiang

2016-01-01

Full Text Available The present study concerns with the secondary electron emission coefficient, γ, of the cathode materials used in the newly developed flat electron emission lamp (FEEL devices, which essentially integrates the concept of using cathode for fluorescent lamp and anode for cathode ray tube (CRT to obtain uniform planar lighting. Three different cathode materials, namely fluorine-doped tin oxide (FTO, aluminum oxide coated FTO (Al2O3/FTO and magnesium oxide coated FTO (MgO/FTO were prepared to investigate how the variations of γ and working gases influence the performance of FEEL devices, especially in lowering the breakdown voltage and pressure of the working gases. The results indicate that the MgO/FTO bilayer cathode exhibited a relatively larger effective secondary electron emission coefficient, resulting in significant reduction of breakdown voltage to about 3kV and allowing the device to be operated at the lower pressure to generate the higher lighting efficiency.

Secondary electron emission characteristics of oxide electrodes in flat electron emission lamp

Energy Technology Data Exchange (ETDEWEB)

Chiang, Chang-Lin, E-mail: CLChiang@itri.org.tw; Li, Chia-Hung [Green Energy and Environment Research Laboratories, Industrial Technology Research Institute, 195, Sec. 4, Chung Hsing Road, Chutung 310, Taiwan (China); Department of Electrophysics, National Chiao Tung University, 1001 Ta Hsueh Road, Hsinchu 300, Taiwan (China); Zeng, Hui-Kai [Department of Electronic Engineering, Chung Yuan Christian University, 200 Chung Pei Road, Chung Li 320, Taiwan (China); Li, Jung-Yu, E-mail: JY-Lee@itri.org.tw; Chen, Shih-Pu; Lin, Yi-Ping [Green Energy and Environment Research Laboratories, Industrial Technology Research Institute, 195, Sec. 4, Chung Hsing Road, Chutung 310, Taiwan (China); Hsieh, Tai-Chiung; Juang, Jenh-Yih, E-mail: jyjuang@cc.nctu.edu.tw [Department of Electrophysics, National Chiao Tung University, 1001 Ta Hsueh Road, Hsinchu 300, Taiwan (China)

2016-01-15

The present study concerns with the secondary electron emission coefficient, γ, of the cathode materials used in the newly developed flat electron emission lamp (FEEL) devices, which essentially integrates the concept of using cathode for fluorescent lamp and anode for cathode ray tube (CRT) to obtain uniform planar lighting. Three different cathode materials, namely fluorine-doped tin oxide (FTO), aluminum oxide coated FTO (Al{sub 2}O{sub 3}/FTO) and magnesium oxide coated FTO (MgO/FTO) were prepared to investigate how the variations of γ and working gases influence the performance of FEEL devices, especially in lowering the breakdown voltage and pressure of the working gases. The results indicate that the MgO/FTO bilayer cathode exhibited a relatively larger effective secondary electron emission coefficient, resulting in significant reduction of breakdown voltage to about 3kV and allowing the device to be operated at the lower pressure to generate the higher lighting efficiency.

Methamphetamine generates peroxynitrite and produces dopaminergic neurotoxicity in mice: protective effects of peroxynitrite decomposition catalyst.

Science.gov (United States)

Imam, S Z; Crow, J P; Newport, G D; Islam, F; Slikker, W; Ali, S F

1999-08-07

Methamphetamine (METH)-induced dopaminergic neurotoxicity is believed to be produced by oxidative stress and free radical generation. The present study was undertaken to investigate if METH generates peroxynitrite and produces dopaminergic neurotoxicity. We also investigated if this generation of peroxynitrite can be blocked by a selective peroxynitrite decomposition catalyst, 5, 10,15, 20-tetrakis(N-methyl-4'-pyridyl)porphyrinato iron III (FeTMPyP) and protect against METH-induced dopaminergic neurotoxicity. Administration of METH resulted in the significant formation of 3-nitrotyrosine (3-NT), an in vivo marker of peroxynitrite generation, in the striatum and also caused a significant increase in the body temperature. METH injection also caused a significant decrease in the concentration of dopamine (DA), 3, 4-dihydroxyphenylacetic acid (DOPAC), and homovanillic acid (HVA) by 76%, 53% and 40%, respectively, in the striatum compared with the control group. Treatment with FeTMPyP blocked the formation of 3-NT by 66% when compared with the METH group. FeTMPyP treatment also provided significant protection against the METH-induced hyperthermia and depletion of DA, DOPAC and HVA. Administration of FeTMPyP alone neither resulted in 3-NT formation nor had any significant effect on DA or its metabolite concentrations. These findings indicate that peroxynitrite plays a role in METH-induced dopaminergic neurotoxicity and also suggests that peroxynitrite decomposition catalysts may be beneficial for the management of psychostimulant abuse. Copyright 1999 Published by Elsevier Science B.V.

Taxane-Induced Peripheral Neurotoxicity

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Roser Velasco

2015-04-01

Full Text Available Taxane-derived agents are chemotherapy drugs widely employed in cancer treatment. Among them, paclitaxel and docetaxel are most commonly administered, but newer formulations are being investigated. Taxane antineoplastic activity is mainly based on the ability of the drugs to promote microtubule assembly, leading to mitotic arrest and apoptosis in cancer cells. Peripheral neurotoxicity is the major non-hematological adverse effect of taxane, often manifested as painful neuropathy experienced during treatment, and it is sometimes irreversible. Unfortunately, taxane-induced neurotoxicity is an uncertainty prior to the initiation of treatment. The present review aims to dissect current knowledge on real incidence, underlying pathophysiology, clinical features and predisposing factors related with the development of taxane-induced neuropathy.

Titanium oxidation-reduction at low oxygen pressure under electron bombardment

International Nuclear Information System (INIS)

Brasca, R.; Passeggi, M.C.G.; Ferron, J.

2006-01-01

The effect of the electron bombardment on the first stages of the titanium oxidation process has been studied by means of Auger Electron Spectroscopy. Using Factor Analysis and the valence electron dependence behaviour of the titanium LMV Auger transition, we found that the process is strongly dependent on the oxygen pressure and electron current density. Depending on the irradiation conditions, films of different thickness and Ti oxidized states are obtained

Protective activities of Vaccinium antioxidants with potential relevance to mitochondrial dysfunction and neurotoxicity.

Science.gov (United States)

Yao, Yu; Vieira, Amandio

2007-01-01

Both the neurotransmitter dopamine (DA) and a neurotoxic metabolite, 6-hydroxy DA, can be oxidized to generate hydrogen peroxide and other reactive species (ROS). ROS promote oxidative stress and have been implicated in dopaminergic neurodegeneration, e.g., Parkinson's disease (PD). There is also evidence for a relation between catecholamine-mediated oxidative damage in dopaminergic neurons and the effects of these neurotransmitters on the redox state of cytochrome c (Cytc). In neurons and other cells, oxidative stress may be enhanced by abnormal release of Cytc and other mitochondrial proteins into the cytoplasm. Cytc release can result in apoptosis; but sub-apoptogenic-threshold release can also occur, and may be highly damaging in the presence of DA metabolites. Loss of mitochondrial membrane integrity, a pathological situation of relevance to several aging-related neurodegenerative disorders including PD, contributes to release of Cytc; and the level of such release is known to be indicative of the extent of mitochondrial dysfunction. In this context, we have used a Cytc-enhanced 6-hydroxy DA oxidation reaction to gauge dietary antioxidant activities. Anthocyanin-rich preparations of Vaccinium species (Vaccinium myrtillus, Vaccinium corymbosum, and Vaccinium oxycoccus) as well as a purified glycosylated anthocyanidin were compared. The most potent inhibition of oxidation was observed with V. myrtillus preparation: 50% inhibition with 7 microM of total anthocyanins. This activity was 1.5-4 times higher than that for the other preparations or for the purified anthocyanin. Ascorbate (Vitamin C), at up to 4-fold higher concentrations, did not result in significant inhibition in this assay. Antioxidant activity in the assay correlated strongly (r2>0.91, PVaccinium content of anthocyanins and total cyanidins, but not quercetin or myricetin. The results provide evidence for the high potency of anthocyanins towards a potentially neurotoxic reaction, and provide a basis

Acrylamide neurotoxicity on the cerebrum of weaning rats

Directory of Open Access Journals (Sweden)

Su-min Tian

2015-01-01

Full Text Available The mechanism underlying acrylamide-induced neurotoxicity remains controversial. Previous studies have focused on acrylamide-induced toxicity in adult rodents, but neurotoxicity in weaning rats has not been investigated. To explore the neurotoxic effect of acrylamide on the developing brain, weaning rats were gavaged with 0, 5, 15, and 30 mg/kg acrylamide for 4 consecutive weeks. No obvious neurotoxicity was observed in weaning rats in the low-dose acrylamide group (5 mg/kg. However, rats from the moderate- and high-dose acrylamide groups (15 and 30 mg/kg had an abnormal gait. Furthermore, biochemical tests in these rats demonstrated that glutamate concentration was significantly reduced, and γ-aminobutyric acid content was significantly increased and was dependent on acrylamide dose. Immunohistochemical staining showed that in the cerebral cortex, γ-aminobutyric acid, glutamic acid decarboxylase and glial fibrillary acidic protein expression increased remarkably in the moderate- and high-dose acrylamide groups. These results indicate that in weaning rats, acrylamide is positively associated with neurotoxicity in a dose-dependent manner, which may correlate with upregulation of γ-aminobutyric acid and subsequent neuronal degeneration after the initial acrylamide exposure.

Serotonergic neurotoxic metabolites of ecstasy identified in rat brain.

Science.gov (United States)

Jones, Douglas C; Duvauchelle, Christine; Ikegami, Aiko; Olsen, Christopher M; Lau, Serrine S; de la Torre, Rafael; Monks, Terrence J

2005-04-01

The selective serotonergic neurotoxicity of 3,4-methylenedioxyamphetamine (MDA) and 3,4-methylenedioxymethamphetamine (MDMA, ecstasy) depends on their systemic metabolism. We have recently shown that inhibition of brain endothelial cell gamma-glutamyl transpeptidase (gamma-GT) potentiates the neurotoxicity of both MDMA and MDA, indicating that metabolites that are substrates for this enzyme contribute to the neurotoxicity. Consistent with this view, glutathione (GSH) and N-acetylcysteine conjugates of alpha-methyl dopamine (alpha-MeDA) are selective neurotoxicants. However, neurotoxic metabolites of MDMA or MDA have yet to be identified in brain. Using in vivo microdialysis coupled to liquid chromatography-tandem mass spectroscopy and a high-performance liquid chromatography-coulometric electrode array system, we now show that GSH and N-acetylcysteine conjugates of N-methyl-alpha-MeDA are present in the striatum of rats administered MDMA by subcutaneous injection. Moreover, inhibition of gamma-GT with acivicin increases the concentration of GSH and N-acetylcysteine conjugates of N-methyl-alpha-MeDA in brain dialysate, and there is a direct correlation between the concentrations of metabolites in dialysate and the extent of neurotoxicity, measured by decreases in serotonin (5-HT) and 5-hydroxyindole acetic (5-HIAA) levels. Importantly, the effects of acivicin are independent of MDMA-induced hyperthermia, since acivicin-mediated potentiation of MDMA neurotoxicity occurs in the context of acivicin-mediated decreases in body temperature. Finally, we have synthesized 5-(N-acetylcystein-S-yl)-N-methyl-alpha-MeDA and established that it is a relatively potent serotonergic neurotoxicant. Together, the data support the contention that MDMA-mediated serotonergic neurotoxicity is mediated by the systemic formation of GSH and N-acetylcysteine conjugates of N-methyl-alpha-MeDA (and alpha-MeDA). The mechanisms by which such metabolites access the brain and produce selective

Electron transfer oxidation of DNA radicals by paranitroacetophenone

Energy Technology Data Exchange (ETDEWEB)

Whillans, D W; Adams, G E [Mount Vernon Hospital, Northwood (UK)

1975-12-01

The reaction of a typical electron-affinic sensitizer, paranitroacetophenone (PNAP) with the model compounds thymine, thymidine, thymidylic acid, deoxyribose and single and double-stranded DNA has been investigated by pulse radiolysis. Radicals formed by one-electron reduction of the bases and of DNA reacted rapidly and efficiently with PNAP by electron transfer. A small yield of transfer (< 10 per cent) was also observed arising from oxidation of the radicals formed by the small proportion of OH which reacted at the sugar moieties in DNA. In contrast, electron transfer oxidation by PNAP of radicals formed by the addition of OH to the base moieties, e.g. thymine, was not an efficient process. Further, addition of the sensitizer to the thymine OH-adduct proceeded at a rate that was too low to measure the pulse radiolysis. We conclude that, since the major sites of OH reaction by DNA are the heterocyclic bases (> 80 per cent), oxidation of the resultant radicals is unlikely to be a major step in the mechanism of sensitization by this typical hypoxic-cell sensitizer.

A plastic stabilizer dibutyltin dilaurate induces subchronic neurotoxicity in rats☆

Science.gov (United States)

Jin, Minghua; Song, Peilin; Li, Na; Li, Xuejun; Chen, Jiajun

2012-01-01

Dibutyltin dilaurate functions as a stabilizer for polyvinyl chloride. In this study, experimental rats were intragastrically administered 5, 10, or 20 mg/kg dibutyltin dilaurate to model sub-chronic poisoning. After exposure, our results showed the activities of superoxide dismutase and glutathione peroxidase decreased in rat brain tissue, while the malondialdehyde and nitric oxide content, as well as nitric oxide synthase activity in rat brain tissue increased. The cell cycle in the right parietal cortex was disordered and the rate of apoptosis increased. DNA damage was aggravated in the cerebral cortex, and the ultrastructure of the right parietal cortex tissues was altered. The above changes became more apparent with exposure to increasing doses of dibutyltin dilaurate. Our experimental findings confirmed the neurotoxicity of dibutyltin dilaurate in rat brain tissues, and demonstrated that the poisoning was dose-dependent. PMID:25538742

Correlation of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine neurotoxicity with blood-brain barrier monoamine oxidase activity

International Nuclear Information System (INIS)

Kalaria, R.N.; Mitchell, M.J.; Harik, S.I.

1987-01-01

Systemic administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) causes parkinsonism in humans and subhuman primates, but not in rats and many other laboratory animals; mice are intermediate in their susceptibility. Since MPTP causes selective dopaminergic neurotoxicity when infused directly into rat substantia nigra, the authors hypothesized that systemic MPTP may be metabolized by monoamine oxidase and/or other enzymes in rat brain capillaries and possibly other peripheral organs and thus prevented from reaching its neuronal sites of toxicity. They tested this hypothesis by assessing monoamine oxidase in isolated cerebral microvessels of humans, rats, and mice by measuring the specific binding of [ 3 H]pargyline, an irreversible monoamine oxidase inhibitor, and by estimating the rates of MPTP and benzylamine oxidation. [ 3 H]Pargyline binding to rat cerebral microvessels was about 10-fold higher than to human or mouse microvessels. Also, MPTP oxidation by rat brain microvessels was about 30-fold greater than by human microvessels; mouse microvessels yielded intermediate values. These results may explain, at least in part, the marked species differences in susceptibility to systemic MPTP. They also suggest the potential importance of enzyme barriers at the blood-brain interface that can metabolize toxins not excluded by structural barriers, and may provide biological bases for developing therapeutic strategies for the prevention of MPTP-induced neurotoxicity and other neurotoxic conditions including, possibly, Parkinson's disease

Electronic properties of hafnium oxide: A contribution from defects and traps

Energy Technology Data Exchange (ETDEWEB)

Gritsenko, Vladimir A., E-mail: grits@isp.nsc.ru; Perevalov, Timofey V.; Islamov, Damir R., E-mail: damir@isp.nsc.ru

2016-02-15

In the present article, we give a review of modern data and latest achievements pertaining to the study of electronic properties of oxygen vacancies in hafnium oxide. Hafnium oxide is a key dielectric for use in many advanced silicon devices. Oxygen vacancies in hafnium oxide largely determine the electronic properties of the material. We show that the electronic transitions between the states due to oxygen vacancies largely determine the optical absorption and luminescent properties of hafnium oxide. We discuss the role of oxygen vacancies as traps that facilitate charge transport in hafnium oxide films. Also, we demonstrate the fact that the electrical conductivity in hafnium oxide is controlled by the phonon-assisted tunnelling of charge carriers between traps that were identified as oxygen vacancies.

Highly n-Type Titanium Oxide as an Electronically Active Support for Platinum in the Catalytic Oxidation of Carbon Monoxide

KAUST Repository

Baker, L. Robert

2011-08-18

The role of the oxide-metal interface in determining the activity and selectivity of chemical reactions catalyzed by metal particles on an oxide support is an important topic in science and industry. A proposed mechanism for this strong metal-support interaction is electronic activation of surface adsorbates by charge carriers. Motivated by the goal of using electronic activation to drive nonthermal chemistry, we investigated the ability of the oxide support to mediate charge transfer. We report an approximately 2-fold increase in the turnover rate of catalytic carbon monoxide oxidation on platinum nanoparticles supported on stoichiometric titanium dioxide (TiO2) when the TiO2 is made highly n-type by fluorine (F) doping. However, for nonstoichiometric titanium oxide (TiOX<2) the effect of F on the turnover rate is negligible. Studies of the titanium oxide electronic structure show that the energy of free electrons in the oxide determines the rate of reaction. These results suggest that highly n-type TiO2 electronically activates adsorbed oxygen (O) by electron spillover to form an active O- intermediate. © 2011 American Chemical Society.

Nanoroses of nickel oxides: Synthesis, electron tomography study, and application in CO oxidation and energy storage

KAUST Repository

Fihri, Aziz; Sougrat, Rachid; Baby, Rakhi Raghavan; Rahal, Raed; Cha, Dong Kyu; Hedhili, Mohamed N.; Bouhrara, Mohamed; Alshareef, Husam N.; Polshettiwar, Vivek

2012-01-01

Nickel oxide and mixed-metal oxide structures were fabricated by using microwave irradiation in pure water. The nickel oxide self-assembled into unique rose-shaped nanostructures. These nickel oxide roses were studied by performing electron

Electronic structure of the high-temperature oxide superconductors

International Nuclear Information System (INIS)

Pickett, W.E.

1989-01-01

Since the discovery of superconductivity above 30 K by Bednorz and Mueller in the La copper oxide system, the critical temperature has been raised to 90 K in YBa 2 Cu 3 O 7 and to 110 and 125 K in Bi-based and Tl-based copper oxides, respectively. In the two years since this Nobel-prize-winning discovery, a large number of electronic structure calculations have been carried out as a first step in understanding the electronic properties of these materials. In this paper these calculations (mostly of the density-functional type) are gathered and reviewed, and their results are compared with the relevant experimental data. The picture that emerges is one in which the important electronic states are dominated by the copper d and oxygen p orbitals, with strong hybridization between them. Photon, electron, and positron spectroscopies provide important information about the electronic states, and comparison with electronic structure calculations indicates that, while many features can be interpreted in terms of existing calculations, self-energy corrections (''correlations'') are important for a more detailed understanding. The antiferromagnetism that occurs in some regions of the phase diagram poses a particularly challenging problem for any detailed theory. The study of structural stability, lattice dynamics, and electron-phonon coupling in the copper oxides is also discussed. Finally, a brief review is given of the attempts so far to identify interaction constants appropriate for a model Hamiltonian treatment of many-body interactions in these materials

Protective effect of quercetin on bupivacaine-induced neurotoxicity ...

African Journals Online (AJOL)

certain side effects, especially neurotoxicity. It has been shown that neurotoxicity caused by local anesthetics such as lidocaine and bupivacaine are related to changes in calcium homeostasis, resulting in intracellular calcium overload [1]. Calcium homeostasis is regulated by many different kinds of calcium channels such.

Metal oxide semiconductor thin-film transistors for flexible electronics

Energy Technology Data Exchange (ETDEWEB)

Petti, Luisa; Vogt, Christian; Büthe, Lars; Cantarella, Giuseppe; Tröster, Gerhard [Electronics Laboratory, Swiss Federal Institute of Technology, Zürich (Switzerland); Münzenrieder, Niko [Electronics Laboratory, Swiss Federal Institute of Technology, Zürich (Switzerland); Sensor Technology Research Centre, University of Sussex, Falmer (United Kingdom); Faber, Hendrik; Bottacchi, Francesca; Anthopoulos, Thomas D. [Department of Physics and Centre for Plastic Electronics, Imperial College London, London (United Kingdom)

2016-06-15

The field of flexible electronics has rapidly expanded over the last decades, pioneering novel applications, such as wearable and textile integrated devices, seamless and embedded patch-like systems, soft electronic skins, as well as imperceptible and transient implants. The possibility to revolutionize our daily life with such disruptive appliances has fueled the quest for electronic devices which yield good electrical and mechanical performance and are at the same time light-weight, transparent, conformable, stretchable, and even biodegradable. Flexible metal oxide semiconductor thin-film transistors (TFTs) can fulfill all these requirements and are therefore considered the most promising technology for tomorrow's electronics. This review reflects the establishment of flexible metal oxide semiconductor TFTs, from the development of single devices, large-area circuits, up to entirely integrated systems. First, an introduction on metal oxide semiconductor TFTs is given, where the history of the field is revisited, the TFT configurations and operating principles are presented, and the main issues and technological challenges faced in the area are analyzed. Then, the recent advances achieved for flexible n-type metal oxide semiconductor TFTs manufactured by physical vapor deposition methods and solution-processing techniques are summarized. In particular, the ability of flexible metal oxide semiconductor TFTs to combine low temperature fabrication, high carrier mobility, large frequency operation, extreme mechanical bendability, together with transparency, conformability, stretchability, and water dissolubility is shown. Afterward, a detailed analysis of the most promising metal oxide semiconducting materials developed to realize the state-of-the-art flexible p-type TFTs is given. Next, the recent progresses obtained for flexible metal oxide semiconductor-based electronic circuits, realized with both unipolar and complementary technology, are reported. In

Δ9-tetrahydrocannabinol prevents methamphetamine-induced neurotoxicity.

Directory of Open Access Journals (Sweden)

M Paola Castelli

Full Text Available Methamphetamine (METH is a potent psychostimulant with neurotoxic properties. Heavy use increases the activation of neuronal nitric oxide synthase (nNOS, production of peroxynitrites, microglia stimulation, and induces hyperthermia and anorectic effects. Most METH recreational users also consume cannabis. Preclinical studies have shown that natural (Δ9-tetrahydrocannabinol, Δ9-THC and synthetic cannabinoid CB1 and CB2 receptor agonists exert neuroprotective effects on different models of cerebral damage. Here, we investigated the neuroprotective effect of Δ9-THC on METH-induced neurotoxicity by examining its ability to reduce astrocyte activation and nNOS overexpression in selected brain areas. Rats exposed to a METH neurotoxic regimen (4 × 10 mg/kg, 2 hours apart were pre- or post-treated with Δ9-THC (1 or 3 mg/kg and sacrificed 3 days after the last METH administration. Semi-quantitative immunohistochemistry was performed using antibodies against nNOS and Glial Fibrillary Acidic Protein (GFAP. Results showed that, as compared to corresponding controls (i METH-induced nNOS overexpression in the caudate-putamen (CPu was significantly attenuated by pre- and post-treatment with both doses of Δ9-THC (-19% and -28% for 1 mg/kg pre- and post-treated animals; -25% and -21% for 3 mg/kg pre- and post-treated animals; (ii METH-induced GFAP-immunoreactivity (IR was significantly reduced in the CPu by post-treatment with 1 mg/kg Δ9-THC1 (-50% and by pre-treatment with 3 mg/kg Δ9-THC (-53%; (iii METH-induced GFAP-IR was significantly decreased in the prefrontal cortex (PFC by pre- and post-treatment with both doses of Δ9-THC (-34% and -47% for 1 mg/kg pre- and post-treated animals; -37% and -29% for 3 mg/kg pre- and post-treated animals. The cannabinoid CB1 receptor antagonist SR141716A attenuated METH-induced nNOS overexpression in the CPu, but failed to counteract the Δ9-THC-mediated reduction of METH-induced GFAP-IR both in the PFC and CPu. Our

Hard X-ray PhotoElectron Spectroscopy of transition metal oxides: Bulk compounds and device-ready metal-oxide interfaces

International Nuclear Information System (INIS)

Borgatti, F.; Torelli, P.; Panaccione, G.

2016-01-01

Highlights: • Hard X-ray PhotoElectron Spectroscopy (HAXPES) applied to buried interfaces of systems involving Transition Metal Oxides. • Enhanced contribution of the s states at high kinetic energies both for valence and core level spectra. • Sensitivity to chemical changes promoted by electric field across metal-oxide interfaces in resistive switching devices. - Abstract: Photoelectron spectroscopy is one of the most powerful tool to unravel the electronic structure of strongly correlated materials also thanks to the extremely large dynamic range in energy, coupled to high energy resolution that this form of spectroscopy covers. The kinetic energy range typically used for photoelectron experiments corresponds often to a strong surface sensitivity, and this turns out to be a disadvantage for the study of transition metal oxides, systems where structural and electronic reconstruction, different oxidation state, and electronic correlation may significantly vary at the surface. We report here selected Hard X-ray PhotoElectron Spectroscopy (HAXPES) results from transition metal oxides, and from buried interfaces, where we highlight some of the important features that such bulk sensitive technique brings in the analysis of electronic properties of the solids.

Hard X-ray PhotoElectron Spectroscopy of transition metal oxides: Bulk compounds and device-ready metal-oxide interfaces

Energy Technology Data Exchange (ETDEWEB)

Borgatti, F., E-mail: francesco.borgatti@cnr.it [Istituto per lo Studio dei Materiali Nanostrutturati (ISMN), Consiglio Nazionale delle Ricerche (CNR), via P. Gobetti 101, Bologna I-40129 (Italy); Torelli, P.; Panaccione, G. [Istituto Officina dei Materiali (IOM)-CNR, Laboratorio TASC, Area Science Park, Trieste I-34149 (Italy)

2016-04-15

Highlights: • Hard X-ray PhotoElectron Spectroscopy (HAXPES) applied to buried interfaces of systems involving Transition Metal Oxides. • Enhanced contribution of the s states at high kinetic energies both for valence and core level spectra. • Sensitivity to chemical changes promoted by electric field across metal-oxide interfaces in resistive switching devices. - Abstract: Photoelectron spectroscopy is one of the most powerful tool to unravel the electronic structure of strongly correlated materials also thanks to the extremely large dynamic range in energy, coupled to high energy resolution that this form of spectroscopy covers. The kinetic energy range typically used for photoelectron experiments corresponds often to a strong surface sensitivity, and this turns out to be a disadvantage for the study of transition metal oxides, systems where structural and electronic reconstruction, different oxidation state, and electronic correlation may significantly vary at the surface. We report here selected Hard X-ray PhotoElectron Spectroscopy (HAXPES) results from transition metal oxides, and from buried interfaces, where we highlight some of the important features that such bulk sensitive technique brings in the analysis of electronic properties of the solids.

Localized conductive patterning via focused electron beam reduction of graphene oxide

Energy Technology Data Exchange (ETDEWEB)

Kim, Songkil; Henry, Mathias [George W. Woodruff School of Mechanical Engineering, Georgia Institute of Technology, Atlanta, Georgia 30332 (United States); Kulkarni, Dhaval D.; Zackowski, Paul; Jang, Seung Soon; Tsukruk, Vladimir V. [School of Materials Science and Engineering, Georgia Institute of Technology, Atlanta, Georgia 30332 (United States); Fedorov, Andrei G., E-mail: agf@gatech.edu [George W. Woodruff School of Mechanical Engineering, Georgia Institute of Technology, Atlanta, Georgia 30332 (United States); Parker H. Petit Institute for Bioengineering and Bioscience, Georgia Institute of Technology, Atlanta, Georgia 30332 (United States)

2015-03-30

We report on a method for “direct-write” conductive patterning via reduction of graphene oxide (GO) sheets using focused electron beam induced deposition (FEBID) of carbon. FEBID treatment of the intrinsically dielectric graphene oxide between two metal terminals opens up the conduction channel, thus enabling a unique capability for nanoscale conductive domain patterning in GO. An increase in FEBID electron dose results in a significant increase of the domain electrical conductivity with improving linearity of drain-source current vs. voltage dependence, indicative of a change of graphene oxide electronic properties from insulating to semiconducting. Density functional theory calculations suggest a possible mechanism underlying this experimentally observed phenomenon, as localized reduction of graphene oxide layers via interactions with highly reactive intermediates of electron-beam-assisted dissociation of surface-adsorbed hydrocarbon molecules. These findings establish an unusual route for using FEBID as nanoscale lithography and patterning technique for engineering carbon-based nanomaterials and devices with locally tailored electronic properties.

Protective effect of ashwagandha (Withania somnifera against neurotoxicity induced by aluminum chloride in rats

Directory of Open Access Journals (Sweden)

Mohamed E Elhadidy

2018-01-01

Full Text Available Objective: To evaluate the neuroprotective effect of ashwagandha extract against aluminum chloride-induced neurotoxicity in rats. Methods: Rats were divided into control, aluminum-intoxicated rats treated daily with aluminum trichloride (AlCl3 (100 mg/kg, orally for 30 d and aluminum-intoxicated animals protected by receiving daily ashwagandha extract (200 mg/kg, orally one hour before AlCl3 administration for 30 d. Levels of lipid peroxidation, nitric oxide, reduced glutathione and tumor necrosis factor-α were measured in the cortex, hippocampus and striatum. In addition, the activities of Na+, K+, ATPase and acetylcholinesterase were determined in the three studied brain regions. Results: Aluminum increased the levels of lipid peroxidation and nitric oxide in the cortex, hippocampus and striatum and decreased the reduced glutathione level in the hippocampus and striatum. In rats protected with ashwagandha extract, non significant changes were observed in lipid peroxidation, nitric oxide and reduced glutathione. In addition, ashwagandha extracts prevented the increased activity of acetylcholinesterase and Na+, K+, ATPase induced by AlCl3 in the cortex, hippocampus and striatum. The present findings also showed that the significant increase in tumor necrosis factor-α induced by AlCl3 in the cortex and hippocampus was prevented by ashwagandha extract. Conclusions: The present results suggest that ashwagandha extract possesses antioxidant and anti-inflammatory effects against aluminum neurotoxicity. In addition, ashwagandha extract could prevent the decline in cholinergic activity by maintaining normal acetylcholinesterase activity. The later effect could recommend the use of ashwagandha as a memory enhancer.

C-Phycocyanin protects against acute tributyltin chloride neurotoxicity by modulating glial cell activity along with its anti-oxidant and anti-inflammatory property: A comparative efficacy evaluation with N-acetyl cysteine in adult rat brain.

Science.gov (United States)

Mitra, Sumonto; Siddiqui, Waseem A; Khandelwal, Shashi

2015-08-05

Spirulina is a widely used health supplement and is a dietary source of C-Phycocyanin (CPC), a potent anti-oxidant. We have previously reported the neurotoxic potential of tributyltin chloride (TBTC), an environmental pollutant and potent biocide. In this study, we have evaluated the protective efficacy of CPC against TBTC induced neurotoxicity. To evaluate the extent of neuroprotection offered by CPC, its efficacy was compared with the degree of protection offered by N-acetylcysteine (NAC) (a well known neuroprotective drug, taken as a positive control). Male Wistar rats (28 day old) were administered with 20mg/kg TBTC (oral) and 50mg/kg CPC or 50mg/kg NAC (i.p.), alone or in combination, and various parameters were evaluated. These include blood-brain barrier (BBB) damage; redox parameters (ROS, GSH, redox pathway associated enzymes, oxidative stress markers); inflammatory, cellular, and stress markers; apoptotic proteins and in situ cell death assay (TUNEL). We observed increased CPC availability in cortical tissue following its administration. Although BBB associated proteins like claudin-5, p-glycoprotein and ZO-1 were restored, CPC/NAC failed to protect against TBTC induced overall BBB permeability (Evans blue extravasation). Both CPC and NAC remarkably reduced oxidative stress and inflammation. NAC effectively modulated redox pathway associated enzymes whereas CPC countered ROS levels efficiently. Interestingly, CPC and NAC were equivalently capable of reducing apoptotic markers, astroglial activation and cell death. This study illustrates the various pathways involved in CPC mediated neuroprotection against this environmental neurotoxicant and highlights its capability to modulate glial cell activity. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.

Participation of Low Molecular Weight Electron Carriers in Oxidative Protein Folding

Directory of Open Access Journals (Sweden)

József Mandl

2009-03-01

Full Text Available Oxidative protein folding is mediated by a proteinaceous electron relay system, in which the concerted action of protein disulfide isomerase and Ero1 delivers the electrons from thiol groups to the final acceptor. Oxygen appears to be the final oxidant in aerobic living organisms, although the existence of alternative electron acceptors, e.g. fumarate or nitrate, cannot be excluded. Whilst the protein components of the system are well-known, less attention has been turned to the role of low molecular weight electron carriers in the process. The function of ascorbate, tocopherol and vitamin K has been raised recently. In vitro and in vivo evidence suggests that these redox-active compounds can contribute to the functioning of oxidative folding. This review focuses on the participation of small molecular weight redox compounds in oxidative protein folding.

Current status of developmental neurotoxicity: regulatory view

DEFF Research Database (Denmark)

Hass, Ulla

2003-01-01

in the testing strategy for new and existing substances, and biocides. Hopefully, this will lead to an improved database for risk assessment of potential developmental neurotoxicants. However, the regulatory authorities and toxicologists will also be faced with the challenge that decisions have to be made......The need for developmental neurotoxicity testing has been recognized for decades and guidelines are available, as the USEPA guideline and the OECD draft TG 426. Regulatory testing of industrial chemicals for developmental neurotoxicity is required to some extent, especially for pesticides in the US....... Until recently, however, developmental neurotoxicity testing of industrial chemicals has not been a clear regulatory requirement in EU, probably due to the lack of an accepted OECD TG. The revised EU Technical Guidance Document for Risk Assessment (EU-TGD) has now included the OECD draft TG 426...

Mitigation of acrylamide-induced behavioral deficits, oxidative impairments and neurotoxicity by oral supplements of geraniol (a monoterpene) in a rat model.

Science.gov (United States)

Prasad, Sathya N; Muralidhara

2014-11-05

In the recent past, several phytoconstituents are being explored for their potential neuromodulatory effects in neurological diseases. Repeated exposure of acrylamide (ACR) leads to varying degree of neuronal damage in experimental animals and humans. In view of this, the present study investigated the efficacy of geraniol (GE, a natural monoterpene) to mitigate acrylamide (ACR)-induced oxidative stress, mitochondrial dysfunction and neurotoxicity in a rat model and compared its efficacy to that of curcumin (CU, a spice active principle with multiple biological activities). ACR administration (50mg/kg bw, i.p. 3times/week) for 4weeks to growing rats caused typical symptoms of neuropathy. ACR rats provided with daily oral supplements of phytoconstituents (GE: 100mg/kg bw/d; CU: 50mg/kg bw/d, 4weeks) exhibited marked improvement in behavioral tests. Both phytoconstituents markedly attenuated ACR-induced oxidative stress as evidenced by the diminished levels of reactive oxygen species, malondialdehyde and nitric oxide and restored the reduced glutathione levels in sciatic nerve (SN) and brain regions (cortex - Ct, cerebellum - Cb). Further, both phytoconstituents effectively diminished ACR-induced elevation in cytosolic calcium levels in SN and Cb. Furthermore, diminution in the levels of oxidative markers in the mitochondria was associated with elevation in the activities of antioxidant enzymes. While ACR mediated elevation in the acetylcholinesterase activity was reduced by both actives, the depletion in dopamine levels was restored only by CU in brain regions. Taken together our findings for the first time demonstrate that the neuromodulatory propensity of GE is indeed comparable to that of CU and may be exploited as a therapeutic adjuvant in the management of varied human neuropathy conditions. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.

Relation between electron- and photon-caused oxidation in EUVL optics

Science.gov (United States)

Malinowski, Michael E.; Steinhaus, Charles A.; Meeker, Donald E.; Clift, W. Miles; Klebanoff, Leonard E.; Bajt, Sasa

2003-06-01

Extreme ultraviolet (EUV)-induced oxidation of silicon-capped, [Mo/Si] multilayer mirrors in the presence of background levels of water vapor is recognized as one of the most serious threats to multilayer lifetime since oxidation of the top silicon layer is an irreversible process. The current work directly compares the oxidation on a silicon-capped, [Mo/Si] multilayers caused by EUV photons with the oxidation caused by 1 keV electrons in the presence of the same water vapor environment (2 x 10-6 Torr). Similar, 4 nm, silicon-capped, [Mo/Si] multilayer mirror samples were exposed to photons (95.3 eV) + water vapor at the ALS, LBNL, and also to a 1 keV electron beam + water vapor in separate experimental systems. The results of this work showed that the oxidation produced by ~1 µA of e-beam current was found to be equivalent to that produced by ~1 mW of EUV exposure. These results will help allow the use of 1 keV electrons beams, instead of EUV photons, to perform environmental testing of multilayers in a low-pressure water environment and to more accurately determine projected mirror lifetimes based on the electron beam exposures.

Self-limited kinetics of electron doping in correlated oxides

International Nuclear Information System (INIS)

Chen, Jikun; Zhou, You; Jiang, Jun; Shi, Jian; Ramanathan, Shriram; Middey, Srimanta; Chakhalian, Jak; Chen, Nuofu; Chen, Lidong; Shi, Xun; Döbeli, Max

2015-01-01

Electron doping by hydrogenation can reversibly modify the electrical properties of complex oxides. We show that in order to realize large, fast, and reversible response to hydrogen, it is important to consider both the electron configuration on the transition metal 3d orbitals, as well as the thermodynamic stability in nickelates. Specifically, large doping-induced resistivity modulations ranging several orders of magnitude change are only observed for rare earth nickelates with small ionic radii on the A-site, in which case both electron correlation effects and the meta-stability of Ni 3+ are important considerations. Charge doping via metastable incorporation of ionic dopants is of relevance to correlated oxide-based devices where advancing approaches to modify the ground state electronic properties is an important problem

Local Anesthetic-Induced Neurotoxicity

NARCIS (Netherlands)

Verlinde, Mark; Hollmann, Markus W.; Stevens, Markus F.; Hermanns, Henning; Werdehausen, Robert; Lirk, Philipp

2016-01-01

This review summarizes current knowledge concerning incidence, risk factors, and mechanisms of perioperative nerve injury, with focus on local anesthetic-induced neurotoxicity. Perioperative nerve injury is a complex phenomenon and can be caused by a number of clinical factors. Anesthetic risk

Cyanobacterial Xenobiotics as Evaluated by a Caenorhabditis elegans Neurotoxicity Screening Test

Science.gov (United States)

Ju, Jingjuan; Saul, Nadine; Kochan, Cindy; Putschew, Anke; Pu, Yuepu; Yin, Lihong; Steinberg, Christian E. W.

2014-01-01

In fresh waters cyanobacterial blooms can produce a variety of toxins, such as microcystin variants (MCs) and anatoxin-a (ANA). ANA is a well-known neurotoxin, whereas MCs are hepatotoxic and, to a lesser degree, also neurotoxic. Neurotoxicity applies especially to invertebrates lacking livers. Current standardized neurotoxicity screening methods use rats or mice. However, in order to minimize vertebrate animal experiments as well as experimental time and effort, many investigators have proposed the nematode Caenorhabditis elegans as an appropriate invertebrate model. Therefore, four known neurotoxic compounds (positive compounds: chlorpyrifos, abamectin, atropine, and acrylamide) were chosen to verify the expected impacts on autonomic (locomotion, feeding, defecation) and sensory (thermal, chemical, and mechanical sensory perception) functions in C. elegans. This study is another step towards successfully establishing C. elegans as an alternative neurotoxicity model. By using this protocol, anatoxin-a adversely affected locomotive behavior and pharyngeal pumping frequency and, most strongly, chemotactic and thermotactic behavior, whereas MC-LR impacted locomotion, pumping, and mechanical behavior, but not chemical sensory behavior. Environmental samples can also be screened in this simple and fast way for neurotoxic characteristics. The filtrate of a Microcystis aeruginosa culture, known for its hepatotoxicity, also displayed mild neurotoxicity (modulated short-term thermotaxis). These results show the suitability of this assay for environmental cyanotoxin-containing samples. PMID:24776722

Transparent Oxide Semiconductors for Emerging Electronics

KAUST Repository

Caraveo-Frescas, Jesus Alfonso

2013-11-01

Transparent oxide electronics have emerged as promising materials to shape the future of electronics. While several n-type oxides have been already studied and demonstrated feasibility to be used as active materials in thin film transistors, high performance p-type oxides have remained elusive. This dissertation is devoted to the study of transparent p-type oxide semiconductor tin monoxide and its use in the fabrication of field effect devices. A complete study on the deposition of tin monoxide thin films by direct current reactive magnetron sputtering is performed. Carrier density, carrier mobility and conductivity are studied over a set of deposition conditions where p-type conduction is observed. Density functional theory simulations are performed in order to elucidate the effect of native defects on carrier mobility. The findings on the electrical properties of SnO thin films are then translated to the fabrication of thin films transistors. The low processing temperature of tin monoxide thin films below 200 oC is shown advantageous for the fabrication of fully transparent and flexible thin film transistors. After careful device engineering, including post deposition annealing temperature, gate dielectric material, semiconductor thickness and source and drain electrodes material, thin film transistors with record device performance are demonstrated, achieving a field effect mobility >6.7 cm2V-1s-1. Device performance is further improved to reach a field effect mobility of 10.8 cm2V-1s-1 in SnO nanowire field effect transistors fabricated from the sputtered SnO thin films and patterned by electron beam lithography. Downscaling device dimension to nano scale is shown beneficial for SnO field effect devices not only by achieving a higher hole mobility but enhancing the overall device performance including better threshold voltage, subthreshold swing and lower number of interfacial defects. Use of p-type semiconductors in nonvolatile memory applications is then

Transmission Electron Microscopy Studies of Electron-Selective Titanium Oxide Contacts in Silicon Solar Cells

KAUST Repository

Ali, Haider; Yang, Xinbo; Weber, Klaus; Schoenfeld, Winston V.; Davis, Kristopher O.

2017-01-01

In this study, the cross-section of electron-selective titanium oxide (TiO2) contacts for n-type crystalline silicon solar cells were investigated by transmission electron microscopy. It was revealed that the excellent cell efficiency of 21

Changes in gene expression linked to methamphetamine-induced dopaminergic neurotoxicity.

Science.gov (United States)

Xie, Tao; Tong, Liqiong; Barrett, Tanya; Yuan, Jie; Hatzidimitriou, George; McCann, Una D; Becker, Kevin G; Donovan, David M; Ricaurte, George A

2002-01-01

The purpose of these studies was to examine the role of gene expression in methamphetamine (METH)-induced dopamine (DA) neurotoxicity. First, the effects of the mRNA synthesis inhibitor, actinomycin-D, and the protein synthesis inhibitor, cycloheximide, were examined. Both agents afforded complete protection against METH-induced DA neurotoxicity and did so independently of effects on core temperature, DA transporter function, or METH brain levels, suggesting that gene transcription and mRNA translation play a role in METH neurotoxicity. Next, microarray technology, in combination with an experimental approach designed to facilitate recognition of relevant gene expression patterns, was used to identify gene products linked to METH-induced DA neurotoxicity. This led to the identification of several genes in the ventral midbrain associated with the neurotoxic process, including genes for energy metabolism [cytochrome c oxidase subunit 1 (COX1), reduced nicotinamide adenine dinucleotide ubiquinone oxidoreductase chain 2, and phosphoglycerate mutase B], ion regulation (members of sodium/hydrogen exchanger and sodium/bile acid cotransporter family), signal transduction (adenylyl cyclase III), and cell differentiation and degeneration (N-myc downstream-regulated gene 3 and tau protein). Of these differentially expressed genes, we elected to further examine the increase in COX1 expression, because of data implicating energy utilization in METH neurotoxicity and the known role of COX1 in energy metabolism. On the basis of time course studies, Northern blot analyses, in situ hybridization results, and temperature studies, we now report that increased COX1 expression in the ventral midbrain is linked to METH-induced DA neuronal injury. The precise role of COX1 and other genes in METH neurotoxicity remains to be elucidated.

Electronic structure investigation of oxidized aluminium films with electron momentum spectroscopy

International Nuclear Information System (INIS)

Guo, X.; Canney, S.; Kheifets, A.S.; Vos, M.; Fang, Z.; Utteridge, S.; McCarthy, I.E.; Weigold, E.

1996-09-01

Electron momentum spectroscopy (EMS) of (e, 2e) measurements with oxidized aluminium thin films have been performed. Due to the surface sensitive mature of the EMS spectrometer employed the measured (e, 2e) events come from the front oxidized layer as viewed by the electron detectors. The measurements show clearly two major features in the spectral momentum density distribution and they are related to the upper valence band and the lower valence band of aluminum oxide. The first is a 'dual parabola' energy-momentum dispersion pattern spanning about 8 eV in the upper valence band. This 'dual parabola' pattern has been qualitatively reproduced by a linear muffin-tin orbital (LMTO) calculation on spherically averaged α-A1 2 O 3 with nearly the same energy span. In the lower valence band, the LMTO calculation indicates a dispersion spanning about 5 eV, and the measured spectral momentum density plot shows a similar 'bowl' shape but with less dispersion. The possible causes which blur the dispersion in the lower valence band are discussed. Other features in the spectral momentum density distribution are also discussed and compared with the LMTO calculation. 45 refs., 1 tab., 10 figs

Latest progress in gallium-oxide electronic devices

Science.gov (United States)

Higashiwaki, Masataka; Wong, Man Hoi; Konishi, Keita; Nakata, Yoshiaki; Lin, Chia-Hung; Kamimura, Takafumi; Ravikiran, Lingaparthi; Sasaki, Kohei; Goto, Ken; Takeyama, Akinori; Makino, Takahiro; Ohshima, Takeshi; Kuramata, Akito; Yamakoshi, Shigenobu; Murakami, Hisashi; Kumagai, Yoshinao

2018-02-01

Gallium oxide (Ga2O3) has emerged as a new competitor to SiC and GaN in the race toward next-generation power switching and harsh environment electronics by virtue of the excellent material properties and the relative ease of mass wafer production. In this proceedings paper, an overview of our recent development progress of Ga2O3 metal-oxide-semiconductor field-effect transistors and Schottky barrier diodes will be reported.

Developmental neurotoxicity of pyrethroid insecticides in zebrafish embryos.

Science.gov (United States)

DeMicco, Amy; Cooper, Keith R; Richardson, Jason R; White, Lori A

2010-01-01

Pyrethroid insecticides are one of the most commonly used residential and agricultural insecticides. Based on the increased use of pyrethroids and recent studies showing that pregnant women and children are exposed to pyrethroids, there are concerns over the potential for developmental neurotoxicity. However, there have been relatively few studies on the developmental neurotoxicity of pyrethroids. In this study, we sought to investigate the developmental toxicity of six common pyrethroids, three type I compounds (permethrin, resmethrin, and bifenthrin) and three type II compounds (deltamethrin, cypermethrin, and lambda-cyhalothrin), and to determine whether zebrafish embryos may be an appropriate model for studying the developmental neurotoxicity of pyrethroids. Exposure of zebrafish embryos to pyrethroids caused a dose-dependent increase in mortality and pericardial edema, with type II compounds being the most potent. At doses approaching the LC(50), permethrin and deltamethrin caused craniofacial abnormalities. These findings are consistent with mammalian studies demonstrating that pyrethroids are mildly teratogenic at very high doses. However, at lower doses, body axis curvature and spasms were observed, which were reminiscent of the classic syndromes observed with pyrethroid toxicity. Treatment with diazepam ameliorated the spasms, while treatment with the sodium channel antagonist MS-222 ameliorated both spasms and body curvature, suggesting that pyrethroid-induced neurotoxicity is similar in zebrafish and mammals. Taken in concert, these data suggest that zebrafish may be an appropriate alternative model to study the mechanism(s) responsible for the developmental neurotoxicity of pyrethroid insecticides and aid in identification of compounds that should be further tested in mammalian systems.

Structural changes in graphene oxide thin film by electron-beam irradiation

Energy Technology Data Exchange (ETDEWEB)

Tyagi, Chetna, E-mail: tchetna91@gmail.com [Materials Science Group, Inter University Accelerator Centre, New Delhi 67 (India); Lakshmi, G.B.V.S.; Kumar, Sunil; Tripathi, Ambuj [Materials Science Group, Inter University Accelerator Centre, New Delhi 67 (India); Avasthi, D.K. [Amity University, Noida 201313, Uttar Pradesh (India)

2016-07-15

Although we have a whole class of 2D materials, graphene has drawn much attention for its excellent electronic, optical, thermal and mechanical properties. Recent researches have shown its large scale production by the reduction of graphene oxide either thermally, chemically or electrochemically. Although the structure of graphene oxide is inhomogeneous and hence complicated due to the presence of organic moieties e.g. epoxy, carboxylic acid, hydroxyl groups etc., its properties can be tuned by reduction according to desired application. The aim of this work is to synthesize continuous thin film of graphene oxide using commercially available graphene oxide solution and to study its reduction by 25 keV electron beam irradiation at fluences varying from 2 × 10{sup 11} to 2 × 10{sup 13} e{sup −}/cm{sup 2}. Our studies using X-ray diffraction, Raman microscopy and UV–Vis spectroscopy showed that electron-beam irradiation is an effective tool for reduction of graphene oxide and for tuning its band gap.

Inhibitors of Microglial Neurotoxicity: Focus on Natural Products

Directory of Open Access Journals (Sweden)

Kyoungho Suk

2011-01-01

Full Text Available Microglial cells play a dual role in the central nervous system as they have both neurotoxic and neuroprotective effects. Uncontrolled and excessive activation of microglia often contributes to inflammation-mediated neurodegeneration. Recently, much attention has been paid to therapeutic strategies aimed at inhibiting neurotoxic microglial activation. Pharmacological inhibitors of microglial activation are emerging as a result of such endeavors. In this review, natural products-based inhibitors of microglial activation will be reviewed. Potential neuroprotective activity of these compounds will also be discussed. Future works should focus on the discovery of novel drug targets that specifically mediate microglial neurotoxicity rather than neuroprotection. Development of new drugs based on these targets may require a better understanding of microglial biology and neuroinflammation at the molecular, cellular, and systems levels.

Tantalum surface oxidation: Bond relaxation, energy entrapment, and electron polarization

Energy Technology Data Exchange (ETDEWEB)

Guo, Yongling [Key Laboratory of Low-Dimensional Materials and Application Technologies (Ministry of Education), Hunan Provincial Key Laboratory of Thin Film Materials and Devices, Faculty of Materials Science and Engineering, Xiangtan University, Hunan 411105 (China); Bo, Maolin [Yangtze Normal University, College of Mechanical and Electrical Engineering, Chongqing 408100 (China); Wang, Yan [School of Information and Electronic Engineering, Hunan University of Science and Technology, Hunan 411201 (China); Liu, Yonghui [Key Laboratory of Low-Dimensional Materials and Application Technologies (Ministry of Education), Hunan Provincial Key Laboratory of Thin Film Materials and Devices, Faculty of Materials Science and Engineering, Xiangtan University, Hunan 411105 (China); Sun, Chang Q. [NOVITAS, School of Electrical and Electronic Engineering, Nanyang Technological University, Singapore 639798 (Singapore); Huang, Yongli, E-mail: huangyongli@xtu.edu.cn [Key Laboratory of Low-Dimensional Materials and Application Technologies (Ministry of Education), Hunan Provincial Key Laboratory of Thin Film Materials and Devices, Faculty of Materials Science and Engineering, Xiangtan University, Hunan 411105 (China)

2017-02-28

Graphical abstract: The bond, electron and energy relaxation result in core level energy shift, local densification, quantum entrapment and electron polarization of bonding electrons. - Highlights: • Increasing the oxygen coverage lowers the adsorption energy associated with lattice reconstruction. • Electrons transfer from Ta surface atoms to sp-hydrated oxygen, creating dipole moment that decreases the work function. • Oxygen chemisorption modified valence density-of-state (DOS) for Ta with four excessive DOS features: O−Ta bonding, O{sup 2−} lone pairs, Ta+ electron holes, and the lone-pair polarized Ta dipoles. • The bond, electron and energy relaxation between surface undercoordinated atoms are responsible for core level energy shift, local densification, quantum entrapment and electron polarization of bonding electrons. - Abstract: A combination of photoelectron spectrometric analysis and density functional theory calculations has enabled reconciliation of the bond-energy-electron relaxation for the Ta(100, 110, 111) surfaces chemisorbed with oxygen at different coverages. Results show that increasing oxygen coverage lowers the adsorption energy associated with lattice reconstruction. Valence electrons transfer from Ta surface atoms to oxygen to create four excessive DOS features in terms of O−Ta bonding, lone pairs of oxygen, Ta{sup +} electron holes, and polarized Ta dipoles. Oxidation proceeds in the following dynamics: oxygen gets electrons from two neighboring Ta atoms left behind Ta{sup +}; the sp{sup 3}-orbital hybridization takes place with additional two electron lone pairs, the lone pairs polarize the other two Ta neighbors becoming dipoles. X-ray photoelectron spectral analysis results in the 4f binding energy of an isolated Ta atom and its shift upon bond formation and oxidation. Exercises provide not only a promising numerical approach for the quantitative information about the bond and electronic behavior but also consistent

Tantalum surface oxidation: Bond relaxation, energy entrapment, and electron polarization

International Nuclear Information System (INIS)

Guo, Yongling; Bo, Maolin; Wang, Yan; Liu, Yonghui; Sun, Chang Q.; Huang, Yongli

2017-01-01

Graphical abstract: The bond, electron and energy relaxation result in core level energy shift, local densification, quantum entrapment and electron polarization of bonding electrons. - Highlights: • Increasing the oxygen coverage lowers the adsorption energy associated with lattice reconstruction. • Electrons transfer from Ta surface atoms to sp-hydrated oxygen, creating dipole moment that decreases the work function. • Oxygen chemisorption modified valence density-of-state (DOS) for Ta with four excessive DOS features: O−Ta bonding, O"2"− lone pairs, Ta+ electron holes, and the lone-pair polarized Ta dipoles. • The bond, electron and energy relaxation between surface undercoordinated atoms are responsible for core level energy shift, local densification, quantum entrapment and electron polarization of bonding electrons. - Abstract: A combination of photoelectron spectrometric analysis and density functional theory calculations has enabled reconciliation of the bond-energy-electron relaxation for the Ta(100, 110, 111) surfaces chemisorbed with oxygen at different coverages. Results show that increasing oxygen coverage lowers the adsorption energy associated with lattice reconstruction. Valence electrons transfer from Ta surface atoms to oxygen to create four excessive DOS features in terms of O−Ta bonding, lone pairs of oxygen, Ta"+ electron holes, and polarized Ta dipoles. Oxidation proceeds in the following dynamics: oxygen gets electrons from two neighboring Ta atoms left behind Ta"+; the sp"3-orbital hybridization takes place with additional two electron lone pairs, the lone pairs polarize the other two Ta neighbors becoming dipoles. X-ray photoelectron spectral analysis results in the 4f binding energy of an isolated Ta atom and its shift upon bond formation and oxidation. Exercises provide not only a promising numerical approach for the quantitative information about the bond and electronic behavior but also consistent insight into the

Oxide-cathode activation and surface temperature calculation of electron cooler

International Nuclear Information System (INIS)

Li Jie; Yang Xiaodong; Mao Lijun; Li Guohong; Yuan Youjin; Liu Zhanwen; Zhang Junhui; Yang Xiaotian; Ma Xiaoming; Yan Tailai

2011-01-01

The pollution on electron gun ceramic insulation of electron cooler restricted the operation of electron cooler at HIRFL-CSR main ring. To cool and accumulate ion beam well, the pollution was cleared and a new oxide-coated cathode was assembled. The processes of cathode replacement,vacuum chamber baking-out, and thermal decomposition of coating binders and alkaline earth metal carbonates, and cathode activation are presented. The electron gun perveance of 10.6 μA/V 1.5 was attained under the heating power of 60 W. The typical surface temperature of oxide-coated cathode that is calculated through grey-body radiation is 1 108 K which shows a comparable result to the experimental measurement 1 078 K. The perveance growth of electron gun during the electron cooler operation is also explained by partial activation of the cathode. (authors)

Assessing the Developmental Neurotoxicity of 27 ...

Science.gov (United States)

Assessing the Developmental Neurotoxicity of 27 Organophosphorus Pesticides Using a Zebrafish Behavioral Assay, Waalkes, M., Hunter, D.L., Jarema, K., Mundy, W., and S. Padilla. The U.S. Environmental Protection Agency is evaluating methods to screen and prioritize organophosphorus pesticides for developmental neurotoxicity. As such, we are exploring a behavioral testing paradigm that can assess the effects of sublethal and subteratogenic concentrations of developmental neurotoxicants on zebrafish (Danio rerio). This in vivo assay quantifies the locomotor response to light stimuli under tandem light and dark conditions in a 96-well plate using a video tracking system on 6 day post fertilization zebrafish larvae. Each of twenty-seven organophosphorus pesticides was tested for their developmental neurotoxic potential by exposing zebrafish embryos/larvae to the pesticide at several concentrations (≤ 100 μM nominal concentration) during the first five days of development, followed by 24 hours of depuration and then behavioral testing. Approximately 22% of the chemicals (Acephate, Dichlorvos, Diazoxon, Bensulide,Tribufos, Tebupirimfos) did not produce any behavioral changes after developmental exposure, while many (Malaoxon Fosthiazate, Dimethoate, Dicrotophos, Ethoprop, Malathion, Naled, Diazinon, Methamidophos, Terbufos, Trichlorfon, Phorate, Pirimiphos-methyl, Profenofos, Z-Tetrachlorvinphos, Chlorpyrifos, Coumaphos, Phosmet, Omethoate) produced changes in swi

Neurotoxicity of fragrance compounds: A review.

Science.gov (United States)

Pinkas, Adi; Gonçalves, Cinara Ludvig; Aschner, Michael

2017-10-01

Fragrance compounds are chemicals belonging to one of several families, which are used frequently and globally in cosmetics, household products, foods and beverages. A complete list of such compounds is rarely found on the ingredients-list of such products, as "fragrance mixtures" are defined as "trade secrets" and thus protected by law. While some information regarding the general toxicity of some of these compounds is available, their neurotoxicity is known to a lesser extent. Here, we discuss the prevalence and neurotoxicity of fragrance compounds belonging to the three most common groups: phthalates, synthetic musks and chemical sensitizers. Copyright © 2017 Elsevier Inc. All rights reserved.

Neurotoxic shellfish poisoning: A review

NARCIS (Netherlands)

Apeldoorn ME van; Egmond HP van; Speijers GJA; CSR; ARO

2001-01-01

Dit literatuuroverzicht bevat informatie betreffende het "neurotoxic shellfish poisoning" (NSP) syndroom en de veroorzakende toxines, nl.de brevetoxines, welke geproduceerd worden door de dinoflagellaat Gymnodinium breve. Chemische structuren en detectie-methodes van de brevetoxines,

Neurite outgrowth in human induced pluripotent stem cell-derived neurons as a high-throughput screen for developmental neurotoxicity or neurotoxicity.

Science.gov (United States)

Ryan, Kristen R; Sirenko, Oksana; Parham, Fred; Hsieh, Jui-Hua; Cromwell, Evan F; Tice, Raymond R; Behl, Mamta

2016-03-01

Due to the increasing prevalence of neurological disorders and the large number of untested compounds in the environment, there is a need to develop reliable and efficient screening tools to identify environmental chemicals that could potentially affect neurological development. Herein, we report on a library of 80 compounds screened for their ability to inhibit neurite outgrowth, a process by which compounds may elicit developmental neurotoxicity, in a high-throughput, high-content assay using human neurons derived from induced pluripotent stem cells (iPSC). The library contains a diverse set of compounds including those that have been known to be associated with developmental neurotoxicity (DNT) and/or neurotoxicity (NT), environmental compounds with unknown neurotoxic potential (e.g., polycyclic aromatic hydrocarbons (PAHs) and flame retardants (FRs)), as well as compounds with no documented neurotoxic potential. Neurons were treated for 72h across a 6-point concentration range (∼0.3-100μM) in 384-well plates. Effects on neurite outgrowth were assessed by quantifying total outgrowth, branches, and processes. We also assessed the number ofviable cells per well. Concentration-response profiles were evaluated using a Hill model to derive benchmark concentration (BMC) values. Assay performance was evaluated using positive and negative controls and test replicates. Compounds were ranked by activity and selectivity (i.e., specific effects on neurite outgrowth in the absence of concomitant cytotoxicity) and repeat studies were conducted to confirm selectivity. Among the 80 compounds tested, 38 compounds were active, of which 16 selectively inhibited neurite outgrowth. Of these 16 compounds, 12 were known to cause DNT/NT and the remaining 4 compounds included 3 PAHs and 1 FR. In independent repeat studies, 14/16 selective compounds were reproducibly active in the assay, of which only 6 were selective for inhibition of neurite outgrowth. These 6 compounds were

A comparison between different oxide dispersion strengthened ferritic steel ongoing in situ oxide dissolution in High Voltage Electron Microscope

International Nuclear Information System (INIS)

Monnet, I.; Van den Berghe, T.; Dubuisson, Ph.

2012-01-01

ODS materials are considered for nuclear applications but previous experimental studies have shown a partial dissolution of some oxides under neutron irradiation. In this work, electron irradiations were used to evaluate the stability of the oxides depending on the chemical composition of the oxide dispersion. Four ferritic steels based on EM10 (Fe–9Cr–1Mo) and reinforced respectively by Al 2 O 3 , MgO, MgAl 2 O 4 and Y 2 O 3 , were studied. These materials were irradiated with 1 MeV or 1.2 MeV electrons in a High Voltage Electron Microscope. This technique allows to follow one single oxide and to determine the evolution of its size during the irradiation. In situ HVEM observations indicate that the dissolution rate depends on the chemical composition of the oxide, on the temperature and on the irradiation dose.

Hyperforin prevents beta-amyloid neurotoxicity and spatial memory impairments by disaggregation of Alzheimer's amyloid-beta-deposits.

Science.gov (United States)

Dinamarca, M C; Cerpa, W; Garrido, J; Hancke, J L; Inestrosa, N C

2006-11-01

The major protein constituent of amyloid deposits in Alzheimer's disease (AD) is the amyloid beta-peptide (Abeta). In the present work, we have determined the effect of hyperforin an acylphloroglucinol compound isolated from Hypericum perforatum (St John's Wort), on Abeta-induced spatial memory impairments and on Abeta neurotoxicity. We report here that hyperforin: (1) decreases amyloid deposit formation in rats injected with amyloid fibrils in the hippocampus; (2) decreases the neuropathological changes and behavioral impairments in a rat model of amyloidosis; (3) prevents Abeta-induced neurotoxicity in hippocampal neurons both from amyloid fibrils and Abeta oligomers, avoiding the increase in reactive oxidative species associated with amyloid toxicity. Both effects could be explained by the capacity of hyperforin to disaggregate amyloid deposits in a dose and time-dependent manner and to decrease Abeta aggregation and amyloid formation. Altogether these evidences suggest that hyperforin may be useful to decrease amyloid burden and toxicity in AD patients, and may be a putative therapeutic agent to fight the disease.

OXIDATION OF POLYCHLORINATED BIPHENYLS BY LIVER TISSUE SLICES FROM PHENOBARBITAL-PRETREATED MICE IS CONGENER-SPECIFIC AND ATROPSELECTIVE

OpenAIRE

Wu, Xianai; Duffel, Michael; Lehmler, Hans-Joachim

2013-01-01

Mouse models are powerful tools to study the developmental neurotoxicity of polychlorinated biphenyls (PCBs); however, studies of the oxidation of chiral PCB congeners to potentially neurotoxic hydroxylated metabolites (OH-PCBs) in mice have not been reported. Here we investigate the atropselective oxidation of chiral PCB 91 (2,2',3,4',6-pentachlorobiphenyl), PCB 95 (2,2',3,5',6-pentachlorobiphenyl), PCB 132 (2,2',3,3',4,6'-hexachlorobiphenyl), PCB 136 (2,2',3,3',6,6'-hexachlorobiphenyl) and ...

Electron small polarons and their mobility in iron (oxyhydr)oxide nanoparticles

DEFF Research Database (Denmark)

Katz, Jordan E; Zhang, Xiaoyi; Attenkofer, Klaus

2012-01-01

Electron mobility within iron (oxyhydr)oxides enables charge transfer between widely separated surface sites. There is increasing evidence that this internal conduction influences the rates of interfacial reactions and the outcomes of redox-driven phase transformations of environmental interest....... To determine the links between crystal structure and charge-transport efficiency, we used pump-probe spectroscopy to study the dynamics of electrons introduced into iron(III) (oxyhydr)oxide nanoparticles via ultrafast interfacial electron transfer. Using time-resolved x-ray spectroscopy and ab initio...

Microplastics cause neurotoxicity, oxidative damage and energy-related changes and interact with the bioaccumulation of mercury in the European seabass, Dicentrarchus labrax (Linnaeus, 1758).

Science.gov (United States)

Barboza, Luís Gabriel Antão; Vieira, Luís Russo; Branco, Vasco; Figueiredo, Neusa; Carvalho, Felix; Carvalho, Cristina; Guilhermino, Lúcia

2018-02-01

Microplastics pollution is a global paradigm that raises concern in relation to environmental and human health. This study investigated toxic effects of microplastics and mercury in the European seabass (Dicentrarchus labrax), a marine fish widely used as food for humans. A short-term (96 h) laboratory bioassay was done by exposing juvenile fish to microplastics (0.26 and 0.69 mg/L), mercury (0.010 and 0.016 mg/L) and binary mixtures of the two substances using the same concentrations, through test media. Microplastics alone and mercury alone caused neurotoxicity through acetylcholinesterase (AChE) inhibition, increased lipid oxidation (LPO) in brain and muscle, and changed the activities of the energy-related enzymes lactate dehydrogenase (LDH) and isocitrate dehydrogenase (IDH). All the mixtures caused significant inhibition of brain AChE activity (64-76%), and significant increase of LPO levels in brain (2.9-3.4 fold) and muscle (2.2-2.9 fold) but not in a concentration-dependent manner; mixtures containing low and high concentrations of microplastics caused different effects on IDH and LDH activity. Mercury was found to accumulate in the brain and muscle, with bioaccumulation factors of 4-7 and 25-40, respectively. Moreover, in the analysis of mercury concentrations in both tissues, a significant interaction between mercury and microplastics was found. The decay of mercury in the water increased with microplastics concentration, and was higher in the presence of fish than in their absence. Overall, these results indicate that: microplastics influence the bioaccumulation of mercury by D. labrax juveniles; microplastics, mercury and their mixtures (ppb range concentrations) cause neurotoxicity, oxidative stress and damage, and changes in the activities of energy-related enzymes in juveniles of this species; mixtures with the lowest and highest concentrations of their components induced different effects on some biomarkers. These findings and other published

Tricyclic sesquiterpene copaene prevents H2O2-induced neurotoxicity

Directory of Open Access Journals (Sweden)

Hasan Turkez

2014-02-01

Full Text Available Aim: Copaene (COP, a tricyclic sesquiterpene, is present in several essential oils of medicinal and aromatic plants and has antioxidant and anticarcinogenic features. But, very little information is known about the effects of COP on oxidative stress induced neurotoxicity. Method: We used hydrogen peroxide (H2O2 exposure for 6 h to model oxidative stress. Therefore, this experimental design allowed us to explore the neuroprotective potential of COP in H2O2-induced toxicity in rat cerebral cortex cell cultures for the first time. For this purpose, methyl thiazolyl tetrazolium (MTT and lactate dehydrogenase (LDH release assays were carried out to evaluate cytotoxicity. Total antioxidant capacity (TAC and total oxidative stress (TOS parameters were used to evaluate oxidative changes. In addition to determining of 8-hydroxy-2-deoxyguanosine (8-OH-dG levels, the single cell gel electrophoresis (SCGE or comet assay was also performed for measuring the resistance of neuronal DNA to H2O2-induced challenge. Result: The results of this study showed that survival and TAC levels of the cells decreased, while TOS, 8-OH-dG levels and the mean values of the total scores of cells showing DNA damage increased in the H2O2 alone treated cultures. But pre-treatment of COP suppressed the cytotoxicity, genotoxicity and oxidative stress which were increased by H2O2. Conclusion: It is proposed that COP as a natural product with an antioxidant capacity in mitigating oxidative injuries in the field of neurodegenerative diseases. [J Intercult Ethnopharmacol 2014; 3(1.000: 21-28

Silver nanoparticles reduce brain inflammation and related neurotoxicity through induction of H2S-synthesizing enzymes

Science.gov (United States)

Gonzalez-Carter, Daniel A.; Leo, Bey Fen; Ruenraroengsak, Pakatip; Chen, Shu; Goode, Angela E.; Theodorou, Ioannis G.; Chung, Kian Fan; Carzaniga, Raffaella; Shaffer, Milo S. P.; Dexter, David T.; Ryan, Mary P.; Porter, Alexandra E.

2017-03-01

Silver nanoparticles (AgNP) are known to penetrate into the brain and cause neuronal death. However, there is a paucity in studies examining the effect of AgNP on the resident immune cells of the brain, microglia. Given microglia are implicated in neurodegenerative disorders such as Parkinson’s disease (PD), it is important to examine how AgNPs affect microglial inflammation to fully assess AgNP neurotoxicity. In addition, understanding AgNP processing by microglia will allow better prediction of their long term bioreactivity. In the present study, the in vitro uptake and intracellular transformation of citrate-capped AgNPs by microglia, as well as their effects on microglial inflammation and related neurotoxicity were examined. Analytical microscopy demonstrated internalization and dissolution of AgNPs within microglia and formation of non-reactive silver sulphide (Ag2S) on the surface of AgNPs. Furthermore, AgNP-treatment up-regulated microglial expression of the hydrogen sulphide (H2S)-synthesizing enzyme cystathionine-γ-lyase (CSE). In addition, AgNPs showed significant anti-inflammatory effects, reducing lipopolysaccharide (LPS)-stimulated ROS, nitric oxide and TNFα production, which translated into reduced microglial toxicity towards dopaminergic neurons. Hence, the present results indicate that intracellular Ag2S formation, resulting from CSE-mediated H2S production in microglia, sequesters Ag+ ions released from AgNPs, significantly limiting their toxicity, concomitantly reducing microglial inflammation and related neurotoxicity.

Electronic-Reconstruction-Enhanced Tunneling Conductance at Terrace Edges of Ultrathin Oxide Films.

Science.gov (United States)

Wang, Lingfei; Kim, Rokyeon; Kim, Yoonkoo; Kim, Choong H; Hwang, Sangwoon; Cho, Myung Rae; Shin, Yeong Jae; Das, Saikat; Kim, Jeong Rae; Kalinin, Sergei V; Kim, Miyoung; Yang, Sang Mo; Noh, Tae Won

2017-11-01

Quantum mechanical tunneling of electrons across ultrathin insulating oxide barriers has been studied extensively for decades due to its great potential in electronic-device applications. In the few-nanometers-thick epitaxial oxide films, atomic-scale structural imperfections, such as the ubiquitously existed one-unit-cell-high terrace edges, can dramatically affect the tunneling probability and device performance. However, the underlying physics has not been investigated adequately. Here, taking ultrathin BaTiO 3 films as a model system, an intrinsic tunneling-conductance enhancement is reported near the terrace edges. Scanning-probe-microscopy results demonstrate the existence of highly conductive regions (tens of nanometers wide) near the terrace edges. First-principles calculations suggest that the terrace-edge geometry can trigger an electronic reconstruction, which reduces the effective tunneling barrier width locally. Furthermore, such tunneling-conductance enhancement can be discovered in other transition metal oxides and controlled by surface-termination engineering. The controllable electronic reconstruction can facilitate the implementation of oxide electronic devices and discovery of exotic low-dimensional quantum phases. © 2017 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

Neuroprotective effects of statins against amyloid β-induced neurotoxicity

Directory of Open Access Journals (Sweden)

Hsin-Hua Li

2018-01-01

Full Text Available A growing body of evidence suggests that disruption of the homeostasis of lipid metabolism affects the pathogenesis of Alzheimer's disease (AD. In particular, dysregulation of cholesterol homeostasis in the brain has been reported to considerably increase the risk of developing AD. Thus, dysregulation of lipid homeostasis may increase the amyloid β (Aβ levels by affecting amyloid precursor protein (APP cleavage, which is the most important risk factor involved in the pathogenesis of AD. Previous research demonstrated that Aβ can trigger neuronal insulin resistance, which plays an important role in response to Aβ-induced neurotoxicity in AD. Epidemiological studies also suggested that statin use is associated with a decreased incidence of AD. Therefore, statins are believed to be a good candidate for conferring neuroprotective effects against AD. Statins may play a beneficial role in reducing Aβ-induced neurotoxicity. Their effect involves a putative mechanism beyond its cholesterol-lowering effects in preventing Aβ-induced neurotoxicity. However, the underlying molecular mechanisms of the protective effect of statins have not been clearly determined in Aβ-induced neurotoxicity. Given that statins may provide benefits beyond the inhibition of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA reductase, these drugs may also improve the brain. Thus, statins may have beneficial effects on impaired insulin signaling by activating AMP-activated protein kinase (AMPK in neuronal cells. They play a potential therapeutic role in targeting Aβ-mediated neurotoxicity.

Oxide bipolar electronics: materials, devices and circuits

International Nuclear Information System (INIS)

Grundmann, Marius; Klüpfel, Fabian; Karsthof, Robert; Schlupp, Peter; Schein, Friedrich-Leonhard; Splith, Daniel; Yang, Chang; Bitter, Sofie; Von Wenckstern, Holger

2016-01-01

We present the history of, and the latest progress in, the field of bipolar oxide thin film devices. As such we consider primarily pn-junctions in which at least one of the materials is a metal oxide semiconductor. A wide range of n-type and p-type oxides has been explored for the formation of such bipolar diodes. Since most oxide semiconductors are unipolar, challenges and opportunities exist with regard to the formation of heterojunction diodes and band lineups. Recently, various approaches have led to devices with high rectification, namely p-type ZnCo 2 O 4 and NiO on n-type ZnO and amorphous zinc-tin-oxide. Subsequent bipolar devices and applications such as photodetectors, solar cells, junction field-effect transistors and integrated circuits like inverters and ring oscillators are discussed. The tremendous progress shows that bipolar oxide electronics has evolved from the exploration of various materials and heterostructures to the demonstration of functioning integrated circuits. Therefore a viable, facile and high performance technology is ready for further exploitation and performance optimization. (topical review)

Multiple mechanisms of PCB neurotoxicity

Energy Technology Data Exchange (ETDEWEB)

Carpenter, D.O.; Stoner, C.T.; Lawrence, D.A. [Univ. of New York, Albany, NY (United States)] [and others

1996-12-31

Polychlorinated biphenyls (PCBs) have been implicated in cancer, but many of the symptoms in humans exposed to PCBs are related to the nervous system and behavior. We demonstrated three different direct mechanisms whereby PCBs are neurotoxic in rats. By using flow cytometry, we demonstrated that the orthosubstituted PCB congener 2,4,4{prime}, but neither TCDD nor the coplanar PCB congener 3,4,5,3{prime},4{prime}, causes rapid death of cerebellar granule cells. The ortho-substituted congener 2,4,4{prime} reduced long-term potentiation, an indicator of cognitive potential, in hippocampal brain slices, but a similar effect was observed for the coplanar congener 3,4,3{prime},4{prime}, indicating that this effect may be caused by both ortho- and coplanar congeners by mechanisms presumably not mediated via the Ah receptor. It was previously shown that some ortho-substituted PCB congeners cause a reduction in levels of the neurotransmitter dopamine, and we present in vitro and in vivo evidence that this is due to reduction of synthesis of dopamine via inhibition of the enzyme tyrosine hydroxylase. Thus, PCBs have a variety of mechanisms of primary neurotoxicity, and neurotoxicity is a characteristic of ortho-substituted, non-dioxin-like congeners as well as some coplanar congeners. The relative contribution of each of these mechanisms to the loss of cognitive function in humans exposed to PCBs remains to be determined. 42 refs., 3 figs., 1 tab.

Cooperative electrocatalytic alcohol oxidation with electron-proton-transfer mediators

Science.gov (United States)

Badalyan, Artavazd; Stahl, Shannon S.

2016-07-01

The electrochemical oxidation of alcohols is a major focus of energy and chemical conversion efforts, with potential applications ranging from fuel cells to biomass utilization and fine-chemical synthesis. Small-molecule electrocatalysts for processes of this type are promising targets for further development, as demonstrated by recent advances in nickel catalysts for electrochemical production and oxidation of hydrogen. Complexes with tethered amines that resemble the active site of hydrogenases have been shown both to catalyse hydrogen production (from protons and electrons) with rates far exceeding those of such enzymes and to mediate reversible electrocatalytic hydrogen production and oxidation with enzyme-like performance. Progress in electrocatalytic alcohol oxidation has been more modest. Nickel complexes similar to those used for hydrogen oxidation have been shown to mediate efficient electrochemical oxidation of benzyl alcohol, with a turnover frequency of 2.1 per second. These compounds exhibit poor reactivity with ethanol and methanol, however. Organic nitroxyls, such as TEMPO (2,2,6,6-tetramethyl-1-piperidine N-oxyl), are the most widely studied electrocatalysts for alcohol oxidation. These catalysts exhibit good activity (1-2 turnovers per second) with a wide range of alcohols and have great promise for electro-organic synthesis. Their use in energy-conversion applications, however, is limited by the high electrode potentials required to generate the reactive oxoammonium species. Here we report (2,2‧-bipyridine)Cu/nitroxyl co-catalyst systems for electrochemical alcohol oxidation that proceed with much faster rates, while operating at an electrode potential a half-volt lower than that used for the TEMPO-only process. The (2,2‧-bipyridine)Cu(II) and TEMPO redox partners exhibit cooperative reactivity and exploit the low-potential, proton-coupled TEMPO/TEMPOH redox process rather than the high-potential TEMPO/TEMPO+ process. The results show how

Neurotoxic shellfish poisoning: A review

NARCIS (Netherlands)

Apeldoorn ME van; Egmond HP van; Speijers GJA; CSR; ARO

2001-01-01

This review contains information on the neurotoxic shellfish poisoning (NSP) syndrome and the provoking toxins called brevetoxins, produced by the dinoflagellate Gymnodinium breve. Data on chemical structures and detection methods for brevetoxins, sources for brevetoxins, marine organisms associated

Oxidative stress and superoxide dismutase activity in brain of rats ...

African Journals Online (AJOL)

The present study was envisaged to investigate the possible role of oxidative stress in permethrin neurotoxicity and to evaluate the protective effect of superoxide dismutase (SOD) activity in brain homogenates of Wistar rats. Oxidative stress measured as thiobarbituric acid reacting substances (TBARS) was found to ...

Nanoroses of nickel oxides: Synthesis, electron tomography study, and application in CO oxidation and energy storage

KAUST Repository

Fihri, Aziz

2012-04-11

Nickel oxide and mixed-metal oxide structures were fabricated by using microwave irradiation in pure water. The nickel oxide self-assembled into unique rose-shaped nanostructures. These nickel oxide roses were studied by performing electron tomography with virtual cross-sections through the particles to understand their morphology from their interior to their surface. These materials exhibited promising performance as nanocatalysts for CO oxidation and in energy storage devices. Copyright © 2012 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

Electronic Structure Control of Tungsten Oxide Activated by Ni for Ultrahigh-Performance Supercapacitors.

Science.gov (United States)

Meng, Tian; Kou, Zongkui; Amiinu, Ibrahim Saana; Hong, Xufeng; Li, Qingwei; Tang, Yongfu; Zhao, Yufeng; Liu, Shaojun; Mai, Liqiang; Mu, Shichun

2018-04-17

Tuning the electron structure is of vital importance for designing high active electrode materials. Here, for boosting the capacitive performance of tungsten oxide, an atomic scale engineering approach to optimize the electronic structure of tungsten oxide by Ni doping is reported. Density functional theory calculations disclose that through Ni doping, the density of state at Fermi level for tungsten oxide can be enhanced, thus promoting its electron transfer. When used as electrode of supercapacitors, the obtained Ni-doped tungsten oxide with 4.21 at% Ni exhibits an ultrahigh mass-specific capacitance of 557 F g -1 at the current density of 1 A g -1 and preferable durability in a long-term cycle test. To the best of knowledge, this is the highest supercapacitor performance reported so far in tungsten oxide and its composites. The present strategy demonstrates the validity of the electronic structure control in tungsten oxide via introducing Ni atoms for pseudocapacitors, which can be extended to other related fields as well. © 2018 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

Ultrafast electron and energy transfer in dye-sensitized iron oxide and oxyhydroxide nanoparticles

DEFF Research Database (Denmark)

Gilbert, Benjamin; Katz, Jordan E.; Huse, Nils

2013-01-01

photo-initiated interfacial electron transfer. This approach enables time-resolved study of the fate and mobility of electrons within the solid phase. However, complete analysis of the ultrafast processes following dye photoexcitation of the sensitized iron(iii) oxide nanoparticles has not been reported....... We addressed this topic by performing femtosecond transient absorption (TA) measurements of aqueous suspensions of uncoated and DCF-sensitized iron oxide and oxyhydroxide nanoparticles, and an aqueous iron(iii)–dye complex. Following light absorption, excited state relaxation times of the dye of 115...... a four-state model of the dye-sensitized system, finding electron and energy transfer to occur on the same ultrafast timescale. The interfacial electron transfer rates for iron oxides are very close to those previously reported for DCF-sensitized titanium dioxide (for which dye–oxide energy transfer...

A peptide disrupting the D2R-DAT interaction protects against dopamine neurotoxicity.

Science.gov (United States)

Su, Ping; Liu, Fang

2017-09-01

Dopamine reuptake from extracellular space to cytosol leads to accumulation of dopamine, which triggers neurotoxicity in dopaminergic neurons. Previous studies have shown that both dopamine D2 receptor (D2R) and dopamine transporter (DAT) are involved in dopamine neurotoxicity. However, blockade of either D2R or DAT causes side effects due to antagonism of other physiological functions of these two proteins. We previously found that DAT can form a protein complex with D2R and its cell surface expression is facilitated via D2R-DAT interaction, which regulates dopamine reuptake and intracellular dopamine levels. Here we found that an interfering peptide (DAT-S1) disrupting the D2R-DAT interaction protects neurons against dopamine neurotoxicity, and this effect is mediated by inhibiting DAT cell surface expression and inhibiting both caspase-3 and PARP-1 cleavage. This study demonstrates the role of the D2R-DAT complex in dopamine neurotoxicity and investigated the potential mechanisms, which might help better understand the mechanisms of dopamine neurotoxicity. The peptide may provide some insights to improve treatments for dopamine neurotoxicity and related diseases, such as Parkinson's disease, as well as methamphetamine- and 3,4-methsylenedioxy methamphetamine-induced neurotoxicity. Copyright © 2017. Published by Elsevier Inc.

Role of mitochondrial dysfunction in neurotoxicity of MPP+: partial protection of PC12 cells by acetyl-L-carnitine.

Science.gov (United States)

Virmani, Ashraf; Gaetani, Franco; Binienda, Zbigniew; Xu, Alex; Duhart, Helen; Ali, Syed F

2004-10-01

The damage to the central nervous system that is observed after administration of either methamphetamine (METH) or 1-methyl-4-phenylpyridinium (MPP+), the neurotoxic metabolite of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), is known to be linked to dopamine (DA). The underlying neurotoxicity mechanism for both METH and MPP+ seem to involve free radical formation and impaired mitochondrial function. The MPP+ is thought to selectively kill nigrostriatal dopaminergic neurons by inhibiting mitochondrial complex I, with cell death being attributed to oxidative stress damage to these vulnerable DA neurons. In the present study, MPP+ was shown to significantly inhibit the response to MTT by cultured PC12 cells. This inhibitory action of MPP+ could be partially reversed by the co-incubation of the cells with the acetylated form of carnitine, acetyl-L-carnitine (ALC). Since at least part of the toxic action of MPP+ is related to mitochondrial inhibition, the partial reversal of the inhibition of MTT response by ALC could involve a partial restoration of mitochondrial function. The role carnitine derivatives, such as ALC, play in attenuating MPP+ and METH-evoked toxicity is still under investigation to elucidate the contribution of mitochondrial dysfunction in mechanisms of neurotoxicity.

Graphene oxide and reduced graphene oxide studied by the XRD, TEM and electron spectroscopy methods

International Nuclear Information System (INIS)

Stobinski, L.; Lesiak, B.; Malolepszy, A.; Mazurkiewicz, M.; Mierzwa, B.; Zemek, J.; Jiricek, P.; Bieloshapka, I.

2014-01-01

Highlights: • Graphene oxide (FL-GOc) and reduced graphene oxide (FL-RGOc): XRD, TEM, XPS, REELS. • FL-GOc: stacking nanostructure—22 × 6 nm (DxH), 0.9 nm layers separation (XRD). • FL-RGOc: stacking nanostructure—8 × 1 nm (DxH), 0.4 nm layers separation (XRD). • Reduction: oxygen group degradation, decreasing distance between graphene layers. • Number of graphene layers in stacking nanostructure: 6–7 (FL-GOc), 2–3 (FL-RGOc). - Abstract: The commercial and synthesised few-layer graphene oxide, prepared using oxidation reactions, and few-layer reduced graphene oxide samples were structurally and chemically investigated by the X-ray diffraction (XRD), transmission electron microscopy (TEM) and electron spectroscopy methods, i.e. X-ray photoelectron spectroscopy (XPS) and reflection electron energy loss spectroscopy (REELS). The commercial graphene oxide (FL-GOc) shows a stacking nanostructure of about 22 × 6 nm average diameter by height with the distance of 0.9 nm between 6-7 graphene layers, whereas the respective reduced graphene oxide (FL-RGOc)—about 8 × 1 nm average diameter by height stacking nanostructure with the distance of 0.4 nm between 2-3 graphene layers (XRD). The REELS results are consistent with those by the XRD indicating 8 (FL-GOc) and 4 layers (FL-RGOc). In graphene oxide and reduced graphene oxide prepared from the graphite the REELS indicates 8–11 and 7–10 layers. All graphene oxide samples show the C/O ratio of 2.1–2.3, 26.5–32.1 at% of C sp 3 bonds and high content of functional oxygen groups (hydroxyl—C-OH, epoxy—C-O-C, carbonyl—C=O, carboxyl—C-OOH, water) (XPS). Reduction increases the C/O ratio to 2.8–10.3, decreases C sp 3 content to 11.4–20.3 at% and also the content of C-O-C and C=O groups, accompanied by increasing content of C-OH and C-OOH groups. Formation of additional amount of water due to functional oxygen group reduction leads to layer delamination. Removing of functional oxygen groups

Mechanistic insight into neurotoxicity induced by developmental insults

International Nuclear Information System (INIS)

Tamm, Christoffer; Ceccatelli, Sandra

2017-01-01

Epidemiological and/or experimental studies have shown that unfavorable prenatal environmental factors, such as stress or exposure to certain neurotoxic environmental contaminants, may have adverse consequences for neurodevelopment. Alterations in neurogenesis can have harmful effects not only for the developing nervous system, but also for the adult brain where neurogenesis is believed to play a role in learning, memory, and even in depression. Many recent advances in the understanding of the complex process of nervous system development can be integrated into the field of neurotoxicology. In the past 15 years we have been using cultured neural stem or progenitor cells to investigate the effects of neurotoxic stimuli on cell survival, proliferation and differentiation, with special focus on heritable effects. This is an overview of the work performed by our group in the attempt to elucidate the mechanisms of developmental neurotoxicity and possibly provide relevant information for the understanding of the etiopathogenesis of complex brain disorders. - Highlights: • The developing nervous system is highly sensitive to toxic insults. • Neural stem cells are relevant models for mechanistic studies as well as for identifying heritable effects due to epigenetic changes. • Depending on the dose, the outcome of exposure to neurotoxicants ranges from altered proliferation and differentiation to cell death. • The elucidation of neurotoxicity mechanisms is relevant for understanding the etiopathogenesis of developmental and adult nervous system disorders.

Biomarkers of cytokine release syndrome and neurotoxicity related to CAR-T cell therapy.

Science.gov (United States)

Wang, Zhenguang; Han, Weidong

2018-01-01

Severe cytokine release syndrome (CRS) and neurotoxicity following chimeric antigen receptor T cell (CAR-T) therapy can be life-threatening in some cases, and management of those toxicities is still a great challenge for physicians. Researchers hope to understand the pathophysiology of CRS and neurotoxicity, and identify predictive biomarkers that can forecast those toxicities in advance. Some risk factors for severe CRS and/or neurotoxicity including patient and treatment characteristics have been identified in multiple clinical trials of CAR-T cell therapy. Moreover, several groups have identified some predictive biomarkers that are able to determine beforehand which patients may suffer severe CRS and/or neurotoxicity during CAR-T cell therapy, facilitating testing of early intervention strategies for those toxicities. However, further studies are needed to better understand the biology and related risk factors for CRS and/or neurotoxicity, and determine if those identified predictors can be extrapolated to other series. Herein, we review the pathophysiology of CRS and neurotoxicity, and summarize the progress of predictive biomarkers to improve CAR-T cell therapy in cancer.

Protective Effects of N-Acetyl-L-cystein on 3,4-Methylene Dioxymethamphetamie-Induced Neurotoxicity in Cerebellum of Male Rats

Directory of Open Access Journals (Sweden)

Sara Soleimani Asl

2011-10-01

Full Text Available Introduction: 3-4, methylenedioxymethamphetamine (MDMA causes apoptosis in nervous system and several studies suggest that oxidative stress contributes to MDMA-induced neurotoxicity. The aim of this study is to examine the effects of N-acetyl-L-Cystein (NAC as an antioxidant on MDMA-induced apoptosis. Methods: 21 Sprague dawley male rats (200-250mg were treated with MDMA (2×0,5mg/kg or MDMA plus NAC (100mg/kg IP for 7 day. After last administration of MDMA, rats were killed, cerebellum was removed and Bax and Bcl-2 expression was assessed by western blotting method. Results: The results of this study showed that MDMA causes up-regulation of Bax and down-regulation of Bcl-2 and NAC administration attenuated MDMA-induced apoptosis. Discussion: The present study suggests that NAC treatment may improve MDMA-induced neurotoxicity.

Diffusion abnormalities of the globi pallidi in manganese neurotoxicity

Energy Technology Data Exchange (ETDEWEB)

McKinney, Alexander M.; Filice, Ross W.; Teksam, Mehmet; Casey, Sean; Truwit, Charles; Clark, H. Brent; Woon, Carolyn; Liu, Hai Ying [Department of Radiology, Medical School, Box 292, 420 Delaware Street S.E., 55455, Minneapolis, MN (United States)

2004-04-01

Manganese is an essential trace metal required for normal central nervous system function, which is toxic when in excess amounts in serum. Manganese neurotoxicity has been demonstrated in patients with chronic liver/biliary failure where an inability to excrete manganese via the biliary system causes increased serum levels, and in patients on total parenteral nutrition (TPN), occupational/inhalational exposure, or other source of excess exogenous manganese. Manganese has been well described in the literature to deposit selectively in the globi pallidi and to induce focal neurotoxicity. We present a case of a 53-year-old woman who presented for a brain MR 3 weeks after liver transplant due to progressively decreasing level of consciousness. The patient had severe liver failure by liver function tests and bilirubin levels, and had also been receiving TPN since the transplant. The MR demonstrated symmetric hyperintensity on T1-weighted images in the globi pallidi. Apparent diffusion coefficient (ADC) map indicated restricted diffusion in the globi pallidi bilaterally. The patient eventually succumbed to systemic aspergillosis 3 days after the MR. The serum manganese level was 195 mcg/l (micrograms per liter) on postmortem exam (over 20 times the upper limits of normal). The patient was presumed to have suffered from manganese neurotoxicity since elevated serum manganese levels have been shown in the literature to correlate with hyperintensity on T1-weighted images, neurotoxicity symptoms, and focal concentration of manganese in the globi pallidi. Neuropathologic sectioning of the globi pallidi at autopsy was also consistent with manganese neurotoxicity. (orig.)

Fingerprinting of neurotoxic compounds using a mouse embryonic stem cell dual luminescence reporter assay

NARCIS (Netherlands)

Colaianna, M.; Ilmjärv, S.; Peterson, H.; Ilse Kern, I.; Julien, S.; Baquié, M.; allocca, G.; Bosgra, S.; Sachinidis, A.; Hengstler, J.G.; Leist, M.; Krause, K.H.

2017-01-01

Identification of neurotoxic drugs and environmental chemicals is an important challenge. However, only few tools to address this topic are available. The aim of this study was to develop a neurotoxicity/developmental neurotoxicity (DNT) test system, using the pluripotent mouse embryonic stem cell

The influence of oxidation properties on the electron emission characteristics of porous silicon

International Nuclear Information System (INIS)

He, Li; Zhang, Xiaoning; Wang, Wenjiang; Wei, Haicheng

2016-01-01

Highlights: • Evaluated the oxidation properties of porous silicon from semi-quantitative methods. • Discovered the relationship between oxidation properties and emission characteristics. • Revealed the micro-essence of the electron emission of the porous silicon. - Abstract: In order to investigate the influence of oxidation properties such as oxygen content and its distribution gradient on the electron emission characteristics of porous silicon (PS) emitters, emitters with PS thickness of 8 μm, 5 μm, and 3 μm were prepared and then oxidized by electrochemical oxidation (ECO) and ECO-RTO (rapid thermal oxidation) to get different oxidation properties. The experimental results indicated that the emission current density, efficiency, and stability of the PS emitters are mainly determined by oxidation properties. The higher oxygen content and the smaller oxygen distribution gradient in the PS layer, the larger emission current density and efficiency we noted. The most favorable results occurred for the PS emitter with the smallest oxygen distribution gradient and the highest level of oxygen content, with an emission current density of 212.25 μA/cm"2 and efficiency of 59.21‰. Additionally, it also demonstrates that thick PS layer benefits to the emission stability due to its longer electron acceleration tunnel. The FN fitting plots indicated that the effective emission areas of PS emitters can be enlarged and electron emission thresholds is decreased because of the higher oxygen content and smaller distribution gradient, which were approved by the optical micrographs of top electrode of PS emitters before and after electron emission.

The influence of oxidation properties on the electron emission characteristics of porous silicon

Energy Technology Data Exchange (ETDEWEB)

He, Li [Key Laboratory of Physical Electronics and Devices of the Ministry of Education, Xi’an Jiaotong University, Xi’an 710049 (China); Zhang, Xiaoning, E-mail: znn@mail.xjtu.edu.cn [Key Laboratory of Physical Electronics and Devices of the Ministry of Education, Xi’an Jiaotong University, Xi’an 710049 (China); Wang, Wenjiang [Key Laboratory of Physical Electronics and Devices of the Ministry of Education, Xi’an Jiaotong University, Xi’an 710049 (China); Wei, Haicheng [School of Electrical and Information Engineering, Beifang University of Nationalities, Yinchuan750021 (China)

2016-09-30

Highlights: • Evaluated the oxidation properties of porous silicon from semi-quantitative methods. • Discovered the relationship between oxidation properties and emission characteristics. • Revealed the micro-essence of the electron emission of the porous silicon. - Abstract: In order to investigate the influence of oxidation properties such as oxygen content and its distribution gradient on the electron emission characteristics of porous silicon (PS) emitters, emitters with PS thickness of 8 μm, 5 μm, and 3 μm were prepared and then oxidized by electrochemical oxidation (ECO) and ECO-RTO (rapid thermal oxidation) to get different oxidation properties. The experimental results indicated that the emission current density, efficiency, and stability of the PS emitters are mainly determined by oxidation properties. The higher oxygen content and the smaller oxygen distribution gradient in the PS layer, the larger emission current density and efficiency we noted. The most favorable results occurred for the PS emitter with the smallest oxygen distribution gradient and the highest level of oxygen content, with an emission current density of 212.25 μA/cm{sup 2} and efficiency of 59.21‰. Additionally, it also demonstrates that thick PS layer benefits to the emission stability due to its longer electron acceleration tunnel. The FN fitting plots indicated that the effective emission areas of PS emitters can be enlarged and electron emission thresholds is decreased because of the higher oxygen content and smaller distribution gradient, which were approved by the optical micrographs of top electrode of PS emitters before and after electron emission.

Occupational Neurotoxic Diseases in Taiwan

Directory of Open Access Journals (Sweden)

Chi-Hung Liu

2012-12-01

Full Text Available Occupational neurotoxic diseases have become increasingly common in Taiwan due to industrialization. Over the past 40 years, Taiwan has transformed from an agricultural society to an industrial society. The most common neurotoxic diseases also changed from organophosphate poisoning to heavy metal intoxication, and then to organic solvent and semiconductor agent poisoning. The nervous system is particularly vulnerable to toxic agents because of its high metabolic rate. Neurological manifestations may be transient or permanent, and may range from cognitive dysfunction, cerebellar ataxia, Parkinsonism, sensorimotor neuropathy and autonomic dysfunction to neuromuscular junction disorders. This study attempts to provide a review of the major outbreaks of occupational neurotoxins from 1968 to 2012. A total of 16 occupational neurotoxins, including organophosphates, toxic gases, heavy metals, organic solvents, and other toxic chemicals, were reviewed. Peer-reviewed articles related to the electrophysiology, neuroimaging, treatment and long-term follow up of these neurotoxic diseases were also obtained. The heavy metals involved consisted of lead, manganese, organic tin, mercury, arsenic, and thallium. The organic solvents included n-hexane, toluene, mixed solvents and carbon disulfide. Toxic gases such as carbon monoxide, and hydrogen sulfide were also included, along with toxic chemicals including polychlorinated biphenyls, tetramethylammonium hydroxide, organophosphates, and dimethylamine borane. In addition we attempted to correlate these events to the timeline of industrial development in Taiwan. By researching this topic, the hope is that it may help other developing countries to improve industrial hygiene and promote occupational safety and health care during the process of industrialization.

Clinical Neurotoxic Disorders : Past, Present and Future

Directory of Open Access Journals (Sweden)

Nag Devika

2001-01-01

Full Text Available Neurotoxins have existed on the earth from times immemorial. Old neurotoxic disorders were due to ingestion/ exposure of heavy metals and food like lathyrus sativus over a long period of time. The 20th Century with rapid industrialsation and expanding chemical and drug industry has spawned several new, hitherto unknown disorders. Old disorders continue to exist e.g. fluorosis, arsenicosis, lathyrism, manganism and lead neuropathy, along with new diseases like Minamata disease, subacute myelo optic neuropathy (SMON, MPTP-Parkinsonian syndorme, triorthcresyl phosphate (TOCP neuroparalytic disease, pesticide induced seizures, tremor and neuropathy, solvent encephalopthy, antipileptic drug foetal syndrome and excitotoxin induced behavioural disorders. Studies on pesticides Organochlorine and organophosphates, synthetic pyrethrins, solvents, heavy metals and substances abuse in the Indian context confirm the neurotoxic nature of many synthetic substances. Future problems envisaged are of concern to clinical neurologists as many of these neurotoxic disorders mimic syndromes of well known neurological disease. The new millenium poses a challenge to the clinician as newer compounds in industry, food, drugs and chemical war agents are being developed. Molecular genetics has advanced rapidly with release of the human genome map. Animal cloning and genetically modified plant products have entered the food chain. How safe are these new inventions for the central nervous system is a big question? India cannot afford disasters like Union Carbide′s Bhopal gas leak nor be a silent spectator to manipulative biotechnology. Unless it is proven beyond all doubt to be a safe innovation, Chemicals have to be cautiously introduced in our environment. To Study, ascertain and confirm safety or neurotoxicity is an exciting challenge for the neuroscientists of the 21st century.

Effect of pressure on f-electron delocalization and oxidation in actinide dioxides

Energy Technology Data Exchange (ETDEWEB)

Petit, L., E-mail: leon.petit@stfc.ac.uk [Daresbury Laboratory, Daresbury, Warrington WA4 4AD (United Kingdom); Szotek, Z.; Temmerman, W.M. [Daresbury Laboratory, Daresbury, Warrington WA4 4AD (United Kingdom); Stocks, G.M. [Materials Science and Technology Division and Center for Defect Physics, Oak Ridge National Laboratory, Oak Ridge, TN 37831 (United States); Svane, A. [Department of Physics and Astronomy, University of Aarhus, DK-8000 Aarhus C (Denmark)

2014-08-01

Using first principles calculations, we have investigated f-electron delocalization and oxidation in the actinide dioxides under pressure. Whilst UO{sub 2} is found on the verge of an insulator to metal transition at the equilibrium volume, increasingly larger pressures are required to delocalize f-electrons in NpO{sub 2}, PuO{sub 2}, and AmO{sub 2}, respectively 49, 112, and 191 GPa. Compared to this broad range of pressures, the experimentally observed structural transitions, in all four dioxides, occur between 30 and 40 GPa, which leads us to conclude that the associated volume collapse is not due to f-electron delocalization. In contrast, oxidation of the dioxides is found to be linked to the degree of f-electron localization, but it emerges that for naturally occurring pressures (<10 GPa), higher oxides only exist for UO{sub 2}.

Interpretation of electron beam induced charging of oxide layers in a transistor studied using electron holography

DEFF Research Database (Denmark)

Ubaldi, F; Pozzi, G; Kasama, Takeshi

2010-01-01

Off-axis electron holography has been used to characterize a linear array of transistors, which was prepared for examination in cross-sectional geometry in the transmission electron microscope using focused ion beam milling. In reconstructed phase images, regions of silicon oxide that are located...... into account the mean inner potential of the specimen and the perturbed vacuum reference wave. The simulations suggest that the oxide layers contain a uniform volume density of positive charge and that the elliptical contours result from the combined effect of the electrostatic potential in the specimen...

The Dynamics of Autism Spectrum Disorders: How Neurotoxic Compounds and Neurotransmitters Interact

Directory of Open Access Journals (Sweden)

Margot Van de Bor

2013-08-01

Full Text Available In recent years concern has risen about the increasing prevalence of Autism Spectrum Disorders (ASD. Accumulating evidence shows that exposure to neurotoxic compounds is related to ASD. Neurotransmitters might play a key role, as research has indicated a connection between neurotoxic compounds, neurotransmitters and ASD. In the current review a literature overview with respect to neurotoxic exposure and the effects on neurotransmitter systems is presented. The aim was to identify mechanisms and related factors which together might result in ASD. The literature reported in the current review supports the hypothesis that exposure to neurotoxic compounds can lead to alterations in the GABAergic, glutamatergic, serotonergic and dopaminergic system which have been related to ASD in previous work. However, in several studies findings were reported that are not supportive of this hypothesis. Other factors also might be related, possibly altering the mechanisms at work, such as time and length of exposure as well as dose of the compound. Future research should focus on identifying the pathway through which these factors interact with exposure to neurotoxic compounds making use of human studies.

Effects of 7-nitroindazole, an NOS inhibitor on methamphetamine-induced dopaminergic and serotonergic neurotoxicity in mice.

Science.gov (United States)

Ali, S F; Itzhak, Y

1998-05-30

Methamphetamine (METH) is one of the major drugs of abuse that is postulated to cause neurotoxicity by depleting dopamine (DA) and its metabolites, high-affinity DA uptake sites, and the activity of tyrosine hydroxylase. The present study was undertaken to investigate whether the relatively selective, neuronal nitric oxide synthase (NOS) inhibitor, 7-nitroindazole (7-NI), protects against METH-induced neurotoxicity. Male Swiss Webster mice received the following injections intraperitoneally (i.p.) 3 times (every 3 hr): (i) vehicle/saline, (ii) 7-NI (25 mg/kg)/saline, (iii) vehicle/METH (5 mg/kg), and (iv) 7-NI (25 mg/kg)/METH (5 mg/kg). On the second day, groups (i) and (iii) received two vehicle injections and groups (ii) and (iv) received two 7-NI injections (25 mg/kg each). The administration of vehicle/METH resulted in 68, 44 and 55% decreases in the concentration of DA, dihydroxyphenylacetic acid (DOPAC), and homovanillic acid (HVA), respectively, and a 48% decrease in the number of [3H]mazindol binding sites in the striatum compared to control values. The treatment with 7-NI (group iv) provided a full protection against the depletion of DA and its metabolites, and the loss of dopamine transporter binding sites. Multiple injection of METH caused a significant decrease in the concentration of serotonin (5-HT) and its metabolite 5-hydroxyindole acetic acid (5-HIAA). Treatment with 7-NI partially blocked the depletion of 5-HT and completely blocked the reduction in 5-HIAA levels. The administration of 7-NI/saline (group ii) affected neither the tissue concentration of DA, 5-HT and their metabolites (DOPAC, HVA and 5-HIAA) nor the binding parameters of [3H]-mazindol compared to control (vehicle/saline) values. 7-NI had no significant effect on the animals' body temperature, and it did not affect METH-induced hyperthermia. These findings indicate a role for nitric oxide in METH-induced neurotoxicity and also suggest that blockage of NOS may be beneficial for the

Effects of 7-Nitroindazole, an NOS Inhibitor on Methamphetamine-Induced Dopaminergic and Serotonergic Neurotoxicity in Micea.

Science.gov (United States)

Ali, Syed F; Itzhak, Yossef

1998-05-01

Methamphetamine (METH) is one of the major drugs of abuse that is postulated to cause neurotoxicity by depleting dopamine (DA) and its metabolites, high-affinity DA uptake sites, and the activity of tyrosine hydroxylase. The present study was undertaken to investigate whether the relatively selective, neuronal nitric oxide synthase (NOS) inhibitor, 7-nitroindazole (7-NI), protects against METH-induced neurotoxicity. Male Swiss Webster mice received the following injections intraperitoneally (i.p.) 3 times (every 3 hr): (i) vehicle/saline, (ii) 7-NI (25 mg/kg)/saline, (iii) vehicle/METH (5 mg/kg), and (iv) 7-NI (25 mg/kg)/METH (5 mg/kg). On the second day, groups (i) and (iii) received two vehicle injections and groups (ii) and (iv) received two 7-NI injections (25 mg/kg each). The administration of vehicle/METH resulted in 68, 44 and 55% decreases in the concentration of DA, dihydroxyphenylacetic acid (DOPAC), and homovanillic acid (HVA), respectively, and a 48% decrease in the number of [ 3 H]mazindol binding sites in the striatum compared to control values. The treatment with 7-NI (group iv) provided a full protection against the depletion of DA and its metabolites, and the loss of dopamine transporter binding sites. Multiple injection of METH caused a significant decrease in the concentration of serotonin (5-HT) and its metabolite 5-hydroxyindole acetic acid (5-HIAA). Treatment with 7-NI partially blocked the depletion of 5-HT and completely blocked the reduction in 5-HIAA levels. The administration of 7-NI/saline (group ii) affected neither the tissue concentration of DA, 5-HT and their metabolites (DOPAC, HVA and 5-HIAA) nor the binding parameters of [ 3 H]-mazindol compared to control (vehicle/saline) values. 7-NI had no significant effect on the animals' body temperature, and it did not affect METH-induced hyperthermia. These findings indicate a role for nitric oxide in METH-induced neurotoxicity and also suggest that blockage of NOS may be beneficial for

Graphene oxide overprints for flexible and transparent electronics

Energy Technology Data Exchange (ETDEWEB)

Rogala, M., E-mail: rogala@uni.lodz.pl; Wlasny, I.; Kowalczyk, P. J.; Busiakiewicz, A.; Kozlowski, W.; Klusek, Z. [Department of Solid State Physics, Faculty of Physics and Applied Informatics, University of Lodz, Pomorska 149/153, 90-236 Lodz (Poland); Dabrowski, P.; Lipinska, L.; Jagiello, J.; Aksienionek, M.; Strupinski, W.; Krajewska, A. [Institute of Electronic Materials Technology, Wolczynska 133, 01-919 Warsaw (Poland); Sieradzki, Z. [Electrotechnological Company QWERTY Ltd., Siewna 21, 94-250 Lodz (Poland); Krucinska, I.; Puchalski, M.; Skrzetuska, E. [Department of Material and Commodity Sciences and Textile Metrology, Lodz University of Technology, Zeromskiego 116, 90-924 Lodz (Poland)

2015-01-26

The overprints produced in inkjet technology with graphene oxide dispersion are presented. The graphene oxide ink is developed to be fully compatible with standard industrial printers and polyester substrates. Post-printing chemical reduction procedure is proposed, which leads to the restoration of electrical conductivity without destroying the substrate. The presented results show the outstanding potential of graphene oxide for rapid and cost efficient commercial implementation to production of flexible electronics. Properties of graphene-based electrodes are characterized on the macro- and nano-scale. The observed nano-scale inhomogeneity of overprints' conductivity is found to be essential in the field of future industrial applications.

Electronically conductive perovskite-based oxide nanoparticles and films for optical sensing applications

Science.gov (United States)

Ohodnicki, Jr., Paul R; Schultz, Andrew M

2015-04-28

The disclosure relates to a method of detecting a change in a chemical composition by contacting a electronically conducting perovskite-based metal oxide material with a monitored stream, illuminating the electronically conducting perovskite-based metal oxide with incident light, collecting exiting light, monitoring an optical signal based on a comparison of the incident light and the exiting light, and detecting a shift in the optical signal. The electronically conducting perovskite-based metal oxide has a perovskite-based crystal structure and an electronic conductivity of at least 10.sup.-1 S/cm, where parameters are specified at the gas stream temperature. The electronically conducting perovskite-based metal oxide has an empirical formula A.sub.xB.sub.yO.sub.3-.delta., where A is at least a first element at the A-site, B is at least a second element at the B-site, and where 0.8perovskite-based oxides include but are not limited to La.sub.1-xSr.sub.xCoO.sub.3, La.sub.1-xSr.sub.xMnO.sub.3, LaCrO.sub.3, LaNiO.sub.3, La.sub.1-xSr.sub.xMn.sub.1-yCr.sub.yO.sub.3, SrFeO.sub.3, SrVO.sub.3, La-doped SrTiO.sub.3, Nb-doped SrTiO.sub.3, and SrTiO.sub.3-.delta..

Evidence for Single Metal Two Electron Oxidative Addition and Reductive Elimination at Uranium

OpenAIRE

Gardner, Benedict M; Kefalidis, Christos E; Lu, Erli; Patel, Dipti; Mcinnes, Eric; Tuna, Floriana; Wooles, Ashley; Maron, Laurent; Liddle, Stephen

2017-01-01

Reversible single-metal two-electron oxidative addition and reductive elimination are common fundamental reactions for transition metals that underpin major catalytic transformations. However, these reactions have never been observed together in the f-block because these metals exhibit irreversible one- or multi-electron oxidation or reduction reactions. Here, we report that azobenzene oxidises sterically and electronically unsaturated uranium(III) complexes to afford a uranium(V)-imido compl...

Time-dependence hole and electron trapping effects in SIMOX buried oxides

International Nuclear Information System (INIS)

Boesch, H.E. Jr.; Taylor, T.L.; Hite, L.R.; Bailey, W.E.

1990-01-01

Back-channel threshold shift associated with the buried oxide layers of separation by implanted oxygen (SIMOX) and zone-melted recrystallization (ZMR) field-effect transistors (FETs) was measured following pulsed irradiation as a function of temperature and back-gate bias using a fast time-resolved I-V measurement technique. The SIMOX FETs showed large initial negative voltage shifts at 0.2 ms after irradiation followed by temperature- and bias-dependent additional negative shifts to 800s. Analysis and modeling of the results indicate efficient deep trapping of radiation-generated holes in the bulk of the oxide, substantial initial trapping of radiation-generated electrons in the oxide, and rapid removal of the trapped electrons by a thermal detrapping process. The ZMR FETs showed evidence of substantial trapping of holes alone in the oxide bulk

Differential response of nNOS knockout mice to MDMA ("ecstasy")- and methamphetamine-induced psychomotor sensitization and neurotoxicity.

Science.gov (United States)

Itzhak, Yossef; Anderson, Karen L; Ali, Syed F

2004-10-01

It has been shown that mice deficient in neuronal nitric oxide synthase (nNOS) gene are resistant to cocaine-induced psychomotor sensitization and methamphetamine (METH)-induced dopaminergic neurotoxicity. The present study was undertaken to investigate the hypothesis that nNOS has a major role in dopamine (DA)- but not serotonin (5-hydroxytryptamine; 5-HT)-mediated effects of psychostimulants. The response of nNOS knockout (KO) and wild-type (WT) mice to the psychomotor-stimulating and neurotoxic effects of 3,4-methylenedioxymethamphetamine (MDMA; "Ecstasy") and METH were investigated. Repeated administration of MDMA for 5 days resulted in psychomotor sensitization in both WT and nNOS KO mice, while repeated administration of METH caused psychomotor sensitization in WT but not in KO mice. Sensitization to both MDMA and METH was persistent for 40 days in WT mice, but not in nNOS KO mice. These findings suggest that the induction of psychomotor sensitization to MDMA and METH is NO independent and NO dependent, respectively, while the persistence of sensitization to both drugs is NO dependent. For the neurochemical studies, a high dose of MDMA caused marked depletion of 5-HT in several brain regions of both WT and KO mice, suggesting that the absence of the nNOS gene did not afford protection against MDMA-induced depletion of 5-HT. Striatal dopaminergic neurotoxicity caused by high doses of MDMA and METH in WT mice was partially prevented in KO mice administered with MDMA, but it was fully precluded in KO mice administered with METH. The differential response of nNOS KO mice to the behavioral and neurotoxic effects of MDMA and METH suggests that the nNOS gene is required for the expression and persistence of DA-mediated effects of METH and MDMA, while 5-HT-mediated effects of MDMA (induction of sensitization and 5-HT depletion) are not dependent on nNOS.

Developmental neurotoxic effects of two pesticides: Behavior and biomolecular studies on chlorpyrifos and carbaryl

International Nuclear Information System (INIS)

Lee, Iwa; Eriksson, Per; Fredriksson, Anders; Buratovic, Sonja; Viberg, Henrik

2015-01-01

In recent times, an increased occurrence of neurodevelopmental disorders, such as neurodevelopmental delays and cognitive abnormalities has been recognized. Exposure to pesticides has been suspected to be a possible cause of these disorders, as these compounds target the nervous system of pests. Due to the similarities of brain development and composition, these pesticides may also be neurotoxic to humans. We studied two different pesticides, chlorpyrifos and carbaryl, which specifically inhibit acetylcholinesterase (AChE) in the nervous system. The aim of the study was to investigate if the pesticides can induce neurotoxic effects, when exposure occurs during a period of rapid brain growth and maturation. The results from the present study show that both compounds can affect protein levels in the developing brain and induce persistent adult behavior and cognitive impairments, in mice neonatally exposed to a single oral dose of chlorpyrifos (0.1, 1.0 or 5 mg/kg body weight) or carbaryl (0.5, 5.0 or 20.0 mg/kg body weight) on postnatal day 10. The results also indicate that the developmental neurotoxic effects induced are not related to the classical mechanism of acute cholinergic hyperstimulation, as the AChE inhibition level (8–12%) remained below the threshold for causing systemic toxicity. The neurotoxic effects are more likely caused by a disturbed neurodevelopment, as similar behavioral neurotoxic effects have been reported in studies with pesticides such as organochlorines, organophosphates, pyrethroids and POPs, when exposed during a critical window of neonatal brain development. - Highlights: • A single neonatal exposure to chlorpyrifos or carbaryl induced developmental neurotoxic effects. • The neurotoxic effects were not caused by acute AChE inhibition. • The neurotoxic effects manifested as altered levels of neuroproteins in the developing brain. • The neurotoxic effects manifested as adult persistent aberrant behavior and cognitive function. �

Developmental neurotoxic effects of two pesticides: Behavior and biomolecular studies on chlorpyrifos and carbaryl

Energy Technology Data Exchange (ETDEWEB)

Lee, Iwa; Eriksson, Per; Fredriksson, Anders; Buratovic, Sonja; Viberg, Henrik, E-mail: henrik.viberg@ebc.uu.se

2015-11-01

In recent times, an increased occurrence of neurodevelopmental disorders, such as neurodevelopmental delays and cognitive abnormalities has been recognized. Exposure to pesticides has been suspected to be a possible cause of these disorders, as these compounds target the nervous system of pests. Due to the similarities of brain development and composition, these pesticides may also be neurotoxic to humans. We studied two different pesticides, chlorpyrifos and carbaryl, which specifically inhibit acetylcholinesterase (AChE) in the nervous system. The aim of the study was to investigate if the pesticides can induce neurotoxic effects, when exposure occurs during a period of rapid brain growth and maturation. The results from the present study show that both compounds can affect protein levels in the developing brain and induce persistent adult behavior and cognitive impairments, in mice neonatally exposed to a single oral dose of chlorpyrifos (0.1, 1.0 or 5 mg/kg body weight) or carbaryl (0.5, 5.0 or 20.0 mg/kg body weight) on postnatal day 10. The results also indicate that the developmental neurotoxic effects induced are not related to the classical mechanism of acute cholinergic hyperstimulation, as the AChE inhibition level (8–12%) remained below the threshold for causing systemic toxicity. The neurotoxic effects are more likely caused by a disturbed neurodevelopment, as similar behavioral neurotoxic effects have been reported in studies with pesticides such as organochlorines, organophosphates, pyrethroids and POPs, when exposed during a critical window of neonatal brain development. - Highlights: • A single neonatal exposure to chlorpyrifos or carbaryl induced developmental neurotoxic effects. • The neurotoxic effects were not caused by acute AChE inhibition. • The neurotoxic effects manifested as altered levels of neuroproteins in the developing brain. • The neurotoxic effects manifested as adult persistent aberrant behavior and cognitive function. �

The Effects of IGF-1 on Trk Expressing DRG Neurons with HIV-gp120- Induced Neurotoxicity.

Science.gov (United States)

Li, Hao; Liu, Zhen; Chi, Heng; Bi, Yanwen; Song, Lijun; Liu, Huaxiang

2016-01-01

HIV envelope glycoprotein gp120 is the main protein that causes HIVassociated sensory neuropathy. However, the underlying mechanisms of gp120-induced neurotoxicity are still unclear. There are lack effective treatments for relieving HIV-related neuropathic symptoms caused by gp120-induced neurotoxicity. In the present study, tyrosine kinase receptor (Trk)A, TrkB, and TrkC expression in primary cultured dorsal root ganglion (DRG) neurons with gp120-induced neurotoxicity was investigated. The effects of IGF-1 on distinct Trk-positive DRG neurons with gp120-induced neurotoxicity were also determined. The results showed that gp120 not only dose-dependently induced DRG neuronal apoptosis and inhibited neuronal survival and neurite outgrowth, but also decreased distinct Trk expression levels. IGF-1 rescued DRG neurons from apoptosis and improved neuronal survival of gp120 neurotoxic DRG neurons in vitro. IGF-1 also improved TrkA and TrkB, but not TrkC, expression in gp120 neurotoxic conditions. The effects of IGF-1 could be blocked by preincubation with the phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002. These results suggested that gp120 may have a wide range of neurotoxicity on different subpopulations of DRG neurons, while IGF-1 might only relieve some subpopulations of DRG neurons with gp120-induced neurotoxicity. These data provide novel information of mechanisms of gp120 neurotoxicity on primary sensory neurons and the potential therapeutic effects of IGF-1 on gp120-induced neurotoxicity.

Protective Effects of N-Acetyl-L-cystein on 3,4-Methylene Dioxymethamphetamie-Induced Neurotoxicity in Cerebellum of Male Rats

Directory of Open Access Journals (Sweden)

Sara Soleimani Asl

2011-10-01

Full Text Available Objective(s: 3-4, methylenedioxymethamphetamine (MDMA causes apoptosis in nervous system and several studies suggest that oxidative stress contributes to MDMA-induced neurotoxicity. The aim of this study is to examine the effects of N-acetyl-L-Cystein (NAC as an antioxidant on MDMA-induced apoptosis. Materials and Methods: 21 Sprague dawley male rats (200-250mg were treated with MDMA (2×0,5mg/kg or MDMA plus NAC (100mg/kg IP for 7 day. After last administration of MDMA, rats were killed, cerebellum was removed and Bax and Bcl-2 expression was assessed by western blotting method. Results: The results of this study showed that MDMA causes up-regulation of Bax and down-regulation of Bcl-2 and NAC administration attenuated MDMA-induced apoptosis. Conclusion: The present study suggests that NAC treatment may improve MDMA-induced neurotoxicity.

Light-Enhanced Antibacterial Activity of Graphene Oxide, Mainly via Accelerated Electron Transfer.

Science.gov (United States)

Chong, Yu; Ge, Cuicui; Fang, Ge; Wu, Renfei; Zhang, He; Chai, Zhifang; Chen, Chunying; Yin, Jun-Jie

2017-09-05

Before graphene derivatives can be exploited as next-generation antimicrobials, we must understand their behavior under environmental conditions. Here, we demonstrate how exposure to simulated sunlight significantly enhances the antibacterial activity of graphene oxide (GO) and reveal the underlying mechanism. Our measurements of reactive oxygen species (ROS) showed that only singlet oxygen ( 1 O 2 ) is generated by GO exposed to simulated sunlight, which contributes only slightly to the oxidation of antioxidant biomolecules. Unexpectedly, we find the main cause of oxidation is light-induced electron-hole pairs generated on the surface of GO. These light-induced electrons promote the reduction of GO, introducing additional carbon-centered free radicals that may also enhance the antibacterial activities of GO. We conclude that GO-mediated oxidative stress mainly is ROS-independent; simulated sunlight accelerates the transfer of electrons from antioxidant biomolecules to GO, thereby destroying bacterial antioxidant systems and causing the reduction of GO. Our insights will help support the development of graphene for antibacterial applications.

Plasmonically sensitized metal-oxide electron extraction layers for organic solar cells.

Science.gov (United States)

Trost, S; Becker, T; Zilberberg, K; Behrendt, A; Polywka, A; Heiderhoff, R; Görrn, P; Riedl, T

2015-01-16

ZnO and TiOx are commonly used as electron extraction layers (EELs) in organic solar cells (OSCs). A general phenomenon of OSCs incorporating these metal-oxides is the requirement to illuminate the devices with UV light in order to improve device characteristics. This may cause severe problems if UV to VIS down-conversion is applied or if the UV spectral range (λ work, silver nanoparticles (AgNP) are used to plasmonically sensitize metal-oxide based EELs in the vicinity (1-20 nm) of the metal-oxide/organic interface. We evidence that plasmonically sensitized metal-oxide layers facilitate electron extraction and afford well-behaved highly efficient OSCs, even without the typical requirement of UV exposure. It is shown that in the plasmonically sensitized metal-oxides the illumination with visible light lowers the WF due to desorption of previously ionosorbed oxygen, in analogy to the process found in neat metal oxides upon UV exposure, only. As underlying mechanism the transfer of hot holes from the metal to the oxide upon illumination with hν < Eg is verified. The general applicability of this concept to most common metal-oxides (e.g. TiOx and ZnO) in combination with different photoactive organic materials is demonstrated.

Oxidation under electron bombardment. A tool for studying the initial states of silicon oxidation

Energy Technology Data Exchange (ETDEWEB)

Carriere, B.; Deville, J.P.; El Maachi, A.

1987-06-01

The exciting beam of an Auger electron spectrometer has been used to monitor the oxidation of silicon single crystals at room temperature and very low pressures of oxygen (approx. 10/sup -7/ Torr). This process allows us to build ultra-thin layers of silica on silicon (down to 30 A) but it is mostly used to investigate the mechanisms of the initial stages of oxidation. Auger spectra recorded continuously during the oxidation process provide information on (1) the nature of the silicon-oxygen chemical bonds which are interpreted through fine structure in the Auger peak, and (2) the kinetics of oxide formation which are deduced from curves of Auger signal versus time. An account is given of the contribution of these Auger studies to the description of the intermediate oxide layer during the reaction between silicon and oxygen and the influence of surface structural disorder, induced mainly by argon-ion bombardment, is discussed in terms of reactivity and oxide coverage.

Spirulina maxima extract prevents cell death through BDNF activation against amyloid beta 1-42 (Aβ1-42) induced neurotoxicity in PC12 cells.

Science.gov (United States)

Koh, Eun-Jeong; Kim, Kui-Jin; Choi, Jia; Kang, Do-Hyung; Lee, Boo-Yong

2018-04-23

Spirulina maxima is a blue-green micro alga that contains abundant amounts of proteins (60-70%), vitamins, chlorophyll a, and C-phycocyanin (C-PC). It has been shown to reduce oxidative stress, and prevent diabetes and non-alcoholic fatty liver disease. However, it is unclear whether Spirulina maxima 70% ethanol extract (SM70EE), chlorophyll a, and C-PC prevent Aβ 1-42 -induced neurotoxicity in PC12 cells. The aim of this study was to investigate whether SM70EE, chlorophyll a, and C-PC prevent Aβ 1-42 -induced cell death. SM70EE, chlorophyll a, and C-PC suppressed the Aβ 1-42 -induced increase in poly-ADP ribose polymerase-1 (PARP-1) cleavage and reduced Aβ 1-42 -induced decreases in glutathione and its associated factors. The level of brain-derived neurotrophic factor (BDNF), which plays a critical role in neuronal survival and neuroprotection, was increased by SM70EE, chlorophyll a, and C-PC in Aβ 1-42 -treated cells. SM70EE treatment decreased oxidative stress and cell death in response to Aβ 1-42 treatment, while simultaneously suppressing PARP cleavage and increasing the levels of glutathione (GSH) and its associated factors. Moreover, SM70EE lowered the levels of APP and BACE1, two major factors involved in APP processing, and increased BDNF expression during Aβ 1-42 -induced neurotoxicity in PC12 cells. We suggest that SM70EE prevents cell death caused by Aβ 1-42 -induced neurotoxicity via the activation of BDNF signaling. Copyright © 2018 Elsevier B.V. All rights reserved.

Synaptic contacts impaired by styrene-7,8-oxide toxicity

International Nuclear Information System (INIS)

Corsi, P.; D'Aprile, A.; Nico, B.; Costa, G.L.; Assennato, G.

2007-01-01

Styrene-7,8-oxide (SO), a chemical compound widely used in industrial applications, is a potential hazard for humans, particularly in occupational settings. Neurobehavioral changes are consistently observed in occupationally exposed individuals and alterations of neurotransmitters associated with neuronal loss have been reported in animal models. Although the toxic effects of styrene have been extensively documented, the molecular mechanisms responsible for SO-induced neurotoxicity are still unclear. A possible dopamine-mediated effect of styrene neurotoxicity has been previously demonstrated, since styrene oxide alters dopamine neurotransmission in the brain. Thus, the present study hypothesizes that styrene neurotoxicity may involve synaptic contacts. Primary striatal neurons were exposed to styrene oxide at different concentrations (0.1-1 mM) for different time periods (8, 16, and 24 h) to evaluate the dose able to induce synaptic impairments. The expression of proteins crucial for synaptic transmission such as Synapsin, Synaptophysin, and RAC-1 were considered. The levels of Synaptophysin and RAC-1 decreased in a dose-dependent manner. Accordingly, morphological alterations, observed at the ultrastructural level, primarily involved the pre-synaptic compartment. In SO-exposed cultures, the biochemical cascade of caspases was activated affecting the cytoskeleton components as their target. Thus the impairments in synaptic contacts observed in SO-exposed cultures might reflect a primarily morphological alteration of neuronal cytoskeleton. In addition, our data support the hypothesis developed by previous authors of reactive oxygen species (ROS) initiating events of SO cytotoxicity

Electrodes as Terminal Electron Acceptors in Anaerobic Ammonium Oxidation

Science.gov (United States)

Ruiz-Urigüen, M.; Jaffe, P. R.

2017-12-01

Anaerobic ammonium (NH4+) oxidation under iron (Fe) reducing conditions is a microbial- mediated process known as Feammox. This is a novel pathway in the nitrogen cycle, and a key process for alleviating NH4+ accumulation in anoxic soils, wetlands, and wastewater. Acidimicrobiaceae-bacterium A6, phylum Actinobacteria, are one type of autotrophic bacteria linked to this process. The Feammox-bacteria obtain their energy by oxidizing NH4+ and transferring the electrons to a terminal electron acceptor (TEA). Under environmental conditions, iron oxides are the TEAs. However, in this study we show that electrodes in Microbial Electrolysis Cells (MECs) or electrodes set in the field can be used as TEAs by Feammox-bacteria. The potential difference between electrodes is the driving force for electron transfer, making the reaction energetically feasible. Our results show that MECs containing Feammox cultures can remove NH4+ up to 3.5 mg/L in less than 4 hours, compared to an average of 9 mg/L in 2 weeks when cultured under traditional conditions. Concomitantly, MECs produce an average current of 30.5 A/m3 whilst dead bacteria produced low (Actinobacteria when compared to bulk soil. Electrodes as TEAs enhance electrogenic bacteria recovery and culturing. The use of MECs for the productions of Feammox-bacteria eliminates the dependence of Fe, a finite electron acceptor, therefore, allowing for continuous NH4+ removal. Finally, Fe-free Feammox-bacteria can be applied to reduce other metals of environmental concern; therefore, opening the range of possible application of Feammox-bacteria.

Nickel exposure induces oxidative damage to mitochondrial DNA in Neuro2a cells: the neuroprotective roles of melatonin.

Science.gov (United States)

Xu, Shang-Cheng; He, Min-Di; Lu, Yong-Hui; Li, Li; Zhong, Min; Zhang, Yan-Wen; Wang, Yuan; Yu, Zheng-Ping; Zhou, Zhou

2011-11-01

Recent studies suggest that oxidative stress and mitochondrial dysfunction play important roles in the neurotoxicity of nickel. Because mitochondrial DNA (mtDNA) is highly vulnerable to oxidative stress and melatonin can efficiently protect mtDNA against oxidative damage in various pathological conditions, the aims of this study were to determine whether mtDNA oxidative damage was involved in the neurotoxicity of nickel and to assay the neuroprotective effects of melatonin in mtDNA. In this study, we exposed mouse neuroblastoma cell lines (Neuro2a) to different concentrations of nickel chloride (NiCl(2), 0.125, 0.25, and 0.5 mm) for 24 hr. We found that nickel significantly increased reactive oxygen species (ROS) production and mitochondrial superoxide levels. In addition, nickel exposure increased mitochondrial 8-hydroxyguanine (8-OHdG) content and reduced mtDNA content and mtDNA transcript levels. Consistent with this finding, nickel was found to destroy mtDNA nucleoid structure and decrease protein levels of Tfam, a key protein component for nucleoid organization. However, all the oxidative damage to mtDNA induced by nickel was efficiently attenuated by melatonin pretreatment. Our results suggest that oxidative damage to mtDNA may account for the neurotoxicity of nickel. Melatonin has great pharmacological potential in protecting mtDNA against the adverse effects of nickel in the nervous system. © 2011 John Wiley & Sons A/S.

Environmental Chemicals and Human Neurotoxicity: Magnitude ...

African Journals Online (AJOL)

Olaleye

altered neurocthemical, electrophysiological or behavioural functions. The adverse effects of neurotoxicity are among the most feared ill health in humans ... chemicals through air, food, or drinking water. The infamous ..... environment can disrupt the neurological control .... that perception and memory gradually fade,.

Reversible metronidazole-induced neurotoxicity after 10 weeks of therapy.

Science.gov (United States)

AlDhaleei, Wafa; AlMarzooqi, Ayesha; Gaber, Nouran

2018-04-20

Metronidazole is a commonly used antimicrobial worldwide. The most common side effects that have been reported are nausea, vomiting and hypersensitivity reactions. However, neurotoxicity has been reported with the use of metronidazole but rather rare. The most common neurological manifestation is peripheral neuropathy involvement in the form of sensory loss. It is worth mentioning that central neurotoxicity is a rare side effect of metronidazole use but reversible. The manifestations vary from a headache, altered mental status to focal neurological deficits. The diagnosis is mainly by neuroimaging in the setting of acute neurological change in the patient status. Here, we report a case of metronidazole-induced neurotoxicity in a 38-year-old male patient who was admitted with a brain abscess and was started on metronidazole for more than 10 weeks. © BMJ Publishing Group Ltd (unless otherwise stated in the text of the article) 2018. All rights reserved. No commercial use is permitted unless otherwise expressly granted.

Severe Dopaminergic Neurotoxicity in Primates After a Common Recreational Dose Regimen of MDMA (``Ecstasy'')

Science.gov (United States)

Ricaurte, George A.; Yuan, Jie; Hatzidimitriou, George; Cord, Branden J.; McCann, Una D.

2002-09-01

The prevailing view is that the popular recreational drug (+/-)3,4-methylenedioxymethamphetamine (MDMA, or ``ecstasy'') is a selective serotonin neurotoxin in animals and possibly in humans. Nonhuman primates exposed to several sequential doses of MDMA, a regimen modeled after one used by humans, developed severe brain dopaminergic neurotoxicity, in addition to less pronounced serotonergic neurotoxicity. MDMA neurotoxicity was associated with increased vulnerability to motor dysfunction secondary to dopamine depletion. These results have implications for mechanisms of MDMA neurotoxicity and suggest that recreational MDMA users may unwittingly be putting themselves at risk, either as young adults or later in life, for developing neuropsychiatric disorders related to brain dopamine and/or serotonin deficiency.

Cedrin identified from Cedrus deodara (Roxb.) G. Don protects PC12 cells against neurotoxicity induced by Aβ1-42.

Science.gov (United States)

Zhao, Zhiwei; Dong, Zhanfei; Ming, Jie; Liu, Yan

2018-06-01

Alzheimer's disease is a severe neurodegenerative disease affecting elder worldwide and closely related to the neurotoxicity induced by amyloid β. To find efficient therapeutics, we have investigated the protective effects of cedrin from Cedrus deodara (Roxb.) G. Don on PC12 cells against the neurotoxicity induced by amyloid β 1-42 . The results have shown the viability of PC12 cells injured by amyloid β 1-42 can be improved by cedrin. Cedrin can reduce reacrive oxygen species overproduction, increase the activity of superoxide dismutase and decrease malondialdehyde content. Meanwhile, the loss of mitochondrial membrane potential and mitochondrial permeability transition pore opening in PC12 cells, and elevated Caspase-3 activity, downregulated Bcl-2 and upregulated Bax are meliorated. These results demonstrate the protective effect of cedrin is related to the inhibition of oxidative stress, improvement of mitochondrial dysfunction and suppression of apoptosis. This investigation gives evidences for the application of cedrin in practice and further investigation in vivo.

In situ Reduction and Oxidation of Nickel from Solid Oxide Fuel Cells in a Transmission Electron Microscope

DEFF Research Database (Denmark)

Faes, Antonin; Jeangros, Quentin; Wagner, Jakob Birkedal

2009-01-01

Environmental transmission electron microscopy was used to characterize in situ the reduction and oxidation of nickel from a Ni/YSZ solid oxide fuel cell anode support between 300-500{degree sign}C. The reduction is done under low hydrogen pressure. The reduction initiates at the NiO/YSZ interface...

Ginger and Propolis Exert Neuroprotective Effects against Monosodium Glutamate-Induced Neurotoxicity in Rats

Directory of Open Access Journals (Sweden)

Usama K. Hussein

2017-11-01

Full Text Available Central nervous system cytotoxicity is linked to neurodegenerative disorders. The objective of the study was to investigate whether monosodium glutamate (MSG neurotoxicity can be reversed by natural products, such as ginger or propolis, in male rats. Four different groups of Wistar rats were utilized in the study. Group A served as a normal control, whereas group B was orally administered with MSG (100 mg/kg body weight, via oral gavage. Two additional groups, C and D, were given MSG as group B along with oral dose (500 mg/kg body weight of either ginger or propolis (600 mg/kg body weight once a day for two months. At the end, the rats were sacrificed, and the brain tissue was excised and levels of neurotransmitters, ß-amyloid, and DNA oxidative marker 8-OHdG were estimated in the brain homogenates. Further, formalin-fixed and paraffin-embedded brain sections were used for histopathological evaluation. The results showed that MSG increased lipid peroxidation, nitric oxide, neurotransmitters, and 8-OHdG as well as registered an accumulation of ß-amyloid peptides compared to normal control rats. Moreover, significant depletions of glutathione, superoxide dismutase, and catalase as well as histopathological alterations in the brain tissue of MSG-treated rats were noticed in comparison with the normal control. In contrast, treatment with ginger greatly attenuated the neurotoxic effects of MSG through suppression of 8-OHdG and β-amyloid accumulation as well as alteration of neurotransmitter levels. Further improvements were also noticed based on histological alterations and reduction of neurodegeneration in the brain tissue. A modest inhibition of the neurodegenerative markers was observed by propolis. The study clearly indicates a neuroprotective effect of ginger and propolis against MSG-induced neurodegenerative disorders and these beneficial effects could be attributed to the polyphenolic compounds present in these natural products.

HIV-1 Myristoylated Nef Treatment of Murine Microglial Cells Activates Inducible Nitric Oxide Synthase, NO2 Production and Neurotoxic Activity.

Directory of Open Access Journals (Sweden)

Giorgio Mangino

Full Text Available The potential role of the human immunodeficiency virus-1 (HIV-1 accessory protein Nef in the pathogenesis of neuroAIDS is still poorly understood. Nef is a molecular adapter that influences several cellular signal transduction events and membrane trafficking. In human macrophages, Nef expression induces the production of extracellular factors (e.g. pro-inflammatory chemokines and cytokines and the recruitment of T cells, thus favoring their infection and its own transfer to uninfected cells via exosomes, cellular protrusions or cell-to-cell contacts. Murine cells are normally not permissive for HIV-1 but, in transgenic mice, Nef is a major disease determinant. Both in human and murine macrophages, myristoylated Nef (myr+Nef treatment has been shown to activate NF-κB, MAP kinases and interferon responsive factor 3 (IRF-3, thereby inducing tyrosine phosphorylation of signal transducers and activator of transcription (STAT-1, STAT-2 and STAT-3 through the production of proinflammatory factors.We report that treatment of BV-2 murine microglial cells with myr+Nef leads to STAT-1, -2 and -3 tyrosine phosphorylation and upregulates the expression of inducible nitric oxide synthase (iNOS with production of nitric oxide. We provide evidence that extracellular Nef regulates iNOS expression through NF-κB activation and, at least in part, interferon-β (IFNβ release that acts in concert with Nef. All of these effects require both myristoylation and a highly conserved acidic cluster in the viral protein. Finally, we report that Nef induces the release of neurotoxic factors in the supernatants of microglial cells.These results suggest a potential role of extracellular Nef in promoting neuronal injury in the murine model. They also indicate a possible interplay between Nef and host factors in the pathogenesis of neuroAIDS through the production of reactive nitrogen species in microglial cells.

Electron molecular beam epitaxy: Layer-by-layer growth of complex oxides via pulsed electron-beam deposition

International Nuclear Information System (INIS)

Comes, Ryan; Liu Hongxue; Lu Jiwei; Gu, Man; Khokhlov, Mikhail; Wolf, Stuart A.

2013-01-01

Complex oxide epitaxial film growth is a rich and exciting field, owing to the wide variety of physical properties present in oxides. These properties include ferroelectricity, ferromagnetism, spin-polarization, and a variety of other correlated phenomena. Traditionally, high quality epitaxial oxide films have been grown via oxide molecular beam epitaxy or pulsed laser deposition. Here, we present the growth of high quality epitaxial films using an alternative approach, the pulsed electron-beam deposition technique. We demonstrate all three epitaxial growth modes in different oxide systems: Frank-van der Merwe (layer-by-layer); Stranski-Krastanov (layer-then-island); and Volmer-Weber (island). Analysis of film quality and morphology is presented and techniques to optimize the morphology of films are discussed.

Electronic structure and ionicity of actinide oxides from first principles

DEFF Research Database (Denmark)

Petit, Leon; Svane, Axel; Szotek, Z.

2010-01-01

The ground-state electronic structures of the actinide oxides AO, A2O3, and AO2 (A=U, Np, Pu, Am, Cm, Bk, and Cf) are determined from first-principles calculations, using the self-interaction corrected local spin-density approximation. Emphasis is put on the degree of f-electron localization, whi...

Involvement of glial cells in the neurotoxicity of parathion and chlorpyrifos

International Nuclear Information System (INIS)

Zurich, M.-G.; Honegger, P.; Schilter, B.; Costa, L.G.; Monnet-Tschudi, F.

2004-01-01

An in vitro model, the aggregating brain cell culture of fetal rat telencephalon, has been used to investigate the influence of glial cells on the neurotoxicity of two organophosphorus pesticides (OPs), chlorpyrifos and parathion. Mixed-cell aggregate cultures were treated continuously for 10 days between DIV 5 and 15. Parathion induced astrogliosis at concentration at which MAP-2 immunostaining, found here to be more sensitive than neuron-specific enzyme activities, was not affected. In contrast, chlorpyrifos induced a comparatively weak gliotic reaction, and only at concentrations at which neurons were already affected. After similar treatments, increased neurotoxicity of parathion and chlorpyrifos was found in aggregate cultures deprived of glial cells. These results suggest that glial cells provide neuroprotection against OPs toxicity. To address the question of the difference in toxicity between parathion and chlorpyrifos, the toxic effects of their leaving groups, p-nitrophenol and trichloropyridinol, were studied in mixed-cell aggregates. General cytotoxicity was more pronounced for trichloropyridinol and both compounds had similar toxic effects on neuron-specific enzyme activities. In contrast, trichloropyridinol induced a much stronger decrease in glutamine synthetase activity, the enzymatic marker of astrocytes. Trichloropyridinol may exert a toxic effect on astrocytes, compromising their neuroprotective function, thus exacerbating the neurotoxicity of chlorpyrifos. This is in line with the suggestion that glial cells may contribute to OPs neurotoxicity, and with the view that OPs may exert their neurotoxic effects through different mechanisms

Fragment C Domain of Tetanus Toxin Mitigates Methamphetamine Neurotoxicity and Its Motor Consequences in Mice.

Science.gov (United States)

Mendieta, Liliana; Granado, Noelia; Aguilera, José; Tizabi, Yousef; Moratalla, Rosario

2016-08-01

The C-terminal domain of the heavy chain of tetanus toxin (Hc-TeTx) is a nontoxic peptide with demonstrated in vitro and in vivo neuroprotective effects against striatal dopaminergic damage induced by 1-methyl-4-phenylpyridinium and 6-hydoxydopamine, suggesting its possible therapeutic potential in Parkinson's disease. Methamphetamine, a widely abused psychostimulant, has selective dopaminergic neurotoxicity in rodents, monkeys, and humans. This study was undertaken to determine whether Hc-TeTx might also protect against methamphetamine-induced dopaminergic neurotoxicity and the consequent motor impairment. For this purpose, we treated mice with a toxic regimen of methamphetamine (4mg/kg, 3 consecutive i.p. injections, 3 hours apart) followed by 3 injections of 40 ug/kg of Hc-TeTx into grastrocnemius muscle at 1, 24, and 48 hours post methamphetamine treatment. We found that Hc-TeTx significantly reduced the loss of dopaminergic markers tyrosine hydroxylase and dopamine transporter and the increases in silver staining (a well stablished degeneration marker) induced by methamphetamine in the striatum. Moreover, Hc-TeTx prevented the increase of neuronal nitric oxide synthase but did not affect microglia activation induced by methamphetamine. Stereological neuronal count in the substantia nigra indicated loss of tyrosine hydroxylase-positive neurons after methamphetamine that was partially prevented by Hc-TeTx. Importantly, impairment in motor behaviors post methamphetamine treatment were significantly reduced by Hc-TeTx. Here we demonstrate that Hc-TeTx can provide significant protection against acute methamphetamine-induced neurotoxicity and motor impairment, suggesting its therapeutic potential in methamphetamine abusers. © The Author 2016. Published by Oxford University Press on behalf of CINP.

Two-electron electrochemical oxidation of quercetin and kaempferol changes only the flavonoid C-ring

DEFF Research Database (Denmark)

Jørgensen, Lars; Cornett, Claus; Justesen, Ulla

1998-01-01

Bulk electrolysis of the antioxidant flavonoids quercetin and kaempferol in acetonitrile both yield a single oxidation product in two-electron processes. The oxidation products are more polar than their parent compounds, with an increased molecular weight of 16g/mol, and were identified as 2......-(3,4-dihydroxybenzoyl)-2,4,6-trihydroxy-3 (2H)-benzofuranone and 2-(4-hydroxybenzoyl)-2,4,6-trihydroxy-3(2H)-benzofuranone for quercetin and kaempferol, respectively. Two-electron oxidation of the parent flavonoid is suggested to yield a 3,4-flavandione with unchanged substitution pattern in the A- and B-ring, which...... may rearrange to form the substituted 3(2H)-benzofuranone through the chalcan-trione ring-chain tautomer. The acidity of the 3-OH group is suggested to determine the fate of the flavonoid phenoxyl radical originally formed by one-electron oxidation, as no well-defined oxidation product of luteolin...

Charging effects during focused electron beam induced deposition of silicon oxide

NARCIS (Netherlands)

de Boer, Sanne K.; van Dorp, Willem F.; De Hosson, Jeff Th. M.

2011-01-01

This paper concentrates on focused electron beam induced deposition of silicon oxide. Silicon oxide pillars are written using 2, 4, 6, 8, 10-pentamethyl-cyclopenta-siloxane (PMCPS) as precursor. It is observed that branching of the pillar occurs above a minimum pillar height. The branching is

Heterojunction oxide thin-film transistors with unprecedented electron mobility grown from solution.

Science.gov (United States)

Faber, Hendrik; Das, Satyajit; Lin, Yen-Hung; Pliatsikas, Nikos; Zhao, Kui; Kehagias, Thomas; Dimitrakopulos, George; Amassian, Aram; Patsalas, Panos A; Anthopoulos, Thomas D

2017-03-01

Thin-film transistors made of solution-processed metal oxide semiconductors hold great promise for application in the emerging sector of large-area electronics. However, further advancement of the technology is hindered by limitations associated with the extrinsic electron transport properties of the often defect-prone oxides. We overcome this limitation by replacing the single-layer semiconductor channel with a low-dimensional, solution-grown In 2 O 3 /ZnO heterojunction. We find that In 2 O 3 /ZnO transistors exhibit band-like electron transport, with mobility values significantly higher than single-layer In 2 O 3 and ZnO devices by a factor of 2 to 100. This marked improvement is shown to originate from the presence of free electrons confined on the plane of the atomically sharp heterointerface induced by the large conduction band offset between In 2 O 3 and ZnO. Our finding underscores engineering of solution-grown metal oxide heterointerfaces as an alternative strategy to thin-film transistor development and has the potential for widespread technological applications.

Heterojunction oxide thin-film transistors with unprecedented electron mobility grown from solution

KAUST Repository

Faber, Hendrik

2017-04-28

Thin-film transistors made of solution-processed metal oxide semiconductors hold great promise for application in the emerging sector of large-area electronics. However, further advancement of the technology is hindered by limitations associated with the extrinsic electron transport properties of the often defect-prone oxides. We overcome this limitation by replacing the single-layer semiconductor channel with a low-dimensional, solution-grown In2O3/ZnO heterojunction. We find that In2O3/ZnO transistors exhibit band-like electron transport, with mobility values significantly higher than single-layer In2O3 and ZnO devices by a factor of 2 to 100. This marked improvement is shown to originate from the presence of free electrons confined on the plane of the atomically sharp heterointerface induced by the large conduction band offset between In2O3 and ZnO. Our finding underscores engineering of solution-grown metal oxide heterointerfaces as an alternative strategy to thin-film transistor development and has the potential for widespread technological applications.

A redox-based mechanism for the neuroprotective and neurodestructive effects of nitric oxide and related nitroso-compounds.

Science.gov (United States)

Lipton, S A; Choi, Y B; Pan, Z H; Lei, S Z; Chen, H S; Sucher, N J; Loscalzo, J; Singel, D J; Stamler, J S

1993-08-12

Congeners of nitrogen monoxide (NO) are neuroprotective and neurodestructive. To address this apparent paradox, we considered the effects on neurons of compounds characterized by alternative redox states of NO: nitric oxide (NO.) and nitrosonium ion (NO+). Nitric oxide, generated from NO. donors or synthesized endogenously after NMDA (N-methyl-D-aspartate) receptor activation, can lead to neurotoxicity. Here, we report that NO.- mediated neurotoxicity is engendered, at least in part, by reaction with superoxide anion (O2.-), apparently leading to formation of peroxynitrite (ONOO-), and not by NO. alone. In contrast, the neuroprotective effects of NO result from downregulation of NMDA-receptor activity by reaction with thiol group(s) of the receptor's redox modulatory site. This reaction is not mediated by NO. itself, but occurs under conditions supporting S-nitrosylation of NMDA receptor thiol (reaction or transfer of NO+). Moreover, the redox versatility of NO allows for its interconversion from neuroprotective to neurotoxic species by a change in the ambient redox milieu. The details of this complex redox chemistry of NO may provide a mechanism for harnessing neuroprotective effects and avoiding neurotoxicity in the central nervous system.

Highly active bidirectional electron transfer by a self-assembled electroactive reduced-graphene-oxide-hybridized biofilm.

Science.gov (United States)

Yong, Yang-Chun; Yu, Yang-Yang; Zhang, Xinhai; Song, Hao

2014-04-22

Low extracellular electron transfer performance is often a bottleneck in developing high-performance bioelectrochemical systems. Herein, we show that the self-assembly of graphene oxide and Shewanella oneidensis MR-1 formed an electroactive, reduced-graphene-oxide-hybridized, three-dimensional macroporous biofilm, which enabled highly efficient bidirectional electron transfers between Shewanella and electrodes owing to high biomass incorporation and enhanced direct contact-based extracellular electron transfer. This 3D electroactive biofilm delivered a 25-fold increase in the outward current (oxidation current, electron flux from bacteria to electrodes) and 74-fold increase in the inward current (reduction current, electron flux from electrodes to bacteria) over that of the naturally occurring biofilms. © 2014 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

Nanosized zinc oxide particles induce neural stem cell apoptosis

International Nuclear Information System (INIS)

Deng Xiaoyong; Luan Qixia; Wu Minghong; Zhang Haijiao; Jiao Zheng; Chen Wenting; Wang Yanli

2009-01-01

Given the intensive application of nanoscale zinc oxide (ZnO) materials in our life, growing concerns have arisen about its unintentional health and environmental impacts. In this study, the neurotoxicity of different sized ZnO nanoparticles in mouse neural stem cells (NSCs) was investigated. A cell viability assay indicated that ZnO nanoparticles manifested dose-dependent, but no size-dependent toxic effects on NSCs. Apoptotic cells were observed and analyzed by confocal microscopy, transmission electron microscopy examination, and flow cytometry. All the results support the viewpoint that the ZnO nanoparticle toxicity comes from the dissolved Zn 2+ in the culture medium or inside cells. Our results highlight the need for caution during the use and disposal of ZnO manufactured nanomaterials to prevent the unintended environmental and health impacts.

Electrochemically oxidized electronic and ionic conducting nanostructured block copolymers for lithium battery electrodes.

Science.gov (United States)

Patel, Shrayesh N; Javier, Anna E; Balsara, Nitash P

2013-07-23

Block copolymers that can simultaneously conduct electronic and ionic charges on the nanometer length scale can serve as innovative conductive binder material for solid-state battery electrodes. The purpose of this work is to study the electronic charge transport of poly(3-hexylthiophene)-b-poly(ethylene oxide) (P3HT-PEO) copolymers electrochemically oxidized with lithium bis(trifluoromethanesulfonyl) imide (LiTFSI) salt in the context of a lithium battery charge/discharge cycle. We use a solid-state three-terminal electrochemical cell that enables simultaneous conductivity measurements and control over electrochemical doping of P3HT. At low oxidation levels (ratio of moles of electrons removed to moles of 3-hexylthiophene moieties in the electrode), the electronic conductivity (σe,ox) increases from 10(-7) S/cm to 10(-4) S/cm. At high oxidation levels, σe,ox approaches 10(-2) S/cm. When P3HT-PEO is used as a conductive binder in a positive electrode with LiFePO4 active material, P3HT is electrochemically active within the voltage window of a charge/discharge cycle. The electronic conductivity of the P3HT-PEO binder is in the 10(-4) to 10(-2) S/cm range over most of the potential window of the charge/discharge cycle. This allows for efficient electronic conduction, and observed charge/discharge capacities approach the theoretical limit of LiFePO4. However, at the end of the discharge cycle, the electronic conductivity decreases sharply to 10(-7) S/cm, which means the "conductive" binder is now electronically insulating. The ability of our conductive binder to switch between electronically conducting and insulating states in the positive electrode provides an unprecedented route for automatic overdischarge protection in rechargeable batteries.

An internal report: Electron Spectroscopy of the Oxidation and Aging of U and Pu

Energy Technology Data Exchange (ETDEWEB)

Tobin, J. G. [Lawrence Livermore National Lab. (LLNL), Livermore, CA (United States)

2015-04-27

Uranium and Plutonium are highly reactive elements that undergo not only chemical reactions but also nuclear reactions. This can lead to possibly significant materials degradation, a matter of potentially great concern. Here, the issue of the electronic structure changes that occur with oxidation and radiological aging will be addressed, in a fairly empirical manner. In essence, the sensitivity of various electron spectroscopic techniques to oxidation and aging will be surveyed and discussed, including the apparent limitations. It will be found that 5d and 4d X-ray absorption and electron energy loss are essentially blind to the changes corresponding to oxidation and aging in U and Pu.

A role for D1 dopamine receptors in striatal methamphetamine-induced neurotoxicity.

Science.gov (United States)

Friend, Danielle M; Keefe, Kristen A

2013-10-25

Methamphetamine (METH) exposure results in long-term damage to the dopamine system in both human METH abusers and animal models. One factor that has been heavily implicated in this METH-induced damage to the dopaminergic system is the activation of D1 dopamine (DA) receptors. However, a significant caveat to the studies investigating the role of the receptor in such toxicity is that genetic and pharmacological manipulations of the D1 DA receptor also mitigate METH-induced hyperthermia. Importantly, METH-induced hyperthermia is tightly associated with the neurotoxicity, such that simply cooling animals during METH exposure protects against the neurotoxicity. Therefore, it is difficult to determine whether D1 DA receptors per se play an important role in METH-induced neurotoxicity or whether the protection observed simply resulted from a mitigation of METH-induced hyperthermia. To answer this important question, the current study infused a D1 DA receptor antagonist into striatum during METH exposure while controlling for METH-induced hyperthermia. Here we found that even when METH-induced hyperthermia is maintained, the coadministration of a D1 DA receptor antagonist protects against METH-induced neurotoxicity, strongly suggesting that D1 DA receptors play an important role in METH-induced neurotoxicity apart from the mitigation of METH-induced hyperthermia. Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.

Evidence for single metal two electron oxidative addition and reductive elimination at uranium.

Science.gov (United States)

Gardner, Benedict M; Kefalidis, Christos E; Lu, Erli; Patel, Dipti; McInnes, Eric J L; Tuna, Floriana; Wooles, Ashley J; Maron, Laurent; Liddle, Stephen T

2017-12-01

Reversible single-metal two-electron oxidative addition and reductive elimination are common fundamental reactions for transition metals that underpin major catalytic transformations. However, these reactions have never been observed together in the f-block because these metals exhibit irreversible one- or multi-electron oxidation or reduction reactions. Here we report that azobenzene oxidises sterically and electronically unsaturated uranium(III) complexes to afford a uranium(V)-imido complex in a reaction that satisfies all criteria of a single-metal two-electron oxidative addition. Thermolysis of this complex promotes extrusion of azobenzene, where H-/D-isotopic labelling finds no isotopomer cross-over and the non-reactivity of a nitrene-trap suggests that nitrenes are not generated and thus a reductive elimination has occurred. Though not optimally balanced in this case, this work presents evidence that classical d-block redox chemistry can be performed reversibly by f-block metals, and that uranium can thus mimic elementary transition metal reactivity, which may lead to the discovery of new f-block catalysis.

Characterization of Li-rich layered oxides by using transmission electron microscope

Directory of Open Access Journals (Sweden)

Hu Zhao

2017-07-01

Full Text Available Lithium-rich layered oxides (LrLOs deliver extremely high specific capacities and are considered to be promising candidates for electric vehicle and smart grid applications. However, the application of LrLOs needs further understanding of the structural complexity and dynamic evolution of monoclinic and rhombohedral phases, in order to overcome the issues including voltage decay, poor rate capability, initial irreversible capacity loss and etc. The development of aberration correction for the transmission electron microscope and concurrent progress in electron spectroscopy, have fueled rapid progress in the understanding of the mechanism of such issues. New techniques based on the transmission electron microscope are first surveyed, and the applications of these techniques for the study of the structure, migration of transition metal, and the activation of oxygen of LrLOs are then explored in detail, with a particular focus on the mechanism of voltage decay. Keywords: Lithium-ion battery, Transmission electron microscope, Lithium-rich layered oxide, Cathode material

The oxidation kinetics for sublimates formed during niobium electron-beam remelting

International Nuclear Information System (INIS)

Chumarev, V.M.; Gulyaeva, R.I.; Mar'evich, V.P.; Upolovnikova, A.G.; Udoeva, L.Yu.

2003-01-01

The oxidation of sublimates of Nb-Al electron beam remelting is investigated under conditions of isothermal and continuous heating in the air. It is stated that basic oxidation products are niobium and aluminium oxides, as well as aluminium niobates of variable composition of Al 2 O 3 · mNb 2 O 5 . The more aluminium enriched sublimates possess an increased resistance to oxidation. Formed in sublimates NbAl 3 intermetallic compound features the highest heat resistance. Oxidation parameters are determined by the method of nonisothermic kinetics. It is noted that the running processes exhibit a multistage nature and are limited by internal diffusion [ru

Thioredoxin-albumin fusion protein prevents copper enhanced zinc-induced neurotoxicity via its antioxidative activity.

Science.gov (United States)

Tanaka, Ken-Ichiro; Shimoda, Mikako; Chuang, Victor T G; Nishida, Kento; Kawahara, Masahiro; Ishida, Tatsuhiro; Otagiri, Masaki; Maruyama, Toru; Ishima, Yu

2018-01-15

Zinc (Zn) is a co-factor for a vast number of enzymes, and functions as a regulator for immune mechanism and protein synthesis. However, excessive Zn release induced in pathological situations such as stroke or transient global ischemia is toxic. Previously, we demonstrated that the interaction of Zn and copper (Cu) is involved in the pathogenesis of Alzheimer's disease and vascular dementia. Furthermore, oxidative stress has been shown to play a significant role in the pathogenesis of various metal ions induced neuronal death. Thioredoxin-Albumin fusion (HSA-Trx) is a derivative of thioredoxin (Trx), an antioxidative protein, with improved plasma retention and stability of Trx. In this study, we examined the effect of HSA-Trx on Cu 2+ /Zn 2+ -induced neurotoxicity. Firstly, HSA-Trx was found to clearly suppress Cu 2+ /Zn 2+ -induced neuronal cell death in mouse hypothalamic neuronal cells (GT1-7 cells). Moreover, HSA-Trx markedly suppressed Cu 2+ /Zn 2+ -induced ROS production and the expression of oxidative stress related genes, such as heme oxygenase-1. In contrast, HSA-Trx did not affect the intracellular levels of both Cu 2+ and Zn 2+ after Cu 2+ /Zn 2+ treatment. Finally, HSA-Trx was found to significantly suppress endoplasmic reticulum (ER) stress response induced by Cu 2+ /Zn 2+ treatment in a dose dependent manner. These results suggest that HSA-Trx counteracted Cu 2+ /Zn 2+ -induced neurotoxicity by suppressing the production of ROS via interfering the related gene expressions, in addition to the highly possible radical scavenging activity of the fusion protein. Based on these findings, HSA-Trx has great potential as a promising therapeutic agent for the treatment of refractory neurological diseases. Copyright © 2017 Elsevier B.V. All rights reserved.

Potential Protection of Coeloglossum viride var. Bracteatum Extract against Oxidative Stress in Rat Cortical Neurons

Directory of Open Access Journals (Sweden)

Zhe Guo

2013-01-01

Full Text Available The present study explored the neuroprotective effect of Coeloglossum viride var. bracteatum extract (CE against oxidative stress in rat cortical neurons. The results demonstrated that administration of CE inhibited hydrogen peroxide-induced neurotoxicity tested by MTT, LDH release, and TUNEL assays. We further found that CE inhibited the activation of caspase-3 (Csp3 induced by hydrogen peroxide. Moreover, CE was found to reverse the hydrogen peroxide-induced downregulation of active AKT and Bcl-2. We then showed that the neuroprotective effect of CE was blocked by adding the AKT inhibitor, Ly294002. Thus, our data strongly indicated that CE played a neuroprotective role against oxidative stress-induced neurotoxicity.

Peripheral Ammonia as a Mediator of Methamphetamine Neurotoxicity

Science.gov (United States)

Halpin, Laura E.; Yamamoto, Bryan K.

2012-01-01

Ammonia is metabolized by the liver and has established neurological effects. The current study examined the possibility that ammonia contributes to the neurotoxic effects of methamphetamine (METH). The results show that a binge dosing regimen of METH to the rat increased plasma and brain ammonia concentrations that were paralleled by evidence of hepatotoxicity. The role of peripheral ammonia in the neurotoxic effects of METH was further substantiated by the demonstration that the enhancement of peripheral ammonia excretion blocked the increases in brain and plasma ammonia and attenuated the long term depletions of dopamine and serotonin typically produced by METH. Conversely, the localized perfusion of ammonia in combination with METH, but not METH alone or ammonia alone, into the striatum recapitulated the neuronal damage produced by the systemic administration of METH. Furthermore, this damage produced by the local administration of ammonia and METH was blocked by the GYKI 52466, an AMPA receptor antagonist. These findings highlight the importance of ammonia derived from the periphery as a small molecule mediator of METH neurotoxicity and more broadly emphasize the importance of peripheral organ damage as a possible mechanism that mediates the neuropathology produced by drugs of abuse and other neuroactive molecules. PMID:22993432

Mitochondrial Ferritin Deletion Exacerbates β-Amyloid-Induced Neurotoxicity in Mice

Directory of Open Access Journals (Sweden)

Peina Wang

2017-01-01

Full Text Available Mitochondrial ferritin (FtMt is a mitochondrial iron storage protein which protects mitochondria from iron-induced oxidative damage. Our previous studies indicate that FtMt attenuates β-amyloid- and 6-hydroxydopamine-induced neurotoxicity in SH-SY5Y cells. To explore the protective effects of FtMt on β-amyloid-induced memory impairment and neuronal apoptosis and the mechanisms involved, 10-month-old wild-type and Ftmt knockout mice were infused intracerebroventricularly (ICV with Aβ25–35 to establish an Alzheimer’s disease model. Knockout of Ftmt significantly exacerbated Aβ25–35-induced learning and memory impairment. The Bcl-2/Bax ratio in mouse hippocampi was decreased and the levels of cleaved caspase-3 and PARP were increased. The number of neuronal cells undergoing apoptosis in the hippocampus was also increased in Ftmt knockout mice. In addition, the levels of L-ferritin and FPN1 in the hippocampus were raised, and the expression of TfR1 was decreased. Increased MDA levels were also detected in Ftmt knockout mice treated with Aβ25–35. In conclusion, this study demonstrated that the neurological impairment induced by Aβ25–35 was exacerbated in Ftmt knockout mice and that this may relate to increased levels of oxidative stress.

Neuroprotective and antioxidant effects of Thalassia testudinum extract BM-21, against acrylamide-induced neurotoxicity in mice

Directory of Open Access Journals (Sweden)

Roberto Menéndez

2014-06-01

Full Text Available Context: Acrylamide (ACR neurotoxicity is associated with the enhancement of lipid peroxidation and the reduction of the antioxidative capacity distal axon and nerve terminal regions. The aqueous ethanolic extract of the marine plant Thalassia testudinum, named BM-21, have shown antioxidant, anti-inflammatory and analgesic properties. Aims: To determine the neuroprotective and the antioxidant effects of BM-21, standardized to thalassiolin B content (5.8 ± 0.9%, on acrylamide (ACR-induced distal axonopathy in male OF-1 mice. Methods: Animals were administered with ACR (70 mg/kg, s.c., 4 weeks, and BM-21 was co-administered p.o at the doses of 4, 40 and 400 mg/kg. The effect of BM-21 on neurobehavioral indexes (rota-rod test, compound muscle action potential (CMAP of the sciatic nerve and oxidative stress parameters were investigated. Results: BM-21 significantly prevented the neurobehavioral sings of neurotoxicity and the alteration of CMAP amplitude and velocity. The lowest dose (4 mg/kg failed to ameliorate these parameters whereas the highest dose (400 mg/kg was the most active. BM-21 (400 mg/kg significantly restored total hydroperoxides (THP and glutathione (GSH in the sciatic nerve as well as superoxide dismutase (SOD and glutathione peroxidase (GSH-Px activities. Additionally, the extract also modified THP, GSH and the activity of SOD in cerebellum and brain towards the standard values. Conclusions: BM-21 given at doses that prevented ACR-induced neurotoxicity also produced antioxidant effect in the sciatic nerve, cerebellum and brain. Thus, the neuroprotective activity of BM-21 in this model seems to be mediated at least partly by its antioxidative properties.

Formation of quinones by one-electron oxidation in the metabolism of benzo[a]pyrene and 6-fluorobenzo[a]pyrene

International Nuclear Information System (INIS)

Cavalieri, E.; Wong, A.; Cremonesi, P.; Warner, C.; Rogan, E.

1986-01-01

Metabolic activation of polycyclic aromatic hydrocarbons (PAH), as well as other chemical carcinogens, occurs by two major pathways: One-electron oxidation and two-electron oxidation, or monooxygenation. One-electron oxidation generates radical cations or radicals, depending on the molecule in which the oxidation occurs, whereas two-electron oxidation produces oxygenated metabolites. Radical cations of PAH are ultimate electrophilic metabolites capable of binding to cellular macromolecules to initiate the tumor process. In this paper the authors will provide evidence that one-electron oxidation is involved not only in PAH carcinogenesis, but also in the formation of certain metabolites. Metabolism of benzo[a]pyrene (BP) by cytochrome P-450 monooxygenase yields three classes of products: phenols, dihydrodiols and the quinones, 1,6-, 3,6- and 6,12- dione

Artificial electron acceptors decouple archaeal methane oxidation from sulfate reduction.

Science.gov (United States)

Scheller, Silvan; Yu, Hang; Chadwick, Grayson L; McGlynn, Shawn E; Orphan, Victoria J

2016-02-12

The oxidation of methane with sulfate is an important microbial metabolism in the global carbon cycle. In marine methane seeps, this process is mediated by consortia of anaerobic methanotrophic archaea (ANME) that live in syntrophy with sulfate-reducing bacteria (SRB). The underlying interdependencies within this uncultured symbiotic partnership are poorly understood. We used a combination of rate measurements and single-cell stable isotope probing to demonstrate that ANME in deep-sea sediments can be catabolically and anabolically decoupled from their syntrophic SRB partners using soluble artificial oxidants. The ANME still sustain high rates of methane oxidation in the absence of sulfate as the terminal oxidant, lending support to the hypothesis that interspecies extracellular electron transfer is the syntrophic mechanism for the anaerobic oxidation of methane. Copyright © 2016, American Association for the Advancement of Science.

Highly n-Type Titanium Oxide as an Electronically Active Support for Platinum in the Catalytic Oxidation of Carbon Monoxide

KAUST Repository

Baker, L. Robert; Hervier, Antoine; Seo, Hyungtak; Kennedy, Griffin; Komvopoulos, Kyriakos; Somorjai, Gabor A.

2011-01-01

-support interaction is electronic activation of surface adsorbates by charge carriers. Motivated by the goal of using electronic activation to drive nonthermal chemistry, we investigated the ability of the oxide support to mediate charge transfer. We report

Changing of the electron structure of dispersed iron oxide during interaction with amines and borofluoride

International Nuclear Information System (INIS)

Hobert, H.; Arnold, D.

1975-01-01

The mechanism of chemisorption on the surface of iron oxide was studied by Moessbauer spectroscopy performed on samples of iron oxide finely dispersed in SiO 2 . It was found from Moessbauer spectra that the interaction of the oxide with amines resulted in a reversible electron transition from the amine to the adsorbent. The interaction with BF 3 brought about an irreversible electron transition from iron to boron. (A.K.)

Secondary electron emission influenced by oxidation on the aluminum surface: the roles of the chemisorbed oxygen and the oxide layer

Science.gov (United States)

Li, Jiangtao; Hoekstra, Bart; Wang, Zhen-Bin; Qiu, Jie; Pu, Yi-Kang

2018-04-01

A relationship between the apparent secondary electron yield ({γ }{{se}}) and the oxygen coverage/oxide layer thickness on an aluminum cathode is obtained in an experiment under a controlled environment. The apparent secondary electron yield ({γ }{{se}}) is deduced from the breakdown voltage between two parallel plate electrodes in a 360 mTorr argon environment using a simple Townsend breakdown model with the assumption that the variation of the apparent secondary electron yield is dominated by the variation of the argon ion induced processes. The oxygen coverage/oxide layer thickness on the aluminum cathode is measured by a semi in situ x-ray photoemission spectroscopy equipment which is directly attached to the discharge chamber. It is found that three phases exist: (1) in the monomonolayer regime, as the oxygen coverage increases from 0 to 0.3, {γ }{{se}} decreases by nearly 40 % , (2) as the oxygen coverage increases from 0.3 to 1, {γ }{{se}} keeps nearly constant, (3) as the oxide layer thickness increases from about 0.3 nm to about 1.1 nm, {γ }{{se}} increases by 150 % . We propose that, in the submonolayer regime, the chemisorbed oxygen on the aluminum surface causes the decrease of {γ }{{se}} by creating a local potential barrier, which reduces the Auger neutralization rate and the energy gained by the Auger electrons. In the multilayer regime, as the oxide layer grows in thickness, there are three proposed mechanisms which cause the increase of {γ }{{se}}: (1) the work function decreases; (2) resonance neutralization and Auger de-excitation may exist. This is served as another channel for secondary electron production; (3) the kinetic energy of Auger electrons is increased on average, leading to a higher probability for electrons to overcome the surface potential barrier.

A first principles investigation of the electronic structure of actinide oxides

DEFF Research Database (Denmark)

Petit, Leon; Svane, Axel; Szotek, Zdzislawa

2010-01-01

The ground state electronic structures of the actinide oxides AO, A2O3 and AO2 (A=U, Np, Pu, Am, Cm, Bk, Cf) are determined from first-principles calculations using the selfinteraction corrected local spin-density approximation. Our study reveals a strong link between preferred oxidation number...... and degree of localization. The ionic nature of the actinide oxides emerges from the fact that those oxides where the ground state is calculated to be metallic do not exist in nature, as the corresponding delocalized f-states favour the accommodation of additional O atoms into the crystal lattice....

Electronic properties of thermally formed thin iron oxide films

International Nuclear Information System (INIS)

Wielant, J.; Goossens, V.; Hausbrand, R.; Terryn, H.

2007-01-01

The oxide layer, present between an organic coating and the substrate, guarantees adhesion of the coating and plays a determinating role in the delamination rate of the organic coating. The purpose of this study is to compare the resistive and semiconducting properties of thermal oxides formed on steel in two different atmospheres at 250 deg. C: an oxygen rich atmosphere, air, and an oxygen deficient atmosphere, N 2 . In N 2 , a magnetite layer grows while in air a duplex oxide film forms composed by an inner magnetite layer and a thin outer hematite scale. The heat treatment for different amounts of time at high temperature was used as method to sample the thickness variation and change in electronic and semiconducting properties of the thermal oxide layers. Firstly, linear voltammetric measurements were performed to have a first insight in the electrochemical behavior of the thermal oxides in a borate buffer solution. Electrochemical impedance spectroscopy in the same buffer combined with the Mott-Schottky analysis were used to determine the semiconducting properties of the thermal oxides. By spectroscopic ellipsometry (SE) and atomic force microscopy (AFM), respectively, the thickness and roughness of the oxide layers were determined supporting the physical interpretation of the voltammetric and EIS data. These measurements clearly showed that oxide layers with different constitution, oxide resistance, flatband potential and doping concentration can be grown by changing the atmosphere

Chemokines, macrophage inflammatory protein-2 and stromal cell-derived factor-1{alpha}, suppress amyloid {beta}-induced neurotoxicity

Energy Technology Data Exchange (ETDEWEB)

Raman, Dayanidhi; Milatovic, Snjezana-Zaja [Department of Cancer Biology, Vanderbilt University, School of Medicine, Nashville, TN 37232 (United States); Milatovic, Dejan [Department of Pediatrics/Pediatric Toxicology, Vanderbilt University, School of Medicine, Nashville, TN 37232 (United States); Splittgerber, Ryan [Department of Cancer Biology, Vanderbilt University, School of Medicine, Nashville, TN 37232 (United States); Fan, Guo-Huang [Department of Neurobiology and Neurotoxicology, Meharry Medical College, Nashville, TN 37221 (United States); Richmond, Ann, E-mail: ann.richmond@vanderbilt.edu [VA Medical Center, Nashville, TN 37232 (United States); Department of Cancer Biology, Vanderbilt University, School of Medicine, Nashville, TN 37232 (United States)

2011-11-15

Alzheimer's disease (AD) is characterized by a progressive cognitive decline and accumulation of neurotoxic oligomeric peptides amyloid-{beta} (A{beta}). Although the molecular events are not entirely known, it has become evident that inflammation, environmental and other risk factors may play a causal, disruptive and/or protective role in the development of AD. The present study investigated the ability of the chemokines, macrophage inflammatory protein-2 (MIP-2) and stromal cell-derived factor-1{alpha} (SDF-1{alpha}), the respective ligands for chemokine receptors CXCR2 and CXCR4, to suppress A{beta}-induced neurotoxicity in vitro and in vivo. Pretreatment with MIP-2 or SDF-1{alpha} significantly protected neurons from A{beta}-induced dendritic regression and apoptosis in vitro through activation of Akt, ERK1/2 and maintenance of metalloproteinase ADAM17 especially with SDF-1{alpha}. Intra-cerebroventricular (ICV) injection of A{beta} led to reduction in dendritic length and spine density of pyramidal neurons in the CA1 area of the hippocampus and increased oxidative damage 24 h following the exposure. The A{beta}-induced morphometric changes of neurons and increase in biomarkers of oxidative damage, F{sub 2}-isoprostanes, were significantly inhibited by pretreatment with the chemokines MIP-2 or SDF-1{alpha}. Additionally, MIP-2 or SDF-1{alpha} was able to suppress the aberrant mislocalization of p21-activated kinase (PAK), one of the proteins involved in the maintenance of dendritic spines. Furthermore, MIP-2 also protected neurons against A{beta} neurotoxicity in CXCR2-/- mice, potentially through observed up regulation of CXCR1 mRNA. Understanding the neuroprotective potential of chemokines is crucial in defining the role for their employment during the early stages of neurodegeneration. -- Research highlights: Black-Right-Pointing-Pointer Neuroprotective ability of the chemokines MIP2 and CXCL12 against A{beta} toxicity. Black-Right-Pointing-Pointer MIP

Chemokines, macrophage inflammatory protein-2 and stromal cell-derived factor-1α, suppress amyloid β-induced neurotoxicity

International Nuclear Information System (INIS)

Raman, Dayanidhi; Milatovic, Snjezana-Zaja; Milatovic, Dejan; Splittgerber, Ryan; Fan, Guo-Huang; Richmond, Ann

2011-01-01

Alzheimer's disease (AD) is characterized by a progressive cognitive decline and accumulation of neurotoxic oligomeric peptides amyloid-β (Aβ). Although the molecular events are not entirely known, it has become evident that inflammation, environmental and other risk factors may play a causal, disruptive and/or protective role in the development of AD. The present study investigated the ability of the chemokines, macrophage inflammatory protein-2 (MIP-2) and stromal cell-derived factor-1α (SDF-1α), the respective ligands for chemokine receptors CXCR2 and CXCR4, to suppress Aβ-induced neurotoxicity in vitro and in vivo. Pretreatment with MIP-2 or SDF-1α significantly protected neurons from Aβ-induced dendritic regression and apoptosis in vitro through activation of Akt, ERK1/2 and maintenance of metalloproteinase ADAM17 especially with SDF-1α. Intra-cerebroventricular (ICV) injection of Aβ led to reduction in dendritic length and spine density of pyramidal neurons in the CA1 area of the hippocampus and increased oxidative damage 24 h following the exposure. The Aβ-induced morphometric changes of neurons and increase in biomarkers of oxidative damage, F 2 -isoprostanes, were significantly inhibited by pretreatment with the chemokines MIP-2 or SDF-1α. Additionally, MIP-2 or SDF-1α was able to suppress the aberrant mislocalization of p21-activated kinase (PAK), one of the proteins involved in the maintenance of dendritic spines. Furthermore, MIP-2 also protected neurons against Aβ neurotoxicity in CXCR2−/− mice, potentially through observed up regulation of CXCR1 mRNA. Understanding the neuroprotective potential of chemokines is crucial in defining the role for their employment during the early stages of neurodegeneration. -- Research highlights: ► Neuroprotective ability of the chemokines MIP2 and CXCL12 against Aβ toxicity. ► MIP-2 or CXCL12 prevented dendritic regression and apoptosis in vitro. ► Neuroprotection through activation of Akt, ERK

FAD oxidizes the ERO1-PDI electron transfer chain: The role of membrane integrity

International Nuclear Information System (INIS)

Papp, Eszter; Nardai, Gabor; Mandl, Jozsef; Banhegyi, Gabor; Csermely, Peter

2005-01-01

The molecular steps of the electron transfer in the endoplasmic reticulum from the secreted proteins during their oxidation are relatively unknown. We present here that flavine adenine dinucleotide (FAD) is a powerful oxidizer of the oxidoreductase system, Ero1 and PDI, besides the proteins of rat liver microsomes and HepG2 hepatoma cells. Inhibition of FAD transport hindered the action of FAD. Microsomal membrane integrity was mandatory for all FAD-related oxidation steps downstream of Ero1. The PDI inhibitor bacitracin could inhibit FAD-mediated oxidation of microsomal proteins and PDI, but did not hinder the FAD-driven oxidation of Ero1. Our data demonstrated that Ero1 can utilize FAD as an electron acceptor and that FAD-driven protein oxidation goes through the Ero1-PDI pathway and requires the integrity of the endoplasmic reticulum membrane. Our findings prompt further studies to elucidate the membrane-dependent steps of PDI oxidation and the role of FAD in redox folding

One-electron oxidation of BD84, an ellipticine antitumor derivative

International Nuclear Information System (INIS)

Sekaki, A.; Gardes-Albert, M.; Houee-Levin, C.; Ferradini, C.; Rivalle, C.; Bisagni, E.; Hickel, B.

1991-01-01

The one-electron oxidation of BD84, an ellipticine-related drug, has been studied by pulse radiolysis using OH· radicals as oxidizing agents. In the absence of oxygen, R· radicals are formed. They disappear by recombination. In the presence of oxygen, R· radicals react with O 2 to give peroxy radicals RO 2 ·, which decay by a second-order process. These results are compared to those obtained for other ellipticine derivatives [fr

Electron momentum spectroscopy of the group I and Il metal and oxides

International Nuclear Information System (INIS)

Ford, M.J.; Dorsett, H.E.; Sashin, V.A.; Bolorizadeh, M.A.; Mikajlo, E.A.; Soule de Bas, B.; Nixon, K.L.; Coleman, V.A.

2002-01-01

Full text: The group I and Il metals and oxides are relatively simple condensed phase systems that are easily accessible to theoretical studies. For this reason they have been the subject of a number of studies using a range of theoretical techniques. Calculated electronic band structures have traditionally been compared with optical, X-ray and photo emissions measurements. While these techniques provide excellent data for testing theoretical predictions they generally probe certain aspects of the electronic structure, such as special point energies or densities of states, or require considerable theoretical input for their interpretation. In this paper we present our electron momentum spectroscopy (EMS) measurements for the lighter group Il metals and oxides and group I oxides. EMS can measure directly the full band dispersions and intensities and provides a sensitive test of theoretical predictions. We compare our measurements with Hartree-Fock (HF) and density functional theory (DFT) calculations carried out within the linear combination of atomic orbitals approximation. As expected HF significantly overestimates the bandwidths and bandgaps. DFT gives reasonable overall agreement, albeit with slight overestimation of bandwidths for the oxides. The intensity distribution for the oxides show a systematic difference from all the calculations which cannot easily be explained by experimental effects such as multiple scattering in the target. This work was funded by the Australian Research Council and Flinders University. EA Mikajlo and K L Nixon acknowledge receipt of SENRAC and Ferry scholarships respectively

Mechanisms for Electron Transfer Through Pili to Fe(III) Oxide in Geobacter

Energy Technology Data Exchange (ETDEWEB)

Lovley, Derek R. [Univ. of Massachusetts, Amherst, MA (United States)

2015-03-09

The purpose of these studies was to aid the Department of Energy in its goal of understanding how microorganisms involved in the bioremediation of metals and radionuclides sustain their activity in the subsurface. This information is required in order to incorporate biological processes into decision making for environmental remediation and long-term stewardship of contaminated sites. The proposed research was designed to elucidate the mechanisms for electron transfer to Fe(III) oxides in Geobacter species because Geobacter species are abundant dissimilatory metal-reducing microorganisms in a diversity of sites in which uranium is undergoing natural attenuation via the reduction of soluble U(VI) to insoluble U(IV) or when this process is artificially stimulated with the addition of organic electron donors. This study investigated the novel, but highly controversial, concept that the final conduit for electron transfer to Fe(III) oxides are electrically conductive pili. The specific objectives were to: 1) further evaluate the conductivity along the pili of Geobacter sulfurreducens and related organisms; 2) determine the mechanisms for pili conductivity; and 3) investigate the role of pili in Fe(III) oxide reduction. The studies demonstrated that the pili of G. sulfurreducens are conductive along their length. Surprisingly, the pili possess a metallic-like conductivity similar to that observed in synthetic organic conducting polymers such as polyaniline. Detailed physical analysis of the pili, as well as studies in which the structure of the pili was genetically modified, demonstrated that the metallic-like conductivity of the pili could be attributed to overlapping pi-pi orbitals of aromatic amino acids. Other potential mechanisms for conductivity, such as electron hopping between cytochromes associated with the pili were definitively ruled out. Pili were also found to be essential for Fe(III) oxide reduction in G. metallireducens. Ecological studies demonstrated

Pseudo-diode based on protonic/electronic hybrid oxide transistor

Science.gov (United States)

Fu, Yang Ming; Liu, Yang Hui; Zhu, Li Qiang; Xiao, Hui; Song, An Ran

2018-01-01

Current rectification behavior has been proved to be essential in modern electronics. Here, a pseudo-diode is proposed based on protonic/electronic hybrid indium-gallium-zinc oxide electric-double-layer (EDL) transistor. The oxide EDL transistors are fabricated by using phosphorous silicate glass (PSG) based proton conducting electrolyte as gate dielectric. A diode operation mode is established on the transistor, originating from field configurable proton fluxes within the PSG electrolyte. Current rectification ratios have been modulated to values ranged between ˜4 and ˜50 000 with gate electrode biased at voltages ranged between -0.7 V and 0.1 V. Interestingly, the proposed pseudo-diode also exhibits field reconfigurable threshold voltages. When the gate is biased at -0.5 V and 0.3 V, threshold voltages are set to ˜-1.3 V and -0.55 V, respectively. The proposed pseudo-diode may find potential applications in brain-inspired platforms and low-power portable systems.

One-electron oxidation of DNA: mechanism and consequences.

Science.gov (United States)

Schuster, Gary B

2009-01-01

All living organisms store the information necessary to maintain life in their DNA. Any process that damages DNA and causes loss or corruption of that information threatens the viability of the organism. One-electron oxidation is such a process. Loss of an electron from DNA generates a radical cation that is located primarily on its nucleobases. The radical cation migrates reversibly through duplex DNA by hopping until it is eventually trapped in an irreversible chemical reaction. The particular sequence of nucleobases in a DNA oligomer determines both the efficiency of hopping and the specific location and nature of the damaging chemical reaction. In its normal aqueous solutions, DNA is a polyanion because of the negative charge carried by its phosphate groups. Counter ions (typically Na(+)) to the phosphate groups play an important role in facilitating both the migration of the radical cation and in its eventual reaction with H(2)O. Irreversible reaction of a radical cation with H(2)O in duplex DNA occurs preferentially at the most reactive site. In normal DNA that is comprised of the four common DNA nucleobases, reaction occurs most commonly at a guanine and results in its conversion primarily to 8-oxo-7,8-dihydroguanine (8-OxoG). Both electronic and steric effects control the outcome of this process. If the DNA oligomer does not contain a suitable guanine, then reaction of the radical cation occurs at the thymine of a TT step primarily by a tandem process. The general outcomes revealed in the one-electron oxidation of DNA oligomers in solution appear to be generally valid also for more complex DNA structures and for the cellular DNA of living organisms.

Alpha 7 nicotinic acetylcholine receptor-mediated protection against ethanol-induced neurotoxicity.

Science.gov (United States)

de Fiebre, NancyEllen C; de Fiebre, Christopher M

2003-11-01

The alpha(7)-selective nicotinic partial agonist 3-[2,4-dimethoxybenzylidene]anabaseine (DMXB) was examined for its ability to modulate ethanol-induced neurotoxicity in primary cultures of rat neurons. Primary cultures of hippocampal neurons were established from Long-Evans, embryonic day (E)-18 rat fetuses and maintained for 7 days. Ethanol (0-150 mM), DMXB (0-56 microM), or both were subsequently co-applied to cultures. Ethanol was added two additional times to the cultures to compensate for evaporation. After 5 days, neuronal viability was assessed with the MTT cell proliferation assay. Results demonstrated that ethanol reduces neuronal viability in a concentration-dependent fashion and that DMXB protects against this ethanol-induced neurotoxicity, also in a concentration-dependent fashion. These results support the suggestion that nicotinic partial agonists may be useful in treating binge drinking-induced neurotoxicity and may provide clues as to why heavy drinkers are usually smokers.

Erythropoietin in the treatment of carbon monoxide neurotoxicity in rat.

Science.gov (United States)

Moallem, Seyed Adel; Mohamadpour, Amir Hooshang; Abnous, Khalil; Sankian, Mojtaba; Sadeghnia, Hamid Reza; Tsatsakis, Aristidis; Shahsavand, Shabnam

2015-12-01

Erythropoietin (EPO) plays a critical role in the development of the nervous system. In this study, the effects of EPO in carbon monoxide (CO) neurotoxicity were examined. Rats were exposed to 3000 ppm CO for 1 h and then different doses of EPO were administrated intraperitoneally. After 24 h, glial fibrillary acidic protein (GFAP) levels in the serum were determined and water content of brain and the extravasation of a tracer (Evans blue) were measured. Brain lipid peroxidation, myeloperoxidase activity Myelin basic protein (MBP) and BAX/BcL2 protein relative expressions were determined. Cation exchange chromatography was used to evaluate MBP alterations. Seven days after exposure, pathological assessment was performed after Klüver-Barrera staining. EPO reduced malondialdehyde levels at all doses (2500, 5000 and 10,000 u/kg). Lower doses of EPO (625, 1250, 2500 u/kg) significantly decreased the elevated serum levels of GFAP. EPO could not reduce the water content of the edematous poisoned brains. However, at 5000 and 10,000 u/kg it protected the blood brain barrier against integrity loss as a result of CO. EPO could significantly decrease the MPO activity. CO-mediated oxidative stress caused chemical alterations in MBP and EPO could partially prevent these biochemical changes. Fewer vacuoles and demyelinated fibers were found in the EPO-treated animals. EPO (5000 u/kg) could restore the MBP density. CO increased brain BAX/Bcl-2 ratio 38.78%. EPO reduced it 38.86%. These results reveal that EPO could relatively prevent different pathways of neurotoxicity by CO poisoning and thus has the potential to be used as a novel approach to manage this poisoning. Copyright © 2015 Elsevier Ltd. All rights reserved.

Neurotoxicity of "ecstasy" and its metabolites in human dopaminergic differentiated SH-SY5Y cells.

Science.gov (United States)

Ferreira, Patrícia Silva; Nogueira, Tiago Bernandes; Costa, Vera Marisa; Branco, Paula Sério; Ferreira, Luísa Maria; Fernandes, Eduarda; Bastos, Maria Lourdes; Meisel, Andreas; Carvalho, Félix; Capela, João Paulo

2013-02-04

"Ecstasy" (3,4-methylenedioxymethamphetamine or MDMA) is a widely abused recreational drug, reported to produce neurotoxic effects, both in laboratory animals and in humans. MDMA metabolites can be major contributors for MDMA neurotoxicity. This work studied the neurotoxicity of MDMA and its catechol metabolites, α-methyldopamine (α-MeDA) and N-methyl-α-methyldopamine (N-Me-α-MeDA) in human dopaminergic SH-SY5Y cells differentiated with retinoic acid and 12-O-tetradecanoyl-phorbol-13-acetate. Differentiation led to SH-SY5Y neurons with higher ability to accumulate dopamine and higher resistance towards dopamine neurotoxicity. MDMA catechol metabolites were neurotoxic to SH-SY5Y neurons, leading to caspase 3-independent cell death in a concentration- and time-dependent manner. MDMA did not show a concentration- and time-dependent death. Pre-treatment with the antioxidant and glutathione precursor, N-acetylcysteine (NAC), resulted in strong protection against the MDMA metabolites' neurotoxicity. Neither the superoxide radical scavenger, tiron, nor the inhibitor of the dopamine (DA) transporter, GBR 12909, prevented the metabolites' toxicity. Cells exposed to α-MeDA showed an increase in intracellular glutathione (GSH) levels, which, at the 48 h time-point, was not dependent in the activity increase of γ-glutamylcysteine synthetase (γ-GCS), revealing a possible transient effect. Importantly, pre-treatment with buthionine sulfoximine (BSO), an inhibitor of γ-GCS, prevented α-MeDA induced increase in GSH levels, but did not augment this metabolite cytotoxicity. Even so, BSO pre-treatment abolished NAC protective effects against α-MeDA neurotoxicity, which were, at least partially, due to GSH de novo synthesis. Inversely, pre-treatment of cells with BSO augmented N-Me-α-MeDA-induced neurotoxicity, but only slightly affected NAC neuroprotection. In conclusion, MDMA catechol metabolites promote differential toxic effects to differentiated dopaminergic human SH

The role of dopamine receptors in the neurotoxicity of methamphetamine.

Science.gov (United States)

Ares-Santos, S; Granado, N; Moratalla, R

2013-05-01

Methamphetamine is a synthetic drug consumed by millions of users despite its neurotoxic effects in the brain, leading to loss of dopaminergic fibres and cell bodies. Moreover, clinical reports suggest that methamphetamine abusers are predisposed to Parkinson's disease. Therefore, it is important to elucidate the mechanisms involved in methamphetamine-induced neurotoxicity. Dopamine receptors may be a plausible target to prevent this neurotoxicity. Genetic inactivation of dopamine D1 or D2 receptors protects against the loss of dopaminergic fibres in the striatum and loss of dopaminergic neurons in the substantia nigra. Protection by D1 receptor inactivation is due to blockade of hypothermia, reduced dopamine content and turnover and increased stored vesicular dopamine in D1R(-/-) mice. However, the neuroprotective impact of D2 receptor inactivation is partially dependent on an effect on body temperature, as well as on the blockade of dopamine reuptake by decreased dopamine transporter activity, which results in reduced intracytosolic dopamine levels in D2R(-/-) mice. © 2013 The Association for the Publication of the Journal of Internal Medicine.

Neurotoxicity of traffic-related air pollution.

Science.gov (United States)

Costa, Lucio G; Cole, Toby B; Coburn, Jacki; Chang, Yu-Chi; Dao, Khoi; Roqué, Pamela J

2017-03-01

The central nervous system is emerging as an important target for adverse health effects of air pollution, where it may contribute to neurodevelopmental and neurodegenerative disorders. Air pollution comprises several components, including particulate matter (PM) and ultrafine particulate matter (UFPM), gases, organic compounds, and metals. An important source of ambient PM and UFPM is represented by traffic-related air pollution, primarily diesel exhaust (DE). Human epidemiological studies and controlled animal studies have shown that exposure to air pollution, and to traffic-related air pollution or DE in particular, may lead to neurotoxicity. In particular, air pollution is emerging as a possible etiological factor in neurodevelopmental (e.g. autism spectrum disorders) and neurodegenerative (e.g. Alzheimer's disease) disorders. The most prominent effects caused by air pollution in both humans and animals are oxidative stress and neuro-inflammation. Studies in mice acutely exposed to DE (250-300μg/m 3 for 6h) have shown microglia activation, increased lipid peroxidation, and neuro-inflammation in various brain regions, particularly the hippocampus and the olfactory bulb. An impairment of adult neurogenesis was also found. In most cases, the effects of DE were more pronounced in male mice, possibly because of lower antioxidant abilities due to lower expression of paraoxonase 2. Copyright © 2015 Elsevier B.V. All rights reserved.

Phosphorene Oxide: Stability and electronic properties of a novel 2D material

OpenAIRE

Wang, Gaoxue; Pandey, Ravindra; Karna, Shashi P.

2014-01-01

Phosphorene, the monolayer form of the (black) phosphorus, was recently exfoliated from its bulk counterpart. Phosphorene oxide, by analogy to graphene oxide, is expected to have novel chemical and electronic properties, and may provide an alternative route to synthesis of phosphorene. In this letter, we investigate physical and chemical properties of the phosphorene oxide including its formation by the oxygen adsorption on the bare phosphorene. Analysis of the phonon dispersion curves finds ...

Nitric Oxide Synthases Reveal a Role for Calmodulin in Controlling Electron Transfer

Science.gov (United States)

Abu-Soud, Husam M.; Stuehr, Dennis J.

1993-11-01

Nitric oxide (NO) is synthesized within the immune, vascular, and nervous systems, where it acts as a wide-ranging mediator of mammalian physiology. The NO synthases (EC 1.14.13.39) isolated from neurons or endothelium are calmodulin dependent. Calmodulin binds reversibly to neuronal NO synthase in response to elevated Ca2+, triggering its NO production by an unknown mechanism. Here we show that calmodulin binding allows NADPH-derived electrons to pass onto the heme group of neuronal NO synthase. Calmodulin-triggered electron transfer to heme was independent of substrate binding, caused rapid enzymatic oxidation of NADPH in the presence of O_2, and was required for NO synthesis. An NO synthase isolated from cytokine-induced macrophages that contains tightly bound calmodulin catalyzed spontaneous electron transfer to its heme, consistent with bound calmodulin also enabling electron transfer within this isoform. Together, these results provide a basis for how calmodulin may regulate NO synthesis. The ability of calmodulin to trigger electron transfer within an enzyme is unexpected and represents an additional function for calcium-binding proteins in biology.

Neuromodulatory Effects of Hesperidin in Mitigating Oxidative Stress in Streptozotocin Induced Diabetes

Directory of Open Access Journals (Sweden)

Mohammad Ashafaq

2014-01-01

Full Text Available Oxidative stress has been implicated in pathogenesis of streptozotocin- (STZ- induced diabetes mellitus and its complication in central nervous system (CNS. Recent studies have provided insights on antioxidants and their emergence as potential therapeutic and nutraceutical. The present study examined the hypothesis that hesperidin (HP ameliorates oxidative stress and may be a limiting factor in the extent of CNS complication following diabetes. To test this hypothesis rats were divided into four groups: control, diabetic, diabetic-HP treated, and vehicle for HP treatment group. Diabetes mellitus was induced by a single injection of STZ (65 mg/kg body weight. Three days after STZ injection, HP was given (50 mg/kg b.wt. orally once daily for four weeks. The results of the present investigation suggest that the significant elevated levels of oxidative stress markers were observed in STZ-treated animals, whereas significant depletion in the activity of nonenzymatic antioxidants and enzymatic antioxidants was witnessed in diabetic rat brain. Neurotoxicity biomarker activity was also altered significantly. HP treatment significantly attenuated the altered levels of oxidative stress and neurotoxicity biomarkers. Our results demonstrate that HP exhibits potent antioxidant and neuroprotective effects on the brain tissue against the diabetic oxidative damage in STZ-induced rodent model.

Microbial Anaerobic Ammonium Oxidation Under Iron Reducing Conditions, Alternative Electron Acceptors

Science.gov (United States)

Ruiz-Urigüen, M.; Jaffe, P. R.

2015-12-01

Autotrophic Acidimicrobiaceae-bacterium named A6 (A6), part of the Actinobacteria phylum have been linked to anaerobic ammonium (NH4+) oxidation under iron reducing conditions. These organisms obtain their energy by oxidizing NH4+ and transferring the electrons to a terminal electron acceptor (TEA). Under environmental conditions, the TEAs are iron oxides [Fe(III)], which are reduced to Fe(II), this process is known as Feammox. Our studies indicate that alternative forms of TEAs can be used by A6, e.g. iron rich clays (i.e. nontronite) and electrodes in bioelectrochemical systems such as Microbial Electrolysis Cells (MECs), which can sustain NH4+removal and A6 biomass production. Our results show that nontronite can support Feammox and promote bacterial cell production. A6 biomass increased from 4.7 x 104 to 3.9 x 105 cells/ml in 10 days. Incubations of A6 in nontronite resulted in up to 10 times more NH4+ removal and 3 times more biomass production than when ferrihydrite is used as the Fe(III) source. Additionally, Fe in nontronite can be reoxidized by aeration and A6 can reutilize it; however, Fe is still finite in the clay. In contrast, in MECs, A6 harvest electrons from NH4+ and use an anode as an unlimited TEA, as a result current is produced. We operated multiple MECs in parallel using a single external power source, as described by Call & Logan (2011). MECs were run with an applied voltage of 0.7V and different growing mediums always containing initial 5mM NH4+. Results show that current production is favored when anthraquinone-2,6-disulfonate (AQDS), an electron shuttled, is present in the medium as it facilitates the transfer of electrons from the bacterial cell to the anode. Additionally, A6 biomass increased from 1 x 104 to 9.77 x 105cells/ml in 14 days of operation. Due to Acidimicrobiaceae-bacterium A6's ability to use various TEAs, MECs represent an alternative, iron-free form, for optimized biomass production of A6 and its application in NH4

Microcystin-LR exposure induces developmental neurotoxicity in zebrafish embryo

International Nuclear Information System (INIS)

Wu, Qin; Yan, Wei; Liu, Chunsheng; Li, Li; Yu, Liqin; Zhao, Sujuan; Li, Guangyu

2016-01-01

Microcystin-LR (MCLR) is a commonly acting potent hepatotoxin and has been pointed out of potentially causing developmental neurotoxicity, but the exact mechanism is little known. In this study, zebrafish embryos were exposed to 0, 0.8, 1.6 or 3.2 mg/L MCLR for 120 h. MCLR exposure through submersion caused serious hatching delay and body length decrease. The content of MCLR in zebrafish larvae was analyzed and the results demonstrated that MCLR can accumulate in zebrafish larvae. The locomotor speed of zebrafish larvae was decreased. Furthermore, the dopamine and acetylcholine (ACh) content were detected to be significantly decreased in MCLR exposure groups. And the acetylcholinesterase (AChE) activity was significantly increased after exposure to 1.6 and 3.2 mg/L MCLR. The transcription pattern of manf, chrnα7 and ache gene was consistent with the change of the dopamine content, ACh content and AChE activity. Gene expression involved in the development of neurons was also measured. α1-tubulin and shha gene expression were down-regulated, whereas mbp and gap43 gene expression were observed to be significantly up-regulated upon exposure to MCLR. The above results indicated that MCLR-induced developmental toxicity might attribute to the disorder of cholinergic system, dopaminergic signaling, and the development of neurons. - Highlights: • MCLR accumulation induces developmental neurotoxicity in zebrafish embryo. • The decrease of dopamine levels might be associated with the MCLR-induced developmental neurotoxicity in zebrafish larvae. • The alternation of cholinergic system might contribute to the change of neurobehavior in zebrafish larvae exposure with MCLR. - MCLR accumulation induces developmental neurotoxicity by affecting cholinergic system, dopaminergic signaling, and the development of neurons in zebrafish embryo.

Squalestatin alters the intracellular trafficking of a neurotoxic prion peptide

Directory of Open Access Journals (Sweden)

Williams Alun

2007-11-01

Full Text Available Abstract Background Neurotoxic peptides derived from the protease-resistant core of the prion protein are used to model the pathogenesis of prion diseases. The current study characterised the ingestion, internalization and intracellular trafficking of a neurotoxic peptide containing amino acids 105–132 of the murine prion protein (MoPrP105-132 in neuroblastoma cells and primary cortical neurons. Results Fluorescence microscopy and cell fractionation techniques showed that MoPrP105-132 co-localised with lipid raft markers (cholera toxin and caveolin-1 and trafficked intracellularly within lipid rafts. This trafficking followed a non-classical endosomal pathway delivering peptide to the Golgi and ER, avoiding classical endosomal trafficking via early endosomes to lysosomes. Fluorescence resonance energy transfer analysis demonstrated close interactions of MoPrP105-132 with cytoplasmic phospholipase A2 (cPLA2 and cyclo-oxygenase-1 (COX-1, enzymes implicated in the neurotoxicity of prions. Treatment with squalestatin reduced neuronal cholesterol levels and caused the redistribution of MoPrP105-132 out of lipid rafts. In squalestatin-treated cells, MoPrP105-132 was rerouted away from the Golgi/ER into degradative lysosomes. Squalestatin treatment also reduced the association between MoPrP105-132 and cPLA2/COX-1. Conclusion As the observed shift in peptide trafficking was accompanied by increased cell survival these studies suggest that the neurotoxicity of this PrP peptide is dependent on trafficking to specific organelles where it activates specific signal transduction pathways.

Effects of keV electron irradiation on the avalanche-electron generation rates of three donors on oxidized silicon

International Nuclear Information System (INIS)

Sah, C.; Sun, J.Y.; Tzou, J.J.

1983-01-01

After keV electron beam irradiation of oxidized silicon, the avalanche-electron-injection generation rates and densities of the bulk compensating donor, the interface states, and the turnaround trap all increase. Heating at 200 0 C can anneal out these three donor-like traps, however, it cannot restore the generation rates back to their original and lower pre-keV electron irradiation values. The experimental results also indicate that all three traps may be related to the same mobile impurity species whose bonds are loosened by the keV electrons and then broken or released by the avalanche injected electrons

Characterization of palladium nanoparticles anchored on graphene oxide obtained by electron beam

Energy Technology Data Exchange (ETDEWEB)

Sobrinho, Luiza F.; Garcia, Rafael H.L.; Silva, Flávia R.O.; Neto, Almir O.; Sakata, Solange K., E-mail: lunnaquimica@usp.br, E-mail: sksakata@ipen.br [Instituto de Pesquisas Energéticas e Nucleares (IPEN/CNEN-SP), São Paulo, SP (Brazil)

2017-07-01

Fuel Cells (FCs) are devices that convert chemical energy directly in electrical and thermal energy. There are two disadvantages in the process that difficult the implementation of these new power supply. The fuel, hydrogen, is highly flammable and it is difficult to transport and the catalyst is costly. FCs have been attracting worldwide attention because they are environmental friendly and potential as clean and efficient power source. However, their durability and cost have being identified as important issues in this power supply. The objective of this work is to provide a new material based on incorporation of palladium graphene oxide as catalyst. Graphene Oxide (GO) was synthesized from graphite by the modified Hummers method, in water/alcohol medium. The one-step method to incorporate nanoparticles on this nanomaterial was developed using by electron beam (EB). Additionally, this method also reduces the Graphene Oxide (GO). This nanocomposite were characterized by thermogravimetry (TG), Fourier transform infrared (FT-IR), transmission electron microscopy (TEM), x-rays diffraction (XRD) and its potential for electro catalysis were performed by cyclic voltammetry (CV) and amperometry (CA). The results showed that the incorporation of Pd on reduced GO (rGO) by electron beam was 20-40 % in mass. The process using EB and Pd nanoparticles supported on graphene oxide as a support are an alternative, in substitution of conventional methods to the production of electrodes for fuel cells. (author)

Characterization of palladium nanoparticles anchored on graphene oxide obtained by electron beam

International Nuclear Information System (INIS)

Sobrinho, Luiza F.; Garcia, Rafael H.L.; Silva, Flávia R.O.; Neto, Almir O.; Sakata, Solange K.

2017-01-01

Fuel Cells (FCs) are devices that convert chemical energy directly in electrical and thermal energy. There are two disadvantages in the process that difficult the implementation of these new power supply. The fuel, hydrogen, is highly flammable and it is difficult to transport and the catalyst is costly. FCs have been attracting worldwide attention because they are environmental friendly and potential as clean and efficient power source. However, their durability and cost have being identified as important issues in this power supply. The objective of this work is to provide a new material based on incorporation of palladium graphene oxide as catalyst. Graphene Oxide (GO) was synthesized from graphite by the modified Hummers method, in water/alcohol medium. The one-step method to incorporate nanoparticles on this nanomaterial was developed using by electron beam (EB). Additionally, this method also reduces the Graphene Oxide (GO). This nanocomposite were characterized by thermogravimetry (TG), Fourier transform infrared (FT-IR), transmission electron microscopy (TEM), x-rays diffraction (XRD) and its potential for electro catalysis were performed by cyclic voltammetry (CV) and amperometry (CA). The results showed that the incorporation of Pd on reduced GO (rGO) by electron beam was 20-40 % in mass. The process using EB and Pd nanoparticles supported on graphene oxide as a support are an alternative, in substitution of conventional methods to the production of electrodes for fuel cells. (author)

Transport of electrons in lead oxide studied by CELIV technique

International Nuclear Information System (INIS)

Semeniuk, O; Juska, G; Oelerich, J O; Jandieri, K; Baranovskii, S D; Reznik, A

2017-01-01

Although polycrystalline lead oxide (PbO) has a long history of application in optoelectronics and imaging, the transport mechanism for electrons in this material has not yet been clarified. Using the photo-generated charge extraction by linear increasing voltage (photo-CELIV) technique, we provide the temperature- and field-dependences of electron mobility in poly-PbO. It is found that electrons undergo dispersive transport, i.e. their mobility decreases in the course of time. Multiple trapping of electrons from the conduction band into the developed band tail is revealed as the dominant transport mechanism. This differs dramatically from the dispersive transport of holes in the same material, dominated by topological factors and not by energy disorder. (paper)

A holistic approach to anesthesia-induced neurotoxicity and its implications for future mechanistic studies.

Science.gov (United States)

Zanghi, Christine N; Jevtovic-Todorovic, Vesna

The year 2016 marked the 15th anniversary since anesthesia-induced developmental neurotoxicity and its resulting cognitive dysfunction were first described. Since that time, multiple scientific studies have supported these original findings and investigated possible mechanisms behind anesthesia-induced neurotoxicity. This paper reviews the existing mechanistic literature on anesthesia-induced neurotoxicity in the context of a holistic approach that emphasizes the importance of both neuronal and non-neuronal cells during early postnatal development. Sections are divided into key stages in early neural development; apoptosis, neurogenesis, migration, differentiation, synaptogenesis, gliogenesis, myelination and blood brain barrier/cerebrovasculature. In addition, the authors combine the established literature in the field of anesthesia-induced neurotoxicity with literature from other related scientific fields to speculate on the potential role of non-neuronal cells and to generate new future hypotheses for understanding anesthetic toxicity and its application to the practice of pediatric anesthesia. Copyright © 2017 Elsevier Inc. All rights reserved.

Positron annihilation induced Auger electron spectroscopic studies of oxide surfaces

Science.gov (United States)

Nadesalingam, Manori

2005-03-01

Defects on oxide surfaces are well known to play a key role in catalysis. TiO2, MgO, SiO2 surfaces were investigated using Time-Of-Flight Positron induced Auger Electron Spectroscopy (TOF-PAES). Previous work in bulk materials has demonstrated that positrons are particularly sensitive to charged defects. In PAES energetic electron emission results from Auger transitions initiated by annihilation of core electrons with positrons trapped in an image-potential well at the surface. Annealed samples in O2 environment show a strong Auger peak of Oxygen. The implication of these results will be discussed

Average electronegativity, electronic polarizability and optical basicity of lanthanide oxides for different coordination numbers

International Nuclear Information System (INIS)

Zhao Xinyu; Wang Xiaoli; Lin Hai; Wang Zhiqiang

2008-01-01

On the basis of new electronegativity values, electronic polarizability and optical basicity of lanthanide oxides are calculated from the concept of average electronegativity given by Asokamani and Manjula. The estimated values are in close agreement with our previous conclusion. Particularly, we attempt to obtain new data of electronic polarizability and optical basicity of lanthanide sesquioxides for different coordination numbers (6-12). The present investigation suggests that both electronic polarizability and optical basicity increase gradually with increasing coordination number. We also looked for another double peak effect, that is, electronic polarizability and optical basicity of trivalent lanthanide oxides show a gradual decrease and then an abrupt increase at the Europia and Ytterbia. Furthermore, close correlations are investigated among average electronegativity, optical basicity, electronic polarizability and coordination number in this paper

Death Adder Envenoming Causes Neurotoxicity Not Reversed by Antivenom - Australian Snakebite Project (ASP-16)

Science.gov (United States)

Johnston, Christopher I.; O'Leary, Margaret A.; Brown, Simon G. A.; Currie, Bart J.; Halkidis, Lambros; Whitaker, Richard; Close, Benjamin; Isbister, Geoffrey K.

2012-01-01

Background Death adders (Acanthophis spp) are found in Australia, Papua New Guinea and parts of eastern Indonesia. This study aimed to investigate the clinical syndrome of death adder envenoming and response to antivenom treatment. Methodology/Principal Findings Definite death adder bites were recruited from the Australian Snakebite Project (ASP) as defined by expert identification or detection of death adder venom in blood. Clinical effects and laboratory results were collected prospectively, including the time course of neurotoxicity and response to treatment. Enzyme immunoassay was used to measure venom concentrations. Twenty nine patients had definite death adder bites; median age 45 yr (5–74 yr); 25 were male. Envenoming occurred in 14 patients. Two further patients had allergic reactions without envenoming, both snake handlers with previous death adder bites. Of 14 envenomed patients, 12 developed neurotoxicity characterised by ptosis (12), diplopia (9), bulbar weakness (7), intercostal muscle weakness (2) and limb weakness (2). Intubation and mechanical ventilation were required for two patients for 17 and 83 hours. The median time to onset of neurotoxicity was 4 hours (0.5–15.5 hr). One patient bitten by a northern death adder developed myotoxicity and one patient only developed systemic symptoms without neurotoxicity. No patient developed venom induced consumption coagulopathy. Antivenom was administered to 13 patients, all receiving one vial initially. The median time for resolution of neurotoxicity post-antivenom was 21 hours (5–168). The median peak venom concentration in 13 envenomed patients with blood samples was 22 ng/mL (4.4–245 ng/mL). In eight patients where post-antivenom bloods were available, no venom was detected after one vial of antivenom. Conclusions/Significance Death adder envenoming is characterised by neurotoxicity, which is mild in most cases. One vial of death adder antivenom was sufficient to bind all circulating venom. The

Morphology and electronic structure of the oxide shell on the surface of iron nanoparticles.

Science.gov (United States)

Wang, Chongmin; Baer, Donald R; Amonette, James E; Engelhard, Mark H; Antony, Jiji; Qiang, You

2009-07-01

An iron (Fe) nanoparticle exposed to air at room temperature will be instantly covered by an oxide shell that is typically approximately 3 nm thick. The nature of this native oxide shell, in combination with the underlying Fe(0) core, determines the physical and chemical behavior of the core-shell nanoparticle. One of the challenges of characterizing core-shell nanoparticles is determining the structure of the oxide shell, that is, whether it is FeO, Fe(3)O(4), gamma-Fe(2)O(3), alpha-Fe(2)O(3), or something else. The results of prior characterization efforts, which have mostly used X-ray diffraction and spectroscopy, electron diffraction, and transmission electron microscopic imaging, have been framed in terms of one of the known Fe-oxide structures, although it is not necessarily true that the thin layer of Fe oxide is a known Fe oxide. In this Article, we probe the structure of the oxide shell on Fe nanoparticles using electron energy loss spectroscopy (EELS) at the oxygen (O) K-edge with a spatial resolution of several nanometers (i.e., less than that of an individual particle). We studied two types of representative particles: small particles that are fully oxidized (no Fe(0) core) and larger core-shell particles that possess an Fe core. We found that O K-edge spectra collected for the oxide shell in nanoparticles show distinct differences from those of known Fe oxides. Typically, the prepeak of the spectra collected on both the core-shell and the fully oxidized particles is weaker than that collected on standard Fe(3)O(4). Given the fact that the origin of this prepeak corresponds to the transition of the O 1s electron to the unoccupied state of O 2p hybridized with Fe 3d, a weak pre-edge peak indicates a combination of the following four factors: a higher degree of occupancy of the Fe 3d orbital; a longer Fe-O bond length; a decreased covalency of the Fe-O bond; and a measure of cation vacancies. These results suggest that the coordination configuration in

Developmental neurotoxicity of Propylthiouracil in rats

DEFF Research Database (Denmark)

Petersen, Marta Axelstad; Hansen, P.; Christiansen, S.

2007-01-01

early in pregnancy may cause adverse effects on the offspring. This has led to increased concern about thyroid hormone disrupting chemicals (TDCs) in our environment. We have studied how developmental exposure to the known antithyroid agent propylthiouracil (PTU) affects the development of rat pups...... behaviour and hearing function. This supports that exposure to TDC's in general may cause long-lasting developmental neurotoxicity....

COMPUTATIONAL ELECTROCHEMISTRY: AQUEOUS ONE-ELECTRON OXIDATION POTENTIALS FOR SUBSTITUTED ANILINES

Science.gov (United States)

Semiempirical molecular orbital theory and density functional theory are used to compute one-electron oxidation potentials for aniline and a set of 21 mono- and di-substituted anilines in aqueous solution. Linear relationships between theoretical predictions and experiment are co...

alpha7 Nicotinic acetylcholine receptor knockout selectively enhances ethanol-, but not beta-amyloid-induced neurotoxicity.

Science.gov (United States)

de Fiebre, Nancyellen C; de Fiebre, Christopher M

2005-01-03

The alpha7 subtype of nicotinic acetylcholine receptor (nAChR) has been implicated as a potential site of action for two neurotoxins, ethanol and the Alzheimer's disease related peptide, beta-amyloid. Here, we utilized primary neuronal cultures of cerebral cortex from alpha7 nAChR null mutant mice to examine the role of this receptor in modulating the neurotoxic properties of subchronic, "binge" ethanol and beta-amyloid. Knockout of the alpha7 nAChR gene selectively enhanced ethanol-induced neurotoxicity in a gene dosage-related fashion. Susceptibility of cultures to beta-amyloid induced toxicity, however, was unaffected by alpha7 nAChR gene null mutation. Further, beta-amyloid did not inhibit the binding of the highly alpha7-selective radioligand, [(125)I]alpha-bungarotoxin. On the other hand, in studies in Xenopus oocytes ethanol efficaciously inhibited alpha7 nAChR function. These data suggest that alpha7 nAChRs modulate the neurotoxic effects of binge ethanol, but not the neurotoxicity produced by beta-amyloid. It is hypothesized that inhibition of alpha7 nAChRs by ethanol provides partial protection against the neurotoxic properties of subchronic ethanol.

Oxidation mechanism of nickel particles studied in an environmental transmission electron microscope

DEFF Research Database (Denmark)

Jeangros, Q.; Hansen, Thomas Willum; Wagner, Jakob Birkedal

2014-01-01

The oxidation of nickel particles was studied in situ in an environmental transmission electron microscope in 3.2 mbar of O2 between ambient temperature and 600°C. Several different transmission electron microscopy imaging techniques, electron diffraction and electron energy-loss spectroscopy were...... diffusion of Ni2+ along NiO grain boundaries, self-diffusion of Ni2+ ions and vacancies, growth of NiO grains and nucleation of voids at Ni/NiO interfaces. We also observed the formation of transverse cracks in a growing NiO film in situ in the electron microscope....

Oxidations of N-(3-indoleethyl) cyclic aliphatic amines by horseradish peroxidase: the indole ring binds to the enzyme and mediates electron-transfer amine oxidation.

Science.gov (United States)

Ling, Ke-Qing; Li, Wen-Shan; Sayre, Lawrence M

2008-01-23

Although oxidations of aromatic amines by horseradish peroxidase (HRP) are well-known, typical aliphatic amines are not substrates of HRP. In this study, the reactions of N-benzyl and N-methyl cyclic amines with HRP were found to be slow, but reactions of N-(3-indoleethyl) cyclic amines were 2-3 orders of magnitude faster. Analyses of pH-rate profiles revealed a dominant contribution to reaction by the amine-free base forms, the only species found to bind to the enzyme. A metabolic study on a family of congeneric N-(3-indoleethyl) cyclic amines indicated competition between amine and indole oxidation pathways. Amine oxidation dominated for the seven- and eight-membered azacycles, where ring size supports the change in hybridization from sp3 to sp2 that occurs upon one-electron amine nitrogen oxidation, whereas only indole oxidation was observed for the six-membered ring congener. Optical difference spectroscopic binding data and computational docking simulations suggest that all the arylalkylamine substrates bind to the enzyme through their aromatic termini with similar binding modes and binding affinities. Kinetic saturation was observed for a particularly soluble substrate, consistent with an obligatory role of an enzyme-substrate complexation preceding electron transfer. The significant rate enhancements seen for the indoleethylamine substrates suggest the ability of the bound indole ring to mediate what amounts to medium long-range electron-transfer oxidation of the tertiary amine center by the HRP oxidants. This is the first systematic investigation to document aliphatic amine oxidation by HRP at rates consistent with normal metabolic turnover, and the demonstration that this is facilitated by an auxiliary electron-rich aromatic ring.

Electrochemical/chemical oxidation of bisphenol A in a four-electron/two-proton process in aprotic organic solvents

International Nuclear Information System (INIS)

Chan, Ya Yun; Yue, Yanni; Li, Yongxin; Webster, Richard D.

2013-01-01

Graphical abstract: - Highlights: • Bisphenol A undergoes a chemically irreversible voltammetric oxidation process. • Chemical oxidation was performed to overcome adsorption effects that cause electrode fouling. • A new product was isolated from chemical oxidation with 4 mol equiv. of the one-electron oxidant, NO + . • The oxidative mechanism was proposed to be a four-electron/two-proton process. - Abstract: The electrochemical behavior of bisphenol A (BPA) was examined using cyclic voltammetry, bulk electrolysis and chemical oxidation in aprotic organic solvents. It was found that BPA undergoes a chemically irreversible voltammetric oxidation process to form compounds that cannot be electrochemically converted back to the starting materials on the voltammetric timescale. To overcome the effects of electrode fouling during controlled potential electrolysis experiments, NO + was used as a one-electron chemical oxidant. A new product, hydroxylated bisdienone was isolated from the chemical oxidation of BPA with 4 mol equiv of NO + SbF 6 − in low water content CH 3 CN. The structure of the cation intermediate species was deduced and it was proposed that BPA is oxidized in a four-electron/two-proton process to form a relatively unstable dication which reacts quickly in the presence of water in acetonitrile (in a mechanism that is similar to phenols in general). However, as the water content of the solvent increased it was found that the chemical oxidation mechanism produced a nitration product in high yield. The findings from this study provide useful insights into the reactions that can occur during oxidative metabolism of BPA and highlight the possibility of the role of a bisdienone cation as a reactive metabolite in biological systems

Melandrii Herba Extract Attenuates H2O2-Induced Neurotoxicity in Human Neuroblastoma SH-SY5Y Cells and Scopolamine-Induced Memory Impairment in Mice

Directory of Open Access Journals (Sweden)

Kwang Min Lee

2017-09-01

Full Text Available Oxidative stress plays a significant role in the etiology of a variety of neurodegenerative diseases. In this study, we found that Melandrii Herba extract (ME attenuated oxidative-induced damage in cells. Mechanistically, ME exhibited protection from H2O2-induced neurotoxicity via caspase-3 inactivation, Bcl-2 downregulation, Bax upregulation, and MAPK activation (ERK 1/2, JNK 1/2, and p38 MAPK in vitro. Moreover, our in vivo data showed that ME was able to attenuate scopolamine-induced cognitive impairment. These results provide in vitro and in vivo evidence that ME exhibits neuroprotective properties against oxidative stress, which suggests that ME is worthy of further investigation as a complementary, or even as an alternative, product for preventing and treating neurodegenerative disorders.

Molecular Computational Investigation of Electron Transfer Kinetics across Cytochrome-Iron Oxide Interfaces

International Nuclear Information System (INIS)

Kerisit, Sebastien N.; Rosso, Kevin M.; Dupuis, Michel; Valiev, Marat

2007-01-01

The interface between electron transfer proteins such as cytochromes and solid phase mineral oxides is central to the activity of dissimilatory-metal reducing bacteria. A combination of potential-based molecular dynamics simulations and ab initio electronic structure calculations are used in the framework of Marcus' electron transfer theory to compute elementary electron transfer rates from a well-defined cytochrome model, namely the small tetraheme cytochrome (STC) from Shewanella oneidensis, to surfaces of the iron oxide mineral hematite (a-Fe2O3). Room temperature molecular dynamics simulations show that an isolated STC molecule favors surface attachment via direct contact of hemes I and IV at the poles of the elongated axis, with electron transfer distances as small as 9 Angstroms. The cytochrome remains attached to the mineral surface in the presence of water and shows limited surface diffusion at the interface. Ab initio electronic coupling matrix element (VAB) calculations of configurations excised from the molecular dynamics simulations reveal VAB values ranging from 1 to 20 cm-1, consistent with nonadiabaticity. Using these results, together with experimental data on the redox potential of hematite and hemes in relevant cytochromes and calculations of the reorganization energy from cluster models, we estimate the rate of electron transfer across this model interface to range from 1 to 1000 s-1 for the most exothermic driving force considered in this work, and from 0.01 to 20 s-1 for the most endothermic. This fairly large range of electron transfer rates highlights the sensitivity of the rate upon the electronic coupling matrix element, which is in turn dependent on the fluctuations of the heme configuration at the interface. We characterize this dependence using an idealized bis-imidazole heme to compute from first principles the VAB variation due to porphyrin ring orientation, electron transfer distance, and mineral surface termination. The electronic

High-Pressure Thermodynamic Properties of f-electron Metals, Transition Metal Oxides, and Half-Metallic Magnets

International Nuclear Information System (INIS)

Richard T. Scalettar; Warren E. Pickett

2005-01-01

This project involves research into the thermodynamic properties of f-electron metals, transition metal oxides, and half-metallic magnets at high pressure. These materials are ones in which the changing importance of electron-electron interactions as the distance between atoms is varied can tune the system through phase transitions from localized to delocalized electrons, from screened to unscreened magnetic moments, and from normal metal to one in which only a single spin specie can conduct. Three main thrusts are being pursued: (1) Mott transitions in transition metal oxides, (2) magnetism in half-metallic compounds, and (3) large volume-collapse transitions in f-band metals

High-Pressure Thermodynamic Properties of f-electron Metals, Transition Metal Oxides, and Half-Metallic Magnets

Energy Technology Data Exchange (ETDEWEB)

Scalettar, Richard T.; Pickett, Warren E.

2004-07-01

This project involves research into the thermodynamic properties of f-electron metals, transition metal oxides, and half-metallic magnets at high pressure. These materials are ones in which the changing importance of electron-electron interactions as the distance between atoms is varied can tune the system through phase transitions from localized to delocalized electrons, from screened to unscreened magnetic moments, and from normal metal to one in which only a single spin specie can conduct. Three main thrusts are being pursued: (1) Mott transitions in transition metal oxides, (2) magnetism in half-metallic compounds, and (3) large volume-collapse transitions in f-band metals.

High-Pressure Thermodynamic Properties of f-electron Metals, Transition Metal Oxides, and Half-Metallic Magnets

Energy Technology Data Exchange (ETDEWEB)

Richard T. Scalettar; Warren E. Pickett

2005-08-02

This project involves research into the thermodynamic properties of f-electron metals, transition metal oxides, and half-metallic magnets at high pressure. These materials are ones in which the changing importance of electron-electron interactions as the distance between atoms is varied can tune the system through phase transitions from localized to delocalized electrons, from screened to unscreened magnetic moments, and from normal metal to one in which only a single spin specie can conduct. Three main thrusts are being pursued: (i) Mott transitions in transition metal oxides, (ii) magnetism in half-metallic compounds, and (iii) large volume-collapse transitions in f-band metals.

Neurotoxicity in long-term survivors of small cell lung cancer

International Nuclear Information System (INIS)

Lee, J.S.; Umsawasdi, T.; Lee, Y.Y.; Barkley, H.T. Jr.; Murphy, W.K.; Welch, S.; Valdivieso, M.

1986-01-01

Chronic central nervous system neurotoxicity was studied in 38 long-term survivors (greater than or equal to 3 years) of small cell lung cancer who were treated at the University of Texas M. D. Anderson Hospital and Tumor Institute at Houston between 1971 and 1980. All but one patient received combination chemotherapy with or without chest irradiation. Twenty-four patients received whole brain irradiation (Group I), 22 for elective and two for therapeutic purposes, while 14 did not (Group II). Abnormalities in computed tomographic (CT) scans of the brain were more frequently observed in Group I than in Group II (70% vs. 0%, p less than 0.01). Clinical central nervous system neurotoxicity developed in three patients in Group I, while none developed in patients in Group II (p less than 0.05). Patients who received methotrexate and procarbazine after whole brain irradiation were at a higher risk for clinical central nervous system neurotoxicity (p less than 0.05), and for development of periventricular white matter changes in CT brain scans (p less than 0.05) than were patients in Group II. Impaired methylation of the myelin sheath is proposed as a possible underlying pathogenic mechanism

In Vivo Evidence of Increased nNOS Activity in Acute MPTP Neurotoxicity: A Functional Pharmacological MRI Study

Directory of Open Access Journals (Sweden)

Tiing Yee Siow

2013-01-01

Full Text Available 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP is a neurotoxin commonly used to produce an animal model of Parkinson’s disease. Previous studies have suggested a critical role for neuronal nitric oxide (NO synthase- (nNOS- derived NO in the pathogenesis of MPTP. However, NO activity is difficult to assess in vivo due to its extremely short biological half-life, and so in vivo evidence of NO involvement in MPTP neurotoxicity remains scarce. In the present study, we utilized flow-sensitive alternating inversion recovery sequences, in vivo localized proton magnetic resonance spectroscopy, and diffusion-weighted imaging to, respectively, assess the hemodynamics, metabolism, and cytotoxicity induced by MPTP. The role of NO in MPTP toxicity was clarified further by administering a selective nNOS inhibitor, 7-nitroindazole (7-NI, intraperitoneally to some of the experimental animals prior to MPTP challenge. The transient increase in cerebral blood flow (CBF in the cortex and striatum induced by systemic injection of MPTP was completely prevented by pretreatment with 7-NI. We provide the first in vivo evidence of increased nNOS activity in acute MPTP-induced neurotoxicity. Although the observed CBF change may be independent of the toxicogenesis of MPTP, this transient hyperperfusion state may serve as an early indicator of neuroinflammation.

Extreme mobility enhancement of two-dimensional electron gases at oxide interfaces by charge-transfer-induced modulation doping

NARCIS (Netherlands)

Chen, Yunzhong; Trier, F.; Wijnands, Tom; Green, R.J.; Gauquelin, N.; Egoavil, R.; Christensen, D.V.; Koster, Gertjan; Huijben, Mark; Bovet, N.; Macke, S.; He, F.; Sutarto, R.; Andersen, N.H.; Sulpizio, J.A.; Honig, M.; Prawiroatmodjo, G.E.D.K.; Jespersen, T.S.; Linderoth, S.; Ilani, S.; Verbeeck, J.; van Tendeloo, G.; Rijnders, Augustinus J.H.M.; Sawatzky, G.A.; Pryds, N.

2015-01-01

Two-dimensional electron gases (2DEGs) formed at the interface of insulating complex oxides promise the development of all-oxide electronic devices. These 2DEGs involve many-body interactions that give rise to a variety of physical phenomena such as superconductivity, magnetism, tunable

Neurotoxic, cytotoxic, apoptotic and antiproliferative effects of some marine algae extracts on the NA2B cell line.

Science.gov (United States)

Kurt, O; Özdal-Kurt, F; Akçora, C M; Özkut, M; Tuğlu, M I

2018-02-01

Oxidative stress contributes to cancer pathologies and to apoptosis. Marine algae exhibit cytotoxic, antiproliferative and apoptotic effects; their metabolites have been used to treat many types of cancer. We investigated in culture extracts of Petalonia fascia, Jania longifurca and Halimeda tuna to determine their effects on mouse neuroblastoma cell line, NA2B. NA2B cells were treated with algae extracts, and the survival and proliferation of NA2B cells were assessed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The effects of algae extracts on oxidative stress in NA2B cells also were investigated using nitric oxide synthase (NOS) immunocytochemistry and apoptosis was assessed using terminal deoxynucleotidyl transferase dUTP nick end labeling. We observed significant neurite inhibition with moderate damage by the neurotoxicity-screening test (NST) at IC 50 dilutions of the extracts. MTT demonstrated that J. longifurca extracts were more toxic than P. fascia and H. tuna extracts. We found an increase of endothelial and inducible NOS immunostaining for oxidative stress and TUNEL analysis revealed increased apoptosis after application of extract. Our findings suggest that the algae we tested may have potential use for treatment of cancer.

Tuning the conductivity threshold and carrier density of two-dimensional electron gas at oxide interfaces through interface engineering

Directory of Open Access Journals (Sweden)

H. J. Harsan Ma

2015-08-01

Full Text Available The two-dimensional electron gas (2DEG formed at the perovskite oxides heterostructures is of great interest because of its potential applications in oxides electronics and nanoscale multifunctional devices. A canonical example is the 2DEG at the interface between a polar oxide LaAlO3 (LAO and non-polar SrTiO3 (STO. Here, the LAO polar oxide can be regarded as the modulating or doping layer and is expected to define the electronic properties of 2DEG at the LAO/STO interface. However, to practically implement the 2DEG in electronics and device design, desired properties such as tunable 2D carrier density are necessary. Here, we report the tuning of conductivity threshold, carrier density and electronic properties of 2DEG in LAO/STO heterostructures by insertion of a La0.5Sr0.5TiO3 (LSTO layer of varying thicknesses, and thus modulating the amount of polarization of the oxide over layers. Our experimental result shows an enhancement of carrier density up to a value of about five times higher than that observed at the LAO/STO interface. A complete thickness dependent metal-insulator phase diagram is obtained by varying the thickness of LAO and LSTO providing an estimate for the critical thickness needed for the metallic phase. The observations are discussed in terms of electronic reconstruction induced by polar oxides.

Dopamine Oxidation and Autophagy

Directory of Open Access Journals (Sweden)

Patricia Muñoz

2012-01-01

Full Text Available The molecular mechanisms involved in the neurodegenerative process of Parkinson's disease remain unclear. Currently, there is a general agreement that mitochondrial dysfunction, α-synuclein aggregation, oxidative stress, neuroinflammation, and impaired protein degradation are involved in the neurodegeneration of dopaminergic neurons containing neuromelanin in Parkinson's disease. Aminochrome has been proposed to play an essential role in the degeneration of dopaminergic neurons containing neuromelanin by inducing mitochondrial dysfunction, oxidative stress, the formation of neurotoxic α-synuclein protofibrils, and impaired protein degradation. Here, we discuss the relationship between the oxidation of dopamine to aminochrome, the precursor of neuromelanin, autophagy dysfunction in dopaminergic neurons containing neuromelanin, and the role of dopamine oxidation to aminochrome in autophagy dysfunction in dopaminergic neurons. Aminochrome induces the following: (i the formation of α-synuclein protofibrils that inactivate chaperone-mediated autophagy; (ii the formation of adducts with α- and β-tubulin, which induce the aggregation of the microtubules required for the fusion of autophagy vacuoles and lysosomes.

Size-dependent single electron transfer and semi-metal-to-insulator transitions in molecular metal oxide electronics

Science.gov (United States)

Balliou, Angelika; Bouroushian, Mirtat; Douvas, Antonios M.; Skoulatakis, George; Kennou, Stella; Glezos, Nikos

2018-07-01

All-inorganic self-arranged molecular transition metal oxide hyperstructures based on polyoxometalate molecules (POMs) are fabricated and tested as electronically tunable components in emerging electronic devices. POM hyperstructures reveal great potential as charging nodes of tunable charging level for molecular memories and as enhancers of interfacial electron/hole injection for photovoltaic stacks. STM, UPS, UV–vis spectroscopy and AFM measurements show that this functionality stems from the films’ ability to structurally tune their HOMO–LUMO levels and electron localization length at room temperature. By adapting POM nanocluster size in solution, self-doping and current modulation of four orders of magnitude is monitored on a single nanocluster on SiO2 at voltages as low as 3 Volt. Structurally driven insulator-to-semi-metal transitions and size-dependent current regulation through single electron tunneling are demonstrated and examined with respect to the stereochemical and electronic structure of the molecular entities. This extends the value of self-assembly as a tool for correlation length and electronic properties tuning and demonstrate POM hyperstructures’ plausibility for on-chip molecular electronics operative at room temperature.

Size-dependent single electron transfer and semi-metal-to-insulator transitions in molecular metal oxide electronics.

Science.gov (United States)

Balliou, Angelika; Bouroushian, Mirtat; Douvas, Antonios M; Skoulatakis, George; Kennou, Stella; Glezos, Nikos

2018-07-06

All-inorganic self-arranged molecular transition metal oxide hyperstructures based on polyoxometalate molecules (POMs) are fabricated and tested as electronically tunable components in emerging electronic devices. POM hyperstructures reveal great potential as charging nodes of tunable charging level for molecular memories and as enhancers of interfacial electron/hole injection for photovoltaic stacks. STM, UPS, UV-vis spectroscopy and AFM measurements show that this functionality stems from the films' ability to structurally tune their HOMO-LUMO levels and electron localization length at room temperature. By adapting POM nanocluster size in solution, self-doping and current modulation of four orders of magnitude is monitored on a single nanocluster on SiO 2 at voltages as low as 3 Volt. Structurally driven insulator-to-semi-metal transitions and size-dependent current regulation through single electron tunneling are demonstrated and examined with respect to the stereochemical and electronic structure of the molecular entities. This extends the value of self-assembly as a tool for correlation length and electronic properties tuning and demonstrate POM hyperstructures' plausibility for on-chip molecular electronics operative at room temperature.

A graphene oxide-carbon nanotube grid for high-resolution transmission electron microscopy of nanomaterials

International Nuclear Information System (INIS)

Zhang Lina; Zhang Haoxu; Zhou Ruifeng; Chen Zhuo; Li Qunqing; Fan Shoushan; Jiang Kaili; Ge Guanglu; Liu Renxiao

2011-01-01

A novel grid for use in transmission electron microscopy is developed. The supporting film of the grid is composed of thin graphene oxide films overlying a super-aligned carbon nanotube network. The composite film combines the advantages of graphene oxide and carbon nanotube networks and has the following properties: it is ultra-thin, it has a large flat and smooth effective supporting area with a homogeneous amorphous appearance, high stability, and good conductivity. The graphene oxide-carbon nanotube grid has a distinct advantage when characterizing the fine structure of a mass of nanomaterials over conventional amorphous carbon grids. Clear high-resolution transmission electron microscopy images of various nanomaterials are obtained easily using the new grids.

Chemistry and electronics of oxides from carbon dioxide to perovskite

International Nuclear Information System (INIS)

Koinuma, Hideomi

2005-01-01

Oxides are thermodynamic stable form of materials in terrestrial conditions to exist as final products of energy consumption proceeding in nature as well as in civilization. The accumulation of heat capacitive CO 2 in atmosphere is becoming a serious environmental problem. Solid oxides as minerals in the earth shell had been used mainly for heat resistant structural materials as well as for raw materials of metals, but recent advanced chemistry and physics have been manifesting new electronic and chemical potentials hidden in oxides. Current interest and studies on oxides are directed towards two main areas: (1) prevention of CO 2 increase in atmosphere by its fixation and/or by saving the consumption of fossil fuels and (2) discovery and utilization of superfunctionality in oxides. Triggered by Bednorz and Muller's discovery of high Tc superconductor, the latter topics have been attracting rapidly growing interest from viewpoints of both fundamental research and practical application. In commemoration of WOE homecoming to the place of inauguration, a founder of WOE appreciates much to the program committee for providing him with this opportunity of briefing the workshop motivation and of reviewing his research career on oxide materials

Electronic structures near surfaces of perovskite type oxides

International Nuclear Information System (INIS)

Hara, Toru

2005-01-01

This work is intended to draw attention to the origin of the electronic structures near surfaces of perovskite type oxides. Deep states were observed by ultraviolet photoelectron spectroscopic measurements. The film thickness dependent electronic structures near surfaces of (Ba 0.5 Sr 0.5 )TiO 3 thin films were observed. As for the 117-308 nm thick (Ba 0.5 Sr 0.5 )TiO 3 films, deep states were lying at 0.20, 0.55, and 0.85 eV below the quasi-fermi level, respectively. However, as for the 40 nm thick (Ba 0.5 Sr 0.5 )TiO 3 film, the states were overlapped. The A-site doping affected electronic structures near surfaces of SrTiO 3 single crystals. No evolution of deep states in non-doped SrTiO 3 single crystal was observed. However, the evolution of deep states in La-doped SrTiO 3 single crystal was observed

Multiple sclerosis, brain radiotherapy, and risk of neurotoxicity: The Mayo Clinic experience

International Nuclear Information System (INIS)

Miller, Robert C.; Lachance, Daniel H.; Lucchinetti, Claudia F.; Keegan, B. Mark; Gavrilova, Ralitza H.; Brown, Paul D.; Weinshenker, Brian G.; Rodriguez, Moses

2006-01-01

Purpose: The aim of this study was a retrospective assessment of neurotoxicity in patients with multiple sclerosis (MS) receiving external beam radiotherapy (EBRT) to the brain. Methods and Materials: We studied 15 consecutively treated patients with MS who received brain EBRT. Neurologic toxicity was assessed with the Common Toxicity Criteria v.3.0. Results: Median follow-up for the 5 living patients was 6.0 years (range, 3.3-27.4 years). No exacerbation of MS occurred in any patient during EBRT. Five patients had Grade 4 neurologic toxicity and 1 had possible Grade 5 toxicity. Kaplan-Meier estimated risk of neurotoxicity greater than Grade 4 at 5 years was 57% (95% confidence interval, 27%-82%). Toxicity occurred at 37.5 to 54.0 Gy at a median of 1.0 year (range, 0.2-4.3 years) after EBRT. Univariate analysis showed an association between opposed-field irradiation of the temporal lobes, central white matter, and brainstem and increased risk of neurotoxicity (p < 0.04). Three of 6 cases of toxicity occurred in patients treated before 1986. Conclusions: External beam radiotherapy of the brain in patients with MS may be associated with an increased risk of neurotoxicity compared with patients without demyelinating illnesses. However, this risk is associated with treatment techniques that may not be comparable to modern, conformal radiotherapy

Involvement of ERK in NMDA receptor-independent cortical neurotoxicity of hydrogen sulfide

International Nuclear Information System (INIS)

Kurokawa, Yuko; Sekiguchi, Fumiko; Kubo, Satoko; Yamasaki, Yoshiko; Matsuda, Sachi; Okamoto, Yukari; Sekimoto, Teruki; Fukatsu, Anna; Nishikawa, Hiroyuki; Kume, Toshiaki; Fukushima, Nobuyuki; Akaike, Akinori; Kawabata, Atsufumi

2011-01-01

Highlights: ► Hydrogen sulfide causes NMDA receptor-independent neurotoxicity in mouse fetal cortical neurons. ► Activation of ERK mediates the toxicity of hydrogen sulfide. ► Apoptotic mechanisms are involved in the hydrogen-induced cell death. -- Abstract: Hydrogen sulfide (H 2 S), a gasotransmitter, exerts both neurotoxicity and neuroprotection, and targets multiple molecules including NMDA receptors, T-type calcium channels and NO synthase (NOS) that might affect neuronal viability. Here, we determined and characterized effects of NaHS, an H 2 S donor, on cell viability in the primary cultures of mouse fetal cortical neurons. NaHS caused neuronal death, as assessed by LDH release and trypan blue staining, but did not significantly reduce the glutamate toxicity. The neurotoxicity of NaHS was resistant to inhibitors of NMDA receptors, T-type calcium channels and NOS, and was blocked by inhibitors of MEK, but not JNK, p38 MAP kinase, PKC and Src. NaHS caused prompt phosphorylation of ERK and upregulation of Bad, followed by translocation of Bax to mitochondria and release of mitochondrial cytochrome c, leading to the nuclear condensation/fragmentation. These effects of NaHS were suppressed by the MEK inhibitor. Our data suggest that the NMDA receptor-independent neurotoxicity of H 2 S involves activation of the MEK/ERK pathway and some apoptotic mechanisms.

Unconventional aspects of electronic transport in delafossite oxides

Science.gov (United States)

Daou, Ramzy; Frésard, Raymond; Eyert, Volker; Hébert, Sylvie; Maignan, Antoine

2017-12-01

The electronic transport properties of the delafossite oxides ? are usually understood in terms of two well-separated entities, namely the triangular ? and (? layers. Here, we review several cases among this extensive family of materials where the transport depends on the interlayer coupling and displays unconventional properties. We review the doped thermoelectrics based on ? and ?, which show a high-temperature recovery of Fermi-liquid transport exponents, as well as the highly anisotropic metals ?, ?, and ?, where the sheer simplicity of the Fermi surface leads to unconventional transport. We present some of the theoretical tools that have been used to investigate these transport properties and review what can and cannot be learned from the extensive set of electronic structure calculations that have been performed.

Electronic interactions decreasing the activation barrier for the hydrogen electro-oxidation reaction

International Nuclear Information System (INIS)

Santos, Elizabeth; Schmickler, Wolfgang

2008-01-01

A unified model for electrochemical electron transfer reactions which explicitly accounts for the electronic structure of the electrode recently proposed by us is applied to the hydrogen oxidation reaction at different metal electrocatalysts. We focus on the changes produced in the transition state (saddle point) as a consequence of the interactions with d-bands. We discuss different empirical correlations between properties of the metal and catalytic activity proposed in the past. We show which role is played by the band structure of the different metals and its interaction with the molecule for decreasing the activation barrier. Finally, we demonstrate why some metals are better electrocatalysts for the hydrogen electro-oxidation reaction than others

Wide and ultra-wide bandgap oxides: where paradigm-shift photovoltaics meets transparent power electronics

Science.gov (United States)

Pérez-Tomás, Amador; Chikoidze, Ekaterine; Jennings, Michael R.; Russell, Stephen A. O.; Teherani, Ferechteh H.; Bove, Philippe; Sandana, Eric V.; Rogers, David J.

2018-03-01

Oxides represent the largest family of wide bandgap (WBG) semiconductors and also offer a huge potential range of complementary magnetic and electronic properties, such as ferromagnetism, ferroelectricity, antiferroelectricity and high-temperature superconductivity. Here, we review our integration of WBG and ultra WBG semiconductor oxides into different solar cells architectures where they have the role of transparent conductive electrodes and/or barriers bringing unique functionalities into the structure such above bandgap voltages or switchable interfaces. We also give an overview of the state-of-the-art and perspectives for the emerging semiconductor β- Ga2O3, which is widely forecast to herald the next generation of power electronic converters because of the combination of an UWBG with the capacity to conduct electricity. This opens unprecedented possibilities for the monolithic integration in solar cells of both self-powered logic and power electronics functionalities. Therefore, WBG and UWBG oxides have enormous promise to become key enabling technologies for the zero emissions smart integration of the internet of things.

Electronic structure of nanoparticles of substoichometric hexagonal tungsten oxides

International Nuclear Information System (INIS)

Khyzhun, O Y; Solonin, Y M

2007-01-01

X-ray photoelectron spectroscopy (XPS), X-ray emission spectroscopy (XES) and X-ray absorption spectroscopy (XAS) methods were used to study the electronic structure of hexagonal h-WO 3 and h-WO 2.8 nanoparticles. For comparison, nanopowder substoichiometric monoclinic tungsten oxides with close content of oxygen atoms, namely m-WO 3 and m-WO 2.77 compounds, were also investigated. For the mentioned oxides, XPS valence-band and corelevel spectra, XES O Kα bands and XAS W L III and O 1s edges were derived. The XPS valence-band spectra and O Kα emission bands in the mentioned hexagonal and monoclinic tungsten oxides were compared on a common energy scale. Both the O Kα bands and XPS valence-band spectra broaden somewhat in the sequences h-WO 3 → h-WO 2.8 and m-WO 3 → m-WO 2.77 , with the half-widths of the spectra being somewhat higher for the hexagonal oxides as compared with those for the monoclinic compounds. The effective positive charge state of tungsten atoms in h-WO 2.8 is very close to that in m-WO 2.77 , but the negative charge states of oxygen atoms are close to each other for all the tungsten oxides under consideration

Neurotoxic effects of ecstasy on the thalamus.

Science.gov (United States)

de Win, Maartje M L; Jager, Gerry; Booij, Jan; Reneman, Liesbeth; Schilt, Thelma; Lavini, Cristina; Olabarriaga, Sílvia D; Ramsey, Nick F; Heeten, Gerard J den; van den Brink, Wim

2008-10-01

Neurotoxic effects of ecstasy have been reported, although it remains unclear whether effects can be attributed to ecstasy, other recreational drugs or a combination of these. To assess specific/independent neurotoxic effects of heavy ecstasy use and contributions of amphetamine, cocaine and cannabis as part of The Netherlands XTC Toxicity (NeXT) study. Effects of ecstasy and other substances were assessed with (1)H-magnetic resonance spectroscopy, diffusion tensor imaging, perfusion weighted imaging and [(123)I]2beta-carbomethoxy-3beta-(4-iodophenyl)-tropane ([(123)I]beta-CIT) single photon emission computed tomography (serotonin transporters) in a sample (n=71) with broad variation in drug use, using multiple regression analyses. Ecstasy showed specific effects in the thalamus with decreased [(123)I]beta-CIT binding, suggesting serotonergic axonal damage; decreased fractional anisotropy, suggesting axonal loss; and increased cerebral blood volume probably caused by serotonin depletion. Ecstasy had no effect on brain metabolites and apparent diffusion coefficients. Converging evidence was found for a specific toxic effect of ecstasy on serotonergic axons in the thalamus.

Application of Degenerately Doped Metal Oxides in the Study of Photoinduced Interfacial Electron Transfer.

Science.gov (United States)

Farnum, Byron H; Morseth, Zachary A; Brennaman, M Kyle; Papanikolas, John M; Meyer, Thomas J

2015-06-18

Degenerately doped In2O3:Sn semiconductor nanoparticles (nanoITO) have been used to study the photoinduced interfacial electron-transfer reactivity of surface-bound [Ru(II)(bpy)2(4,4'-(PO3H2)2-bpy)](2+) (RuP(2+)) molecules as a function of driving force over a range of 1.8 eV. The metallic properties of the ITO nanoparticles, present within an interconnected mesoporous film, allowed for the driving force to be tuned by controlling their Fermi level with an external bias while their optical transparency allowed for transient absorption spectroscopy to be used to monitor electron-transfer kinetics. Photoinduced electron transfer from excited-state -RuP(2+*) molecules to nanoITO was found to be dependent on applied bias and competitive with nonradiative energy transfer to nanoITO. Back electron transfer from nanoITO to oxidized -RuP(3+) was also dependent on the applied bias but without complication from inter- or intraparticle electron diffusion in the oxide nanoparticles. Analysis of the electron injection kinetics as a function of driving force using Marcus-Gerischer theory resulted in an experimental estimate of the reorganization energy for the excited-state -RuP(3+/2+*) redox couple of λ* = 0.83 eV and an electronic coupling matrix element, arising from electronic wave function overlap between the donor orbital in the molecule and the acceptor orbital(s) in the nanoITO electrode, of Hab = 20-45 cm(-1). Similar analysis of the back electron-transfer kinetics yielded λ = 0.56 eV for the ground-state -RuP(3+/2+) redox couple and Hab = 2-4 cm(-1). The use of these wide band gap, degenerately doped materials provides a unique experimental approach for investigating single-site electron transfer at the surface of oxide nanoparticles.

Protective effect of quercetin on bupivacaine-induced neurotoxicity ...

African Journals Online (AJOL)

... bupivacaine, possibly through inhibition of T-type calcium channel. This finding implies a novel mechanism for neuroprotective effect of quercetin, and its potential for treating toxicity arising from the use of local anesthetic agents. Keywords: Quercetin, Bupivacaine, Local anaesthetic, Neuroprotection, Neurotoxicity, T-type ...

Toxicologic evidence of developmental neurotoxicity of environmental chemicals

DEFF Research Database (Denmark)

Andersen, H R; Nielsen, J B; Grandjean, P

2000-01-01

Developmental neurotoxicity constitutes effects occurring in the offspring primarily as a result of exposure of the mother during pregnancy and lactation. To exert their effect, these chemicals or their metabolites must pass the placenta and/or the blood-brain barrier. In experimental animals, ex...

Hyperammonemia following glufosinate-containing herbicide poisoning: a potential marker of severe neurotoxicity.

Science.gov (United States)

Mao, Yan-Chiao; Wang, Jiaan-Der; Hung, Dong-Zong; Deng, Jou-Fang; Yang, Chen-Chang

2011-01-01

Glufosinate-ammonium (GLA) is the active ingredient of certain widely used non-selective contact herbicides ("e.g.," Basta). Although it is thought to be much less toxic to humans than to plants, deliberate ingestion of GLA could still lead to serious effects ("e.g.," neurotoxicity) or even death. Three cases presented with delayed-onset neurotoxicity including stupor, delirium, seizures, coma, and amnesia after ingesting large amount of Basta. Considering that GLA could irreversibly inhibit glutamine synthetase (GS) in plants, we performed serial measurements of serum ammonia in those patients and revealed marked hyperammonemia in all of them. All patients recovered with the sequelae of persistent amnesia after receiving intensive care and hemodialysis. We speculated that the occurrence of hyperammonemia might at least be partially related to GS inhibition in humans. Moreover, hyperammonemia could serve as a potential marker of severe neurotoxicity, especially prolonged amnesia, following massive ingestion of GLA-containing herbicides. The possible dose-response relation between GLA exposure and serum ammonia level, however, needs more investigations.

The effect of electron beam irradiation on lipid oxidation in sausages

Directory of Open Access Journals (Sweden)

atefeh yousefi

2017-09-01

Full Text Available Introduction: Irradiation treatment is one of the best techniques to extend the shelf-life of meat, without emerging the nutritional properties and sensory quality of irradiated meat products.  However electron -beam  may cause transformations in foods but has been known as to the most easily-applied irradiation technique in food industries. Electron-beam irradiation is an environment friendly, low cost and time effective alternative to other decontamination technologies. Lipid oxidation could produce of irradiated meat. This study aimed at evaluating the state of lipid oxidation of irradiated sausages. Its findings could help the control, improve food safety and quality properties to food industries. Methods: Sausages were purchased in a local supermarket, minced sausages blended for thiobarbituric acid reactive substances (TBARS analysis and divided into 25 g pieces. The samples including one control group and four case groups. Packaged sausage were exposed at doses of 0 (control, 1, 2, 3 and 5 kGy and analyzed on various days 0, 5, 10 and 30. Results: Thiobarbituric acid reactive substances (TBARS has increased as time goes on (P<0.05. A significant relationship was observed on different Doses. But, the maximum of TBARS was observed in 3 kGy. Conclusion: Utilizing of Electron-beam irradiation in low doses does not have significant difference on lipid oxidation. Irradiating of meat products by addition of antioxidants can minimize or avoid the development of rancidity.

Transmission electron microscopy and Raman characterization of copper (I) oxide microspheres composed of nanoparticles

International Nuclear Information System (INIS)

Wang Wenzhong; Tu Ya; Wang Lijuan; Liang Yujie; Shi Honglong

2013-01-01

Highlights: ► Raman spectroscopy of copper (I) oxide microspheres were investigated. ► Infrared active mode is greatly activated in Raman scattering spectrum. ► Infrared active mode shows up in Raman spectrum of copper (I) oxide microspheres. ► The defects existed in spheres could be responsible for the observed Raman property. - Abstract: The high-resolution transmission electron microscope and Raman spectroscopy were used to investigate the microstructures and Raman scattering property of copper (I) oxide microspheres composed of nanoparticles. High-resolution transmission electron microscope images indicate that the copper (I) oxide microspheres are composed of nanoparticles with random growth direction, indicating that there are many defects in microspheres. The Raman spectrum shows that infrared active mode, which must be odd parity and is Raman forbidden for bulk crystal due to its inversion symmetry, is activated and shows up in Raman scattering spectrum. On the basis of investigations of the microstructure features of copper (I) oxide microspheres, we attribute the appearance of IR active mode in Raman scattering spectrum to the breakdown of the symmetry of the lattice due to the presence of defects in the prepared copper (I) oxide microspheres as observed in HRTEM images.

MR findings of cyclosporine neurotoxicity

Energy Technology Data Exchange (ETDEWEB)

Yang, Po Song; Ahn, Kook Jin; Ahn, Bo Young; Jung, Hae An; Kim, Hee Je; Lee, Jae Mun [The Catholic Univ. St Mary' s Hospital, Seoul (Korea, Republic of)

1998-12-01

To analyze the MR findings of cyclosporine-induced neurotoxicity in patients receiving high dose of cyclosporine and to suggest the possible pathogenetic mechanism. The cases of seven patients (2 males, 5 females;18-36 years old) who suffered seizures after receiving high-dose cyclosporine for bone marrow transplantation due to diseases such as aplastic anemia or leukemia were retrospectively reviewed. We evaluated the location and pattern of abnormal signal intensity seen on T2 weighted images, the presence of contrast enhancement, and the changes seen on follow-up MR performed at intervals of 12-30 days after initial MR in five of seven patients. We analyzed levels of blood cyclosporine and magnesium, and investigated the presence of hypertension at the sity of the seizure. Locations of the lesions were bilateral(n=3D5), unilateral(n=3D2), parietal(n=3D6), occipital(n=3D6), temporal(n=3D4), and in the frontal lobe(n=3D3). Frontal lesions showed high signal intensities in the borderline ischemic zone of the frontal lobe between the territory of the anterior and middle cerebral arteries. In six of the seven patients, cortical and subcortical areas including subcortical U-fibers were seen on T2-weighted images to be involved in the parietooccipital lobes. Only one of the seven showed high signal intensity in the left basal ganglia. All lesions showed high signal intensity on T2-weighted images, and iso to low signal intensity on T1-weighted. In five of seven patients there was no definite enhancement, but in the other two, enhancement was slight. In four of seven patients seizures occurred within high therapeutic ranges(250-450ng/ml), while others suffered such attacks at levels below the therapeutic range. After cyclospirine was administered at a reduced dosage or stopped, follow-up MR images showed the complete or near-total disappearance of the abnormal findings previously described. Only two patients had hypertension, and the others normotension. Five of the

MR findings of cyclosporine neurotoxicity

International Nuclear Information System (INIS)

Yang, Po Song; Ahn, Kook Jin; Ahn, Bo Young; Jung, Hae An; Kim, Hee Je; Lee, Jae Mun

1998-01-01

To analyze the MR findings of cyclosporine-induced neurotoxicity in patients receiving high dose of cyclosporine and to suggest the possible pathogenetic mechanism. The cases of seven patients (2 males, 5 females;18-36 years old) who suffered seizures after receiving high-dose cyclosporine for bone marrow transplantation due to diseases such as aplastic anemia or leukemia were retrospectively reviewed. We evaluated the location and pattern of abnormal signal intensity seen on T2 weighted images, the presence of contrast enhancement, and the changes seen on follow-up MR performed at intervals of 12-30 days after initial MR in five of seven patients. We analyzed levels of blood cyclosporine and magnesium, and investigated the presence of hypertension at the sity of the seizure. Locations of the lesions were bilateral(n=3D5), unilateral(n=3D2), parietal(n=3D6), occipital(n=3D6), temporal(n=3D4), and in the frontal lobe(n=3D3). Frontal lesions showed high signal intensities in the borderline ischemic zone of the frontal lobe between the territory of the anterior and middle cerebral arteries. In six of the seven patients, cortical and subcortical areas including subcortical U-fibers were seen on T2-weighted images to be involved in the parietooccipital lobes. Only one of the seven showed high signal intensity in the left basal ganglia. All lesions showed high signal intensity on T2-weighted images, and iso to low signal intensity on T1-weighted. In five of seven patients there was no definite enhancement, but in the other two, enhancement was slight. In four of seven patients seizures occurred within high therapeutic ranges(250-450ng/ml), while others suffered such attacks at levels below the therapeutic range. After cyclospirine was administered at a reduced dosage or stopped, follow-up MR images showed the complete or near-total disappearance of the abnormal findings previously described. Only two patients had hypertension, and the others normotension. Five of the

Oxidative stress and Parkinson’s Disease

OpenAIRE

Javier eBlesa; Javier eBlesa; Javier eBlesa; Ines eTrigo-Damas; Ines eTrigo-Damas; Anna eQuiroga-Varela; Vernice Ruffin Jackson-Lewis

2015-01-01

Parkinson disease is a chronic, progressive neurological disease that is associated with a loss of dopaminergic neurons in the substantia nigra of the brain. The molecular mechanisms underlying the loss of these neurons still remain elusive. Oxidative stress is thought to play an important role in dopaminergic neurotoxicity. Complex I deficiencies of the respiratory chain account for the majority of unfavorable neuronal degeneration in Parkinson’s Disease. Environmental factors, such as neuro...

Lead neurotoxicity: In vitro and in vivo effects

International Nuclear Information System (INIS)

Rowles, T.K.

1989-01-01

Neuroglial cells, in particular astroglia, are thought to play a role in the neurotoxicity of lead. Two hypotheses have been proposed as possible cellular mechanism of this neurotoxicity: (1) lead affects intracellular levels of metals which mediate the toxic effects noted, and (2) lead affects intracellular heme biosynthesis which is then toxic to the cells. Zinc was found to have a profound effect on both intracellular lead levels and on cell numbers in lead-treated rat astroglia. A comparison of bovine and rat astroglia in culture indicated that the bovine cell cultures were not more sensitive to lead, even though calves are more sensitive. Lead was also shown to affect intracellular heme biosynthesis by a decrease in 14 C aminolevulinic acid incorporation into extractable heme in lead-treated rat astroglia. Finally, low levels of lead in immature guinea pigs caused changes in tissue levels of lead, iron, copper, and zinc with no change in weight gain or body:brain weight ratios

Cnidarian Neurotoxic Peptides Affecting Central Nervous System Targets.

Science.gov (United States)

Lazcano-Pérez, Fernando; Hernández-Guzmán, Ulises; Sánchez-Rodríguez, Judith; Arreguín-Espinosa, Roberto

2016-01-01

Natural products from animal venoms have been used widely in the discovery of novel molecules with particular biological activities that enable their use as potential drug candidates. The phylum Cnidaria (jellyfish, sea anemones, corals zoanthids, hydrozoans, etc.) is the most ancient venomous phylum on earth. Its venoms are composed of a complex mixture of peptidic compounds with neurotoxic and cytolitic properties that have shown activity on mammalian systems despite the fact that they are naturally targeted against fish and invertebrate preys, mainly crustaceans. For this reason, cnidarian venoms are an interesting and vast source of molecules with a remarkable activity on central nervous system, targeting mainly voltage-gated ion channels, ASIC channels, and TRPV1 receptors. In this brief review, we list the amino acid sequences of most cnidarian neurotoxic peptides reported to date. Additionally, we propose the inclusion of a new type of voltage-gated sea anemone sodium channel toxins based on the most recent reports.

Neurotoxicity of dental amalgam is mediated by zinc.

Science.gov (United States)

Lobner, D; Asrari, M

2003-03-01

The use of dental amalgam is controversial largely because it contains mercury. We tested whether amalgam caused toxicity in neuronal cultures and whether that toxicity was caused by mercury. In this study, we used cortical cell cultures to show for the first time that amalgam causes nerve cell toxicity in culture. However, the toxicity was not blocked by the mercury chelator, 2,3-dimercaptopropane-1-sulphonate (DMPS), but was blocked by the metal chelator, calcium disodium ethylenediaminetetraacetate (CaEDTA). DMPS was an effective mercury chelator in this system, since it blocked mercury toxicity. Of the components that comprise amalgam (mercury, zinc, tin, copper, and silver), only zinc neurotoxicity was blocked by CaEDTA. These results indicate that amalgam is toxic to nerve cells in culture by releasing zinc. While zinc is known to be neurotoxic, ingestion of zinc is not a major concern because zinc levels in the body are tightly regulated.

The inhibitory effect of manganese on acetylcholinesterase activity enhances oxidative stress and neuroinflammation in the rat brain

International Nuclear Information System (INIS)

Santos, Dinamene; Milatovic, Dejan; Andrade, Vanda; Batoreu, M. Camila; Aschner, Michael; Marreilha dos Santos, A.P.

2012-01-01

Highlights: ► Acetylcholinesterase (AChE) is a target of Mn in the central nervous system. ► Mn inhibits AChE, representing a novel mechanistic finding for its mode of action. ► AChE inhibition may trigger or contribute to the development of oxidative stress. ► Excess Mn can trigger the release of inflammatory mediators. ► AChE activity may serve as an early biomarker of Mn neurotoxicity. -- Abstract: Background: Manganese (Mn) is a naturally occurring element and an essential nutrient for humans and animals. However, exposure to high levels of Mn may cause neurotoxic effects. The pathological mechanisms associated with Mn neurotoxicity are poorly understood, but several reports have established it is mediated, at least in part, by oxidative stress. Objectives: The present study was undertaken to test the hypothesis that a decrease in acetylcholinesterase (AChE) activity mediates Mn-induced neurotoxicity. Methods: Groups of 6 rats received 4 or 8 intraperitoneal (i.p.) injections of 25 mg MnCl 2 /kg/day, every 48 h. Twenty-four hours after the last injection, brain AChE activity and the levels of F 2 -isoprostanes (F 2 -IsoPs) and F 4 -neuroprostanes (F 4 -NPs) (biomarkers of oxidative stress), as well as prostaglandin E 2 (PGE 2 ) (biomarker of neuroinflammation) were analyzed. Results: The results showed that after either 4 or 8 Mn doses, brain AChE activity was significantly decreased (p 2 -IsoPs and PGE 2 levels, but only after 8 doses. In rats treated with 4 Mn doses, a significant increase (p 4 -NPs levels was found. To evaluate cellular responses to oxidative stress, we assessed brain nuclear factor-erythroid 2 p45-related factor 2 (Nrf2) and Mn-superoxide dismutase (Mn-SOD, SOD2) protein expression levels. A significant increase in Mn-SOD protein expression (p < 0.05) and a trend towards increased Nrf2 protein expression was noted in rat brains after 4 Mn doses vs. the control group, but the expression of these proteins was decreased after 8 Mn

Investigation of the aluminium-aluminium oxide reversible transformation as observed by hot stage electron microscopy.

Science.gov (United States)

Grove, C. A.; Judd, G.; Ansell, G. S.

1972-01-01

Thin foils of high purity aluminium and an Al-Al2O3 SAP type of alloy were oxidised in a specially designed hot stage specimen chamber in an electron microscope. Below 450 C, amorphous aluminium oxide formed on the foil surface and was first detectable at foil edges, holes, and pits. Islands of aluminium then nucleated in this amorphous oxide. The aluminium islands displayed either a lateral growth with eventual coalescence with other islands, or a reoxidation process which caused the islands to disappear. The aluminium island formation was determined to be related to the presence of the electron beam. A mechanism based upon electron charging due to the electron beam was proposed to explain the nucleation, growth, coalescence, disappearance, and geometry of the aluminium islands.

What is microglia neurotoxicity (Not)?

DEFF Research Database (Denmark)

Biber, Knut; Owens, Trevor; Boddeke, Erik

2014-01-01

and vulnerable organ like the brain should host numerous potential killers, we here review the concept of microglia neurotoxicity. On one hand it is discussed that most of our understanding about how microglia kill neurons is based on in vitro experiments or correlative staining studies that suffer from...... the difficulty to discriminate microglia and peripheral myeloid cells in the diseased brain. On the other hand it is described that a more functional approach by mutating, inactivating or deleting microglia is seldom associated with a beneficial outcome in an acute injury situation, suggesting that microglia...

Exocytosis: using amperometry to study presynaptic mechanisms of neurotoxicity

NARCIS (Netherlands)

Westerink, R.H.S.

2004-01-01

The development of carbon fiber microelectrode amperometry enabled detailed investigation of the presynaptic response at the single cell level with single vesicle resolution. Consequently, amperometry allowed for detailed studies into the presynaptic mechanisms underlying neurotoxicity. This review

Acute D2/D3 dopaminergic agonism but chronic D2/D3 antagonism prevents NMDA antagonist neurotoxicity.

Science.gov (United States)

Farber, Nuri B; Nemmers, Brian; Noguchi, Kevin K

2006-09-15

Antagonists of the N-methyl-D-aspartate (NMDA) glutamate receptor, most likely by producing disinhibtion in complex circuits, acutely produce psychosis and cognitive disturbances in humans, and neurotoxicity in rodents. Studies examining NMDA Receptor Hypofunction (NRHypo) neurotoxicity in animals, therefore, may provide insights into the pathophysiology of psychotic disorders. Dopaminergic D2 and/or D3 agents can modify psychosis over days to weeks, suggesting involvement of these transmitter system(s). We studied the ability of D2/D3 agonists and antagonists to modify NRHypo neurotoxicity both after a one-time acute exposure and after chronic daily exposure. Here we report that D2/D3 dopamine agonists, probably via D3 receptors, prevent NRHypo neurotoxicity when given acutely. The protective effect with D2/D3 agonists is not seen after chronic daily dosing. In contrast, the antipsychotic haloperidol does not affect NRHypo neurotoxicity when given acutely at D2/D3 doses. However, after chronic daily dosing of 1, 3, or 5 weeks, haloperidol does prevent NRHypo neurotoxicity with longer durations producing greater protection. Understanding the changes that occur in the NRHypo circuit after chronic exposure to dopaminergic agents could provide important clues into the pathophysiology of psychotic disorders.

p73 gene in dopaminergic neurons is highly susceptible to manganese neurotoxicity.

Science.gov (United States)

Kim, Dong-Suk; Jin, Huajun; Anantharam, Vellareddy; Gordon, Richard; Kanthasamy, Arthi; Kanthasamy, Anumantha G

2017-03-01

Chronic exposure to elevated levels of manganese (Mn) has been linked to a Parkinsonian-like movement disorder, resulting from dysfunction of the extrapyramidal motor system within the basal ganglia. However, the exact cellular and molecular mechanisms of Mn-induced neurotoxicity remain elusive. In this study, we treated C57BL/6J mice with 30mg/kg Mn via oral gavage for 30 days. Interestingly, in nigral tissues of Mn-exposed mice, we found a significant downregulation of the truncated isoform of p73 protein at the N-terminus (ΔNp73). To further determine the functional role of Mn-induced p73 downregulation in Mn neurotoxicity, we examined the interrelationship between the effect of Mn on p73 gene expression and apoptotic cell death in an N27 dopaminergic neuronal model. Consistent with our animal study, 300μM Mn treatment significantly suppressed p73 mRNA expression in N27 dopaminergic cells. We further determined that protein levels of the ΔNp73 isoform was also reduced in Mn-treated N27 cells and primary striatal cultures. Furthermore, overexpression of ΔNp73 conferred modest cellular protection against Mn-induced neurotoxicity. Taken together, our results demonstrate that Mn exposure downregulates p73 gene expression resulting in enhanced susceptibility to apoptotic cell death. Thus, further characterization of the cellular mechanism underlying p73 gene downregulation will improve our understanding of the molecular underpinnings of Mn neurotoxicity. Copyright © 2016 Elsevier B.V. All rights reserved.

Surface and Core Electronic Structure of Oxidized Silicon Nanocrystals

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Noor A. Nama

2010-01-01

Full Text Available Ab initio restricted Hartree-Fock method within the framework of large unit cell formalism is used to simulate silicon nanocrystals between 216 and 1000 atoms (1.6–2.65 nm in diameter that include Bravais and primitive cell multiples. The investigated properties include core and oxidized surface properties. Results revealed that electronic properties converge to some limit as the size of the nanocrystal increases. Increasing the size of the core of a nanocrystal resulted in an increase of the energy gap, valence band width, and cohesive energy. The lattice constant of the core and oxidized surface parts shows a decreasing trend as the nanocrystal increases in a size that converges to 5.28 Ǻ in a good agreement with the experiment. Surface and core convergence to the same lattice constant reflects good adherence of oxide layer at the surface. The core density of states shows highly degenerate states that split at the oxygenated (001-(1×1 surface due to symmetry breaking. The nanocrystal surface shows smaller gap and higher valence and conduction bands when compared to the core part, due to oxygen surface atoms and reduced structural symmetry. The smaller surface energy gap shows that energy gap of the nanocrystal is controlled by the surface part. Unlike the core part, the surface part shows a descending energy gap that proves its obedience to quantum confinement effects. Nanocrystal geometry proved to have some influence on all electronic properties including the energy gap.

Phosphorene oxide: stability and electronic properties of a novel two-dimensional material.

Science.gov (United States)

Wang, Gaoxue; Pandey, Ravindra; Karna, Shashi P

2015-01-14

Phosphorene, the monolayer form of (black) phosphorus, was recently exfoliated from its bulk counterpart. Phosphorene oxide, by analogy to graphene oxide, is expected to have novel chemical and electronic properties, and may provide an alternative route to the synthesis of phosphorene. In this research, the physical and chemical properties of phosphorene oxide including its formation by oxygen adsorption on the bare phosphorene was investigated. Analysis of the phonon dispersion curves finds stoichiometric and non-stoichiometric oxide configurations to be stable at ambient conditions, thus suggesting that the oxygen adsorption may not degrade the phosphorene. The nature of the band gap of the oxides depends on the degree of functionalization of phosphorene; an indirect gap is predicted for the non-stoichiometric configurations, whereas a direct gap is predicted for the stoichiometric oxide. Application of mechanical strain or an external electric field leads to tunability of the band gap of the phosphorene oxide. In contrast to the case of the bare phosphorene, dependence of the diode-like asymmetric current-voltage response on the degree of stoichiometry is predicted for the phosphorene oxide.

Endothelial Activation and Blood-Brain Barrier Disruption in Neurotoxicity after Adoptive Immunotherapy with CD19 CAR-T Cells.

Science.gov (United States)

Gust, Juliane; Hay, Kevin A; Hanafi, Laïla-Aïcha; Li, Daniel; Myerson, David; Gonzalez-Cuyar, Luis F; Yeung, Cecilia; Liles, W Conrad; Wurfel, Mark; Lopez, Jose A; Chen, Junmei; Chung, Dominic; Harju-Baker, Susanna; Özpolat, Tahsin; Fink, Kathleen R; Riddell, Stanley R; Maloney, David G; Turtle, Cameron J

2017-12-01

Lymphodepletion chemotherapy followed by infusion of CD19-targeted chimeric antigen receptor-modified T (CAR-T) cells can be complicated by neurologic adverse events (AE) in patients with refractory B-cell malignancies. In 133 adults treated with CD19 CAR-T cells, we found that acute lymphoblastic leukemia, high CD19 + cells in bone marrow, high CAR-T cell dose, cytokine release syndrome, and preexisting neurologic comorbidities were associated with increased risk of neurologic AEs. Patients with severe neurotoxicity demonstrated evidence of endothelial activation, including disseminated intravascular coagulation, capillary leak, and increased blood-brain barrier (BBB) permeability. The permeable BBB failed to protect the cerebrospinal fluid from high concentrations of systemic cytokines, including IFNγ, which induced brain vascular pericyte stress and their secretion of endothelium-activating cytokines. Endothelial activation and multifocal vascular disruption were found in the brain of a patient with fatal neurotoxicity. Biomarkers of endothelial activation were higher before treatment in patients who subsequently developed grade ≥4 neurotoxicity. Significance: We provide a detailed clinical, radiologic, and pathologic characterization of neurotoxicity after CD19 CAR-T cells, and identify risk factors for neurotoxicity. We show endothelial dysfunction and increased BBB permeability in neurotoxicity and find that patients with evidence of endothelial activation before lymphodepletion may be at increased risk of neurotoxicity. Cancer Discov; 7(12); 1404-19. ©2017 AACR. See related commentary by Mackall and Miklos, p. 1371 This article is highlighted in the In This Issue feature, p. 1355 . ©2017 American Association for Cancer Research.

Scutellarin Mitigates Aβ-Induced Neurotoxicity and Improves Behavior Impairments in AD Mice

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Yue-Qin Zeng

2018-04-01

Full Text Available Alzheimer’s disease (AD is pathologically characterized by excessive accumulation of amyloid-beta (Aβ within extracellular spaces of the brain. Aggregation of Aβ has been shown to trigger oxidative stress, inflammation, and neurotoxicity resulting in cognitive dysfunction. In this study, we use models of cerebral Aβ amyloidosis to investigate anti-amyloidogenic effects of scutellarin in vitro and in vivo. Our results show that scutellarin, through binding to Aβ42, efficiently inhibits oligomerization as well as fibril formation and reduces Aβ oligomer-induced neuronal toxicity in cell line SH-SY5Y. After nine months of treatment in APP/PS1 double-transgenic mice, scutellarin significantly improves behavior, reduces soluble and insoluble Aβ levels in the brain and plasma, decreases Aβ plaque associated gliosis and levels of proinflammatory cytokines TNF-α and IL-6, attenuates neuroinflammation, displays anti-amyloidogenic effects, and highlights the beneficial effects of intervention on development or progression of AD-like neuropathology.

Comparative developmental neurotoxicity of flame-retardants, polybrominated flame-retardants and organophosphorous compounds, in mice

Energy Technology Data Exchange (ETDEWEB)

Eriksson, P.; Johansson, N.; Viberg, H.; Fischer, C.; Fredriksson, A. [Dept. of Environmental Toxicology, Uppsala Univ. (Sweden)

2004-09-15

Recently we have reported that certain PBDEs, such as 2,2',4,4'-tetrabromodiphenyl ether (PBDE 47), 2,2',4,4',5- pentabromodiphenyl ether (PBDE 99), 2,2',4,4',5,5'-hexabromodiphenyl ether (PBDE153) and 2,2',3,3',4,4',5,5',6,6'-decabromodiphenyl ether (PBDE 209) can cause developmental neurotoxic effects when given to neonatal mice. The developmental neurotoxic effects after neonatal exposure to PBDE 209 are suggested to be caused by a metabolite (possible de-brominated one). Neonatal exposure HBCDD has also been shown to cause developmental neurotoxic effects. Neonatal exposure to PBDE 99, PBDE 153 and HBCDD was also found to affect learning and memory in the adult animal. The induction of permanent aberration in spontaneous behaviour was induced during limited period of the neonatal brain development. The altered spontaneous behaviour was also seen to worsen with age. In these studies we have also found that the cholinergic system is one target that is affected, observed as changes in the response of the cholinergic system and a decrease in cholinergic receptors, and is one of the mechanisms underlying the observed behavioural changes. BFRs so far studied TBBPA appears not to cause developmental neurotoxic effects when administered at the same dose levels to neonatal mice. In the present studies we have investigated whether neonatal exposure to three highly brominated dipehenyl ethers, 2,2',3,4,4',5',6'-heptabromodiphenyl ether (PBDE183), 2,2',3'4'4',5,5',6- octabromodiphenyl ether (PBDE 203) and 2,2',3,3',4,4',5',6'-nonabromodiphenyl ether (PBDE 206) can induce developmental neurotoxic effects, such as aberrations in spontaneous behaviour and in learning and memory. Furthermore, neonatal developmental neurotoxicity effects were also studied for two OPs used as FR, triphenyl phosphate and tris(2-chloro-ethyl)phosphate.

Neurotoxicity profile of supermethrin, a new pyrethroid insecticide.

Science.gov (United States)

Hornychova, M; Frantik, E; Kubat, J; Formanek, J

1995-11-01

The use of a standard two-tier neurotoxicity screening procedure in the context of risk assessment is exemplified. Testing of a new pyrethroid in rats addressed the following sequence of questions: Does the substance evoke neurotoxic symptoms in sublethal doses? Do these symptoms reflect a primary neurotropic action? What are the dynamic characteristics of injury, the clinical profile of effect, and the relative potency of the tested substance compared to similar compounds? - The testing protocol is an animal analogue of a systematic neurological and psychological examination in man. First tier tests (structured observation, motor activity measurement, simple neurological examination) were applied after the first dose, during repeated dosing phase and in the restitution phase. Facultative tests for the second-tier examination (motor activity pattern, learning/retention test, evoked potentials, dynamic motor performance) were selected on the basis of effects revealed by the first-tier testing. Supermethrin evoked acute neurotoxicity in sublethal doses, ranging from 1/30 to 1/15 of LD50. The clinical pattern was similar to other cyano-substituted pyrethroids. Behavioural inhibition was transient and complete tolerance to it developed after 4-week repeated dosing. No indications of long-lasting changes in neuronal excitability or in learning and memory processes were found. Ataxia and excitomotoric phenomena dominated both the acute and the subchronic picture. Marked and persistent motor disturbances, including symptoms of lower motoneuron injury, were limited to individual animals of the highest, near-lethal dose group (27 mg-kg-1). Compared to lambda-cyhalothrin, the effects of supermethrin were 2 to 3 times weaker, disappeared more rapidly, cumulated less, and had higher tendency to tolerance.

Molecular mechanisms of aluminium ions neurotoxicity in brain cells of fish from various pelagic areas

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E. V. Sukharenko

2017-07-01

Full Text Available Neurotoxic effects of aluminum chloride in higher than usual environment concentration (10 mg/L were studied in brains of fishes from various pelagic areas, especially in sunfish (Lepomis macrochirus Rafinesque, 1819, roach (Rutilus rutilus Linnaeus, 1758, crucian carp (Carasius carasius Linnaeus, 1758, goby (Neogobius fluviatilis Pallas, 1811. The intensity of oxidative stress and the content of both cytoskeleton protein GFAP and cytosol Ca-binding protein S100β were determined. The differences in oxidative stress data were observed in the liver and brain of fish during 45 days of treatment with aluminum chloride. The data indicated that in the modeling of aluminum intoxication in mature adult fishes the level of oxidative stress was noticeably higher in the brain than in the liver. This index was lower by1.5–2.0 times on average in the liver cells than in the brain. The obtained data evidently demonstrate high sensitivity to aluminum ions in neural tissue cells of fish from various pelagic areas. Chronic intoxication with aluminum ions induced intense astrogliosis in the fish brain. Astrogliosis was determined as result of overexpression of both cytoskeleton and cytosole markers of astrocytes – GFAP and protein S100β (on 75–112% and 67–105% accordingly. Moreover, it was shown that the neurotixic effect of aluminum ions is closely related to metabolism of astroglial intermediate filaments. The results of western blotting showed a considerable increase in the content of the lysis protein products of GFAP with a range of molecular weight from 40–49 kDa. A similar metabolic disturbance was determined for the upregulation protein S100β expression and particularly in the increase in the content of polypeptide fragments of this protein with molecular weight 24–37 kDa. Thus, the obtained results allow one to presume that aluminum ions activate in the fish brain intracellular proteases which have a capacity to destroy the proteins of

Study of the electronic structure of pure aluminium, aluminium oxide and nitride by spectroscopy of electrons excited under electronic and photonic bombardment (X and UV)

International Nuclear Information System (INIS)

Gautier-Soyer, Martine

1985-01-01

This research thesis reports the use of electron spectroscopy with electrons excited under electronic or photonic (X or UV) bombardment for the study of electronic state density of aluminium, aluminium oxide (Al 2 O 3 ) and aluminium nitride (AlN). The objective is to get an insight into phenomena related to technological problems of adherence, wear, lubrication, corrosion or breakdown met in metals, insulators and semiconductors. The author highlighted the presence of occupied surface states on Al(111) and Al(100), and electronic levels localised in the forbidden band of Al 2 O 3 and AlN, induced by structural defects which promote surface reactivity [fr

Prion infections and anti-PrP antibodies trigger converging neurotoxic pathways.

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Uli S Herrmann

2015-02-01

Full Text Available Prions induce lethal neurodegeneration and consist of PrPSc, an aggregated conformer of the cellular prion protein PrPC. Antibody-derived ligands to the globular domain of PrPC (collectively termed GDL are also neurotoxic. Here we show that GDL and prion infections activate the same pathways. Firstly, both GDL and prion infection of cerebellar organotypic cultured slices (COCS induced the production of reactive oxygen species (ROS. Accordingly, ROS scavenging, which counteracts GDL toxicity in vitro and in vivo, prolonged the lifespan of prion-infected mice and protected prion-infected COCS from neurodegeneration. Instead, neither glutamate receptor antagonists nor inhibitors of endoplasmic reticulum calcium channels abolished neurotoxicity in either model. Secondly, antibodies against the flexible tail (FT of PrPC reduced neurotoxicity in both GDL-exposed and prion-infected COCS, suggesting that the FT executes toxicity in both paradigms. Thirdly, the PERK pathway of the unfolded protein response was activated in both models. Finally, 80% of transcriptionally downregulated genes overlapped between prion-infected and GDL-treated COCS. We conclude that GDL mimic the interaction of PrPSc with PrPC, thereby triggering the downstream events characteristic of prion infection.

First-principles analysis of structural and opto-electronic properties of indium tin oxide

Science.gov (United States)

Tripathi, Madhvendra Nath; Shida, Kazuhito; Sahara, Ryoji; Mizuseki, Hiroshi; Kawazoe, Yoshiyuki

2012-05-01

Density functional theory (DFT) and DFT + U (DFT with on-site Coulomb repulsion corrections) calculations have been carried out to study the structural and opto-electronic properties of indium tin oxide (ITO) for both the oxidized and reduced environment conditions. Some of the results obtained by DFT calculations differ from the experimental observations, such as uncertain indication for the site preference of tin atom to replace indium atom at b-site or d-site, underestimation of local inward relaxation in the first oxygen polyhedra around tin atom, and also the improper estimation of electronic density of states and hence resulting in an inappropriate optical spectra of ITO. These discrepancies of theoretical outcomes with experimental observations in ITO arise mainly due to the underestimation of the cationic 4d levels within standard DFT calculations. Henceforth, the inclusion of on-site corrections within DFT + U framework significantly modifies the theoretical results in better agreement to the experimental observations. Within this framework, our calculations show that the indium b-site is preferential site over d-site for tin atom substitution in indium oxide under both the oxidized and reduced conditions. Moreover, the calculated average inward relaxation value of 0.16 Å around tin atom is in good agreement with the experimental value of 0.18 Å. Furthermore, DFT + U significantly modify the electronic structure and consequently induce modifications in the calculated optical spectra of ITO.

Electrochemical One-Electron Oxidation of Low-Generation Polyamidoamine-Type Dendrimers with a 1,4-Phenylenediamine Core

DEFF Research Database (Denmark)

Hammerich, Ole; Hansen, Thomas; Thorvildsen, Asbjørn

2009-01-01

voltammetry (DPV) in methanol, acetonitrile, dichloromethane, and dimethyl sulfoxide. The dendrimers are more difficult to oxidize than N,N,N',N'-tetramethyl-p-phenylenediamine (TMePD). The oxidation potentials decrease with increasing dendrimer generation up to G0.5, after which the potential is essentially......A series of polyamidoamine (PAMAM)-type dendrimers with a 1,4-phenylenediamine (PD) core is prepared from PD by procedures including Michael addition of methyl acrylate followed by aminolysis with 1,2-ethanediamine. Their one-electron oxidation potentials are determined by differential pulse......,N,N',N'-tetra-n-alkyl-p-phenylenediamines, including a planar arrangement of the atoms linked to the two PD nitrogen atoms. Thus, the effect of chain size on the oxidation potential appears to be caused primarily by a simple electronic effect. The calculations indicate considerable reorientation of the dendrimer side chains on oxidation, presumably...

[Toxicodynamic properties of liquids used for the cooling of high-power turbines. III. Neurotoxic effects].

Science.gov (United States)

Florek, E; Malendowicz, L; Seńczuk, W

1984-01-01

Results of neurotoxicity studies indicate that preparations IWiOL -3-n, IWiOL -3-e and OMTI administered intragastrically or intraperitoneally induce neurotoxic effects in hens. Those effects are, however, weaker than those of the standard substance, i.e. triorthocresyl . Yet, they get increased in result of IWiOL -3-e, as compared to IWiOL -3-n administration.

Oxidative mechanisms contributing to the developmental neurotoxicity of nicotine and chlorpyrifos

International Nuclear Information System (INIS)

Qiao, Dan; Seidler, Frederic J.; Slotkin, Theodore A.

2005-01-01

Nicotine and chlorpyrifos are developmental neurotoxicants that, despite their differences in structure and mechanism of action, share many aspects for damage to the developing brain. Both are thought to generate oxidative radicals; in the current study, we evaluated their ability to produce lipid peroxidation in two in vitro models of neural cell development (PC12 and SH-SY5Y cells) and for nicotine, with treatment of adolescent rats in vivo. Nicotine and chlorpyrifos, in concentrations relevant to human exposures, elicited an increase in thiobarbituric-acid-reactive species (TBARS) in undifferentiated cells, an effect that was prevented by addition of the antioxidant, Vitamin E. Initiating differentiation with nerve growth factor, which enhances nicotinic acetylcholine receptor expression, increased the TBARS response to nicotine but not chlorpyrifos, suggesting that the two agents act by different originating mechanisms to converge on the endpoint of oxidative damage. Furthermore, nicotine protected the cells from oxidative damage evoked by chlorpyrifos and similarly blocked the antimitotic effect of chlorpyrifos. Treatment of adolescent rats with nicotine elicited increases in TBARS in multiple brain regions when given in doses that simulate plasma nicotine concentrations found in smokers or at one-tenth the dose. Our results indicate that nicotine and chlorpyrifos elicit oxidative damage to developing neural cells both in vitro and in vivo, a mechanism that explains some of the neurodevelopmental endpoints that are common to the two agents. The balance between neuroprotectant and neurotoxicant actions of nicotine may be particularly important in situations where exposure to tobacco smoke is combined with other prooxidant insults

3-nitropropionic acid neurotoxicity in hippocampal slice cultures

DEFF Research Database (Denmark)

Noer, Helle; Kristensen, Bjarne W; Noraberg, Jens

2002-01-01

: CA1 > CA3 > fascia dentata. In low glucose much lower concentrations of 3-NP (25 microM) triggered neurotoxicity. One-week-old cultures were less susceptible to 3-NP toxicity than 3-week-old cultures, but the dentate granule cells were relatively more affected in the immature cultures. We found...

One-electron oxidation reactions of purine and pyrimidine bases in cellular DNA.

Science.gov (United States)

Cadet, Jean; Wagner, J Richard; Shafirovich, Vladimir; Geacintov, Nicholas E

2014-06-01

The aim of this survey is to critically review the available information on one-electron oxidation reactions of nucleobases in cellular DNA with emphasis on damage induced through the transient generation of purine and pyrimidine radical cations. Since the indirect effect of ionizing radiation mediated by hydroxyl radical is predominant in cells, efforts have been made to selectively ionize bases using suitable one-electron oxidants that consist among others of high intensity UVC laser pulses. Thus, the main oxidation product in cellular DNA was found to be 8-oxo-7,8-dihydroguanine as a result of direct bi-photonic ionization of guanine bases and indirect formation of guanine radical cations through hole transfer reactions from other base radical cations. The formation of 8-oxo-7,8-dihydroguanine and other purine and pyrimidine degradation products was rationalized in terms of the initial generation of related radical cations followed by either hydration or deprotonation reactions in agreement with mechanistic pathways inferred from detailed mechanistic studies. The guanine radical cation has been shown to be implicated in three other nucleophilic additions that give rise to DNA-protein and DNA-DNA cross-links in model systems. Evidence was recently provided for the occurrence of these three reactions in cellular DNA. There is growing evidence that one-electron oxidation reactions of nucleobases whose mechanisms have been characterized in model studies involving aqueous solutions take place in a similar way in cells. It may also be pointed out that the above cross-linked lesions are only produced from the guanine radical cation and may be considered as diagnostic products of the direct effect of ionizing radiation.

Electron Band Alignment at Interfaces of Semiconductors with Insulating Oxides: An Internal Photoemission Study

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Valeri V. Afanas'ev

2014-01-01

Full Text Available Evolution of the electron energy band alignment at interfaces between different semiconductors and wide-gap oxide insulators is examined using the internal photoemission spectroscopy, which is based on observations of optically-induced electron (or hole transitions across the semiconductor/insulator barrier. Interfaces of various semiconductors ranging from the conventional silicon to the high-mobility Ge-based (Ge, Si1-xGex, Ge1-xSnx and AIIIBV group (GaAs, InxGa1-xAs, InAs, GaP, InP, GaSb, InSb materials were studied revealing several general trends in the evolution of band offsets. It is found that in the oxides of metals with cation radii larger than ≈0.7 Å, the oxide valence band top remains nearly at the same energy (±0.2 eV irrespective of the cation sort. Using this result, it becomes possible to predict the interface band alignment between oxides and semiconductors as well as between dissimilar insulating oxides on the basis of the oxide bandgap width which are also affected by crystallization. By contrast, oxides of light elements, for example, Be, Mg, Al, Si, and Sc exhibit significant shifts of the valence band top. General trends in band lineup variations caused by a change in the composition of semiconductor photoemission material are also revealed.

In situ studies of oxide nucleation, growth, and transformation using slow electrons

Science.gov (United States)

Flege, Jan Ingo; Grinter, David C.

2018-05-01

Surface processes such as metal oxidation and metal oxide growth invariably influence the physical and chemical properties of materials and determine their interaction with their surroundings and hence their functionality in many technical applications. On a fundamental level, these processes are found to be governed by a complex interplay of thermodynamic variables and kinetic constraints, resulting in a rich variety of material-specific phenomena. In this review article, we discuss recent results and insights on transition metal oxidation and rare-earth oxide growth acquired by low-energy electron microscopy and related techniques. We demonstrate that the use of in situ surface sensitive methods is a prerequisite to gaining a deeper understanding of the underlying concepts and the mechanisms responsible for the emerging oxide structure and morphology. Furthermore, examples will be provided on how structural and chemical modifications of the oxide films and nanostructures can be followed in real-time and analyzed in terms of local reactivity and cooperative effects relevant for heterogeneous model catalysis.

The Potential Neurotoxic Effects of Low-Dose Sarin Exposure in a Guinea Pig Model

Science.gov (United States)

2002-01-01

1 THE POTENTIAL NEUROTOXIC EFFECTS OF LOW-DOSE SARIN EXPOSURE IN A GUINEA PIG MODEL Melinda R. Roberson, PhD, Michelle B. Schmidt...Proving Ground, MD 21010 USA ABSTRACT This study is assessing the effects in guinea pigs of repeated low-dose exposure to the nerve...COVERED - 4. TITLE AND SUBTITLE The Potential Neurotoxic Effects Of Low-Dose Sarin Exposure In A Guinea Pig Model 5a. CONTRACT NUMBER 5b

A study of internal oxidation in carburized steels by glow discharge optical emission spectroscopy and scanning electron microscopy

CERN Document Server

An, X; Rainforth, W M; Chen, L

2003-01-01

The internal oxidation of Cr-Mn carburizing steel was studied. Internal oxidation was induced using a commercial carburizing process. Sputter erosion coupled with glow discharge optical emission spectroscopy (GDOES) was used to determine the depth profile elemental distribution within the internal oxidation layer (<10 mu m). In addition, scanning electron microscopy (SEM) equipped with energy dispersive spectrometer (EDS) studies were carried out on selected sputter eroded surfaces. Oxide type was identified primarily by transmission electron microscopy (TEM). The carburized surface was found to consist of a continuous oxide layer, followed by a complex internal oxidation layer, where Cr and Mn oxides were found to populate grain boundaries in a globular form in the near surface region. At greater depths (5-10 mu m), Si oxides formed as a grain boundary network. The internal oxides (mainly complex oxides) grew quickly during the initial stages of the carburizing process (2 h, 800 deg. C+3 h, 930 deg. C). G...

Conversion of sulfur and nitrogen oxides in air under exposure to microsecond electron beams

International Nuclear Information System (INIS)

Denisov, G.V.; Kuznetsov, D.L.; Novoselov, Yu.N.; Tkachenko, R.M.

2002-01-01

Flue gases of power plants realizing sulfur and nitrogen oxides into the atmosphere represent one of the environmental pollution sources. Paper presents the results of experimental investigations of conversion of sulfur and nitrogen oxides in the ionized gas mixture simulating composition of off-gases of thermal power stations. Pulse beam of microsecond duration electrons was used as a source of ionization. Mutual influence of both types of oxides on process of their conversion is shown. One studied possible kinetic mechanisms to remove sulfur and nitrogen oxides from gaseous mixture [ru

Electronic, vibrational and related properties of group IV metal oxides by ab initio calculations

International Nuclear Information System (INIS)

Leite Alves, H.W.; Silva, C.C.; Lino, A.T.; Borges, P.D.; Scolfaro, L.M.R.; Silva, E.F. da

2008-01-01

We present our theoretical results for the structural, electronic, vibrational and optical properties of MO 2 (M = Sn, Zr, Hf and Ti) obtained by first-principles calculations. Relativistic effects are demonstrated to be important for a realistic description of the detailed structure of the electronic frequency-dependent dielectric function, as well as of the carrier effective masses. Based on our results, we found that the main contribution of the high values calculated for the oxides dielectric constants arises from the vibrational properties of these oxides, and the vibrational static dielectric constant values diminish with increasing pressure

Attenuation of arsenic neurotoxicity by curcumin in rats

International Nuclear Information System (INIS)

Yadav, Rajesh S.; Sankhwar, Madhu Lata; Shukla, Rajendra K.; Chandra, Ramesh; Pant, Aditya B.; Islam, Fakhrul; Khanna, Vinay K.

2009-01-01

In view of continued exposure to arsenic and associated human health risk including neurotoxicity, neuroprotective efficacy of curcumin, a polyphenolic antioxidant, has been investigated in rats. A significant decrease in locomotor activity, grip strength (26%) and rota-rod performance (82%) was observed in rats treated with arsenic (sodium arsenite, 20 mg/kg body weight, p.o., 28 days) as compared to controls. The arsenic treated rats also exhibited a decrease in the binding of striatal dopamine receptors (32%) and tyrosine hydroxylase (TH) immunoreactivity (19%) in striatum. Increased arsenic levels in corpus striatum (6.5 fold), frontal cortex (6.3 fold) and hippocampus (7.0 fold) associated with enhanced oxidative stress in these brain regions, as evident by an increase in lipid perioxidation, protein carbonyl and a decrease in the levels of glutathione and activity of superoxide dismutase, catalase and glutathione peroxidase with differential effects were observed in arsenic treated rats compared to controls. Simultaneous treatment with arsenic (sodium arsenite, 20 mg/kg body weight, p.o., 28 days) and curcumin (100 mg/kg body weight, p.o., 28 days) caused an increase in locomotor activity and grip strength and improved the rota-rod performance in comparison to arsenic treated rats. Binding of striatal dopamine receptors and TH expression increased while arsenic levels and oxidative stress decreased in these brain regions in co-treated rats as compared to those treated with arsenic alone. No significant effect on any of these parameters was observed in rats treated with curcumin (100 mg/kg body weight, p.o., 28 days) alone compared to controls. A significant protection in behavioral, neurochemical and immunohistochemical parameters in rats simultaneously treated with arsenic and curcumin suggest the neuroprotective efficacy of curcumin.

Radioprotective efficacy of bisarylidene cyclopentanone on electron beam radiation induced oxidative stress in Drosophila melanogaster

International Nuclear Information System (INIS)

Darshan Raj, C.G.; Sarojini, B.K.; Musthafa Khaleel, V.; Ramesh, S.R.; Ramakrishna, M.K.; Narayana, B.; Sanjeev, Ganesh

2010-01-01

Present study was carried out for evaluating the radioprotective effect of bischalcone (2E, 5E) - 2,5-bis (3-methoxy-4-hydroxy-benzylidene) cyclopentanone (curcumin analog (CA)), on electron beam radiation induced oxidative stress in Drosophila melanogaster adults. The oxidative stress markers and antioxidants included superoxide dismutase (SOD) and catalase (CAT). The oxidative stress was induced at 1.5 Gy. (author)

Scoping review: Awareness of neurotoxicity from anesthesia in children in otolaryngology literature.

Science.gov (United States)

Earley, Marisa A; Pham, Liem T; April, Max M

2017-08-01

Review otolaryngology literature for awareness of neurotoxicity from general anesthesia in children. Recently, there has been increasing focus in anesthesia literature on the long-term effects of general anesthesia on neurodevelopment. Multiple animal models have demonstrated evidence of neurotoxicity from both inhalational and intravenous anesthetics. Cohort studies also have revealed modestly increased risk of adverse neurodevelopmental outcomes in children exposed to a single episode of general anesthesia prior to 3 to 4 years of age, with stronger evidence for multiple exposures in this age range. Otolaryngologists may subject children to general anesthesia via procedures or tests, including computed tomography, magnetic resonance imaging, and auditory brainstem response. PubMed, Embase, Scopus, and Web of Science Review. A scoping review using the above databases was performed limited to January 2005 through December 2015. Articles were screened and reviewed based on predefined inclusion and exclusion criteria. Initial search generated 3,909 articles. After 72 full text articles were reviewed, only seven articles mentioned neurotoxicity as a risk of general anesthesia in pediatric patients. Despite the high volume of pediatric otolaryngologic procedures performed annually, there remains limited awareness in our literature discussing neurotoxicity as an outcome. Prospective data from anesthesia literature is still pending; therefore, specific recommendations cannot be made at this time. Otolaryngologists should be aware of the concerns and work toward defining elective procedures, combining surgical procedures with other procedures or imaging, and reassessing the timing and frequency of various interventions under general anesthesia in young children. Laryngoscope, 127:1930-1937, 2017. © 2017 The American Laryngological, Rhinological and Otological Society, Inc.

Lithium-mediated protection against ethanol neurotoxicity

Directory of Open Access Journals (Sweden)

Jia Luo

2010-06-01

Full Text Available Lithium has long been used as a mood stabilizer in the treatment of manic-depressive (bipolar disorder. Recent studies suggest that lithium has neuroprotective properties and may be useful in the treatment of acute brain injuries such as ischemia and chronic neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease and amyotrophic lateral sclerosis. One of the most important neuroprotective properties of lithium is its anti-apoptotic action. Ethanol is a neuroteratogen and fetal alcohol spectrum disorders (FASD are caused by maternal ethanol exposure during pregnancy. FASD is the leading cause of mental retardation. Ethanol exposure causes neuroapoptosis in the developing brain. Ethanol-induced loss of neurons in the central nervous system underlies many of the behavioral deficits observed in FASD. Excessive alcohol consumption is also associated with Wernicke–Korsakoff syndrome and neurodegeneration in the adult brain. Recent in vivo and in vitro studies indicate that lithium is able to ameliorate ethanol-induced neuroapoptosis. Lithium is an inhibitor of glycogen synthase kinase 3 (GSK3 which has recently been identified as a mediator of ethanol neurotoxicity. Lithium’s neuroprotection may be mediated by its inhibition of GSK3. In addition, lithium also affects many other signaling proteins and pathways that regulate neuronal survival and differentiation. This review discusses the recent evidence of lithium-mediated protection against ethanol neurotoxicity and potential underlying mechanisms.

The effect of energetic electron precipitation on the nitric oxide density in the lower thermosphere

International Nuclear Information System (INIS)

Saetre, Camilla

2006-12-01

The objective of this thesis has been the study of the chemical effects of the electron precipitation in the upper atmosphere, and mainly the increase of thermospheric nitric oxide (NO). NO plays an important role in the temperature balance for the mesosphere and thermosphere.In this project auroral electron precipitation data, derived from the Polar Ionospheric X-ray Imaging Experiment (PIXIE) and the Ultraviolet Imager (UVI) on board the Polar satellite, have been used together with NO density measurements from the Student Nitric Oxide Explorer (SNOE)

The one-electron oxidation of a dithiolate molecule: the importance of chemical intuition.

Science.gov (United States)

Bushnell, Eric A C; Burns, Thomas D; Boyd, Russell J

2014-05-14

A series of nine commonly used density functional methods were assessed to accurately predict the oxidation potential of the (C2H2S2(-2)/C2H2S2(•-)) redox couple. It was found that due to their greater tendency for charge delocalization the GGA functionals predict a structure where the radical electron is delocalized within the alkene backbone of C2H2S2(•-), whereas the hybrid functionals and the reference QCISD/cc-pVTZ predict that the radical electron remains localized on the sulfurs. However, chemical intuition suggests that the results obtained with the GGA functionals should be correct. Indeed, with the use of the geometries obtained at the HCTH/6-311++G(3df,3pd) level of theory both the QCISD and hybrid DFT methods yield a molecule with a delocalized electron. Notably, this new molecule lies at least 53 kJ mol(-1) lower in energy than the previously optimized one that had a localized radical. Using these new structures the calculated oxidation potential was found to be 2.71-2.97 V for the nine DFT functionals tested. The M06-L functional provided the best agreement with the QCISD/cc-pVTZ reference oxidation potential of 3.28 V.

Atmospheric nitrous oxide produced by solar protons and relativistic electrons

International Nuclear Information System (INIS)

Prasad, S.S.; Zipf, E.C.

1981-01-01

An alternative means of nitric oxide production in the stratosphere to that of direct formation in the upper atmosphere by solar proton (SP) events and by relativistic electron precipitation (REP) events from the Earth's radiation belt, is described. It is suggested that nitrous oxide is produced in the mesosphere and then migrates downward and is converted in the stratosphere to NO by the reaction N 2 O + O( 1 D) → 2 NO. Such a process could amplify the direct NO production by >10%. Mesospheric nitrous oxide mixing ratios increase to values as high as 6 x 10 -7 due to REP- and SP- related production. Lateral transport will reduce these high values but mesospheric mixing ratios of N 2 O in the high latitudes would approach 10 -7 , considerably greater than those expected on the basis of theories which neglect REP- and SP-related production of this species. (U.K.)

Oxide nanomembrane hybrids with enhanced mechano- and thermo-sensitivity for semitransparent epidermal electronics.

Science.gov (United States)

Park, Minjoon; Do, Kyungsik; Kim, Jaemin; Son, Donghee; Koo, Ja Hoon; Park, Jinkyung; Song, Jun-Kyul; Kim, Ji Hoon; Lee, Minbaek; Hyeon, Taeghwan; Kim, Dae-Hyeong

2015-05-01

Oxide nanomembrane hybrids with enhanced mechano- and thermo-sensitivity for semitransparent epidermal electronics are developed. The use of nanomaterials (single wall nanotubes and silver nanoparticles) embedded in the oxide nanomembranes significantly enhances mechanical and thermal sensitivities. These mechanical and thermal sensors are utilized in wheelchair control and hypothermia detection, which are useful for patients with strokes. © 2015 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

Electronic structure and charge transport in nonstoichiometric tantalum oxide

Science.gov (United States)

Perevalov, T. V.; Gritsenko, V. A.; Gismatulin, A. A.; Voronkovskii, V. A.; Gerasimova, A. K.; Aliev, V. Sh; Prosvirin, I. A.

2018-06-01

The atomic and electronic structure of nonstoichiometric oxygen-deficient tantalum oxide TaO x<2.5 grown by ion beam sputtering deposition was studied. The TaO x film content was analyzed by x-ray photoelectron spectroscopy and by quantum-chemistry simulation. TaO x is composed of Ta2O5, metallic tantalum clusters and tantalum suboxides. A method for evaluating the stoichiometry parameter of TaO x from the comparison of experimental and theoretical photoelectron valence band spectra is proposed. The charge transport properties of TaO x were experimentally studied and the transport mechanism was quantitatively analyzed with four theoretical dielectric conductivity models. It was found that the charge transport in almost stoichiometric and nonstoichiometric tantalum oxide can be consistently described by the phonon-assisted tunneling between traps.

The electronic structure and metal-insulator transitions in vanadium oxides

International Nuclear Information System (INIS)

Mossanek, Rodrigo Jose Ochekoski

2010-01-01

The electronic structure and metal-insulator transitions in vanadium oxides (SrVO_3, CaVO_3, LaVO_3 and YVO_3) are studied here. The purpose is to show a new interpretation to the spectra which is coherent with the changes across the metal-insulator transition. The main experimental techniques are the X-ray photoemission (PES) and X-ray absorption (XAS) spectroscopies. The spectra are interpreted with cluster model, band structure and atomic multiplet calculations. The presence of charge-transfer satellites in the core-level PES spectra showed that these vanadium oxides cannot be classified in the Mott-Hubbard regime. Further, the valence band and core-level spectra presented a similar behavior across the metal insulator transition. In fact, the structures in the spectra and their changes are determined by the different screening channels present in the metallic or insulating phases. The calculated spectral weight showed that the coherent fluctuations dominate the spectra at the Fermi level and give the metallic character to the SrVO_3 and CaVO_3 compounds. The vanishing of this charge fluctuation and the replacement by the Mott-Hubbard screening in the LaVO_3 and YVO_3 systems is ultimately responsible for the opening of a band gap and the insulating character. Further, the correlation effects are, indeed, important to the occupied electronic structure (coherent and incoherent peaks). On the other hand, the unoccupied electronic structure is dominated by exchange and crystal field effects (t2g and eg sub-bands of majority and minority spins). The optical conductivity spectrum was obtained by convoluting the removal and addition states. It showed that the oxygen states, as well as the crystal field and exchange effects are necessary to correctly compare and interpret the experimental results. Further, a correlation at the charge-transfer region of the core-level and valence band optical spectra was observed, which could be extended to other transition metal oxides

Functional, Structural, and Neurotoxicity Biomarkers in Integrative Assessment of Concussions

Directory of Open Access Journals (Sweden)

Svetlana A Dambinova

2016-10-01

Full Text Available Concussion is a complex, heterogenous process affecting the brain. Accurate assessment and diagnosis and appropriate management of concussion are essential to ensure athletes do not prematurely return to play or others to work or active military duty, risking re-injury. To date, clinical diagnosis relies primarily on evaluating subjects for functional impairment using instruments that include neurocognitive testing, subjective symptom report, and neurobehavioral assessments, such as balance and vestibular-ocular reflex testing. Structural biomarkers, defined as advanced neuroimaging techniques and biomarkers assessing neurotoxicity and immunoexcitotoxicity may complement the use of functional biomarkers. We hypothesize that neurotoxicity AMPA, NMDA, and kainite receptor biomarkers might be utilized as a part of comprehensive approach to concussion evaluations, with the goal of increasing diagnostic accuracy and facilitating treatment planning and prognostic assessment.

Spectroscopy study of electron spin resonance of coal oxidation of different rank

International Nuclear Information System (INIS)

Enciso Prieto, Hector Manuel

1992-01-01

The present work constitutes an initial step for the knowledge of the coal oxidation, with the purpose of preventing the adverse influences caused by this phenomenon in the physical-chemical characteristics and in the tendency to the spontaneous combustion. Since the knowledge the influence of the free radicals in this process, their relative concentration was measured by means of the use of the technique of resonance spin electron. This technique measures the absorption of electromagnetic radiation, generally in the microwaves region, for the materials that not have electrons matched up in a strong magnetic field. In the essays of oxidation three coal of different range and different characteristics of mass were used and it was studied the influence of the temperature, particle size and the range. The results showed that the coal of Guacheta (bituminous low in volatile) it presents bigger concentration of free radicals, after the reaction with the atmospheric oxygen, with regard to the coal of the Cerrejon (bituminous high in volatile B) and Amaga (bituminous high in volatile C). Although this doesn't indicate that the coal of Guacheta is that more easily is oxidized, but rather it possibly presents stabilization of radicals for resonance. It concluded that there are differences in the oxidation mechanism between coal of different rank and different agglomeration properties

Protective effects of antioxidants and anti-inflammatory agents against manganese-induced oxidative damage and neuronal injury

International Nuclear Information System (INIS)

Milatovic, Dejan; Gupta, Ramesh C.; Yu, Yingchun; Zaja-Milatovic, Snjezana; Aschner, Michael

2011-01-01

Exposure to excessive manganese (Mn) levels leads to neurotoxicity, referred to as manganism, which resembles Parkinson's disease (PD). Manganism is caused by neuronal injury in both cortical and subcortical regions, particularly in the basal ganglia. The basis for the selective neurotoxicity of Mn is not yet fully understood. However, several studies suggest that oxidative damage and inflammatory processes play prominent roles in the degeneration of dopamine-containing neurons. In the present study, we assessed the effects of Mn on reactive oxygen species (ROS) formation, changes in high-energy phosphates and associated neuronal dysfunctions both in vitro and in vivo. Results from our in vitro study showed a significant (p 2 -isoprostanes (F 2 -IsoPs), as well as the depletion of ATP in primary rat cortical neurons following exposure to Mn (500 μM) for 2 h. These effects were protected when neurons were pretreated for 30 min with 100 of an antioxidant, the hydrophilic vitamin E analog, trolox (6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid), or an anti-inflammatory agent, indomethacin. Results from our in vivo study confirmed a significant increase in F 2 -IsoPs levels in conjunction with the progressive spine degeneration and dendritic damage of the striatal medium spiny neurons (MSNs) of mice exposed to Mn (100 mg/kg, s.c.) 24 h. Additionally, pretreatment with vitamin E (100 mg/kg, i.p.) or ibuprofen (140 μg/ml in the drinking water for two weeks) attenuated the Mn-induced increase in cerebral F 2 -IsoPs? and protected the MSNs from dendritic atrophy and dendritic spine loss. Our findings suggest that the mediation of oxidative stress/mitochondrial dysfunction and the control of alterations in biomarkers of oxidative injury, neuroinflammation and synaptodendritic degeneration may provide an effective, multi-pronged therapeutic strategy for protecting dysfunctional dopaminergic transmission and slowing of the progression of Mn-induced neurodegenerative

Protective effects of antioxidants and anti-inflammatory agents against manganese-induced oxidative damage and neuronal injury

Energy Technology Data Exchange (ETDEWEB)

Milatovic, Dejan, E-mail: dejan.milatovic@vanderbilt.edu [Vanderbilt University School of Medicine, Department of Pediatrics, Nashville, TN (United States); Gupta, Ramesh C. [Murray State University, Breathitt Veterinary Center, Hopkinsville, KY (United States); Yu, Yingchun; Zaja-Milatovic, Snjezana [Vanderbilt University School of Medicine, Department of Pediatrics, Nashville, TN (United States); Aschner, Michael [Vanderbilt University School of Medicine, Department of Pediatrics, Nashville, TN (United States); Pharmacology and the Kennedy Center for Research on Human Development, Nashville, TN (United States)

2011-11-15

Exposure to excessive manganese (Mn) levels leads to neurotoxicity, referred to as manganism, which resembles Parkinson's disease (PD). Manganism is caused by neuronal injury in both cortical and subcortical regions, particularly in the basal ganglia. The basis for the selective neurotoxicity of Mn is not yet fully understood. However, several studies suggest that oxidative damage and inflammatory processes play prominent roles in the degeneration of dopamine-containing neurons. In the present study, we assessed the effects of Mn on reactive oxygen species (ROS) formation, changes in high-energy phosphates and associated neuronal dysfunctions both in vitro and in vivo. Results from our in vitro study showed a significant (p < 0.01) increase in biomarkers of oxidative damage, F{sub 2}-isoprostanes (F{sub 2}-IsoPs), as well as the depletion of ATP in primary rat cortical neurons following exposure to Mn (500 {mu}M) for 2 h. These effects were protected when neurons were pretreated for 30 min with 100 of an antioxidant, the hydrophilic vitamin E analog, trolox (6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid), or an anti-inflammatory agent, indomethacin. Results from our in vivo study confirmed a significant increase in F{sub 2}-IsoPs levels in conjunction with the progressive spine degeneration and dendritic damage of the striatal medium spiny neurons (MSNs) of mice exposed to Mn (100 mg/kg, s.c.) 24 h. Additionally, pretreatment with vitamin E (100 mg/kg, i.p.) or ibuprofen (140 {mu}g/ml in the drinking water for two weeks) attenuated the Mn-induced increase in cerebral F{sub 2}-IsoPs? and protected the MSNs from dendritic atrophy and dendritic spine loss. Our findings suggest that the mediation of oxidative stress/mitochondrial dysfunction and the control of alterations in biomarkers of oxidative injury, neuroinflammation and synaptodendritic degeneration may provide an effective, multi-pronged therapeutic strategy for protecting dysfunctional

Effect of Gestational Intake of Fisetin (3,3',4',7-Tetrahydroxyflavone) on Developmental Methyl Mercury Neurotoxicity in F1 Generation Rats.

Science.gov (United States)

Jacob, Sherin; Thangarajan, Sumathi

2017-06-01

Methyl mercury (MeHg) is a developmental neurotoxin that causes irreversible cognitive damage in offspring of gestationally exposed mothers. Currently, no preventive drugs are established against MeHg developmental neurotoxicity. The neuroprotective effect of gestational administration of a flavanoid against in utero toxicity of MeHg is not explored much. Hence, the present study validated the effect of a bioactive flavanoid, fisetin, on MeHg developmental neurotoxicity outcomes in rat offspring at postnatal weaning age. Pregnant Wistar rats were simultaneously given MeHg (1.5 mg/kg b.w.) and two doses of fisetin (10 and 50 mg/kg b.w. in two separate groups) orally from gestational day (GD) 5 till parturition. Accordingly, after parturition, on postnatal day (PND) 24, weaning F 1 generation rats were studied for motor and cognitive behavioural changes. Biochemical and histopathological changes were also studied in the cerebral cortex, cerebellum and hippocampus on PND 25. Administration of fisetin during pregnancy prevented behavioural impairment due to transplacental MeHg exposure in weaning rats. Fisetin decreased the levels of oxidative stress markers, increased enzymatic and non-enzymatic antioxidant levels and increased the activity of membrane-bound ATPases and cholinergic function in F 1 generation rats. In light microscopic studies, fisetin treatment protected the specific offspring brain regions from significant morphological aberrations. Between the two doses of fisetin studied, 10 mg/kg b.w. was found to be more satisfactory and effective than 50 mg/kg b.w. The present study shows that intake of fisetin during pregnancy in rats ameliorated in utero MeHg exposure-induced neurotoxicity outcomes in postnatal weaning F 1 generation rats.

Electronic Structure of the Perylene / Zinc Oxide Interface: A Computational Study of Photoinduced Electron Transfer and Impact of Surface Defects

KAUST Repository

Li, Jingrui

2015-07-29

The electronic properties of dye-sensitized semiconductor surfaces consisting of pery- lene chromophores chemisorbed on zinc oxide via different spacer-anchor groups, have been studied at the density-functional-theory level. The energy distributions of the donor states and the rates of photoinduced electron transfer from dye to surface are predicted. We evaluate in particular the impact of saturated versus unsaturated aliphatic spacer groups inserted between the perylene chromophore and the semiconductor as well as the influence of surface defects on the electron-injection rates.

Electronic Structure of the Perylene / Zinc Oxide Interface: A Computational Study of Photoinduced Electron Transfer and Impact of Surface Defects

KAUST Repository

Li, Jingrui; Li, Hong; Winget, Paul; Bredas, Jean-Luc

2015-01-01

The electronic properties of dye-sensitized semiconductor surfaces consisting of pery- lene chromophores chemisorbed on zinc oxide via different spacer-anchor groups, have been studied at the density-functional-theory level. The energy distributions of the donor states and the rates of photoinduced electron transfer from dye to surface are predicted. We evaluate in particular the impact of saturated versus unsaturated aliphatic spacer groups inserted between the perylene chromophore and the semiconductor as well as the influence of surface defects on the electron-injection rates.

Epitaxial Lift-Off of Centimeter-Scaled Spinel Ferrite Oxide Thin Films for Flexible Electronics.

Science.gov (United States)

Shen, Lvkang; Wu, Liang; Sheng, Quan; Ma, Chunrui; Zhang, Yong; Lu, Lu; Ma, Ji; Ma, Jing; Bian, Jihong; Yang, Yaodong; Chen, Aiping; Lu, Xiaoli; Liu, Ming; Wang, Hong; Jia, Chun-Lin

2017-09-01

Mechanical flexibility of electronic devices has attracted much attention from research due to the great demand in practical applications and rich commercial value. Integration of functional oxide materials in flexible polymer materials has proven an effective way to achieve flexibility of functional electronic devices. However, the chemical and mechanical incompatibilities at the interfaces of dissimilar materials make it still a big challenge to synthesize high-quality single-crystalline oxide thin film directly on flexible polymer substrates. This study reports an improved method that is employed to successfully transfer a centimeter-scaled single-crystalline LiFe 5 O 8 thin film on polyimide substrate. Structural characterizations show that the transferred films have essentially no difference in comparison with the as-grown films with respect to the microstructure. In particular, the transferred LiFe 5 O 8 films exhibit excellent magnetic properties under various mechanical bending statuses and show excellent fatigue properties during the bending cycle tests. These results demonstrate that the improved transfer method provides an effective way to compose single-crystalline functional oxide thin films onto flexible substrates for applications in flexible and wearable electronics. © 2017 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

Topotactic reduction yielding black titanium oxide nanostructures as metallic electronic conductors.

Science.gov (United States)

Tominaka, Satoshi

2012-10-01

Detailed analyses of reduced, single crystal, rutile-type TiO(2) via high-resolution transmission electron microscopy (TEM) are reported which reveal that the reduction proceeds topotactically via interstitial diffusion of Ti ions at low temperature, around 350 °C. This important finding encouraged the production of various nanostructured reduced titanium oxides from TiO(2) precursors with morphology retention, and in the process, the synthesis of black titanium oxide nanorods using TiO(2) nanorods was demonstrated. Interestingly, as opposed to the semiconductive behavior of Ti(2)O(3) synthesized at high temperature, topotactically synthesized Ti(2)O(3) exhibits metallic electrical resistance, and the value at room temperature is quite low (topotactically synthesized Ti(2)O(3). This work shows that topotactically reduced titanium oxides can have fascinating properties as well as nanostructures.

Transmission electron microscopy characterization of Zircaloy-4 and ZIRLO™ oxide layers

International Nuclear Information System (INIS)

Gabory, Benoit de; Motta, Arthur T.; Wang, Ke

2015-01-01

Waterside corrosion of zirconium alloy nuclear fuel cladding varies markedly from one alloy to another. In addition, for a given alloy, the corrosion rate evolves during the corrosion process, most notably when the oxide loses its stability at the oxide transition. In an effort to understand the mechanism resulting in the variations of corrosion rate observed at the oxide transition, oxide layers formed on Zircaloy-4 and ZIRLO™ in high temperature water autoclave environments, and archived before and after the transition, are characterized using transmission electron microscopy. The study characterizes and compares the oxide morphology in both alloys at different times during the corrosion process, in an effort to understand the oxide growth mechanism for these alloys. Results show that the oxide is mainly composed of monoclinic ZrO 2 , with a preponderance of columnar oxide grains which extend to the oxide/metal interface. The oxide formed right after the transition has occurred, exhibits a 150 nm-wide layer of small equiaxed grains with high tetragonal oxide fraction. This layer has a similar morphology and structure as the first oxide layer formed (observed near the oxide/water interface). A study of the oxygen-rich region near the oxide/metal interface reveals a complex structure of different phases at different stages of corrosion. The interface exhibits an intermediate layer, identified as ZrO, a discontinuous layer of “blocky” Zr 3 O grains embedded in the ZrO layer, and a suboxide layer corresponding to an oxygen saturated solid solution in the metal matrix side. The thickness of this interfacial layer decreased markedly at the transition. Hydrides are also observed in that region, with a definite orientation relationship with the matrix. The observations of the oxide/metal interface are qualitatively similar for the two alloys but quantitatively different. The incorporation of intermetallic precipitates into the oxide layer is also studied, and

L-ascorbate attenuates methamphetamine neurotoxicity through enhancing the induction of endogenous heme oxygenase-1.

Science.gov (United States)

Huang, Ya-Ni; Wang, Jiz-Yuh; Lee, Ching-Tien; Lin, Chih-Hung; Lai, Chien-Cheng; Wang, Jia-Yi

2012-12-01

Methamphetamine (METH) is a drug of abuse which causes neurotoxicity and increased risk of developing neurodegenerative diseases. We previously found that METH induces heme oxygenase (HO)-1 expression in neurons and glial cells, and this offers partial protection against METH toxicity. In this study, we investigated the effects of l-ascorbate (vitamin C, Vit. C) on METH toxicity and HO-1 expression in neuronal/glial cocultures. Cell viability and damage were evaluated by 3-(4,5-dimethylthianol-2-yl)-2,5 diphenyl tetrazolium bromide (MTT) reduction and lactate dehydrogenase (LDH) release, respectively. Neuronal and glial localization of HO-1 were identified by double immunofluorescence staining. Reactive oxygen species (ROS) production was measured using the fluorochrome 2',7'-dichlorofluorescin diacetate. HO-1 mRNA and protein expression were examined by RT-qPCR and Western blotting, respectively. Results show that Vit. C induced HO-1 mRNA and protein expressions in time- and concentration-dependent manners. Inhibition of p38 mitogen-activated protein kinase (MAPK) but not extracellular signal-regulated kinase (ERK) significantly blocked induction of HO-1 by Vit. C. HO-1 mRNA and protein expressions were significantly elevated by a combination of Vit. C and METH, compared to either Vit. C or METH alone. Pretreatment with Vit. C enhanced METH-induced HO-1 expression and attenuated METH-induced ROS production and neurotoxicity. Pharmacological inhibition of HO activity abolished suppressive effects of Vit. C on METH-induced ROS production and attenuated neurotoxicity. We conclude that induction of HO-1 expression contributes to the attenuation of METH-induced ROS production and neurotoxicity by Vit. C. We suggest that HO-1 induction by Vit. C may serve as a strategy to alleviate METH neurotoxicity. Copyright © 2012 Elsevier Inc. All rights reserved.

Modifying welding process parameters can reduce the neurotoxic potential of manganese-containing welding fumes.

Science.gov (United States)

Sriram, Krishnan; Lin, Gary X; Jefferson, Amy M; Stone, Samuel; Afshari, Aliakbar; Keane, Michael J; McKinney, Walter; Jackson, Mark; Chen, Bean T; Schwegler-Berry, Diane; Cumpston, Amy; Cumpston, Jared L; Roberts, Jenny R; Frazer, David G; Antonini, James M

2015-02-03

Welding fumes (WF) are a complex mixture of toxic metals and gases, inhalation of which can lead to adverse health effects among welders. The presence of manganese (Mn) in welding electrodes is cause for concern about the potential development of Parkinson's disease (PD)-like neurological disorder. Consequently, from an occupational safety perspective, there is a critical need to prevent adverse exposures to WF. As the fume generation rate and physicochemical characteristics of welding aerosols are influenced by welding process parameters like voltage, current or shielding gas, we sought to determine if changing such parameters can alter the fume profile and consequently its neurotoxic potential. Specifically, we evaluated the influence of voltage on fume composition and neurotoxic outcome. Rats were exposed by whole-body inhalation (40 mg/m(3); 3h/day × 5 d/week × 2 weeks) to fumes generated by gas-metal arc welding using stainless steel electrodes (GMA-SS) at standard/regular voltage (25 V; RVSS) or high voltage (30 V; HVSS). Fumes generated under these conditions exhibited similar particulate morphology, appearing as chain-like aggregates; however, HVSS fumes comprised of a larger fraction of ultrafine particulates that are generally considered to be more toxic than their fine counterparts. Paradoxically, exposure to HVSS fumes did not elicit dopaminergic neurotoxicity, as monitored by the expression of dopaminergic and PD-related markers. We show that the lack of neurotoxicity is due to reduced solubility of Mn in HVSS fumes. Our findings show promise for process control procedures in developing prevention strategies for Mn-related neurotoxicity during welding; however, it warrants additional investigations to determine if such modifications can be suitably adapted at the workplace to avert or reduce adverse neurological risks. Published by Elsevier Ireland Ltd.

Modifying welding process parameters can reduce the neurotoxic potential of manganese-containing welding fumes

International Nuclear Information System (INIS)

Sriram, Krishnan; Lin, Gary X.; Jefferson, Amy M.; Stone, Samuel; Afshari, Aliakbar; Keane, Michael J.; McKinney, Walter; Jackson, Mark; Chen, Bean T.; Schwegler-Berry, Diane; Cumpston, Amy; Cumpston, Jared L.; Roberts, Jenny R.; Frazer, David G.; Antonini, James M.

2015-01-01

Welding fumes (WF) are a complex mixture of toxic metals and gases, inhalation of which can lead to adverse health effects among welders. The presence of manganese (Mn) in welding electrodes is cause for concern about the potential development of Parkinson’s disease (PD)-like neurological disorder. Consequently, from an occupational safety perspective, there is a critical need to prevent adverse exposures to WF. As the fume generation rate and physicochemical characteristics of welding aerosols are influenced by welding process parameters like voltage, current or shielding gas, we sought to determine if changing such parameters can alter the fume profile and consequently its neurotoxic potential. Specifically, we evaluated the influence of voltage on fume composition and neurotoxic outcome. Rats were exposed by whole-body inhalation (40 mg/m 3 ; 3 h/day × 5 d/week × 2 weeks) to fumes generated by gas–metal arc welding using stainless steel electrodes (GMA-SS) at standard/regular voltage (25 V; RVSS) or high voltage (30 V; HVSS). Fumes generated under these conditions exhibited similar particulate morphology, appearing as chain-like aggregates; however, HVSS fumes comprised of a larger fraction of ultrafine particulates that are generally considered to be more toxic than their fine counterparts. Paradoxically, exposure to HVSS fumes did not elicit dopaminergic neurotoxicity, as monitored by the expression of dopaminergic and PD-related markers. We show that the lack of neurotoxicity is due to reduced solubility of Mn in HVSS fumes. Our findings show promise for process control procedures in developing prevention strategies for Mn-related neurotoxicity during welding; however, it warrants additional investigations to determine if such modifications can be suitably adapted at the workplace to avert or reduce adverse neurological risks

Effect of oxygen deficiency on electronic properties and local structure of amorphous tantalum oxide thin films

Energy Technology Data Exchange (ETDEWEB)

Denny, Yus Rama [Department of Physics Education, University of Sultan Ageng Tirtayasa, Banten 42435 (Indonesia); Firmansyah, Teguh [Department of Electrical Engineering, University of Sultan Ageng Tirtayasa, Banten 42435 (Indonesia); Oh, Suhk Kun [Department of Physics, Chungbuk National University, Cheongju 28644 (Korea, Republic of); Kang, Hee Jae, E-mail: hjkang@cbu.ac.kr [Department of Physics, Chungbuk National University, Cheongju 28644 (Korea, Republic of); Yang, Dong-Seok [Department of Physics Education, Chungbuk National University, Cheongju 28644 (Korea, Republic of); Heo, Sung; Chung, JaeGwan; Lee, Jae Cheol [Analytical Engineering Center, Samsung Advanced Institute of Technology, Suwon 16678 (Korea, Republic of)

2016-10-15

Highlights: • The effect of oxygen flow rate on electronic properties and local structure of tantalum oxide thin films was studied. • The oxygen deficiency induced the nonstoichiometric state a-TaOx. • A small peak at 1.97 eV above the valence band side appeared on nonstoichiometric Ta{sub 2}O{sub 5} thin films. • The oxygen flow rate can change the local electronic structure of tantalum oxide thin films. - Abstract: The dependence of electronic properties and local structure of tantalum oxide thin film on oxygen deficiency have been investigated by means of X-ray photoelectron spectroscopy (XPS), Reflection Electron Energy Loss Spectroscopy (REELS), and X-ray absorption spectroscopy (XAS). The XPS results showed that the oxygen flow rate change results in the appearance of features in the Ta 4f at the binding energies of 23.2 eV, 24.4 eV, 25.8, and 27.3 eV whose peaks are attributed to Ta{sup 1+}, Ta{sup 2+}, Ta{sup 3+}/Ta{sup 4+}, and Ta{sup 5+}, respectively. The presence of nonstoichiometric state from tantalum oxide (TaOx) thin films could be generated by the oxygen vacancies. In addition, XAS spectra manifested both the increase of coordination number of the first Ta-O shell and a considerable reduction of the Ta-O bond distance with the decrease of oxygen deficiency.

A study of internal oxidation in carburized steels by glow discharge optical emission spectroscopy and scanning electron microscopy

International Nuclear Information System (INIS)

An, X; Cawley, J.; Rainforth, W.M.; Chen, L.

2003-01-01

The internal oxidation of Cr-Mn carburizing steel was studied. Internal oxidation was induced using a commercial carburizing process. Sputter erosion coupled with glow discharge optical emission spectroscopy (GDOES) was used to determine the depth profile elemental distribution within the internal oxidation layer (<10 μm). In addition, scanning electron microscopy (SEM) equipped with energy dispersive spectrometer (EDS) studies were carried out on selected sputter eroded surfaces. Oxide type was identified primarily by transmission electron microscopy (TEM). The carburized surface was found to consist of a continuous oxide layer, followed by a complex internal oxidation layer, where Cr and Mn oxides were found to populate grain boundaries in a globular form in the near surface region. At greater depths (5-10 μm), Si oxides formed as a grain boundary network. The internal oxides (mainly complex oxides) grew quickly during the initial stages of the carburizing process (2 h, 800 deg. C+3 h, 930 deg. C). GDOES proved to be an excellent tool for the quantification of oxidation and element distribution as a function of depth, particularly when combined with SEM and TEM to identify oxide type and morphology

Uranium oxide nanocrystals by microwave-assisted thermal decomposition. Electronic and structural properties

Energy Technology Data Exchange (ETDEWEB)

Leduc, Jennifer; Mathur, Sanjay [Institute of Inorganic Chemistry, University of Cologne (Germany); Pacold, Joseph I.; Shuh, David K. [Chemical Sciences Division, The Glenn T. Seaborg Center, Lawrence Berkeley National Laboratory, Berkeley, CA (United States); Dong, Chung-Li [Department of Physics, Tamkang University, Tamsui, Taiwan (China)

2018-01-17

Uranium oxides have attracted much attention not only in the context of nuclear energy generation but also for their application as pristine catalysts or as supports for other (transition metal) oxides and (precious) metals. Their propensity to adopt high coordination numbers and manifest multiple oxidation states (from +II to +VI) makes them attractive candidates for catalyzed transformation reactions. Herein, we report a new synthesis route to phase-pure, crystalline UO{sub 2} nanoparticles via microwave-assisted decomposition of a molecular uranium(IV) precursor. The electronic structure and optical absorption properties of these nanocrystals were investigated using spectroscopic methods to evaluate their suitability for photo(electro)catalytic applications. (copyright 2018 WILEY-VCH Verlag GmbH and Co. KGaA, Weinheim)

Uranium oxide nanocrystals by microwave-assisted thermal decomposition. Electronic and structural properties

International Nuclear Information System (INIS)

Leduc, Jennifer; Mathur, Sanjay; Pacold, Joseph I.; Shuh, David K.; Dong, Chung-Li

2018-01-01

Uranium oxides have attracted much attention not only in the context of nuclear energy generation but also for their application as pristine catalysts or as supports for other (transition metal) oxides and (precious) metals. Their propensity to adopt high coordination numbers and manifest multiple oxidation states (from +II to +VI) makes them attractive candidates for catalyzed transformation reactions. Herein, we report a new synthesis route to phase-pure, crystalline UO 2 nanoparticles via microwave-assisted decomposition of a molecular uranium(IV) precursor. The electronic structure and optical absorption properties of these nanocrystals were investigated using spectroscopic methods to evaluate their suitability for photo(electro)catalytic applications. (copyright 2018 WILEY-VCH Verlag GmbH and Co. KGaA, Weinheim)

Reduced coupling of oxidative phosphorylation in vivo precedes electron transport chain defects due to mild oxidative stress in mice.

Directory of Open Access Journals (Sweden)

Michael P Siegel

Full Text Available Oxidative stress and mitochondrial function are at the core of many degenerative conditions. However, the interaction between oxidative stress and in vivo mitochondrial function is unclear. We used both pharmacological (2 week paraquat (PQ treatment of wild type mice and transgenic (mice lacking Cu, Zn-superoxide dismutase (SOD1(-/- models to test the effect of oxidative stress on in vivo mitochondrial function in skeletal muscle. Magnetic resonance and optical spectroscopy were used to measure mitochondrial ATP and oxygen fluxes and cell energetic state. In both models of oxidative stress, coupling of oxidative phosphorylation was significantly lower (lower P/O at rest in vivo in skeletal muscle and was dose-dependent in the PQ model. Despite this reduction in efficiency, in vivo mitochondrial phosphorylation capacity (ATPmax was maintained in both models, and ex vivo mitochondrial respiration in permeabilized muscle fibers was unchanged following PQ treatment. In association with the reduced P/O, PQ treatment led to a dose-dependent reduction in PCr/ATP ratio and increased phosphorylation of AMPK. These results indicate that oxidative stress uncouples oxidative phosphorylation in vivo and results in energetic stress in the absence of defects in the mitochondrial electron transport chain.

Corneal neurotoxicity due to topical benzalkonium chloride.

Science.gov (United States)

Sarkar, Joy; Chaudhary, Shweta; Namavari, Abed; Ozturk, Okan; Chang, Jin-Hong; Yco, Lisette; Sonawane, Snehal; Khanolkar, Vishakha; Hallak, Joelle; Jain, Sandeep

2012-04-06

The aim of this study was to determine and characterize the effect of topical application of benzalkonium chloride (BAK) on corneal nerves in vivo and in vitro. Thy1-YFP+ neurofluorescent mouse eyes were treated topically with vehicle or BAK (0.01% or 0.1%). Wide-field stereofluorescence microscopy was performed to sequentially image the treated corneas in vivo every week for 4 weeks, and changes in stromal nerve fiber density (NFD) and aqueous tear production were determined. Whole-mount immunofluorescence staining of corneas was performed with antibodies to axonopathy marker SMI-32. Western immunoblot analyses were performed on trigeminal ganglion and corneal lysates to determine abundance of proteins associated with neurotoxicity and regeneration. Compartmental culture of trigeminal ganglion neurons was performed in Campenot devices to determine whether BAK affects neurite outgrowth. BAK-treated corneas exhibited significantly reduced NFD and aqueous tear production, and increased inflammatory cell infiltration and fluorescein staining at 1 week (P reduction in neurites occurred after BAK addition to compartmental cultures of dissociated trigeminal ganglion cells. Although both BAK doses (0.0001% and 0.001%) reduced nerve fiber length, the reduction was significantly more with the higher dose (P < 0.001). Topical application of BAK to the eye causes corneal neurotoxicity, inflammation, and reduced aqueous tear production.

Ameliorating effects of aged garlic extracts against Aβ-induced neurotoxicity and cognitive impairment

Science.gov (United States)

2013-01-01

Background In vitro antioxidant activities and neuron-like PC12 cell protective effects of solvent fractions from aged garlic extracts were investigated to evaluate their anti-amnesic functions. Ethyl acetate fractions of aged garlic had higher total phenolics than other fractions. Methods Antioxidant activities of ethyl acetate fractions from aged garlic were examined using 2,2'-azino-bis(3-ethylbenzthiazoline-6-sulfonic acid) diammonium salt (ABTS) and malondialdehyde (MDA) inhibitory effect using mouse whole brain homogenates. Levels of cellular oxidative stress as reactive oxygen species (ROS) accumulation were measured using 2',7'-dichlorofluorescein diacetate (DCF-DA). PC12 cell viability was investigated by 3-[4,5-dimethythiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MTT) and lactate dehydtrogenase (LDH) assay. The learning and memory impairment in institute of cancer research (ICR) mice was induced by neurotoxic amyloid beta protein (Aβ) to investigate in vivo anti-amnesic effects of aged garlic extracts by using Y-maze and passive avoidance tests. Results We discovered that ethyl acetate fractions showed the highest ABTS radical scavenging activity and MDA inhibitory effect. Intracellular ROS accumulation resulting from Aβ treatment in PC12 cells was significantly reduced when ethyl acetate fractions were presented in the medium compare to PC12 cells which was only treated with Aβ only. Ethyl acetate fractions from aged garlic extracts showed protection against Aβ-induced neurotoxicity. Pre-administration with aged garlic extracts attenuated Aβ-induced learning and memory deficits in both in vivo tests. Conclusions Our findings suggest that aged garlic extracts with antioxidant activities may improve cognitive impairment against Aβ-induced neuronal deficit, and possess a wide range of beneficial activities for neurodegenerative disorders, notably Alzheimer's disease (AD). PMID:24134394

The one-electron oxidation of a dithiolate molecule: The importance of chemical intuition

International Nuclear Information System (INIS)

Bushnell, Eric A. C.; Burns, Thomas D.; Boyd, Russell J.

2014-01-01

A series of nine commonly used density functional methods were assessed to accurately predict the oxidation potential of the (C 2 H 2 S 2 −2 /C 2 H 2 S 2 •− ) redox couple. It was found that due to their greater tendency for charge delocalization the GGA functionals predict a structure where the radical electron is delocalized within the alkene backbone of C 2 H 2 S 2 •− , whereas the hybrid functionals and the reference QCISD/cc-pVTZ predict that the radical electron remains localized on the sulfurs. However, chemical intuition suggests that the results obtained with the GGA functionals should be correct. Indeed, with the use of the geometries obtained at the HCTH/6-311++G(3df,3pd) level of theory both the QCISD and hybrid DFT methods yield a molecule with a delocalized electron. Notably, this new molecule lies at least 53 kJ mol −1 lower in energy than the previously optimized one that had a localized radical. Using these new structures the calculated oxidation potential was found to be 2.71–2.97 V for the nine DFT functionals tested. The M06-L functional provided the best agreement with the QCISD/cc-pVTZ reference oxidation potential of 3.28 V

The one-electron oxidation of a dithiolate molecule: The importance of chemical intuition

Energy Technology Data Exchange (ETDEWEB)

Bushnell, Eric A. C.; Burns, Thomas D.; Boyd, Russell J., E-mail: russell.boyd@dal.ca [Department of Chemistry, Dalhousie University, Halifax, Nova Scotia B3H 4R2 (Canada)

2014-05-14

A series of nine commonly used density functional methods were assessed to accurately predict the oxidation potential of the (C{sub 2}H{sub 2}S{sub 2}{sup −2}/C{sub 2}H{sub 2}S{sub 2}{sup •−}) redox couple. It was found that due to their greater tendency for charge delocalization the GGA functionals predict a structure where the radical electron is delocalized within the alkene backbone of C{sub 2}H{sub 2}S{sub 2}{sup •−}, whereas the hybrid functionals and the reference QCISD/cc-pVTZ predict that the radical electron remains localized on the sulfurs. However, chemical intuition suggests that the results obtained with the GGA functionals should be correct. Indeed, with the use of the geometries obtained at the HCTH/6-311++G(3df,3pd) level of theory both the QCISD and hybrid DFT methods yield a molecule with a delocalized electron. Notably, this new molecule lies at least 53 kJ mol{sup −1} lower in energy than the previously optimized one that had a localized radical. Using these new structures the calculated oxidation potential was found to be 2.71–2.97 V for the nine DFT functionals tested. The M06-L functional provided the best agreement with the QCISD/cc-pVTZ reference oxidation potential of 3.28 V.

TRANSFORMATION OF DEVELOPMENTAL NEUROTOXICITY DATA INTO STRUCTURE-SEARCHABLE TOXML DATABASE IN SUPPORT OF STRUCTURE-ACTIVITY RELATIONSHIP (SAR) WORKFLOW.

Science.gov (United States)

Early hazard identification of new chemicals is often difficult due to lack of data on the novel material for toxicity endpoints, including neurotoxicity. At present, there are no structure searchable neurotoxicity databases. A working group was formed to construct a database to...

Intracystic interferon-α treatment leads to neurotoxicity in craniopharyngioma: case report.

Science.gov (United States)

Sharma, Julia; Bonfield, Christopher M; Singhal, Ash; Hukin, Juliette; Steinbok, Paul

2015-09-01

Craniopharyngioma is a benign, cystic suprasellar tumor that can be treated with intracystic chemotherapy. Interferon-α (IFN-α) has been gaining popularity as an intracystic treatment for craniopharyngioma because of its efficacy and supposed benign neurotoxicity profile. In this case report the authors describe a patient who, while receiving intracystic IFN-α, suffered a neurological event, which was believed to be related to drug leakage outside the cyst. This is the first report of a focal neurological deficit potentially attributable to intracystic IFN-α therapy, highlighting the fact that IFN-α may have neurotoxic effects on the central nervous system. Given this case and the results of a literature review, the authors suggest that a positive leak test is a relative contraindication to intracystic IFN-α treatment.

Insights into Parkinson's disease models and neurotoxicity using non-invasive imaging

International Nuclear Information System (INIS)

Sanchez-Pernaute, Rosario; Brownell, Anna-Liisa; Jenkins, Bruce G.; Isacson, Ole

2005-01-01

Loss of dopamine in the nigrostriatal system causes a severe impairment in motor function in patients with Parkinson's disease and in experimental neurotoxic models of the disease. We have used non-invasive imaging techniques such as positron emission tomography (PET) and functional magnetic resonance imaging (MRI) to investigate in vivo the changes in the dopamine system in neurotoxic models of Parkinson's disease. In addition to classic neurotransmitter studies, in these models, it is also possible to characterize associated and perhaps pathogenic factors, such as the contribution of microglia activation and inflammatory responses to neuronal damage. Functional imaging techniques are instrumental to our understanding and modeling of disease mechanisms, which should in turn lead to development of new therapies for Parkinson's disease and other neurodegenerative disorders

Oxide Thin-Film Electronics using All-MXene Electrical Contacts

KAUST Repository

Wang, Zhenwei

2018-02-23

2D MXenes have shown great promise in electrochemical and electromagnetic shielding applications. However, their potential use in electronic devices is significantly less explored. The unique combination of metallic conductivity and hydrophilic surface suggests that MXenes can also be promising in electronics and sensing applications. Here, it is shown that metallic Ti3C2 MXene with work function of 4.60 eV can make good electrical contact with both zinc oxide (ZnO) and tin monoxide (SnO) semiconductors, with negligible band offsets. Consequently, both n-type ZnO and p-type SnO thin-film transistors (TFTs) have been fabricated entirely using large-area MXene (Ti3C2) electrical contacts, including gate, source, and drain. The n- and p-type TFTs show balanced performance, including field-effect mobilities of 2.61 and 2.01 cm2 V−1 s−1 and switching ratios of 3.6 × 106 and 1.1 × 103, respectively. Further, complementary metal oxide semiconductor (CMOS) inverters are demonstrated. The CMOS inverters show large voltage gain of 80 and excellent noise margin of 3.54 V, which is 70.8% of the ideal value. Moreover, the operation of CMOS inverters is shown to be very stable under a 100 Hz square waveform input. The current results suggest that MXene (Ti3C2) can play an important role as contact material in nanoelectronics.

Ferrocene-Functionalized Graphene Oxide Nanosheets: Efficient Electronic Communication between Ferrocene Centers across Graphene Nanosheets

International Nuclear Information System (INIS)

Lu, Yizhong; Jiang, Yuanyuan; Wu, Haibin; Chen, Wei

2015-01-01

Highlights: • Graphene oxide (GO) nanosheets functionalized with ferrocenyl moieties (GO-Fc) are fabricated. • GO-Fc shows efficient electronic communication between ferrocene centers. • GO-Fc exhibits two pairs of voltammetric peaks with a large potential spacing of 0.515 V. • GO-Fc shows a broad absorption peak in the near-infrared range (∼ 1428 nm) at mixed valence. - Abstract: Graphene oxide (GO) nanosheets functionalized with ferrocenyl moieties (GO-Fc) were fabricated through strong covalent C−C bonds. The resulting hybrid showed efficient electronic communication between ferrocene centers due to the strong electron delocalization facilitated by the large pi-pi conjugated structure of graphene sheets. The obtained hybrid exhibited two pairs of voltammetric peaks with a large potential spacing of 0.515 V and a broad absorption peak in the near-infrared range (∼ 1428 nm) at mixed valence. The electrochemical and near IR spectroscopic features suggested a Class II/III behavior of the intervalence charge transfer. This work indicates clearly that strong electronic coupling between ferrocene centers can be easily realized across graphene nanosheets with sp 2 -hybridized carbon

Tuning of electronic properties and dynamical stability of graphene oxide with different functional groups

Science.gov (United States)

Dabhi, Shweta D.; Jha, Prafulla K.

2017-09-01

The structural, electronic and vibrational properties of graphene oxide (GO) with varying proportion of epoxy and hydroxyl functional groups have been studied using density functional theory. The functional groups and oxygen density have an obvious influence on the electronic and vibrational properties. The dependence of band gap on associated functional groups and oxygen density shows a possibility of tuning the band gap of graphene by varying the functional groups as well as oxidation level. The absorption of high oxygen content in graphene leads to the gap opening and resulting in a transition from semimetal to semiconductor. Phonon dispersion curves show no imaginary frequency or no softening of any phonon mode throughout the Brillouin zone which confirms the dynamical stability of all considered GO models. Different groups and different oxygen density result into the varying characteristics of phonon modes. The computed results show good agreement with the experimental observations. Our results present interesting possibilities for engineering the electronic properties of graphene and GO and impact the fabrication of new electronics.

Autophagy activation is involved in 3,4-methylenedioxymethamphetamine ('ecstasy'--induced neurotoxicity in cultured cortical neurons.

Directory of Open Access Journals (Sweden)

I-Hsun Li

Full Text Available Autophagic (type II cell death, characterized by the massive accumulation of autophagic vacuoles in the cytoplasm of cells, has been suggested to play pathogenetic roles in cerebral ischemia, brain trauma, and neurodegenerative disorders. 3,4-Methylenedioxymethamphetamine (MDMA or ecstasy is an illicit drug causing long-term neurotoxicity in the brain. Apoptotic (type I and necrotic (type III cell death have been implicated in MDMA-induced neurotoxicity, while the role of autophagy in MDMA-elicited neurotoxicity has not been investigated. The present study aimed to evaluate the occurrence and contribution of autophagy to neurotoxicity in cultured rat cortical neurons challenged with MDMA. Autophagy activation was monitored by expression of microtubule-associated protein 1 light chain 3 (LC3; an autophagic marker using immunofluorescence and western blot analysis. Here, we demonstrate that MDMA exposure induced monodansylcadaverine (MDC- and LC3B-densely stained autophagosome formation and increased conversion of LC3B-I to LC3B-II, coinciding with the neurodegenerative phase of MDMA challenge. Autophagy inhibitor 3-methyladenine (3-MA pretreatment significantly attenuated MDMA-induced autophagosome accumulation, LC3B-II expression, and ameliorated MDMA-triggered neurite damage and neuronal death. In contrast, enhanced autophagy flux by rapamycin or impaired autophagosome clearance by bafilomycin A1 led to more autophagosome accumulation in neurons and aggravated neurite degeneration, indicating that excessive autophagosome accumulation contributes to MDMA-induced neurotoxicity. Furthermore, MDMA induced phosphorylation of AMP-activated protein kinase (AMPK and its downstream unc-51-like kinase 1 (ULK1, suggesting the AMPK/ULK1 signaling pathway might be involved in MDMA-induced autophagy activation.

Involvement of Programmed Cell Death in Neurotoxicity of Metallic Nanoparticles: Recent Advances and Future Perspectives

Science.gov (United States)

Song, Bin; Zhou, Ting; Liu, Jia; Shao, LongQuan

2016-11-01

The widespread application of metallic nanoparticles (NPs) or NP-based products has increased the risk of exposure to NPs in humans. The brain is an important organ that is more susceptible to exogenous stimuli. Moreover, any impairment to the brain is irreversible. Recently, several in vivo studies have found that metallic NPs can be absorbed into the animal body and then translocated into the brain, mainly through the blood-brain barrier and olfactory pathway after systemic administration. Furthermore, metallic NPs can cross the placental barrier to accumulate in the fetal brain, causing developmental neurotoxicity on exposure during pregnancy. Therefore, metallic NPs become a big threat to the brain. However, the mechanisms underlying the neurotoxicity of metallic NPs remain unclear. Programmed cell death (PCD), which is different from necrosis, is defined as active cell death and is regulated by certain genes. PCD can be mainly classified into apoptosis, autophagy, necroptosis, and pyroptosis. It is involved in brain development, neurodegenerative disorders, psychiatric disorders, and brain injury. Given the pivotal role of PCD in neurological functions, we reviewed relevant articles and tried to summarize the recent advances and future perspectives of PCD involvement in the neurotoxicity of metallic NPs, with the purpose of comprehensively understanding the neurotoxic mechanisms of NPs.

Nitric oxide: a physiologic messenger.

Science.gov (United States)

Lowenstein, C J; Dinerman, J L; Snyder, S H

1994-02-01

To review the physiologic role of nitric oxide, an unusual messenger molecule that mediates blood vessel relaxation, neurotransmission, and pathogen suppression. A MEDLINE search of articles published from 1987 to 1993 that addressed nitric oxide and the enzyme that synthesizes it, nitric oxide synthase. Animal and human studies were selected from 3044 articles to analyze the clinical importance of nitric oxide. Descriptions of the structure and function of nitric oxide synthase were selected to show how nitric oxide acts as a biological messenger molecule. Biochemical and physiologic studies were analyzed if the same results were found by three or more independent observers. Two major classes of nitric oxide synthase enzymes produce nitric oxide. The constitutive isoforms found in endothelial cells and neurons release small amounts of nitric oxide for brief periods to signal adjacent cells, whereas the inducible isoform found in macrophages releases large amounts of nitric oxide continuously to eliminate bacteria and parasites. By diffusing into adjacent cells and binding to enzymes that contain iron, nitric oxide plays many important physiologic roles. It regulates blood pressure, transmits signals between neurons, and suppresses pathogens. Excess amounts, however, can damage host cells, causing neurotoxicity during strokes and causing the hypotension associated with sepsis. Nitric oxide is a simple molecule with many physiologic roles in the cardiovascular, neurologic, and immune systems. Although the general principles of nitric oxide synthesis are known, further research is necessary to determine what role it plays in causing disease.

From chemolithoautotrophs to electrolithoautotrophs: CO2 fixation by Fe(II)-oxidizing bacteria coupled with direct uptake of electrons from solid electron sources.

Science.gov (United States)

Ishii, Takumi; Kawaichi, Satoshi; Nakagawa, Hirotaka; Hashimoto, Kazuhito; Nakamura, Ryuhei

2015-01-01

At deep-sea vent systems, hydrothermal emissions rich in reductive chemicals replace solar energy as fuels to support microbial carbon assimilation. Until recently, all the microbial components at vent systems have been assumed to be fostered by the primary production of chemolithoautotrophs; however, both the laboratory and on-site studies demonstrated electrical current generation at vent systems and have suggested that a portion of microbial carbon assimilation is stimulated by the direct uptake of electrons from electrically conductive minerals. Here we show that chemolithoautotrophic Fe(II)-oxidizing bacterium, Acidithiobacillus ferrooxidans, switches the electron source for carbon assimilation from diffusible Fe(2+) ions to an electrode under the condition that electrical current is the only source of energy and electrons. Site-specific marking of a cytochrome aa3 complex (aa3 complex) and a cytochrome bc1 complex (bc1 complex) in viable cells demonstrated that the electrons taken directly from an electrode are used for O2 reduction via a down-hill pathway, which generates proton motive force that is used for pushing the electrons to NAD(+) through a bc1 complex. Activation of carbon dioxide fixation by a direct electron uptake was also confirmed by the clear potential dependency of cell growth. These results reveal a previously unknown bioenergetic versatility of Fe(II)-oxidizing bacteria to use solid electron sources and will help with understanding carbon assimilation of microbial components living in electronically conductive chimney habitats.

Magnetic, thermal and luminescence properties in room-temperature nanosecond electron-irradiated various metal oxide nanopowders

Science.gov (United States)

Sokovnin, S. Yu; Balezin, M. E.; Il’ves, V. G.

2018-03-01

By means of pulsed electron beam evaporation in vacuum of targets non-magnetic, in bulk state, Al2O3 and YSZ (ZrO2-8% Y2O3) oxides, magnetic nanopowders (NPs) with a high specific surface were produced. The NPs were subsequently irradiated in air by electrons with energy of 700 keV, using a URT-1 accelerator for 15 and 30 minutes. The magnetic, thermal, and pulsed cathodoluminescence (PCL) characteristics of NPs were measured before and after irradiation. It was established that the electron irradiation non-monotonically changes the magnetization of the pristine samples. To the contrary, a clear correlation between the intensity of PCL and the irradiation doses is found in the oxides. There was a decrease in the intensity of PCL after irradiation. Luminescent and thermal properties reflect the transformation of structural defects in NPs more strongly after the exposure to a pulsed electron beam in comparison with corresponding changes of the NPs magnetic response.

On the nature of organic and inorganic centers that bifurcate electrons, coupling exergonic and endergonic oxidation-reduction reactions.

Science.gov (United States)

Peters, John W; Beratan, David N; Schut, Gerrit J; Adams, Michael W W

2018-04-19

Bifurcating electrons to couple endergonic and exergonic electron-transfer reactions has been shown to have a key role in energy conserving redox enzymes. Bifurcating enzymes require a redox center that is capable of directing electron transport along two spatially separate pathways. Research into the nature of electron bifurcating sites indicates that one of the keys is the formation of a low potential oxidation state to satisfy the energetics required of the endergonic half reaction, indicating that any redox center (organic or inorganic) that can exist in multiple oxidation states with sufficiently separated redox potentials should be capable of electron bifurcation. In this Feature Article, we explore a paradigm for bifurcating electrons down independent high and low potential pathways, and describe redox cofactors that have been demonstrated or implicated in driving this unique biochemistry.

A novel method for qualitative analysis of edible oil oxidation using an electronic nose.

Science.gov (United States)

Xu, Lirong; Yu, Xiuzhu; Liu, Lei; Zhang, Rui

2016-07-01

An electronic nose (E-nose) was used for rapid assessment of the degree of oxidation in edible oils. Peroxide and acid values of edible oil samples were analyzed using data obtained by the American Oil Chemists' Society (AOCS) Official Method for reference. Qualitative discrimination between non-oxidized and oxidized oils was conducted using the E-nose technique developed in combination with cluster analysis (CA), principal component analysis (PCA), and linear discriminant analysis (LDA). The results from CA, PCA and LDA indicated that the E-nose technique could be used for differentiation of non-oxidized and oxidized oils. LDA produced slightly better results than CA and PCA. The proposed approach can be used as an alternative to AOCS Official Method as an innovative tool for rapid detection of edible oil oxidation. Copyright © 2016 Elsevier Ltd. All rights reserved.

Investigating the potential neurotoxicity of Ecstasy (MDMA): an imaging approach

NARCIS (Netherlands)

Reneman, Liesbeth; Booij, Jan; Majoie, Charles B. L. M.; van den Brink, Wim; den Heeten, Gerard J.

2001-01-01

Human users of 3,4-methylenedioxymethamphetamine (MDMA, 'Ecstasy') users may be at risk of developing MDMA-induced neuronal injury. Previously, no methods were available for directly evaluating the neurotoxic effects of MDMA in the living human brain. However, development of in vivo neuroimaging

Developmental neurotoxicity of different pesticides in PC-12 cells in vitro

Energy Technology Data Exchange (ETDEWEB)

Christen, Verena [University of Applied Sciences and Arts Northwestern Switzerland, School of Life Sciences, Gründenstrasse 40, CH-4132, Muttenz (Switzerland); Rusconi, Manuel; Crettaz, Pierre [Federal Office of Public Health, Division Chemical Products, 3003 Bern (Switzerland); Fent, Karl, E-mail: karl.fent@bluewin.ch [University of Applied Sciences and Arts Northwestern Switzerland, School of Life Sciences, Gründenstrasse 40, CH-4132, Muttenz (Switzerland); Swiss Federal Institute of Technology Zürich (ETH Zürich), Department of Environmental Systems Sciences, Institute of Biogeochemistry and Pollution Dynamics, CH-8092 Zürich (Switzerland)

2017-06-15

The detection of developmental neurotoxicity (DNT) of chemicals has high relevance for protection of human health. However, DNT of many pesticides is only little known. Furthermore, validated in vitro systems for assessment of DNT are not well established. Here we employed the rat phaeochromocytoma cell line PC-12 to evaluate DNT of 18 frequently used pesticides of different classes, including neonicotinoids, pyrethroids, organophosphates, organochlorines, as well as quaternary ammonium compounds, the organic compound used in pesticides, piperonyl butoxide, as well as the insect repellent diethyltoluamide (DEET). We determined the outgrowth of neurites in PC-12 cells co-treated with nerve growth factor and different concentrations of biocides for 5 days. Furthermore, we determined transcriptional alterations of selected genes that may be associated with DNT, such as camk2α and camk2β, gap-43, neurofilament-h, tubulin-α and tubulin-β. Strong and dose- dependent inhibition of neurite outgrowth was induced by azamethiphos and chlorpyrifos, and dieldrin and heptachlor, which was correlated with up-regulation of gap-43. No or only weak effects on neurite outgrowth and transcriptional alterations occurred for neonicotinoids acetamiprid, clothianidin, imidacloprid and thiamethoxam, the pyrethroids λ-cyhalothrin, cyfluthrin, deltamethrin, and permethrin, the biocidal disinfectants C12-C14-alkyl(ethylbenzyl)dimethylammonium (BAC), benzalkonium chloride and barquat (dimethyl benzyl ammonium chloride), and piperonyl butoxide and DEET. Our study confirms potential developmental neurotoxicity of some pesticides and provides first evidence that azamethiphos has the potential to act as a developmental neurotoxic compound. We also demonstrate that inhibition of neurite outgrowth and transcriptional alterations of gap-43 expression correlate, which suggests the employment of gap-43 expression as a biomarker for detection and initial evaluation of potential DNT of chemicals

Developmental neurotoxicity of different pesticides in PC-12 cells in vitro

International Nuclear Information System (INIS)

Christen, Verena; Rusconi, Manuel; Crettaz, Pierre; Fent, Karl

2017-01-01

The detection of developmental neurotoxicity (DNT) of chemicals has high relevance for protection of human health. However, DNT of many pesticides is only little known. Furthermore, validated in vitro systems for assessment of DNT are not well established. Here we employed the rat phaeochromocytoma cell line PC-12 to evaluate DNT of 18 frequently used pesticides of different classes, including neonicotinoids, pyrethroids, organophosphates, organochlorines, as well as quaternary ammonium compounds, the organic compound used in pesticides, piperonyl butoxide, as well as the insect repellent diethyltoluamide (DEET). We determined the outgrowth of neurites in PC-12 cells co-treated with nerve growth factor and different concentrations of biocides for 5 days. Furthermore, we determined transcriptional alterations of selected genes that may be associated with DNT, such as camk2α and camk2β, gap-43, neurofilament-h, tubulin-α and tubulin-β. Strong and dose- dependent inhibition of neurite outgrowth was induced by azamethiphos and chlorpyrifos, and dieldrin and heptachlor, which was correlated with up-regulation of gap-43. No or only weak effects on neurite outgrowth and transcriptional alterations occurred for neonicotinoids acetamiprid, clothianidin, imidacloprid and thiamethoxam, the pyrethroids λ-cyhalothrin, cyfluthrin, deltamethrin, and permethrin, the biocidal disinfectants C12-C14-alkyl(ethylbenzyl)dimethylammonium (BAC), benzalkonium chloride and barquat (dimethyl benzyl ammonium chloride), and piperonyl butoxide and DEET. Our study confirms potential developmental neurotoxicity of some pesticides and provides first evidence that azamethiphos has the potential to act as a developmental neurotoxic compound. We also demonstrate that inhibition of neurite outgrowth and transcriptional alterations of gap-43 expression correlate, which suggests the employment of gap-43 expression as a biomarker for detection and initial evaluation of potential DNT of chemicals

Microfabrication of passive electronic components with printed graphene-oxide deposition

Science.gov (United States)

Sinar, Dogan; Knopf, George K.; Nikumb, Suwas

2014-03-01

Flexible electronic circuitry is an emerging technology that will significantly impact the future of healthcare and medicine, food safety inspection, environmental monitoring, and public security. Recent advances in drop-on-demand printing technology and electrically conductive inks have enabled simple electronic circuits to be fabricated on mechanically flexible polymers, paper, and bioresorbable silk. Research has shown that graphene, and its derivative formulations, can be used to create low-cost electrically conductive inks. Graphene is a one atom thick two-dimensional layer composed of carbon atoms arranged in a hexagonal lattice forming a material with very high fracture strength, high Young's Modulus, and low electrical resistance. Non-conductive graphene-oxide (GO) inks can also be synthesized from inexpensive graphite powders. Once deposited on the flexible substrate the electrical conductivity of the printed GO microcircuit traces can be restored through thermal reduction. In this paper, a femtosecond laser with a wavelength of 775nm and pulse width of 120fs is used to transform the non-conductive printed GO film into electrically conductive oxygen reduced graphene-oxide (rGO) passive electronic components by the process of laser assisted thermal reduction. The heat affected zone produced during the process was minimized because of the femtosecond pulsed laser. The degree of conductivity exhibited by the microstructure is directly related to the laser power level and exposure time. Although rGO films have higher resistances than pristine graphene, the ability to inkjet print capacitive elements and modify local resistive properties provides for a new method of fabricating sensor microcircuits on a variety of substrate surfaces.

Heterojunction oxide thin-film transistors with unprecedented electron mobility grown from solution

KAUST Repository

Faber, Hendrik; Das, Satyajit; Lin, Yen-Hung; Pliatsikas, Nikos; Zhao, Kui; Kehagias, Thomas; Dimitrakopulos, George; Amassian, Aram; Patsalas, Panos A.; Anthopoulos, Thomas D.

2017-01-01

with the extrinsic electron transport properties of the often defect-prone oxides. We overcome this limitation by replacing the single-layer semiconductor channel with a low-dimensional, solution-grown In2O3/ZnO heterojunction. We find that In2O3/ZnO transistors

Transmission Electron Microscopy Studies of Electron-Selective Titanium Oxide Contacts in Silicon Solar Cells

KAUST Repository

Ali, Haider

2017-08-15

In this study, the cross-section of electron-selective titanium oxide (TiO2) contacts for n-type crystalline silicon solar cells were investigated by transmission electron microscopy. It was revealed that the excellent cell efficiency of 21.6% obtained on n-type cells, featuring SiO2/TiO2/Al rear contacts and after forming gas annealing (FGA) at 350°C, is due to strong surface passivation of SiO2/TiO2 stack as well as low contact resistivity at the Si/SiO2/TiO2 heterojunction. This can be attributed to the transformation of amorphous TiO2 to a conducting TiO2-x phase. Conversely, the low efficiency (9.8%) obtained on cells featuring an a-Si:H/TiO2/Al rear contact is due to severe degradation of passivation of the a-Si:H upon FGA.

In Zucker Diabetic Fatty Rats, Subclinical Diabetic Neuropathy Increases In Vivo Lidocaine Block Duration But Not In Vitro Neurotoxicity

NARCIS (Netherlands)

Lirk, Philipp; Flatz, Magdalena; Haller, Ingrid; Hausott, Barbara; Blumenthal, Stephan; Stevens, Markus F.; Suzuki, Suzuko; Klimaschewski, Lars; Gerner, Peter

2012-01-01

Background and Objectives: Application of local anesthetics may lead to nerve damage. Increasing evidence suggests that risk of neurotoxicity is higher in patients with diabetic peripheral neuropathy. In addition, block duration may be prolonged in neuropathy. We sought to investigate neurotoxicity

Two nitro derivatives of azabenzo[a]pyrene N-oxide: Electronic properties and their relation to mutagenic activity

Energy Technology Data Exchange (ETDEWEB)

Ostojić, Bojana D., E-mail: bostojic@chem.bg.ac.rs; Đorđević, Dragana S.

2015-03-21

Highlights: • Molecular properties of nitro isomers of azabenzo[a]pyrene N-oxide are investigated. • Stability, ionization potential, electron affinity, and polarizability are determined. • High quality DFT methods are employed. • Nitroreduction, oxidation, and polarizability are not crucial for mutagenicity. • Dipole moment and electronic charge distribution are important for characterization. - Abstract: The equilibrium geometries, relative energies, IR and Raman spectra, vertical ionization potentials (IP), vertical electron affinities (EA), dipole moments (μ), electronic dipole polarizabilities (α), and molecular electrostatic potentials (MEP) of two species that show very high mutagenicity, 1-nitro-6-azabenzo[a]pyrene N-oxide (1-N-6-ABPO) and 3-nitro-6-azabenzo[a]pyrene N-oxide (3-N-6-ABPO), are investigated by means of Density Functional Theory (DFT) using B3LYP functional with different basis sets. The 3-N-6-ABPO isomer was estimated to be much more mutagenic in Salmonella typhimurium tester strain TA98 (396 000 revertants/nmol) than 1-N-6-ABPO (36 100 revertants/nmol) (Fukuhara et al., 1992). The results show that for both isomers the structural, energetic, and vibrational properties are similar. The orientation of the nitro group with respect to the plane of the aromatic system as well as the nitroreduction and oxidation reaction and polarizability seem not be important for the determination of different mutagenic behavior of these isomers. However, the dipole moment of 3-N-6-ABPO is about 3 times that of 1-N-6-ABPO. The larger dipole moment and the different electronic charge distribution of 3-N-6-ABPO compared to 1-N-6-ABPO imply stronger electrostatic and inductive molecular interactions so that the active site of the enzyme involved in the mutagenic activation can more effectively bind 3-N-6-ABPO compared to 1-N-6-ABPO.

Enhanced oxidative stress and aberrant mitochondrial biogenesis in human neuroblastoma SH-SY5Y cells during methamphetamine induced apoptosis

International Nuclear Information System (INIS)

Wu, C.-W.; Ping, Y.-H.; Yen, J.-C.; Chang, C.-Y.; Wang, S.-F.; Yeh, C.-L.; Chi, C.-W.; Lee, H.-C.

2007-01-01

Methamphetamine (METH) is an abused drug that may cause psychiatric and neurotoxic damage, including degeneration of monoaminergic terminals and apoptosis of non-monoaminergic cells in Brain. The cellular and molecular mechanisms underlying these METH-induced neurotoxic effects remain to be clarified. In this study, we performed a time course assessment to investigate the effects of METH on intracellular oxidative stress and mitochondrial alterations in a human dopaminergic neuroblastoma SH-SY5Y cell line. We characterized that METH induces a temporal sequence of several cellular events including, firstly, a decrease in mitochondrial membrane potential within 1 h of the METH treatment, secondly, an extensive decline in mitochondrial membrane potential and increase in the level of reactive oxygen species (ROS) after 8 h of the treatment, thirdly, an increase in mitochondrial mass after the drug treatment for 24 h, and finally, a decrease in mtDNA copy number and mitochondrial proteins per mitochondrion as well as the occurrence of apoptosis after 48 h of the treatment. Importantly, vitamin E attenuated the METH-induced increases in intracellular ROS level and mitochondrial mass, and prevented METH-induced cell death. Our observations suggest that enhanced oxidative stress and aberrant mitochondrial biogenesis may play critical roles in METH-induced neurotoxic effects

Peroxisomes contribute to oxidative stress in neurons during doxorubicin-based chemotherapy.

Science.gov (United States)

Moruno-Manchon, Jose F; Uzor, Ndidi-Ese; Kesler, Shelli R; Wefel, Jeffrey S; Townley, Debra M; Nagaraja, Archana Sidalaghatta; Pradeep, Sunila; Mangala, Lingegowda S; Sood, Anil K; Tsvetkov, Andrey S

2018-01-01

Doxorubicin, a commonly used anti-neoplastic agent, causes severe neurotoxicity. Doxorubicin promotes thinning of the brain cortex and accelerates brain aging, leading to cognitive impairment. Oxidative stress induced by doxorubicin contributes to cellular damage. In addition to mitochondria, peroxisomes also generate reactive oxygen species (ROS) and promote cell senescence. Here, we investigated if doxorubicin affects peroxisomal homeostasis in neurons. We demonstrate that the number of peroxisomes is increased in doxorubicin-treated neurons and in the brains of mice which underwent doxorubicin-based chemotherapy. Pexophagy, the specific autophagy of peroxisomes, is downregulated in neurons, and peroxisomes produce more ROS. 2-hydroxypropyl-β-cyclodextrin (HPβCD), an activator of the transcription factor TFEB, which regulates expression of genes involved in autophagy and lysosome function, mitigates damage of pexophagy and decreases ROS production induced by doxorubicin. We conclude that peroxisome-associated oxidative stress induced by doxorubicin may contribute to neurotoxicity, cognitive dysfunction, and accelerated brain aging in cancer patients and survivors. Peroxisomes might be a valuable new target for mitigating neuronal damage caused by chemotherapy drugs and for slowing down brain aging in general. Copyright © 2017 Elsevier Inc. All rights reserved.

Neurotoxicity induced by alkyl nitrites: Impairment in learning/memory and motor coordination.

Science.gov (United States)

Cha, Hye Jin; Kim, Yun Ji; Jeon, Seo Young; Kim, Young-Hoon; Shin, Jisoon; Yun, Jaesuk; Han, Kyoungmoon; Park, Hye-Kyung; Kim, Hyung Soo

2016-04-21

Although alkyl nitrites are used as recreational drugs, there is only little research data regarding their effects on the central nervous system including their neurotoxicity. This study investigated the neurotoxicity of three representative alkyl nitrites (isobutyl nitrite, isoamyl nitrite, and butyl nitrite), and whether it affected learning/memory function and motor coordination in rodents. Morris water maze test was performed in mice after administrating the mice with varying doses of the substances in two different injection schedules of memory acquisition and memory retention. A rota-rod test was then performed in rats. All tested alkyl nitrites lowered the rodents' capacity for learning and memory, as assessed by both the acquisition and retention tests. The results of the rota-rod test showed that isobutyl nitrite in particular impaired motor coordination in chronically treated rats. The mice chronically injected with isoamyl nitrite also showed impaired function, while butyl nitrite had no significant effect. The results of the water maze test suggest that alkyl nitrites may impair learning and memory. Additionally, isoamyl nitrite affected the rodents' motor coordination ability. Collectively, our findings suggest that alkyl nitrites may induce neurotoxicity, especially on the aspect of learning and memory function. Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.

Age dependence of organophosphate and carbamate neurotoxicity in the postnatal rat: extrapolation to the human

International Nuclear Information System (INIS)

Vidair, Charles A.

2004-01-01

One important aspect of risk assessment for the organophosphate and carbamate pesticides is to determine whether their neurotoxicity occurs at lower dose levels in human infants compared to adults. Because these compounds probably exert their neurotoxic effects through the inhibition of acetylcholinesterase (AChE), the above question can be narrowed to whether the cholinesterase inhibition and neurotoxicity they produce is age-dependent, both in terms of the effects produced and potency. The rat is the animal model system most commonly used to address these issues. This paper first discusses the adequacy of the postnatal rat to serve as a model for neurodevelopment in the postnatal human, concluding that the two species share numerous pathways of postnatal neurodevelopment, and that the rat in the third postnatal week is the neurodevelopmental equivalent of the newborn human. Then, studies are discussed in which young and adult rats were dosed by identical routes with organophosphates or carbamates. Four pesticides were tested in rat pups in their third postnatal week: aldicarb, chlorpyrifos, malathion, and methamidophos. The first three, but not methamidophos, caused neurotoxicity at dose levels that ranged from 1.8- to 5.1-fold lower (mean 2.6-fold lower) in the 2- to 3-week-old rat compared to the adult. This estimate in the rat, based on a limited data set of three organophosphates and a single carbamate, probably represents the minimum difference in the neurotoxicity of an untested cholinesterase-inhibiting pesticide that should be expected between the human neonate and adult. For the organophosphates, the greater sensitivity of postnatal rats, and, by analogy, that expected for human neonates, is correlated with generally lower levels of the enzymes involved in organophosphate deactivation

iTRAQ proteomics analysis reveals that PI3K is highly associated with bupivacaine-induced neurotoxicity pathways.

Science.gov (United States)

Zhao, Wei; Liu, Zhongjie; Yu, Xujiao; Lai, Luying; Li, Haobo; Liu, Zipeng; Li, Le; Jiang, Shan; Xia, Zhengyuan; Xu, Shi-yuan

2016-02-01

Bupivacaine, a commonly used local anesthetic, has potential neurotoxicity through diverse signaling pathways. However, the key mechanism of bupivacaine-induced neurotoxicity remains unclear. Cultured human SH-SY5Y neuroblastoma cells were treated (bupivacaine) or untreated (control) with bupivacaine for 24 h. Compared to the control group, bupivacaine significantly increased cyto-inhibition, cellular reactive oxygen species, DNA damage, mitochondrial injury, apoptosis (increased TUNEL-positive cells, cleaved caspase 3, and Bcl-2/Bax), and activated autophagy (enhanced LC3II/LC3I ratio). To explore changes in protein expression and intercommunication among the pathways involved in bupivacaine-induced neurotoxicity, an 8-plex iTRAQ proteomic technique and bioinformatics analysis were performed. Compared to the control group, 241 differentially expressed proteins were identified, of which, 145 were up-regulated and 96 were down-regulated. Bioinformatics analysis of the cross-talk between the significant proteins with altered expression in bupivacaine-induced neurotoxicity indicated that phosphatidyl-3-kinase (PI3K) was the most frequently targeted protein in each of the interactions. We further confirmed these results by determining the downstream targets of the identified signaling pathways (PI3K, Akt, FoxO1, Erk, and JNK). In conclusion, our study demonstrated that PI3K may play a central role in contacting and regulating the signaling pathways that contribute to bupivacaine-induced neurotoxicity. © 2015 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

Rutin improves spatial memory in Alzheimer's disease transgenic mice by reducing Aβ oligomer level and attenuating oxidative stress and neuroinflammation.

Science.gov (United States)

Xu, Peng-Xin; Wang, Shao-Wei; Yu, Xiao-Lin; Su, Ya-Jing; Wang, Teng; Zhou, Wei-Wei; Zhang, He; Wang, Yu-Jiong; Liu, Rui-Tian

2014-05-01

Alzheimer's disease (AD) is a progressive, neurodegenerative disease characterized by extracellular β-amyloid (Aβ) plaques and intracellular neurofibrillary tangles in the brain. Aβ aggregation is closely associated with neurotoxicity, oxidative stress, and neuronal inflammation. The soluble Aβ oligomers are believed to be the most neurotoxic form among all forms of Aβ aggregates. We have previously reported a polyphenol compound rutin that could inhibit Aβ aggregation and cytotoxicity, attenuate oxidative stress, and decrease the production of nitric oxide and proinflammatory cytokines in vitro. In the current study, we investigated the effect of rutin on APPswe/PS1dE9 transgenic mice. Results demonstrated that orally administered rutin significantly attenuated memory deficits in AD transgenic mice, decreased oligomeric Aβ level, increased super oxide dismutase (SOD) activity and glutathione (GSH)/glutathione disulfide (GSSG) ratio, reduced GSSG and malondialdehyde (MDA) levels, downregulated microgliosis and astrocytosis, and decreased interleukin (IL)-1β and IL-6 levels in the brain. These results indicated that rutin is a promising agent for AD treatment because of its antioxidant, anti-inflammatory, and reducing Aβ oligomer activities. Copyright © 2014 Elsevier B.V. All rights reserved.

Tuning the Electronic Structure of Titanium Oxide Support to Enhance the Electrochemical Activity of Platinum Nanoparticles

KAUST Repository

Shi, Feifei

2013-09-11

Two times higher activity and three times higher stability in methanol oxidation reaction, a 0.12 V negative shift of the CO oxidation peak potential, and a 0.07 V positive shift of the oxygen reaction potential compared to Pt nanoparticles on pristine TiO2 support were achieved by tuning the electronic structure of the titanium oxide support of Pt nanoparticle catalysts. This was accomplished by adding oxygen vacancies or doping with fluorine. Experimental trends are interpreted in the context of an electronic structure model, showing an improvement in electrochemical activity when the Fermi level of the support material in Pt/TiOx systems is close to the Pt Fermi level and the redox potential of the reaction. The present approach provides guidance for the selection of the support material of Pt/TiOx systems and may be applied to other metal-oxide support materials, thus having direct implications in the design and optimization of fuel cell catalyst supports. © 2013 American Chemical Society.

Calcium-activated butyrylcholinesterase in human skin protects acetylcholinesterase against suicide inhibition by neurotoxic organophosphates

International Nuclear Information System (INIS)

Schallreuter, Karin U.; University of Bradford; Elwary, Souna M.; Parkin, Susan M.; Wood, John M.

2007-01-01

The human epidermis holds an autocrine acetylcholine production and degradation including functioning membrane integrated and cytosolic butyrylcholinesterase (BuchE). Here we show that BuchE activities increase 9-fold in the presence of calcium (0.5 x 10 -3 M) via a specific EF-hand calcium binding site, whereas acetylcholinesterase (AchE) is not affected. 45 Calcium labelling and computer simulation confirmed the presence of one EF-hand binding site per subunit which is disrupted by H 2 O 2 -mediated oxidation. Moreover, we confirmed the faster hydrolysis by calcium-activated BuchE using the neurotoxic organophosphate O-ethyl-O-(4-nitrophenyl)-phenylphosphonothioate (EPN). Considering the large size of the human skin with 1.8 m 2 surface area with its calcium gradient in the 10 -3 M range, our results implicate calcium-activated BuchE as a major protective mechanism against suicide inhibition of AchE by organophosphates in this non-neuronal tissue

Localized and collectivized behaviour of d-electrons in complicated titanium, vanadium and niobium oxides

International Nuclear Information System (INIS)

Bazuev, G.V.; Shvejkin, G.P.

1980-01-01

On the basis of investigation of electric and magnetic properties of oxide compounds of transition metals made are the conclusions on the degree of localization and delocalization of d-electrons in them. Generalized are the investigation results of complicated titanium, vanadium, niobium oxide compounds in low degrees of oxidation with rare earth and alkaline earth elements belonging to the two structural types: perovskite and pyrochlore. Presented are the results of investigations of perovskite-like solid solutions and of variable-content phases containing cations of transition metals in two different oxidation degrees: oxide niobium bronzes of two-valent europium and titanium bronzes of rare-earth elements, as well as Lnsub(1-x)Msub(x)Vsub(1-x)sup(3+)Vsub(x)sup(4+)Osub(3), where M is an alkaline earth element

Graphene Oxide-TiO2 Nanocomposite Films for Electron Transport Applications

Science.gov (United States)

Saleem, Abida; Ullah, Naveed; Khursheed, Kamran; Iqbal, Tahir; Shah, Saqlain A.; Asjad, Muhammad; Sarwar, Nazim; Saleem, Murtaza; Arshad, Muhammad

2018-03-01

Graphene oxide-titanium dioxide (GO-TiO2) nanocomposite thin films were prepared for application as the window layer of perovskite solar cells. Graphene oxide (GO) was prepared by a modified Hummer's method, and titanium dioxide (TiO2) nanoparticles were synthesized by hydrothermal solution method. Thin films of GO-TiO2 nanocomposite were prepared with different wt.% of GO by spin coating on indium tin oxide (ITO) substrate followed by annealing at 150°C. X-ray diffraction analysis revealed rutile phase of TiO2 nanostructures. The bandgap of the pure TiO2 thin film was found to be 3.5 eV, reducing to 2.9 eV for the GO-TiO2 nanocomposites with a red-shift towards higher wavelength. Furthermore, thermal postannealing at 400°C improved the transparency in the visible region and decreased the sheet resistance. Morphological and elemental analysis was performed by scanning electron microscopy and energy-dispersive x-ray spectroscopy, respectively. The current-voltage characteristic of the GO-TiO2 nanocomposites indicated Ohmic contact with the ITO substrate. The chemical composition of the as-synthesized GO-TiO2 nanocomposites was investigated by x-ray photoelectron spectroscopy (XPS). The results presented herein demonstrate a new, low-temperature solution-processing approach to obtain rGO-TiO2 composite material for use as the electron transport layer of perovskite solar cells.

Neurobehavioural and Neurotoxic Effects of L-ascorbic Acid and L ...

African Journals Online (AJOL)

Background: Lead is an environmental toxicant, occupational and environmental exposures remain a serious problem in developing and industrializing countries. Objective: This study is designed to investigate the effects of L-ascorbic acid and L-tryptophan on the neurotoxicity and neurobehavioural alterations in lead ...

Enhancement of endocannabinoid signaling protects against cocaine-induced neurotoxicity

International Nuclear Information System (INIS)

Vilela, Luciano R.; Gobira, Pedro H.; Viana, Thercia G.; Medeiros, Daniel C.; Ferreira-Vieira, Talita H.; Doria, Juliana G.; Rodrigues, Flávia; Aguiar, Daniele C.; Pereira, Grace S.; Massessini, André R.; Ribeiro, Fabíola M.; Oliveira, Antonio Carlos P. de; Moraes, Marcio F.D.; Moreira, Fabricio A.

2015-01-01

Cocaine is an addictive substance with a potential to cause deleterious effects in the brain. The strategies for treating its neurotoxicity, however, are limited. Evidence suggests that the endocannabinoid system exerts neuroprotective functions against various stimuli. Thus, we hypothesized that inhibition of fatty acid amide hydrolase (FAAH), the main enzyme responsible for terminating the actions of the endocannabinoid anandamide, reduces seizures and cell death in the hippocampus in a model of cocaine intoxication. Male Swiss mice received injections of endocannabinoid-related compounds followed by the lowest dose of cocaine that induces seizures, electroencephalographic activity and cell death in the hippocampus. The molecular mechanisms were studied in primary cell culture of this structure. The FAAH inhibitor, URB597, reduced cocaine-induced seizures and epileptiform electroencephalographic activity. The cannabinoid CB 1 receptor selective agonist, ACEA, mimicked these effects, whereas the antagonist, AM251, prevented them. URB597 also inhibited cocaine-induced activation and death of hippocampal neurons, both in animals and in primary cell culture. Finally, we investigated if the PI3K/Akt/ERK intracellular pathway, a cell surviving mechanism coupled to CB 1 receptor, mediated these neuroprotective effects. Accordingly, URB597 injection increased ERK and Akt phosphorylation in the hippocampus. Moreover, the neuroprotective effect of this compound was reversed by the PI3K inhibitor, LY294002. In conclusion, the pharmacological facilitation of the anandamide/CB1/PI3K signaling protects the brain against cocaine intoxication in experimental models. This strategy may be further explored in the development of treatments for drug-induced neurotoxicity. - Highlights: • Cocaine toxicity is characterized by seizures and hippocampal cell death. • The endocannabinoid anandamide acts as a brain protective mechanism. • Inhibition of anandamide hydrolysis attenuates

Enhancement of endocannabinoid signaling protects against cocaine-induced neurotoxicity

Energy Technology Data Exchange (ETDEWEB)

Vilela, Luciano R. [Graduate Program in Neuroscience, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, MG (Brazil); Gobira, Pedro H.; Viana, Thercia G. [Department of Pharmacology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, MG (Brazil); Medeiros, Daniel C.; Ferreira-Vieira, Talita H. [Department of Physiology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, MG (Brazil); Doria, Juliana G. [Graduate Program in Neuroscience, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, MG (Brazil); Rodrigues, Flávia [Department of Biochemistry and Immunology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, MG (Brazil); Aguiar, Daniele C. [Department of Pharmacology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, MG (Brazil); Pereira, Grace S.; Massessini, André R. [Department of Physiology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, MG (Brazil); Ribeiro, Fabíola M. [Department of Biochemistry and Immunology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, MG (Brazil); Oliveira, Antonio Carlos P. de [Department of Pharmacology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, MG (Brazil); Moraes, Marcio F.D., E-mail: mfdm@icb.ufmg.br [Department of Physiology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, MG (Brazil); Moreira, Fabricio A., E-mail: fabriciomoreira@icb.ufmg.br [Department of Pharmacology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, MG (Brazil)

2015-08-01

Cocaine is an addictive substance with a potential to cause deleterious effects in the brain. The strategies for treating its neurotoxicity, however, are limited. Evidence suggests that the endocannabinoid system exerts neuroprotective functions against various stimuli. Thus, we hypothesized that inhibition of fatty acid amide hydrolase (FAAH), the main enzyme responsible for terminating the actions of the endocannabinoid anandamide, reduces seizures and cell death in the hippocampus in a model of cocaine intoxication. Male Swiss mice received injections of endocannabinoid-related compounds followed by the lowest dose of cocaine that induces seizures, electroencephalographic activity and cell death in the hippocampus. The molecular mechanisms were studied in primary cell culture of this structure. The FAAH inhibitor, URB597, reduced cocaine-induced seizures and epileptiform electroencephalographic activity. The cannabinoid CB{sub 1} receptor selective agonist, ACEA, mimicked these effects, whereas the antagonist, AM251, prevented them. URB597 also inhibited cocaine-induced activation and death of hippocampal neurons, both in animals and in primary cell culture. Finally, we investigated if the PI3K/Akt/ERK intracellular pathway, a cell surviving mechanism coupled to CB{sub 1} receptor, mediated these neuroprotective effects. Accordingly, URB597 injection increased ERK and Akt phosphorylation in the hippocampus. Moreover, the neuroprotective effect of this compound was reversed by the PI3K inhibitor, LY294002. In conclusion, the pharmacological facilitation of the anandamide/CB1/PI3K signaling protects the brain against cocaine intoxication in experimental models. This strategy may be further explored in the development of treatments for drug-induced neurotoxicity. - Highlights: • Cocaine toxicity is characterized by seizures and hippocampal cell death. • The endocannabinoid anandamide acts as a brain protective mechanism. • Inhibition of anandamide hydrolysis

Atropa belladonna neurotoxicity: Implications to neurological disorders.

Science.gov (United States)

Kwakye, Gunnar F; Jiménez, Jennifer; Jiménez, Jessica A; Aschner, Michael

2018-06-01

Atropa belladonna, commonly known as belladonna or deadly nightshade, ranks among one of the most poisonous plants in Europe and other parts of the world. The plant contains tropane alkaloids including atropine, scopolamine, and hyoscyamine, which are used as anticholinergics in Food and Drug Administration (FDA) approved drugs and homeopathic remedies. These alkaloids can be very toxic at high dose. The FDA has recently reported that Hyland's baby teething tablets contain inconsistent amounts of Atropa belladonna that may have adverse effects on the nervous system and cause death in children, thus recalled the product in 2017. A greater understanding of the neurotoxicity of Atropa belladonna and its modification of genetic polymorphisms in the nervous system is critical in order to develop better treatment strategies, therapies, regulations, education of at-risk populations, and a more cohesive paradigm for future research. This review offers an integrated view of the homeopathy and neurotoxicity of Atropa belladonna in children, adults, and animal models as well as its implications to neurological disorders. Particular attention is dedicated to the pharmaco/toxicodynamics, pharmaco/toxicokinetics, pathophysiology, epidemiological cases, and animal studies associated with the effects of Atropa belladonna on the nervous system. Additionally, we discuss the influence of active tropane alkaloids in Atropa belladonna and other similar plants on FDA-approved therapeutic drugs for treatment of neurological disorders. Copyright © 2018. Published by Elsevier Ltd.

Neurotoxicity of cytarabine (Ara-C) in dorsal root ganglion neurons originates from impediment of mtDNA synthesis and compromise of mitochondrial function.

Science.gov (United States)

Zhuo, Ming; Gorgun, Murat F; Englander, Ella W

2018-06-01

Peripheral Nervous System (PNS) neurotoxicity caused by cancer drugs hinders attainment of chemotherapy goals. Due to leakiness of the blood nerve barrier, circulating chemotherapeutic drugs reach PNS neurons and adversely affect their function. Chemotherapeutic drugs are designed to target dividing cancer cells and mechanisms underlying their toxicity in postmitotic neurons remain to be fully clarified. The objective of this work was to elucidate progression of events triggered by antimitotic drugs in postmitotic neurons. For proof of mechanism study, we chose cytarabine (ara-C), an antimetabolite used in treatment of hematological cancers. Ara-C is a cytosine analog that terminates DNA synthesis. To investigate how ara-C affects postmitotic neurons, which replicate mitochondrial but not genomic DNA, we adapted a model of Dorsal Root Ganglion (DRG) neurons. We showed that DNA polymerase γ, which is responsible for mtDNA synthesis, is inhibited by ara-C and that sublethal ara-C exposure of DRG neurons leads to reduction in mtDNA content, ROS generation, oxidative mtDNA damage formation, compromised mitochondrial respiration and diminution of NADPH and GSH stores, as well as, activation of the DNA damage response. Hence, it is plausible that in ara-C exposed DRG neurons, ROS amplified by the high mitochondrial content shifts from physiologic to pathologic levels signaling stress to the nucleus. Combined, the findings suggest that ara-C neurotoxicity in DRG neurons originates in mitochondria and that continuous mtDNA synthesis and reliance on oxidative phosphorylation for energy needs sensitize the highly metabolic neurons to injury by mtDNA synthesis terminating cancer drugs. Copyright © 2018 Elsevier Inc. All rights reserved.

Low-voltage protonic/electronic hybrid indium zinc oxide synaptic transistors on paper substrates

International Nuclear Information System (INIS)

Wu, Guodong; Wan, Changjin; Wan, Qing; Zhou, Jumei; Zhu, Liqiang

2014-01-01

Low-voltage (1.5 V) indium zinc oxide (IZO)-based electric-double-layer (EDL) thin-film transistors (TFTs) gated by nanogranular proton conducting SiO 2 electrolyte films are fabricated on paper substrates. Both enhancement-mode and depletion-mode operation are obtained by tuning the thickness of the IZO channel layer. Furthermore, such flexible IZO protonic/electronic hybrid EDL TFTs can be used as artificial synapses, and synaptic stimulation response and short-term synaptic plasticity function are demonstrated. The protonic/electronic hybrid EDL TFTs on paper substrates proposed here are promising for low-power flexible paper electronics, artificial synapses and bioelectronics. (paper)

Electronic devices containing switchably conductive silicon oxides as a switching element and methods for production and use thereof

Science.gov (United States)

Tour, James M; Yao, Jun; Natelson, Douglas; Zhong, Lin; He, Tao

2013-11-26

In various embodiments, electronic devices containing switchably conductive silicon oxide as a switching element are described herein. The electronic devices are two-terminal devices containing a first electrical contact and a second electrical contact in which at least one of the first electrical contact or the second electrical contact is deposed on a substrate to define a gap region therebetween. A switching layer containing a switchably conductive silicon oxide resides in the the gap region between the first electical contact and the second electrical contact. The electronic devices exhibit hysteretic current versus voltage properties, enabling their use in switching and memory applications. Methods for configuring, operating and constructing the electronic devices are also presented herein.

Effects of soluble flavin on heterogeneous electron transfer between surface-exposed bacterial cytochromes and iron oxides

Energy Technology Data Exchange (ETDEWEB)

Wang, Zheming; Shi, Zhi; Shi, Liang; White, Gaye F.; Richardson, David J.; Clarke, Thomas A.; Fredrickson, Jim K.; Zachara, John M.

2015-08-25

Dissimilatory iron-reducing bacteria can utilize insoluble Fe(Mn)-oxides as a terminal electron acceptor under anaerobic conditions. For Shewanella species specifically, some evidence suggests that iron reduction is associated with the secretion of flavin mononucleotide (FMN) and riboflavin that are proposed to mediate electron transfer (Marsili et al., 2008). In this work, we used methyl viologen (MV•+)-encapsulated, porin-cytochrome complex (MtrCAB) embedded liposomes (MELs) as a synthetic model of the Shewanella outer membrane to investigate the proposed mediating behavior of secreted flavins. The reduction kinetics of goethite, hematite and lepidocrocite (200 µM) by MELs ([MV•+] ~ 42 µM and MtrABC ≤ 1 nM) were determined in the presence FMN at pH 7.0 in N2 atmosphere by monitoring the concentrations of MV•+ and FMN through their characteristic UV-visible absorption spectra. Experiments were performed where i) FMN and Fe(III)-oxide were mixed and then reacted with the reduced MELs and ii) FMN was reacted with the reduced MELs followed by addition of Fe(III)-oxide. The redox reactions proceeded in two steps: a fast step that was completed in a few seconds, and a slower one lasting over 400 seconds. For all three Fe(III)-oxides, the initial reaction rate in the presence of a low concentration of FMN (≤ 1 µM) was at least a factor of five faster than those with MELs alone, and orders of magnitude faster than those by FMNH2, suggesting that FMN may serve as a co-factor that enhances electron transfer from outer-membrane c-cytochromes to Fe(III)-oxides. The rate and extent of the initial reaction followed the order of lepidocrocite > hematite > goethite, the same as their reduction potentials, implying thermodynamic control on reaction rate. However, at higher FMN concentrations (> 1 µM), the reaction rates for both steps decreased and varied inversely with FMN concentration, indicating that FMN inhibited the MEL to Fe(III)-oxide electron transfer

A comprehensible need of zinc oxide varistors in electronics technology

International Nuclear Information System (INIS)

Mehmood, F.S.

2007-01-01

A range of varistors, in terms of break down voltage, is required to protect integrated circuits, automotive systems and other modern electronics against transient over-voltages. There is a progressing need for the development and advancement of rugged and reliable varistor capable and proficient of working in harsh and callous environment like automotive Industry where greater than before use of electronics technology has led to improvements in equipment performance and presentation. There is a comprehensible need to combine triumphant and successable models developed at different length scales into an integrated framework that can be used to drive new research and guide experimental efforts and device development. The review of ZnO varistor in particular and metal-oxide varistors (MOVs) in general is presented In this article. (author)

METAL OXIDE DOPED ANTIBACTERIAL POLYMERIC COATED TEXTILE MATERIALS AND ASSESSEMENT OF ANTIBACTERIAL ACTIVITY WITH ELECTRON SPIN RESONANCE

Directory of Open Access Journals (Sweden)

GEDIK Gorkem

2017-05-01

Full Text Available Antibacterial activity of a food conveyor belt is an essential property in some cases. However, every antibacterial chemical is not suitable to contact with food materials. Many metal oxides are suitable option for this purpose. The aim of this study was to investigate antibacterial properties of zinc oxide doped PVC polymer coated with electron spin resonance technique. Therefore, optimum zinc oxide containing PVC paste was prepared and applied to textile surface. Coating construction was designed as double layered, first layer did not contain antibacterial agent, thin second layer contained zinc oxide at 10-35% concentration. Oxygen radicals released from zinc oxide containing polymeric coated surface were spin trapped with DMPO (dimethylpyrroline-N-oxide spin trap and measured with Electron Spin Resonance (ESR. Besides conveyor belt samples, oxygen radical release from zinc oxide surface was measured with ESR under UV light and dark conditions. Oxygen radical release was determined even at dark conditions. Antibacterial properties were tested with ISO 22196 standard using Listeria innocua species. Measured antibacterial properties were related with ESR results. Higher concentration of zinc oxide resulted in higher antibacterial efficiency. DCFH-DA flourometric assay was carried out to determine oxidative stress insidebacteria. It is tought that, this technique will lead to decrease on the labour and time needed for conventional antibacterial tests.

Pulse radiolysis study of one electron oxidation of riboflavin

International Nuclear Information System (INIS)

Kishore, K.; Moorthy, P.N.; Guha, S.N.

1991-01-01

One electron oxidation of riboflavin (Rf) has been studied using various oxidising species such as Cl 2 -. , SO 4 -. and OH radicals. The transient species produced by the reaction of SO 4 -. with riboflavin gave spectra with λ m at 680 and 640 nm at pHs 4 and 7.1 respectively with a pK a at ∼ 6. Cl 2 -. radicals reacted with riboflavin to give a transient spectrum with λ m at 570 nm. The possibility of two sites viz. C-8 methyl group and the extended π-ring system of the molecule for oxidation reaction are discussed. The reaction of Cl 2 -. with riboflavin is an equilibrium from which the redox potential for the Rf +. /Rf couple has been evaluated to be 2.28 V vs NHE. OH radicals reacted with riboflavin to give a transient spectrum attributable to a mixture of species produced by addition or abstraction reactions. (author)

In-vitro Neurotoxicity of Two Malaysian Krait Species (Bungarus candidus and Bungarus fasciatus Venoms: Neutralization by Monovalent and Polyvalent Antivenoms from Thailand

Directory of Open Access Journals (Sweden)

Muhamad Rusdi Ahmad Rusmili

2014-03-01

Full Text Available Bungarus candidus and Bungarus fasciatus are two species of krait found in Southeast Asia. Envenoming by these snakes is often characterized by neurotoxicity and, without treatment, causes considerable morbidity and mortality. In this study, the in vitro neurotoxicity of each species, and the effectiveness of two monovalent antivenoms and a polyvalent antivenom, against the neurotoxic effects of the venoms, were examined in a skeletal muscle preparation. Both venoms caused concentration-dependent inhibition of indirect twitches, and attenuated responses to exogenous nicotinic receptor agonists, in the chick biventer preparation, with B. candidus venom being more potent than B. fasciatus venom. SDS-PAGE and western blot analysis indicated different profiles between the venoms. Despite these differences, most proteins bands were recognized by all three antivenoms. Antivenom, added prior to the venoms, attenuated the neurotoxic effect of the venoms. Interestingly, the respective monovalent antivenoms did not neutralize the effects of the venom from the other Bungarus species indicating a relative absence of cross-neutralization. Addition of a high concentration of polyvalent antivenom, at the t90 time point after addition of venom, partially reversed the neurotoxicity of B. fasciatus venom but not B. candidus venom. The monovalent antivenoms had no significant effect when added at the t90 time point. This study showed that B. candidus and B. fasciatus venoms display marked in vitro neurotoxicity in the chick biventer preparation and administration of antivenoms at high dose is necessary to prevent or reverse neurotoxicity.

Highly Confined Electronic and Ionic Conduction in Oxide Heterostructures

DEFF Research Database (Denmark)

Pryds, Nini

2015-01-01

The conductance confined at the interface of complex oxide heterostructures provides new opportunities to explore nanoelectronic as well as nanoionic devices. In this talk I will present our recent results both on ionic and electronic conductivity at different heterostructures systems. In the first...... unattainable for Bi2O3-based materials, is achieved[1]. These confined heterostructures provide a playground not only for new high ionic conductivity phenomena that are sufficiently stable but also uncover a large variety of possible technological perspectives. At the second part, I will discuss and show our...

Delayed neurotoxicity - do trichlorphon and/or dichlorvos cause delayed neuropathy in man or in test animals?

Science.gov (United States)

Johnson, M K

1981-01-01

Many, but not all, reports of delayed neuropathy associated with acute poisoning by trichlorphon refer to cases in U.S.S.R. Adulteration of technical trichlorphon with the ethyl analogue would greatly increase the neurotoxic hazard but analysis of a few samples has not revealed such impurities. Simultaneous ingestion of alcohol does not appear to increase neuropathic hazard. In hens double doses of trichlorphon each exceeding unprotected LD50 can produce moderate neuropathy associated with appropriately high inhibitions of neurotoxic esterase. Similar results are obtained with 2 doses of 10 x LD50 of dichlorvos. In vitro the inhibitory power of dichlorvos against neurotoxic esterase of hen brain is 0.02 x the power against acetylcholinesterase. This ratio correlates reasonably with the ratio of LD50/neuropathic dose. The factor for human brain enzymes is 0.06 suggesting that man is more susceptible to neuropathic effects of near-lethal doses of circulating dichlorvos. It is concluded that the only neuropathic hazard to man from good quality trichlorphon arises from rapid ingestion of massive doses. To obtain critical levels of inhibition of neurotoxic esterase and to cause neuropathy in man by repeated doses would require each dose to be severely toxic. Dichlorvos ingested in large doses is likely to kill rather than to cause neuropathy.

Inverse electron-demand 1,3-dipolar cycloaddition of nitrile oxide with common nitriles leading to 3-functionalized 1,2,4-oxadiazoles.

Science.gov (United States)

Nishiwaki, Nagatoshi; Kobiro, Kazuya; Hirao, Shotaro; Sawayama, Jun; Saigo, Kazuhiko; Ise, Yumiko; Okajima, Yoshikazu; Ariga, Masahiro

2011-10-07

A carbamoyl-substituted nitrile oxide was generated upon treatment of easily available 2-methyl-4-nitro-3-isoxazolin-5(2H)-one with THF (not dried); the reaction proceeded efficiently even in the absence of any special reagents and reaction conditions. The nitrile oxide caused 1,3-dipolar cycloaddition with common aliphatic nitriles or electron-rich aromatic nitriles to afford 3-functionalized 1,2,4-oxadiazoles, which are expected to serve as precursors for the preparation of a variety of functional materials by the chemical transformation of the carbamoyl group. While conventional preparative methods for 1,2,4-oxadiazoles involve the cycloaddition of an electron-rich nitrile oxide with an electron-deficient nitrile or a nitrile activated by a Lewis acid, our method employs the complementary combination of an electron-rich nitrile and an electron-deficient nitrile oxide- the inverse electron-demand 1,3-cycloaddition. The DFT calculations using B3LYP 6-31G* supported the abovementioned inverse reactivity, and also suggested the presence of an accelerating effect by the carbamoyl group as a result of hydrogen bond formation with a dipolarophilic nitrile.

Increased interleukin-1β levels following low dose MDMA induces tolerance against the 5-HT neurotoxicity produced by challenge MDMA

Science.gov (United States)

2011-01-01

Background Preconditioning is a phenomenon by which tolerance develops to injury by previous exposure to a stressor of mild severity. Previous studies have shown that single or repeated low dose MDMA can attenuate 5-HT transporter loss produced by a subsequent neurotoxic dose of the drug. We have explored the mechanism of delayed preconditioning by low dose MDMA. Methods Male Dark Agouti rats were given low dose MDMA (3 mg/kg, i.p.) 96 h before receiving neurotoxic MDMA (12.5 mg/kg, i.p.). IL-1β and IL1ra levels and 5-HT transporter density in frontal cortex were quantified at 1 h, 3 h or 7 days. IL-1β, IL-1ra and IL-1RI were determined between 3 h and 96 h after low dose MDMA. sIL-1RI combined with low dose MDMA or IL-1β were given 96 h before neurotoxic MDMA and toxicity assessed 7 days later. Results Pretreatment with low dose MDMA attenuated both the 5-HT transporter loss and elevated IL-1β levels induced by neurotoxic MDMA while producing an increase in IL-1ra levels. Low dose MDMA produced an increase in IL-1β at 3 h and in IL-1ra at 96 h. sIL-1RI expression was also increased after low dose MDMA. Coadministration of sIL-1RI (3 μg, i.c.v.) prevented the protection against neurotoxic MDMA provided by low dose MDMA. Furthermore, IL-1β (2.5 pg, intracortical) given 96 h before neurotoxic MDMA protected against the 5-HT neurotoxicity produced by the drug, thus mimicking preconditioning. Conclusions These results suggest that IL-1β plays an important role in the development of delayed preconditioning by low dose MDMA. PMID:22114930

Increased interleukin-1β levels following low dose MDMA induces tolerance against the 5-HT neurotoxicity produced by challenge MDMA

Directory of Open Access Journals (Sweden)

Mayado Andrea

2011-11-01

Full Text Available Abstract Background Preconditioning is a phenomenon by which tolerance develops to injury by previous exposure to a stressor of mild severity. Previous studies have shown that single or repeated low dose MDMA can attenuate 5-HT transporter loss produced by a subsequent neurotoxic dose of the drug. We have explored the mechanism of delayed preconditioning by low dose MDMA. Methods Male Dark Agouti rats were given low dose MDMA (3 mg/kg, i.p. 96 h before receiving neurotoxic MDMA (12.5 mg/kg, i.p.. IL-1β and IL1ra levels and 5-HT transporter density in frontal cortex were quantified at 1 h, 3 h or 7 days. IL-1β, IL-1ra and IL-1RI were determined between 3 h and 96 h after low dose MDMA. sIL-1RI combined with low dose MDMA or IL-1β were given 96 h before neurotoxic MDMA and toxicity assessed 7 days later. Results Pretreatment with low dose MDMA attenuated both the 5-HT transporter loss and elevated IL-1β levels induced by neurotoxic MDMA while producing an increase in IL-1ra levels. Low dose MDMA produced an increase in IL-1β at 3 h and in IL-1ra at 96 h. sIL-1RI expression was also increased after low dose MDMA. Coadministration of sIL-1RI (3 μg, i.c.v. prevented the protection against neurotoxic MDMA provided by low dose MDMA. Furthermore, IL-1β (2.5 pg, intracortical given 96 h before neurotoxic MDMA protected against the 5-HT neurotoxicity produced by the drug, thus mimicking preconditioning. Conclusions These results suggest that IL-1β plays an important role in the development of delayed preconditioning by low dose MDMA.

Influence of oxidation treatment on ballistic electron surface-emitting display of porous silicon

International Nuclear Information System (INIS)

Du, Wentao; Zhang, Xiaoning; Zhang, Yujuan; Wang, Wenjiang; Duan, Xiaotao

2012-01-01

Two groups of porous silicon (PS) samples are treated by rapid thermal oxidation (RTO) and electrochemical oxidation (ECO), respectively. Scanning electron microscopy images show that PS samples are segmented into two layers. Oxidized film layer is formed on the top surface of PS samples treated by RTO while at the bottom of PS samples treated by ECO. Both ECO and RTO treatment can make emission current density, diode current density, and emission efficiency of PS increase with the bias voltage increasing. The emission current density and the field emission enhancement factor β of PS sample treated by RTO are larger than that treated by ECO. The Fowler–Nordheim curves of RTO and ECO samples are linear which indicates that high electric field exists on the oxidized layer and field emission occurs whether PS is treated by RTO or ECO.

Mutual enhancement of central neurotoxicity induced by ketamine followed by methamphetamine

International Nuclear Information System (INIS)

Ke, J.-J.; Chen, H.-I.; Jen, C.J.; Kuo, Y.-M.; Cherng, C.G.; Tsai, Y.-P.N.; Ho, M.-C.; Tsai, C.-W.; Lung Yu

2008-01-01

We hereby report that repeated administration of ketamine (350 mg/kg in total) and methamphetamine (30 mg/kg in total) causes specific glutamatergic and dopaminergic neuron deficits, respectively, in adult mouse brain. Acute ketamine did not affect basal body temperature or the later methamphetamine-induced hyperthermia. However, pretreatment with repeated doses of ketamine aggravated methamphetamine-induced dopaminergic terminal loss as evidenced by a drastic decrease in the levels of dopamine, 3,4-dihydroxyphenylacetic acid, and dopamine transporter density as well as poor gait balance performance. In contrast, methamphetamine-induced serotonergic depletion was not altered by ketamine pretreatment. Likewise, the subsequent treatment with methamphetamine exacerbated the ketamine-induced glutamatergic damage as indicated by reduced levels of the vesicular glutamate transporter in hippocampus and striatum and poor memory performance in the Morris water maze. Finally, since activation of the D1 and AMPA/kainate receptors has been known to be involved in the release of glutamate and dopamine, we examined the effects of co-administration of SCH23390, a D1 antagonist, and CNQX, an AMPA/kainate antagonist. Intraventricular CNQX infusion abolished ketamine's potentiation of methamphetamine-induced dopamine neurotoxicity, while systemic SCH23390 mitigated methamphetamine's potentiation of ketamine-induced glutamatergic toxicity. We conclude that repeated doses of ketamine potentiate methamphetamine-induced dopamine neurotoxicity via AMPA/kainate activation and that conjunctive use of methamphetamine aggravates ketamine-induced glutamatergic neurotoxicity possibly via D1 receptor activation

Neuro-protective effect of rutin against Cisplatin-induced neurotoxic rat model.

Science.gov (United States)

Almutairi, Mashal M; Alanazi, Wael A; Alshammari, Musaad A; Alotaibi, Moureq Rashed; Alhoshani, Ali R; Al-Rejaie, Salim Salah; Hafez, Mohamed M; Al-Shabanah, Othman A

2017-09-29

Cisplatin is widely used chemotherapeutic agent for cancer treatment with limited uses due to its neurotoxic side effect. The aim of this study was to determine the potential preventive effects of rutin on the brain of cisplatin- neurotoxic rat model. Forty rats were divided into four groups. Group-1 (control group) was intra-peritoneal (IP) injected with 2.5 ml/kg saline. Group-2 (rutin group) was orally administrated 30 mg/kg rutin dissolved in water for 14 days. Group-3 (cisplatin group) was IP received 5 mg/kg cisplatin single dose. Group-4 (rutin and cisplatin group) was orally administrated 30 mg/kg rutin dissolved in water for 14 days with a single dose of 5 mg/kg cisplatin IP on day ten. Brain tissues from frontal cortex was used to extract RNA, the gene expression levels of paraoxonase-1 (PON-1), PON-2, PON-3, peroxisome proliferator-activated receptor delta (PPAR-δ), and glutathione peroxidase (GPx) was investigated by Real-time PCR. Cisplatin significantly decreased the expression levels of PON-1, PON-3, PPAR-δ and GPX whereas significantly increased PON-2 expression levels. Co-administration of Rutin prevented the cisplatin-induced toxicity by restoring the alteration in the studied genes to normal values as in the control group. This study showed that Rutin has neuroprotective effect and reduces cisplatin- neurotoxicity with possible mechanism via the antioxidant pathway.

Electronic States of High-k Oxides in Gate Stack Structures

Science.gov (United States)

Zhu, Chiyu

In this dissertation, in-situ X-ray and ultraviolet photoemission spectroscopy have been employed to study the interface chemistry and electronic structure of potential high-k gate stack materials. In these gate stack materials, HfO2 and La2O3 are selected as high-k dielectrics, VO2 and ZnO serve as potential channel layer materials. The gate stack structures have been prepared using a reactive electron beam system and a plasma enhanced atomic layer deposition system. Three interrelated issues represent the central themes of the research: 1) the interface band alignment, 2) candidate high-k materials, and 3) band bending, internal electric fields, and charge transfer. 1) The most highlighted issue is the band alignment of specific high-k structures. Band alignment relationships were deduced by analysis of XPS and UPS spectra for three different structures: a) HfO2/VO2/SiO2/Si, b) HfO 2-La2O3/ZnO/SiO2/Si, and c) HfO 2/VO2/ HfO2/SiO2/Si. The valence band offset of HfO2/VO2, ZnO/SiO2 and HfO 2/SiO2 are determined to be 3.4 +/- 0.1, 1.5 +/- 0.1, and 0.7 +/- 0.1 eV. The valence band offset between HfO2-La2O3 and ZnO was almost negligible. Two band alignment models, the electron affinity model and the charge neutrality level model, are discussed. The results show the charge neutrality model is preferred to describe these structures. 2) High-k candidate materials were studied through comparison of pure Hf oxide, pure La oxide, and alloyed Hf-La oxide films. An issue with the application of pure HfO2 is crystallization which may increase the leakage current in gate stack structures. An issue with the application of pure La2O3 is the presence of carbon contamination in the film. Our study shows that the alloyed Hf-La oxide films exhibit an amorphous structure along with reduced carbon contamination. 3) Band bending and internal electric fields in the gate stack structure were observed by XPS and UPS and indicate the charge transfer during the growth and process. The oxygen

Investigations of the electronic, magnetic and crystalline structure of perovskite oxides and an oxide-oxide interface

International Nuclear Information System (INIS)

Raisch, Christoph Werner

2013-01-01

Strontium doped LSMO, Calcium doped LCMO and undoped LMO are discussed in chapter 7. The focus lies on a multi-technique approach to correlate changes of one parameter to its effects on others. The characterization of a YBCO / LCMO heterostructure on STO concludes this work (chapter 8). Again it is the electronic, magnetic and crystalline structure at the interface that proves crucial for the properties of this unusual system which artificially combines a superconductor (SC) and a ferromagnet (FM). This structure makes two antagonistic effects meet, the tendency of a superconductor to pair two electrons with different spin into Cooper pairs and the tendency of a ferromagnet to align all spin moments. This fascinating competition shows the wide range of properties that the perovskite oxides offer when they are used accordingly and combined usefully. The above mentioned polar discontinuity at the interface between a manganite and a cuprate is examined. The thesis is completed by a summary and an outlook.

Asiatic acid attenuates methamphetamine-induced neuroinflammation and neurotoxicity through blocking of NF-kB/STAT3/ERK and mitochondria-mediated apoptosis pathway

OpenAIRE

Park, Ji-Hyun; Seo, Young Ho; Jang, Jung-Hee; Jeong, Chul-Ho; Lee, Sooyeun; Park, Byoungduck

2017-01-01

Background Methamphetamine (METH) is a commonly abused drug that may result in neurotoxic effects. Recent studies have suggested that involvement of neuroinflammatory processes in brain dysfunction is induced by misuse of this drug. However, the mechanism underlying METH-induced inflammation and neurotoxicity in neurons is still unclear. In this study, we investigated whether asiatic acid (AA) effected METH-mediated neuroinflammation and neurotoxicity in dopaminergic neuronal cells. And we fu...

The classification of motor neuron defects in the zebrafish embryo toxicity test (ZFET) as an animal alternative approach to assess developmental neurotoxicity.

Science.gov (United States)

Muth-Köhne, Elke; Wichmann, Arne; Delov, Vera; Fenske, Martina

2012-07-01

Rodents are widely used to test the developmental neurotoxicity potential of chemical substances. The regulatory test procedures are elaborate and the requirement of numerous animals is ethically disputable. Therefore, non-animal alternatives are highly desirable, but appropriate test systems that meet regulatory demands are not yet available. Hence, we have developed a new developmental neurotoxicity assay based on specific whole-mount immunostainings of primary and secondary motor neurons (using the monoclonal antibodies znp1 and zn8) in zebrafish embryos. By classifying the motor neuron defects, we evaluated the severity of the neurotoxic damage to individual primary and secondary motor neurons caused by chemical exposure and determined the corresponding effect concentration values (EC₅₀). In a proof-of-principle study, we investigated the effects of three model compounds thiocyclam, cartap and disulfiram, which show some neurotoxicity-indicating effects in vertebrates, and the positive controls ethanol and nicotine and the negative controls 3,4-dichloroaniline (3,4-DCA) and triclosan. As a quantitative measure of the neurotoxic potential of the test compounds, we calculated the ratios of the EC₅₀ values for motor neuron defects and the cumulative malformations, as determined in a zebrafish embryo toxicity test (zFET). Based on this index, disulfiram was classified as the most potent and thiocyclam as the least potent developmental neurotoxin. The index also confirmed the control compounds as positive and negative neurotoxicants. Our findings demonstrate that this index can be used to reliably distinguish between neurotoxic and non-neurotoxic chemicals and provide a sound estimate for the neurodevelopmental hazard potential of a chemical. The demonstrated method can be a feasible approach to reduce the number of animals used in developmental neurotoxicity evaluation procedures. Copyright © 2012 Elsevier Inc. All rights reserved.

Two-Dimensional Electron Gas at SrTiO3-Based Oxide Heterostructures via Atomic Layer Deposition

Directory of Open Access Journals (Sweden)

Sang Woon Lee

2016-01-01

Full Text Available Two-dimensional electron gas (2DEG at an oxide interface has been attracting considerable attention for physics research and nanoelectronic applications. Early studies reported the formation of 2DEG at semiconductor interfaces (e.g., AlGaAs/GaAs heterostructures with interesting electrical properties such as high electron mobility. Besides 2DEG formation at semiconductor junctions, 2DEG was realized at the interface of an oxide heterostructure such as the LaAlO3/SrTiO3 (LAO/STO heterojunction. The origin of 2DEG was attributed to the well-known “polar catastrophe” mechanism in oxide heterostructures, which consist of an epitaxial LAO layer on a single crystalline STO substrate among proposed mechanisms. Recently, it was reported that the creation of 2DEG was achieved using the atomic layer deposition (ALD technique, which opens new functionality of ALD in emerging nanoelectronics. This review is focused on the origin of 2DEG at oxide heterostructures using the ALD process. In particular, it addresses the origin of 2DEG at oxide interfaces based on an alternative mechanism (i.e., oxygen vacancies.

Structural, electronic structure and antibacterial properties of graphene-oxide nano-sheets

Science.gov (United States)

Sharma, Aditya; Varshney, Mayora; Nanda, Sitansu Sekhar; Shin, Hyun Joon; Kim, Namdong; Yi, Dong Kee; Chae, Keun-Hwa; Ok Won, Sung

2018-04-01

Correlation between the structural/electronic structure properties and bio-activity of graphene-based materials need to be thoroughly evaluated before their commercial implementation in the health and environment precincts. To better investigate the local hybridization of sp2/sp3 orbitals of the functional groups of graphene-oxide (GO) and their execution in the antimicrobial mechanism, we exemplify the antibacterial activity of GO sheets towards the Escherichia coli bacteria (E. coli) by applying the field-emission scanning electron microscopy (FESEM), near edge X-ray absorption fine structure (NEXAFS) and scanning transmission X-ray microscope (STXM) techniques. C K-edge and O K-edge NEXAFS spectra have revealed lesser sp2 carbon atoms in the aromatic ring and attachment of functional oxygen groups at GO sheets. Entrapment of E. coli bacteria by GO sheets is evidenced by FESEM investigations and has also been corroborated by nano-scale imaging of bacteria using the STXM. Spectroscopy evidence of functional oxygen moieties with GO sheets and physiochemical entrapment of E. coli bacteria have assisted us to elaborate the mechanism of cellular oxidative stress-induced disruption of bacterial membrane.

Electron spin resonance characterization of trapping centers in Unibond reg-sign buried oxides

International Nuclear Information System (INIS)

Conley, J.F. Jr.; Lenahan, P.M.; Wallace, B.D.

1996-01-01

Electron spin resonance and capacitance vs. voltage measurements are used to evaluate the radiation response of Unibond buried oxides. When damaged by hole injection, it is found that Unibond reg-sign buried oxides exhibit a rough correspondence between E' centers and positive charge as well as generation of P b centers at the Unibond buried oxide/Si interface. In these respects, Unibond buried oxides qualitatively resemble thermal SiO 2 . However, a hydrogen complexed E' center known as the 74 G doublet is also detected in the Unibond buried oxides. This defect is not detectable in thermal SiO 2 under similar circumstances. Since the presence of 74 G doublet center is generally indicative of very high hydrogen content and since hydrogen is clearly a significant participant in radiation damage, this result suggests a qualitative difference between the radiation response of Unibond and thermal SiO 2 . Unibond results are also compared and contrasted with similar investigations on separation-by-implanted-oxygen (SIMOX) buried oxides. Although the charge trapping response of Unibond buried oxides may be inferior to that of radiation hardened thermal SiO 2 , it appears to be more simple and superior to that of SIMOX buried oxides

Electron-electron scattering-induced channel hot electron injection in nanoscale n-channel metal-oxide-semiconductor field-effect-transistors with high-k/metal gate stacks

International Nuclear Information System (INIS)

Tsai, Jyun-Yu; Liu, Kuan-Ju; Lu, Ying-Hsin; Liu, Xi-Wen; Chang, Ting-Chang; Chen, Ching-En; Ho, Szu-Han; Tseng, Tseung-Yuen; Cheng, Osbert; Huang, Cheng-Tung; Lu, Ching-Sen

2014-01-01

This work investigates electron-electron scattering (EES)-induced channel hot electron (CHE) injection in nanoscale n-channel metal-oxide-semiconductor field-effect-transistors (n-MOSFETs) with high-k/metal gate stacks. Many groups have proposed new models (i.e., single-particle and multiple-particle process) to well explain the hot carrier degradation in nanoscale devices and all mechanisms focused on Si-H bond dissociation at the Si/SiO 2 interface. However, for high-k dielectric devices, experiment results show that the channel hot carrier trapping in the pre-existing high-k bulk defects is the main degradation mechanism. Therefore, we propose a model of EES-induced CHE injection to illustrate the trapping-dominant mechanism in nanoscale n-MOSFETs with high-k/metal gate stacks.

A specific 2,4-disubstituted-adamantane interaction with plasma-grown aluminum oxide. Inelastic-electron-tunneling spectroscopy study

NARCIS (Netherlands)

Meijer, E.W.; Raas, M.C.; Velzen, van P.N.T.

1987-01-01

The interaction of several mono- and disubstituted adamantanes with plasma-grown aluminum oxide has been studied using inelastic-electron-tunneling (IET) spectroscopy. The IET spectra evidence the chemisorption of 2,4-adamantanedione onto the aluminum oxide surface as the carboxylate anion of

Hard electronics; Hard electronics

Energy Technology Data Exchange (ETDEWEB)

NONE

1997-03-01

Hard material technologies were surveyed to establish the hard electronic technology which offers superior characteristics under hard operational or environmental conditions as compared with conventional Si devices. The following technologies were separately surveyed: (1) The device and integration technologies of wide gap hard semiconductors such as SiC, diamond and nitride, (2) The technology of hard semiconductor devices for vacuum micro- electronics technology, and (3) The technology of hard new material devices for oxides. The formation technology of oxide thin films made remarkable progress after discovery of oxide superconductor materials, resulting in development of an atomic layer growth method and mist deposition method. This leading research is expected to solve such issues difficult to be easily realized by current Si technology as high-power, high-frequency and low-loss devices in power electronics, high temperature-proof and radiation-proof devices in ultimate electronics, and high-speed and dense- integrated devices in information electronics. 432 refs., 136 figs., 15 tabs.

Electronic structure of indium-tungsten-oxide alloys and their energy band alignment at the heterojunction to crystalline silicon

Science.gov (United States)

Menzel, Dorothee; Mews, Mathias; Rech, Bernd; Korte, Lars

2018-01-01

The electronic structure of thermally co-evaporated indium-tungsten-oxide films is investigated. The stoichiometry is varied from pure tungsten oxide to pure indium oxide, and the band alignment at the indium-tungsten-oxide/crystalline silicon heterointerface is monitored. Using in-system photoelectron spectroscopy, optical spectroscopy, and surface photovoltage measurements, we show that the work function of indium-tungsten-oxide continuously decreases from 6.3 eV for tungsten oxide to 4.3 eV for indium oxide, with a concomitant decrease in the band bending at the hetero interface to crystalline silicon than indium oxide.

Protection against β-amyloid neurotoxicity by a non-toxic endogenous N-terminal β-amyloid fragment and its active hexapeptide core sequence.

Science.gov (United States)

Forest, Kelly H; Alfulaij, Naghum; Arora, Komal; Taketa, Ruth; Sherrin, Tessi; Todorovic, Cedomir; Lawrence, James L M; Yoshikawa, Gene T; Ng, Ho-Leung; Hruby, Victor J; Nichols, Robert A

2018-01-01

High levels (μM) of beta amyloid (Aβ) oligomers are known to trigger neurotoxic effects, leading to synaptic impairment, behavioral deficits, and apoptotic cell death. The hydrophobic C-terminal domain of Aβ, together with sequences critical for oligomer formation, is essential for this neurotoxicity. However, Aβ at low levels (pM-nM) has been shown to function as a positive neuromodulator and this activity resides in the hydrophilic N-terminal domain of Aβ. An N-terminal Aβ fragment (1-15/16), found in cerebrospinal fluid, was also shown to be a highly active neuromodulator and to reverse Aβ-induced impairments of long-term potentiation. Here, we show the impact of this N-terminal Aβ fragment and a shorter hexapeptide core sequence in the Aβ fragment (Aβcore: 10-15) to protect or reverse Aβ-induced neuronal toxicity, fear memory deficits and apoptotic death. The neuroprotective effects of the N-terminal Aβ fragment and Aβcore on Aβ-induced changes in mitochondrial function, oxidative stress, and apoptotic neuronal death were demonstrated via mitochondrial membrane potential, live reactive oxygen species, DNA fragmentation and cell survival assays using a model neuroblastoma cell line (differentiated NG108-15) and mouse hippocampal neuron cultures. The protective action of the N-terminal Aβ fragment and Aβcore against spatial memory processing deficits in amyloid precursor protein/PSEN1 (5XFAD) mice was demonstrated in contextual fear conditioning. Stabilized derivatives of the N-terminal Aβcore were also shown to be fully protective against Aβ-triggered oxidative stress. Together, these findings indicate an endogenous neuroprotective role for the N-terminal Aβ fragment, while active stabilized N-terminal Aβcore derivatives offer the potential for therapeutic application. © 2017 International Society for Neurochemistry.

Lipids and Oxidative Stress Associated with Ethanol-Induced Neurological Damage

Directory of Open Access Journals (Sweden)

José A. Hernández

2016-01-01

Full Text Available The excessive intake of alcohol is a serious public health problem, especially given the severe damage provoked by chronic or prenatal exposure to alcohol that affects many physiological processes, such as memory, motor function, and cognitive abilities. This damage is related to the ethanol oxidation in the brain. The metabolism of ethanol to acetaldehyde and then to acetate is associated with the production of reactive oxygen species that accentuate the oxidative state of cells. This metabolism of ethanol can induce the oxidation of the fatty acids in phospholipids, and the bioactive aldehydes produced are known to be associated with neurotoxicity and neurodegeneration. As such, here we will review the role of lipids in the neuronal damage induced by ethanol-related oxidative stress and the role that lipids play in the related compensatory or defense mechanisms.

A neurotoxicity assessment of high flash aromatic naphtha.

Science.gov (United States)

Douglas, J F; McKee, R H; Cagen, S Z; Schmitt, S L; Beatty, P W; Swanson, M S; Schreiner, C A; Ulrich, C E; Cockrell, B Y

1993-01-01

Catalytic reforming is a refining process that converts naphthenes to aromatics by dehydrogenation to make higher octane gasoline blending components. A portion of this wide-boiling range hydrocarbon stream can be separated by distillation and used for other purposes. One such application is a mixture of predominantly 9-carbon aromatic molecules (C9 Aromatics, primarily isomers of ethyltoluene and trimethylbenzene), which is removed and used as a solvent also known as High Flash Aromatic Naphtha (HFAN). A program was initiated to assess the toxicological properties of HFAN since there may be human exposure, especially in the workplace. The current study was conducted to assess the potential for neurotoxicity in the rat. Adult male Sprague-Dawley rats of approximately 300 grams body weight, in groups of twenty, were exposed by inhalation to HFAN for 90 days at concentrations of 0, 100, 500, and 1500 ppm. During this period the animals were tested monthly for motor activity and in a functional observation battery. After three months of exposure, for 6 hours/day, 5 days/week, 10 animals/group/sex were sacrificed and selected nervous system tissue was examined histopathologically. No signs of neurotoxicity were seen in any of the evaluated parameters, nor was there evidence of pathologic changes in any of the examined tissues.

Electron microscopy and EXAFS studies on oxide-supported gold-silver nanoparticles prepared by flame spray pyrolysis

Energy Technology Data Exchange (ETDEWEB)

Hannemann, Stefan [Institute of Chemical and Bioengineering, Swiss Federal Institute of Technology, ETH Hoenggerberg, CH-8093 Zurich (Switzerland); Grunwaldt, Jan-Dierk [Institute of Chemical and Bioengineering, Swiss Federal Institute of Technology, ETH Hoenggerberg, CH-8093 Zurich (Switzerland)]. E-mail: grunwaldt@chem.ethz.ch; Krumeich, Frank [Laboratory of Inorganic Chemistry, Swiss Federal Institute of Technology, ETH Hoenggerberg, CH-8093 Zurich (Switzerland); Kappen, Peter [Department of Physics, La Trobe University, Victoria 3086 (Australia); Baiker, Alfons [Institute of Chemical and Bioengineering, Swiss Federal Institute of Technology, ETH Hoenggerberg, CH-8093 Zurich (Switzerland)

2006-09-15

Gold and gold-silver nanoparticles prepared by flame spray pyrolysis (FSP) were characterized by electron microscopy, in situ X-ray absorption spectroscopy (XANES and EXAFS), X-ray diffraction (XRD) and their catalytic activity in CO oxidation. Within this one-step flame-synthesis procedure, precursor solutions of dimethyl gold(III) acetylacetonate and silver(I) benzoate together with the corresponding precursor of the silica, iron oxide or titania support, were sprayed and combusted. In order to prepare small metal particles, a low noble metal loading was required. A loading of 0.1-1 wt.% of Au and Ag resulted in 1-6 nm particles. The size of the noble metal particles increased with higher loadings of gold and particularly silver. Both scanning transmission electron microscopy (STEM) combined with energy dispersive X-ray spectroscopy (EDXS) and X-ray absorption spectroscopy (XAS) studies proved the formation of mixed Au-Ag particles. In case of 1% Au-1% Ag/SiO{sub 2}, TEM combined with electron spectroscopic imaging (ESI) using an imaging filter could be used in addition to prove the presence of silver and gold in the same noble metal particle. CO oxidation in the presence of hydrogen was chosen as a test reaction sensitive to small gold particles. Both the influence of the particle size and the alloying of gold and silver were reflected in the CO oxidation activity.

Electron microscopy and EXAFS studies on oxide-supported gold-silver nanoparticles prepared by flame spray pyrolysis

International Nuclear Information System (INIS)

Hannemann, Stefan; Grunwaldt, Jan-Dierk; Krumeich, Frank; Kappen, Peter; Baiker, Alfons

2006-01-01

Gold and gold-silver nanoparticles prepared by flame spray pyrolysis (FSP) were characterized by electron microscopy, in situ X-ray absorption spectroscopy (XANES and EXAFS), X-ray diffraction (XRD) and their catalytic activity in CO oxidation. Within this one-step flame-synthesis procedure, precursor solutions of dimethyl gold(III) acetylacetonate and silver(I) benzoate together with the corresponding precursor of the silica, iron oxide or titania support, were sprayed and combusted. In order to prepare small metal particles, a low noble metal loading was required. A loading of 0.1-1 wt.% of Au and Ag resulted in 1-6 nm particles. The size of the noble metal particles increased with higher loadings of gold and particularly silver. Both scanning transmission electron microscopy (STEM) combined with energy dispersive X-ray spectroscopy (EDXS) and X-ray absorption spectroscopy (XAS) studies proved the formation of mixed Au-Ag particles. In case of 1% Au-1% Ag/SiO 2 , TEM combined with electron spectroscopic imaging (ESI) using an imaging filter could be used in addition to prove the presence of silver and gold in the same noble metal particle. CO oxidation in the presence of hydrogen was chosen as a test reaction sensitive to small gold particles. Both the influence of the particle size and the alloying of gold and silver were reflected in the CO oxidation activity

Correlation between donating or accepting electron behavior of the adsorbed CO or H_2 and its oxidation over TiO_2 under ultraviolet light irradiation

International Nuclear Information System (INIS)

Peng, Xiaoying; He, Zhoujun; Yang, Kai; Chen, Xun; Wang, Xuxu; Dai, Wenxin; Fu, Xianzhi

2016-01-01

Graphical abstract: Although both H_2 and CO can be thermodynamically oxidized by O_2 over TiO_2 under UV irradiation, only CO was oxidized by O_2 over TiO_2 due to its donating electrons to TiO_2, while H_2 was not oxidized by O_2 under the same condition due to its accepting electrons from TiO_2. - Highlights: • CO could but H_2 could not be oxidized over TiO_2 under UV irradiation. • Electron transfer behaviors of species adsorbed at TiO_2 were characterized by gas sensing testing. • Adsorbed CO donated electrons to TiO_2 but adsorbed H_2 accepted electrons from TiO_2 under UV irradiation. • Photocatalytic oxidation of species over TiO_2 maybe depends on the electron transfer direction between species and TiO_2. - Abstract: Although both H_2 and CO can be thermodynamically oxidized by O_2 over TiO_2 under ultraviolet light (UV) irradiation, it was found that CO not H_2 could be oxidized over an anatase TiO_2 in this work. The chemisorption results of CO and H_2 at TiO_2 surface under UV irradiation, investigated by a gas sensing testing, showed that CO adsorption at TiO_2 would cause the decrease of TiO_2 surface impedance, whereas H_2 adsorption would cause its increase. It is proposed that the CO adsorbed at TiO_2 donate electrons to TiO_2 (as a process of CO pre-oxidation), resulting in its oxidation. In contrast, the H_2 adsorbed at TiO_2 accept electrons from TiO_2 (as a process of H_2 pre-reduction), which makes it difficult to be oxidized. This result indicates that the photocatalytic oxidation of a reactant over TiO_2 not only depends on the formation of the photo-generated carriers and the subsequent activated oxidizing species, but maybe also depends on the electron transfer behavior at the interface of the adsorbed reactant and TiO_2.

Effect of crowding, temperature and age on glia activation and dopaminergic neurotoxicity induced by MDMA in the mouse brain.

Science.gov (United States)

Frau, Lucia; Simola, Nicola; Porceddu, Pier Francesca; Morelli, Micaela

2016-09-01

3,4-methylenedyoxymethamphetamine (MDMA or "ecstasy"), a recreational drug of abuse, can induce glia activation and dopaminergic neurotoxicity. Since MDMA is often consumed in crowded environments featuring high temperatures, we studied how these factors influenced glia activation and dopaminergic neurotoxicity induced by MDMA. C57BL/6J adolescent (4 weeks old) and adult (12 weeks old) mice received MDMA (4×20mg/kg) in different conditions: 1) while kept 1, 5, or 10×cage at room temperature (21°C); 2) while kept 5×cage at either room (21°C) or high (27°C) temperature. After the last MDMA administration, immunohistochemistry was performed in the caudate-putamen for CD11b and GFAP, to mark microglia and astroglia, and in the substantia nigra pars compacta for tyrosine hydroxylase, to mark dopaminergic neurons. MDMA induced glia activation and dopaminergic neurotoxicity, compared with vehicle administration. Crowding (5 or 10 mice×cage) amplified MDMA-induced glia activation (in adult and adolescent mice) and dopaminergic neurotoxicity (in adolescent mice). Conversely, exposure to a high environmental temperature (27°C) potentiated MDMA-induced glia activation in adult and adolescent mice kept 5×cage, but not dopaminergic neurotoxicity. Crowding and exposure to a high environmental temperature amplified MDMA-induced hyperthermia, and a positive correlation between body temperature and activation of either microglia or astroglia was found in adult and adolescent mice. These results provide further evidence that the administration setting influences the noxious effects of MDMA in the mouse brain. However, while crowding amplifies both glia activation and dopaminergic neurotoxicity, a high environmental temperature exacerbates glia activation only. Copyright © 2016 Elsevier B.V. All rights reserved.

Mephedrone does not damage dopamine nerve endings of the striatum, but enhances the neurotoxicity of methamphetamine, amphetamine, and MDMA.

Science.gov (United States)

Angoa-Pérez, Mariana; Kane, Michael J; Briggs, Denise I; Francescutti, Dina M; Sykes, Catherine E; Shah, Mrudang M; Thomas, David M; Kuhn, Donald M

2013-04-01

Mephedrone (4-methylmethcathinone) is a β-ketoamphetamine stimulant drug of abuse with close structural and mechanistic similarities to methamphetamine. One of the most powerful actions associated with mephedrone is the ability to stimulate dopamine (DA) release and block its re-uptake through its interaction with the dopamine transporter (DAT). Although mephedrone does not cause toxicity to DA nerve endings, its ability to serve as a DAT blocker could provide protection against methamphetamine-induced neurotoxicity like other DAT inhibitors. To test this possibility, mice were treated with mephedrone (10, 20, or 40 mg/kg) prior to each injection of a neurotoxic regimen of methamphetamine (four injections of 2.5 or 5.0 mg/kg at 2 h intervals). The integrity of DA nerve endings of the striatum was assessed through measures of DA, DAT, and tyrosine hydroxylase levels. The moderate to severe DA toxicity associated with the different doses of methamphetamine was not prevented by any dose of mephedrone but was, in fact, significantly enhanced. The hyperthermia caused by combined treatment with mephedrone and methamphetamine was the same as seen after either drug alone. Mephedrone also enhanced the neurotoxic effects of amphetamine and 3,4-methylenedioxymethamphetamine on DA nerve endings. In contrast, nomifensine protected against methamphetamine-induced neurotoxicity. As mephedrone increases methamphetamine neurotoxicity, the present results suggest that it interacts with the DAT in a manner unlike that of other typical DAT inhibitors. The relatively innocuous effects of mephedrone alone on DA nerve endings mask a potentially dangerous interaction with drugs that are often co-abused with it, leading to heightened neurotoxicity. © 2012 International Society for Neurochemistry.

The electronic and optical properties of warm dense nitrous oxide using quantum molecular dynamics simulations

International Nuclear Information System (INIS)

Zhang Yujuan; Wang Cong; Zhang Ping

2012-01-01

First-principles molecular-dynamics simulations based on density-functional theory have been used to study the electronic and optical properties of fluid nitrous oxide under extreme conditions. Systematic descriptions of pair-correlation function, atomic structure, and the charge density distribution are used to investigate the dissociation of fluid nitrous oxide. The electrical and optical properties are derived from the Kubo-Greenwood formula. It is found that the nonmetal-metal transition for fluid nitrous oxide can be directly associated to the dissociation and has significant influence on the optical properties of the fluid.

3-Nitropropionic acid neurotoxicity in organotypic striatal and corticostriatal slice cultures is dependent on glucose and glutamate

DEFF Research Database (Denmark)

Storgaard, J; Kornblit, B T; Zimmer, J

2000-01-01

of lactate dehydrogenase in the medium and glutamic acid decarboxylase in tissue homogenates. 3-NPA toxicity (25-100 microM in 5 mM glucose, 24-48 h) appeared to be highly dependent on culture medium glucose levels. 3-NPA treatment caused also a dose-dependent lactate increase, reaching a maximum......Mitochondrial inhibition by 3-nitropropionic acid (3-NPA) causes striatal degeneration reminiscent of Huntington's disease. We studied 3-NPA neurotoxicity and possible indirect excitotoxicity in organotypic striatal and corticostriatal slice cultures. Neurotoxicity was quantified by assay...... of threefold increase above control at 100 microM. Both a high dose of glutamate (5 mM) and glutamate uptake blockade by dl-threo-beta-hydroxyaspartate potentiated 3-NPA neurotoxicity in corticostriatal slice cultures. Furthermore, striatum from corticostriatal cocultures was more sensitive to 3-NPA than...

Complexes of uranyl with N-oxides of heterocyclic amines. Electron-vibrational absorption spectra

International Nuclear Information System (INIS)

Jezowska-Trzebiatowska, B.; Wieczorek, M.

1977-01-01

A number of coordination compounds formed by uranyl chloride and nitrate with N-oxides of heterocyclic amines have been prepared and characterized by spectral measurements in the absorption region 20000-50000 cm -1 . The electrons and vibronic transitions have been determined and discussed. (author)

Neurophysiological evidence of methylmercury neurotoxicity

DEFF Research Database (Denmark)

Murata, Katsuyuki; Grandjean, Philippe; Dakeishi, Miwako

2007-01-01

neurotoxicity and to examine the usefulness of those measures. METHODS: The reports addressing both neurophysiological measures and methylmercury exposure in humans were identified and evaluated. RESULTS: The neurological signs and symptoms of MD included paresthesias, constriction of visual fields, impairment...... disease (MD; methylmercury poisoning). In recent years, some of these methods have been used for the risk assessment of low-level methylmercury exposure in asymptomatic children. The objectives of this article were to present an overview of neurophysiological findings involved in methylmercury...... of hearing and speech, mental disturbances, excessive sweating, and hypersalivation. Neuropathological lesions involved visual, auditory, and post- and pre-central cortex areas. Neurophysiological changes involved in methylmercury, as assessed by EPs and HRV, were found to be in accordance with both clinical...

Detection of beryllium in oxides and silicates by electron-probe microanalysis

Directory of Open Access Journals (Sweden)

V. V. Khiller

2017-12-01

Full Text Available The author developed the technique of electron-probe microanalysis for quantitative determination of beryllium content, providing the example of studying natural minerals (aluminosilicates and oxides. This technique allowed to obtain a quantitative content of beryllium (in combination with other elements in the emeralds of the Mariinsky beryllium deposit and in zonal mariinskite-chrysoberyl from the chromitites of the Bazhenov ophiolite complex. All analyzes of minerals were performed on a CAMECA SX 100 electron probe microanalyzer with five wave spectrometers (IGG UB RAS. The pressure in the sample chamber was 2 × 10–4 Pa, in the electron gun region – 4 × 10–6 Pa, in wave spectrometers – 7 Pa. Accelerating voltage was 10 kV, the current of absorbed electrons on the Faraday cylinder (beam current was 100–150 nA. Diameter of the electron beam focused on the sample was 2 μm, the angle of x-ray extraction was 40°. The spectra were obtained on wave spectrometers with TAP crystal analyzers (2d = 25.745 Å, LPET (2d = 8.75 Å, LiF (2d = 4.0226 Å, and PC3 (2d = 211.4 Å, a specialized crystal for determining the content of beryllium and boron; the author carried out all the elements measurements along the Kα-lines. To determine position of the analytical peak and the background from two sides with the minimum possible spectral overlap, the author preliminarily recorded spectra on wave spectrometers. The obtained microprobe analyzes of minerals with quantitative determination of beryllium converge well with the available theoretical compositions of beryl and chrysoberyl, which indicates the high efficiency of the developed technique. By using this technique, we can relatively quickly and reliably determine the quantitative content of beryllium in natural silicates and oxides, which is an acute need for geological researchers studying the mineralogy of beryllium deposits.

Neurotoxicity Induced by Bupivacaine via T-Type Calcium Channels in SH-SY5Y Cells

Science.gov (United States)

Wen, Xianjie; Xu, Shiyuan; Liu, Hongzhen; Zhang, Quinguo; Liang, Hua; Yang, Chenxiang; Wang, Hanbing

2013-01-01

There is concern regarding neurotoxicity induced by the use of local anesthetics. A previous study showed that an overload of intracellular calcium is involved in the neurotoxic effect of some anesthetics. T-type calcium channels, which lower the threshold of action potentials, can regulate the influx of calcium ions. We hypothesized that T-type calcium channels are involved in bupivacaine-induced neurotoxicity. In this study, we first investigated the effects of different concentrations of bupivacaine on SH-SY5Y cell viability, and established a cell injury model with 1 mM bupivacaine. The cell viability of SH-SY5Y cells was measured following treatment with 1 mM bupivacaine and/or different dosages (10, 50, or 100 µM) of NNC 55-0396 dihydrochloride, an antagonist of T-type calcium channels for 24 h. In addition, we monitored the release of lactate dehydrogenase, cytosolic Ca2+ ([Ca2+]i), cell apoptosis and caspase-3 expression. SH-SY5Y cells pretreated with different dosages (10, 50, or 100 µM) of NNC 55-0396 dihydrochloride improved cell viability, reduced lactate dehydrogenase release, inhibited apoptosis, and reduced caspase-3 expression following bupivacaine exposure. However, the protective effect of NNC 55-0396 dihydrochloride plateaued. Overall, our results suggest that T-type calcium channels may be involved in bupivacaine neurotoxicity. However, identification of the specific subtype of T calcium channels involved requires further investigation. PMID:23658789

Neurotoxicity induced by bupivacaine via T-type calcium channels in SH-SY5Y cells.

Directory of Open Access Journals (Sweden)

Xianjie Wen

Full Text Available There is concern regarding neurotoxicity induced by the use of local anesthetics. A previous study showed that an overload of intracellular calcium is involved in the neurotoxic effect of some anesthetics. T-type calcium channels, which lower the threshold of action potentials, can regulate the influx of calcium ions. We hypothesized that T-type calcium channels are involved in bupivacaine-induced neurotoxicity. In this study, we first investigated the effects of different concentrations of bupivacaine on SH-SY5Y cell viability, and established a cell injury model with 1 mM bupivacaine. The cell viability of SH-SY5Y cells was measured following treatment with 1 mM bupivacaine and/or different dosages (10, 50, or 100 µM of NNC 55-0396 dihydrochloride, an antagonist of T-type calcium channels for 24 h. In addition, we monitored the release of lactate dehydrogenase, cytosolic Ca(2+ ([Ca2+]i, cell apoptosis and caspase-3 expression. SH-SY5Y cells pretreated with different dosages (10, 50, or 100 µM of NNC 55-0396 dihydrochloride improved cell viability, reduced lactate dehydrogenase release, inhibited apoptosis, and reduced caspase-3 expression following bupivacaine exposure. However, the protective effect of NNC 55-0396 dihydrochloride plateaued. Overall, our results suggest that T-type calcium channels may be involved in bupivacaine neurotoxicity. However, identification of the specific subtype of T calcium channels involved requires further investigation.

Bulk-surface relationship of an electronic structure for high-throughput screening of metal oxide catalysts

International Nuclear Information System (INIS)

Kweun, Joshua Minwoo; Li, Chenzhe; Zheng, Yongping; Cho, Maenghyo; Kim, Yoon Young; Cho, Kyeongjae

2016-01-01

Graphical abstract: - Highlights: • Bulk-surface relationship was predicted by the ligand field nature of metal oxides. • Antibonding and bonding d-bands occupancy clarified the bulk-surface relationship. • Different surface relaxations were explained by the bulk electronic structures. • Transition from the bulk to the surface state was simulated by oxygen adsorption. - Abstract: Designing metal-oxides consisting of earth-abundant elements has been a crucial issue to replace precious metal catalysts. To achieve efficient screening of metal-oxide catalysts via bulk descriptors rather than surface descriptors, we investigated the relationship between the electronic structure of bulk and that of the surface for lanthanum-based perovskite oxides, LaMO_3 (M = Ti, V, Cr, Mn, Fe, Co, Ni, Cu). Through density functional theory calculations, we examined the d-band occupancy of the bulk and surface transition-metal atoms (n_B_u_l_k and n_S_u_r_f) and the adsorption energy of an oxygen atom (E_a_d_s) on (001), (110), and (111) surfaces. For the (001) surface, we observed strong correlation between the n_B_u_l_k and n_S_u_r_f with an R-squared value over 94%, and the result was interpreted in terms of ligand field splitting and antibonding/bonding level splitting. Moreover, the E_a_d_s on the surfaces was highly correlated with the n_B_u_l_k with an R-squared value of more than 94%, and different surface relaxations could be explained by the bulk electronic structure (e.g., LaMnO_3 vs. LaTiO_3). These results suggest that a bulk-derived descriptor such as n_B_u_l_k can be used to screen metal-oxide catalysts.

The effects of electron-hole separation on the photoconductivity of individual metal oxide nanowires

International Nuclear Information System (INIS)

Prades, J D; Hernandez-Ramirez, F; Jimenez-Diaz, R; Manzanares, M; Andreu, T; Cirera, A; Romano-Rodriguez, A; Morante, J R

2008-01-01

The responses of individual ZnO nanowires to UV light demonstrate that the persistent photoconductivity (PPC) state is directly related to the electron-hole separation near the surface. Our results demonstrate that the electrical transport in these nanomaterials is influenced by the surface in two different ways. On the one hand, the effective mobility and the density of free carriers are determined by recombination mechanisms assisted by the oxidizing molecules in air. This phenomenon can also be blocked by surface passivation. On the other hand, the surface built-in potential separates the photogenerated electron-hole pairs and accumulates holes at the surface. After illumination, the charge separation makes the electron-hole recombination difficult and originates PPC. This effect is quickly reverted after increasing either the probing current (self-heating by Joule dissipation) or the oxygen content in air (favouring the surface recombination mechanisms). The model for PPC in individual nanowires presented here illustrates the intrinsic potential of metal oxide nanowires to develop optoelectronic devices or optochemical sensors with better and new performances.