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Sample records for pyridoxine

  1. Pyridoxine

    Science.gov (United States)

    Pyridoxine, vitamin B6, is required by your body for utilization of energy in the foods you eat, ... Pyridoxine comes in regular and extended-release (long-acting) tablets. It usually is taken once a day. ...

  2. Pyridoxine neuropathy.

    Science.gov (United States)

    Waterston, J A; Gilligan, B S

    1987-06-15

    A case of sensory neuropathy in a young woman due to long-term ingestion of pyridoxine, with subsequent recovery, is described. Pyridoxine neuropathy may occur after the long-term ingestion of doses as low as 200 mg a day. Because of its widespread use in the community, both the general public and the medical community need to be aware of this recently described complication of megavitamin therapy.

  3. [Pyridoxine dependent seizures].

    Science.gov (United States)

    Hansen, K N; Ostergaard, J R; Møller, S M

    1994-10-17

    Pyridoxine dependent seizures is a rare autosomal recessive disorder. Its manifestations are intractable epilepsy leading to death in status epilepticus. Treatment with pyridoxine prevents the seizures and normalizes the EEG. Early diagnosis is important for the intellectual outcome. In Denmark, the disease has occurred in a child of healthy Tamil immigrants, who are first cousins. The child's case story is described and points to awareness of increased occurrence of rare autosomal recessive disorders in immigrants from cultures with traditional consanguinity. We suggest giving a pyridoxine test dosis to all cases of severe epilepsy and status epilepticus in infants younger than 18 months.

  4. Doxylamine and Pyridoxine

    Science.gov (United States)

    The combination of doxylamine and pyridoxine is used to treat nausea and vomiting in pregnant women whose symptoms have not improved after changing their diet or using other non-medicine treatments. Doxylamine is in a class of medications called antihistamines. ...

  5. Genetics Home Reference: pyridoxine-dependent epilepsy

    Science.gov (United States)

    ... Home Health Conditions pyridoxine-dependent epilepsy pyridoxine-dependent epilepsy Enable Javascript to view the expand/collapse boxes. ... PDF Open All Close All Description Pyridoxine-dependent epilepsy is a condition that involves seizures beginning in ...

  6. Pyridoxine supplementation during isoniazid therapy.

    Science.gov (United States)

    Snider, D E

    1980-12-01

    Vitamin B6 (pyridoxine) supplementation during isoniazid (INH) therapy is necessary in some patients to prevent the development of peripheral neuropathy. In vivo pyridoxine is converted into coenzymes which play an essential role in the metabolism of protein, carbohydrates, fatty acids, and several other substances, including brain amines, INH apparently competitively inhibits the action of pyridoxine in these metabolic functions. The reported frequency of INH-induced neuropathy in various studies is reviewed and population groups at relatively high risk of developing this complication are identified. The routine use of pyridoxine supplementation to prevent peripheral neuropathy in high risk populations is recommended.

  7. Low-Dose Pyridoxine Masks Pyridoxine-Dependent Seizures

    OpenAIRE

    2001-01-01

    A 4-month-old male infant with pyridoxine dependency and seizures from birth was controlled with extremely low-dose pyridoxine (0.5 mg/day) given as a vitamin supplement, in a report from Joana de Gusmao Children’s Hospital, Florianopolis, Brazil.

  8. Pyridoxine-dependent seizures and microcephaly.

    Science.gov (United States)

    Tan, Hüseyin; Kardaş, Fatih; Büyükavci, Mustafa; Karakelleoğlu, Cahit

    2004-09-01

    Pyridoxine dependency is a rare autosomal-recessive disorder causing intractable seizures in neonates and infants. This case report describes an infant with pyridoxine-dependent seizures with microcephaly and discusses a probable pathogenetic mechanism of microcephaly in this condition.

  9. 21 CFR 582.5676 - Pyridoxine hydrochloride.

    Science.gov (United States)

    2010-04-01

    ... 21 Food and Drugs 6 2010-04-01 2010-04-01 false Pyridoxine hydrochloride. 582.5676 Section 582.5676 Food and Drugs FOOD AND DRUG ADMINISTRATION, DEPARTMENT OF HEALTH AND HUMAN SERVICES (CONTINUED... Dietary Supplements 1 § 582.5676 Pyridoxine hydrochloride. (a) Product. Pyridoxine hydrochloride....

  10. Pyridoxine and depression: neuroendocrine aspects.

    Science.gov (United States)

    Casacchia, M; Boni, B; Meco, G

    1982-01-01

    Plasma prolactin levels (PRL) were determined in 5 male depressed patients and in 5 controls, after injection of TRH (200 mg i.v.) (first phase), TRH following oral L-DOPA (500 mg) given 90 minutes before (second phase), TRH plus pyridoxine (300 mg i.v.) after same pretreatment with L-Dopa (third phase). L-Dopa induced a statistically significant suppression of TRH, caused PRL release; such suppression appears to be lower when TRH plus pyridoxine were administered simultaneously. PRL profile was not significantly different in the two groups.

  11. Pyridoxine-Induced Sensory Neuropathy

    OpenAIRE

    1995-01-01

    An 18-year-old man with seizures from birth was followed in the Department of Clinical Neurological Sciences, University of Western Ontario, London, and was found to have developed a sensory neuropathy by 2 years of age following treatment with pyridoxine in doses up to 2000 mg/day.

  12. Epidemiology of pyridoxine dependent and pyridoxine responsive seizures in the UK

    OpenAIRE

    1999-01-01

    OBJECTIVE—To study the epidemiology of pyridoxine dependent seizures and other forms of pyridoxine responsive seizures.
DESIGN—Monthly notifications to the British Paediatric Surveillance Unit over two years. Questionnaire follow up.
SETTING—UK and the Republic of Ireland.
PATIENTS—Children aged 15 years or younger whose seizures respond to pyridoxine.
INTERVENTIONS—None.
MAIN OUTCOME MEASURES—Numbers of children with definite, probable, and possible pyridoxine depende...

  13. Sensory neuropathy with low-dose pyridoxine.

    Science.gov (United States)

    Parry, G J; Bredesen, D E

    1985-10-01

    We describe 16 patients with neuropathy associated with pyridoxine abuse. The clinical picture of a pure sensory central-peripheral distal axonopathy was consistent. Pyridoxine dose was 0.2 to 5 g/d, and duration of consumption before symptoms was inversely proportional to the daily intake. In all patients with adequate follow-up, improvement followed discontinuation of pyridoxine. The ready availability of up to 1-gram tablets makes it likely that this neuropathy will continue to be seen.

  14. Pyridoxine-responsive PH1: treatment.

    Science.gov (United States)

    Toussaint, C

    1998-01-01

    Owing to the rarity of PH, the efficacy of pyridoxine therapy has only been tested in very small series of patients. From two recent reports including 18 patients, 50% of patients would be unresponsive to pyridoxine whereas oxaluria would be normalized in 20% of patients and somewhat reduced-but not to normal level-in the remaining 30%. In a few aneodotical cases pyridoxine administration was reported to improve kidney function in patients with renal failure secondary to hyperoxaluria. It is reminded that megadoses of pyridoxine (0.5 to 6 g daily) may induce severe sensory neuropathy.

  15. Pyridoxine in clinical toxicology: a review.

    Science.gov (United States)

    Lheureux, Philippe; Penaloza, Andrea; Gris, Mireille

    2005-04-01

    Pyridoxine (vitamin B6) is a co-factor in many enzymatic pathways involved in amino acid metabolism: the main biologically active form is pyridoxal 5-phosphate. Pyridoxine has been used as an antidote in acute intoxications, including isoniazid overdose, Gyromitra mushroom or false morrel (monomethylhydrazine) poisoning and hydrazine exposure. It is also recommended as a co-factor to improve the conversion of glyoxylic acid into glycine in ethylene glycol poisoning. Other indications are recommended by some sources (for example crimidine poisoning, zipeprol and theophylline-induced seizures, adjunct to d-penicillamine chelation), without significant supporting data. The value of pyridoxine or its congener metadoxine as an agent for hastening ethanol metabolism or improving vigilance in acute alcohol intoxication is controversial. This paper reviews the various indications of pyridoxine in clinical toxicology and the supporting literature. The potential adverse effects of excessive pyridoxine dosage will also be summarized.

  16. Case Report: Intravenous and Oral Pyridoxine Trial for Diagnosis of Pyridoxine-Dependent Epilepsy.

    Science.gov (United States)

    Cirillo, Melissa; Venkatesan, Charu; Millichap, John J; Stack, Cynthia V; Nordli, Douglas R

    2015-07-01

    Pyridoxine-dependent epilepsy is a rare, autosomal recessive, treatable cause of neonatal seizures. Genetic testing can confirm mutations in the ALDH7A1 gene, which encodes antiquitin. To avoid delays in initiating treatment while awaiting confirmatory genetic testing, it is recommended that all neonates with unexplained seizures should receive trial of intravenous (IV) pyridoxine to assess for responsiveness. However, oral pyridoxine is not commonly continued in the absence of the typical EEG changes. Two cases are presented that highlight the potential inadequacy of this single-step approach. One neonate ultimately diagnosed with pyridoxine-dependent seizures had no EEG changes after administration of IV pyridoxine. In contrast, another neonate who did not have this diagnosis had profound EEG changes after pyridoxine administration. We present 2 cases that highlight the difficulties in using initial EEG response to IV pyridoxine in establishing a diagnosis of pyridoxine-dependent seizures in the neonate. Given the availability of biochemical markers and gene testing, we suggest that oral pyridoxine treatment should be continued until biochemical and/or genetic testing has confirmed the presence or absence of pyridoxine-dependent epilepsy.

  17. Pyridoxine deficiency in adult patients with status epilepticus.

    Science.gov (United States)

    Dave, Hina N; Eugene Ramsay, Richard; Khan, Fawad; Sabharwal, Vivek; Irland, Megan

    2015-11-01

    An 8-year-old girl treated at our facility for superrefractory status epilepticus was found to have a low pyridoxine level at 5 μg/L. After starting pyridoxine supplementation, improvement in the EEG for a 24-hour period was seen. We decided to look at the pyridoxine levels in adult patients admitted with status epilepticus. We reviewed the records on patients admitted to the neurological ICU for status epilepticus (SE). Eighty-one adult patients were identified with documented pyridoxine levels. For comparison purposes, we looked at pyridoxine levels in outpatients with epilepsy (n=132). Reported normal pyridoxine range is >10 ng/mL. All but six patients admitted for SE had low normal or undetectable pyridoxine levels. A selective pyridoxine deficiency was seen in 94% of patients with status epilepticus (compared to 39.4% in the outpatients) which leads us to believe that there is a relationship between status epilepticus and pyridoxine levels.

  18. Comparing pyridoxine and doxylamine succinate-pyridoxine HCl for nausea and vomiting of pregnancy: A matched, controlled cohort study.

    Science.gov (United States)

    Pope, Eliza; Maltepe, Caroline; Koren, Gideon

    2015-07-01

    Nausea and vomiting of pregnancy (NVP) is a common gestational condition. This is the first study to compare the use of vitamin B6 (pyridoxine) versus Diclectin (doxylamine succinate-pyridoxine HCl) for NVP symptoms. Participants were pregnant women with NVP who used either pyridoxine or doxylamine succinate-pyridoxine HCl for ≥4 days prior to calling the Motherisk NVP Helpline. Women receiving pyridoxine only (n = 80) were matched to a woman taking doxylamine succinate-pyridoxine HCl only (n = 80), accounting for potential confounders and baseline level of NVP, measured by the Pregnancy Unique Quantification of Emesis (PUQE) score. Change in NVP severity after a week of therapy with either pyridoxine or doxylamine succinate-pyridoxine HCl was quantified using the PUQE-24 scale, which describes NVP symptoms 24 hours prior to their call. Doxylamine succinate-pyridoxine HCl use found a significant reduction in PUQE score, compared with pyridoxine (+0.5 versus -0.2, P doxylamine succinate-pyridoxine HCl use saw a mean improvement of 2.6 versus 0.4 with pyridoxine (P doxylamine succinate-pyridoxine HCl use was associated with fewer women experiencing moderate to severe scores after a week of treatment, compared with the pyridoxine group (7 versus 17, P < .05), despite similar baseline PUQE scores.

  19. Pyridoxal Phosphate vs Pyridoxine for Intractable Seizures

    Directory of Open Access Journals (Sweden)

    J Gordon Millichap

    2005-05-01

    Full Text Available The efficacy of pyridoxal phosphate (PLP compared to pyridoxine (PN in the control of idiopathic intractable epilepsy was studied in 94 children, aged 8 months to 15 years, at the National Taiwan University Hospital, Taipei, Taiwan.

  20. Pyridoxine dependent epilepsy: a suggestive electroclinical pattern

    OpenAIRE

    1999-01-01

    AIMS—To determine if there is an electroencephalographic pattern suggestive of pyridoxine dependent epilepsy that could be used to improve the chances of early diagnosis.
METHODS—A retrospective study was made of all the clinical records and electroencephalograms of neonates identified with pyridoxine dependent seizures between 1983 and 1994, at this hospital. Neonates whose seizures began after more than 28 days of life were excluded; in all, five patients from four fami...

  1. Pyridoxine dependent epilepsy with iatrogenic sensory neuronopathy.

    Science.gov (United States)

    McLachlan, R S; Brown, W F

    1995-02-01

    An 18-year-old man was treated from birth with chronic high dose pyridoxine (vitamin B6) up to 2000 mg per day for pyridoxine-dependent seizures. Within two years of onset of treatment, he developed a sensory neuropathy which did not progress over the following 16 years. Electrophysiological studies were consistent with a pure sensory neuronopathy expressed as centripetal degeneration of processes of the dorsal root ganglion cells.

  2. The EEG response to pyridoxine-IV neither identifies nor excludes pyridoxine-dependent epilepsy.

    NARCIS (Netherlands)

    Bok, L.A.; Maurits, N.M.; Willemsen, M.A.A.P.; Jakobs, C.; Teune, L.K.; Poll-The, B.T.; Coo, I.F.M. de; Toet, M.C.; Hagebeuk, E.E.; Brouwer, O.F.; Hoeven, J.H. van; Sival, D.A.

    2010-01-01

    PURPOSE: Pyridoxine-dependent epilepsy (PDE) is characterized by therapy-resistant seizures (TRS) responding to intravenous (IV) pyridoxine. PDE can be identified by increased urinary alpha-aminoadipic semialdehyde (alpha-AASA) concentrations and mutations in the ALDH7A1 (antiquitin) gene. Prompt re

  3. The EEG response to pyridoxine-IV neither identifies nor excludes pyridoxine-dependent epilepsy

    NARCIS (Netherlands)

    Bok, Levinus A; Maurits, Natasha M; Willemsen, Michèl A; Jakobs, Cornelis; Teune, Laura K; Poll-The, Bwee Tien; de Coo, Irenaeus F; Toet, Mona C; Hagebeuk, Eveline E; Brouwer, Oebele F; van der Hoeven, Johannes H; Sival, Deborah A

    2010-01-01

    PURPOSE: Pyridoxine-dependent epilepsy (PDE) is characterized by therapy-resistant seizures (TRS) responding to intravenous (IV) pyridoxine. PDE can be identified by increased urinary alpha-aminoadipic semialdehyde (α-AASA) concentrations and mutations in the ALDH7A1 (antiquitin) gene. Prompt recogn

  4. Epidemiology of pyridoxine dependent seizures in the Netherlands.

    NARCIS (Netherlands)

    Been, J.V.; Bok, L.A.; Andriessen, P.; Renier, W.O.

    2005-01-01

    BACKGROUND: Pyridoxine dependent epilepsy is a rare cause of seizures in childhood. The diagnosis is made on clinical criteria, that in many cases are never met. Therefore, epidemiological data on pyridoxine dependency are scarce. AIMS: To study the epidemiology of pyridoxine dependent epilepsy in t

  5. Biosynthesis of pyridoxine: origin of the nitrogen atom of pyridoxine in microorganisms.

    Science.gov (United States)

    Tanaka, K; Tazuya, K; Yamada, K; Kumaoka, H

    2000-04-01

    The amide nitrogen atom of glutamine was incorporated into pyridoxine in four eukaryotes, Emericella nidulans, Mucor racemosus, Neurospora crassa and Saccharomyces cerevisiae, and two prokaryotes, Staphylococcus aureus and Bacillus subtilis, but not in the following prokaryotes, Pseudomonas putida, Enterobacter aerogenes and Escherichia coli. On the other hand, the nitrogen atom of glutamate was incorporated into pyridoxine in P. putida, E. aerogenes and E. coli, but not in S. aureus and B. subtilis. These results suggest that there are at least two different biosynthetic routes for pyridoxine and the difference does not depend on prokaryotes and eukaryotes.

  6. Acute sensory neuropathy-neuronopathy from pyridoxine overdose.

    Science.gov (United States)

    Albin, R L; Albers, J W; Greenberg, H S; Townsend, J B; Lynn, R B; Burke, J M; Alessi, A G

    1987-11-01

    We report two patients who developed an acute, profound, and permanent sensory deficit after treatment with massive doses of parenteral pyridoxine. Aside from rapid onset, their clinical picture resembles that described in chronic pyridoxine neurotoxicity. It also is consonant with experimental models of acute pyridoxine intoxication and is probably secondary to a sensory ganglion neuronopathy. These patients also had transient autonomic dysfunction, mild weakness, nystagmus, lethargy, and respiratory depression. These previously undocumented features may be attributable to either the preservative used in the parenteral pyridoxine preparation or to the exceptionally high doses of pyridoxine these patients received.

  7. Pyridoxine (vitamin B6) toxicity: enhancement by uremia in rats.

    Science.gov (United States)

    Levine, S; Saltzman, A

    2002-10-01

    Pyridoxine is not completely innocuous. Large doses can cause a peripheral neuropathy despite renal excretion of this water-soluble vitamin. Renal failure patients are treated with pyridoxine to prevent a deficiency. The safety of pyridoxine treatment in the presence of renal dysfunction has not been studied. Our experiments on anephric rats show that the uremic state, in a mere 3 or 4 days, causes a 5- to 10-fold increase in susceptibility to pyridoxine-induced neuronopathy. These results suggest a need for caution in prescribing pyridoxine to uremic patients who will probably take the vitamin daily for many years.

  8. Intravenous pyridoxine in acute ethanol intoxication.

    Science.gov (United States)

    Mardel, S; Phair, I; O'Dwyer, F; Henry, J A

    1994-05-01

    Intravenous pyridoxine was evaluated as an agent for the reversal of ethanol-induced central nervous depression in a randomised double blind controlled study of 108 patients presenting with a clinical diagnosis of acute ethanol intoxication to two accident and emergency departments. Level of consciousness, measured by a modified Glasgow coma scale, showed no significant change after a single 1 g dose of intravenous pyridoxine when compared to controls given saline. The mean fall in blood alcohol concentration after one hour was 33 mg dl-1 (7.2 mmol l-1) in both groups suggesting that pyridoxine has no antidotal action and no short term effect on the rate of metabolism of ethanol.

  9. Pyridoxine-dependent seizures in an older child.

    Science.gov (United States)

    Yoshikawa, H; Abe, T; Oda, Y

    1999-10-01

    The case of a 12-year-old girl with pyridoxine-dependent seizures is reported. She developed status epilepticus just after birth and ordinary antiepileptic drugs were administered without effect. Her seizures ceased only on the administration of pyridoxine. Status epilepticus associated with the withdrawal of pyridoxine occurred three times, and ceased only after the renewed administration of pyridoxine. She now has mental retardation and mild spastic diplegia. The reported cases of pyridoxine-dependent seizures usually have been neonates and infants. Older patients were not fully investigated, and so we have reviewed these cases of pyridoxine-dependent seizures. As known previously, pediatricians should not forget that pyridoxine should be continued for life.

  10. [Depression, pyridoxine and oral contraception (author's transl)].

    Science.gov (United States)

    Leriche, A M; Romain, J L

    1981-07-01

    Numerous publications have, in recent years, associated the apparition of depressive syndrome with OC (oral contraception). The study of modified triptophane metabolism in OC patients has also involved the study of quantitative modifications of serotonin in certain types of depressive syndrome, as well as the positive effects of vitamin B6 and of pyridoxine administration. On the other hand, there is strong evidence showing that the involvement of OCs in depression cannot always be incriminated, and that, in the majority of cases, the causes are to be found in other, and mostly psychological, factors. Even in these last cases pyridoxine can be prescribed for a limited time without interruption of OC treatment.

  11. Pyridoxine-Dependent Seizures and MRI Abnormality

    OpenAIRE

    J Gordon Millichap

    1996-01-01

    An infant with pyridoxine-dependent seizures and MRI, PET, and EEG evidence of diffuse structural or functional brain disease is reported from the University of New Mexico Health Sciences Center, Albuquerque, NM, and the UCLA School of Medicine, Los Angeles, CA.

  12. Pyridoxine and pyridoxalphosphate-dependent epilepsies.

    Science.gov (United States)

    Plecko, Barbara

    2013-01-01

    To date we know of four inborn errors of autosomal recessive inheritance that lead to vitamin B6-dependent seizures. Among these, pyridoxine-dependent seizures due to antiquitin deficiency is by far the most common, although exact incidence data are lacking. In PNPO deficiency, samples have to be collected prior to treatment, while PDE, hyperprolinemia type II and congenital HPP can be diagnosed while on vitamin B6 supplementation. A vitamin B6 withdrawal for diagnostic purposes is nowadays only indicated in patients with a clear vitamin B6 response but normal biochemical work-up. In the presence of therapy-resistant neonatal seizures, early consideration of a vitamin B6 trial over 3 consecutive days is crucial in order to prevent irreversible brain damage. While PLP would be effective in all four disorders, pyridoxine fails to treat seizures in PNPO deficiency. As PLP is unlicensed within Europe and North America, pyridoxine is widely used as the first line drug, but if it is ineffective it should be followed by a trial with PLP, especially in neonates. As severe apnea has been described in responders, resuscitation equipment should be at hand during a first pyridoxine/PLP administration. Patients and parents have to be informed about the lifelong dependency and recurrence risks in forthcoming pregnancies.

  13. Reversal of prolonged isoniazid-induced coma by pyridoxine.

    Science.gov (United States)

    Brent, J; Vo, N; Kulig, K; Rumack, B H

    1990-08-01

    Isoniazid overdose is known to result in the rapid onset of seizures, metabolic acidosis, and prolonged obtundation. Pyridoxine has been reported to be effective in treating isoniazid-induced seizures. We report three cases of obtundation secondary to isoniazid overdose that was immediately reversed by intravenous pyridoxine. In two of these cases, status seizures were stopped by intravenous pyridoxine administration, but the patients remained comatose for prolonged periods. The comas were immediately reversed by the administration of additional pyridoxine. In the third case, the patient's lethargy was treated by intravenous pyridoxine on presentation and was followed by immediate awakening. Pyridoxine is effective in treating not only isoniazid-induced seizures, but also the mental status changes associated with this overdose. The dose required to induce awakening may be higher than that required to control seizures.

  14. Exacerbation of isoniazid induced peripheral neuropathy by pyridoxine.

    OpenAIRE

    1990-01-01

    Mycobacterium kansasii was isolated from an area of cavitating pneumonia in a man with rheumatoid arthritis. Standard antituberculosis treatment, including isoniazid 300 mg daily, had to be stopped because of peripheral neuropathy. The patient, a slow acetylator, subjectively deteriorated despite withdrawal of isoniazid and treatment with pyridoxine 150 mg daily. Improvement occurred only after the pyridoxine had also been withdrawn. Pyridoxine may cause peripheral neuropathy and this case il...

  15. Seizure recurrence following pyridoxine withdrawal in a patient with pyridoxine-dependent epilepsy.

    Science.gov (United States)

    Tamaura, Moe; Shimbo, Hiroko; Iai, Mizue; Yamashita, Sumimasa; Osaka, Hitoshi

    2015-04-01

    Pyridoxine-dependent epilepsy (PDE) is an autosomal recessive disorder characterized by early onset and recurrent seizures that can be controlled by a high dose of pyridoxine. PDE is caused by mutations in ALDH7A1, which encodes antiquitin. Antiquitin converts α-aminoadipic semialdehyde to α-aminoadipic acid. Seizure recurrence after pyridoxine withdrawal is a criterion for diagnosis, but PDE can be diagnosed conclusively by genetic testing for mutations in the ALDH7A1 gene. In this case study, we report the long-term follow-up of a patient suspected with PDE. She experienced prolonged generalized tonic seizures and was hospitalized in an intensive care unit following pyridoxine withdrawal. Later, we identified a compound heterozygous mutation, c.1216G>A, p.Gly406Arg, and a novel splice donor site mutation, IVS9+5G>A. Confirmation of these mutations would have prevented an unsafe withdrawal test. This case suggests the importance of the genetic determination of PDE to avoid the diagnostic withdrawal of pyridoxine.

  16. Folinic acid-responsive seizures initially responsive to pyridoxine.

    Science.gov (United States)

    Nicolai, Joost; van Kranen-Mastenbroek, Vivianne H J M; Wevers, Ron A; Hurkx, Wilfred A P T; Vles, Johan S H

    2006-02-01

    This report presents a male who developed clonic seizures on the day he was born. The next day, the diagnosis of pyridoxine-dependent seizures was made. However, contradictory to this diagnosis, seizures reappeared despite treatment with pyridoxine. Seizures ceased after folinic acid was initiated. The clinical and biochemical characteristics of folinic acid-responsive seizures are reviewed. Treatment with folinic acid should be considered in neonatal seizures of unknown origin that do not respond to pyridoxine, or manifest a transient response to pyridoxine.

  17. Single high-dose pyridoxine treatment for isoniazid overdose.

    Science.gov (United States)

    Wason, S; Lacouture, P G; Lovejoy, F H

    1981-09-04

    We treated five isoniazid-overdosed patients each with a single dose of pyridoxine hydrochloride equivalent to the gram amount of isoniazid ingested and compared their outcome with that of 41 patients from the literature who received little or no pyridoxine. Recurrent seizures occurred in 60% of patients who had received no pyridoxine vs 0% in our patients. Metabolic acidosis resolved in our cases but was refractory in the literature cases. In our cases, coma lightened more rapidly and was of shorter duration as compared with that in the literature cases (mean, seven hours vs 24 hours). No adverse effects of pyridoxine were seen in our patients.

  18. [Pyridoxine neuropathies. Review of the literature].

    Science.gov (United States)

    Dordain, G; Deffond, D

    1994-01-01

    Daily needs of vitamin B6 are very low (2 mg per day) and widely covered by normal feeding. Pyridoxine deficiencies are exceptional (congenital metabolic abnormalities, drug or toxic-induced perturbations). First described in animal models, human cases of neuropathy had been encountered in the "megavitamin"-syndrome. They are confirmed by rare case-reports of very high doses given in toxic indication. Sensory peripheral neuropathies can also occur with lower doses taken over a long period of time.

  19. CSF glutamate/GABA concentrations in pyridoxine-dependent seizures: etiology of pyridoxine-dependent seizures and the mechanisms of pyridoxine action in seizure control.

    Science.gov (United States)

    Goto, T; Matsuo, N; Takahashi, T

    2001-03-01

    Several lines of evidence suggest that the binding affinity of glutamate decarboxylase (GAD) to the active form of pyridoxine is low in cases of pyridoxine-dependent seizures (PDS) and that a quantitative imbalance between excitatory (i.e. glutamate) and inhibitory (i.e. gamma-aminobutyric acid, GABA) neurotransmitters could cause refractory seizures. However, inconsistent findings with GAD insufficiency have been reported in PDS. We report a case of PDS that is not accompanied by an elevated cerebrospinal fluid (CSF) glutamate concentration. Intravenous pyridoxine phosphate terminated generalized seizures which were otherwise refractory to conventional anti-epileptic medicines. No seizure occurred once oral pyridoxine (13.5 mg/kg per day) was started in combination with phenobarbital sodium (PB, 3.7 mg/kg per day). The electroencephalogram (EEG) normalized approximately 8 months after pyridoxine was started. The patient is gradually acquiring developmental milestones during the 15 months follow-up period. The CSF glutamate and GABA concentrations were determined on three separate occasions: (1) during status epilepticus; (2) during a seizure-free period with administration of pyridoxine and PB; and (3) 6 days after suspension of pyridoxine and PB and immediately before a convulsion. The CSF glutamate level was below the sensitivity of detection (pyridoxine supplementation, were within the normal range. We suggest that (1) PDS is not a discrete disease of single etiology in that insufficient activation of GAD may not account for seizure susceptibility in all cases and (2) mechanism(s) of anti-convulsive effect of pyridoxine, at least in some cases, may be independent of GAD activation.

  20. Folinic acid-responsive seizures initially responsive to pyridoxine.

    NARCIS (Netherlands)

    Nicolai, J.; Kranen-Mastenbroek, V.H. van; Wevers, R.A.; Hurkx, W.A.; Vles, J.S.

    2006-01-01

    This report presents a male who developed clonic seizures on the day he was born. The next day, the diagnosis of pyridoxine-dependent seizures was made. However, contradictory to this diagnosis, seizures reappeared despite treatment with pyridoxine. Seizures ceased after folinic acid was initiated.

  1. Isoniazid overdose treated with high-dose pyridoxine.

    Science.gov (United States)

    Yarbrough, B E; Wood, J P

    1983-05-01

    Large doses of pyridoxine recently have been shown to prevent the seizures and acidosis caused by ingestion of more than two to three grams of isoniazid. We present three cases of massive isoniazid ingestion, producing seizures and acidosis, that were treated successfully by administration of one gram of pyridoxine intravenously for each gram of isoniazid ingested.

  2. No sensory neuropathy during pyridoxine treatment in homocystinuria.

    OpenAIRE

    1991-01-01

    Seventeen patients with cystathionine synthase deficiency homocystinuria were examined clinically and neurophysiologically for evidence of sensory neuropathy. All had received high dose pyridoxine (vitamin B-6) for many years. Absence of neurological disturbance in all cases suggests long term treatment with pyridoxine in the dosages used in homocystinuric patients is not harmful.

  3. No sensory neuropathy during pyridoxine treatment in homocystinuria.

    Science.gov (United States)

    Mpofu, C; Alani, S M; Whitehouse, C; Fowler, B; Wraith, J E

    1991-09-01

    Seventeen patients with cystathionine synthase deficiency homocystinuria were examined clinically and neurophysiologically for evidence of sensory neuropathy. All had received high dose pyridoxine (vitamin B-6) for many years. Absence of neurological disturbance in all cases suggests long term treatment with pyridoxine in the dosages used in homocystinuric patients is not harmful.

  4. Should doxylamine-pyridoxine be used for nausea and vomiting of pregnancy?

    Science.gov (United States)

    Persaud, Navindra; Chin, Jessica; Walker, Mark

    2014-04-01

    Doxylamine-pyridoxine is the first-line agent for the treatment of nausea and vomiting of pregnancy (NVP) according to Canadian guidelines, and this combination is commonly prescribed to pregnant women. There is limited evidence that doxylamine-pyridoxine is more effective than pyridoxine alone. There is stronger support for the safety of pyridoxine monotherapy than for the combination of doxylamine-pyridoxine during pregnancy, and some conflicting evidence links doxylamine-pyridoxine use to pyloric stenosis and childhood malignancies. The role of doxylamine-pyridoxine as the first-line pharmacological treatment for NVP in Canada should be reconsidered.

  5. Biosynthesis of pyridoxine in Saccharomyces cerevisiae--origin of the pyridoxine nitrogen atom differs under anaerobic and aerobic conditions.

    Science.gov (United States)

    Ishida, Shiho; Yamada, Kazuko

    2002-12-01

    The amide nitrogen atom of glutamine is incorporated into pyridoxine in four eukaryotes (i.e., Emericella nidulans, Mucor racemosus, Neurospora crassa and Saccharomyces cerevisiae) and two prokaryotes (i.e., Staphylococcus aureus and Bacillus subtilis). However, in the prokaryotes Pseudomonas putida, Enterobacter aerogenes and Escherichia coli, it is the nitrogen atom of glutamate that is incorporated into pyridoxine (J Nutr Sci Vitaminol (2000) 46, 55-57). As these results were from experiments conducted under aerobic conditions, we investigated the biosynthesis of pyridoxine on S. cerevisiae under anaerobic conditions. The results showed that [amide-15N]L-glutamine was not incorporated into pyridoxine, unlike the results for aerobic conditions. The incorporation of [15N]ammonium salts into pyridoxine was not inhibited in the presence of casamino acids and tryptophan. The results showed that the nitrogen atoms of amino acids are not used for the biosynthesis of pyridoxine. The incorporation of 15N into pyridoxine was inhibited in the presence of adenine, but not in that of hypoxanthine. Thus, the nitrogen atom of pyridoxine may be from the amino group attached to the C-6 of adenine.

  6. INH induced status epilepticus: response to pyridoxine.

    Science.gov (United States)

    Tajender, Vasu; Saluja, Jasjeet

    2006-01-01

    Isoniazid is an effective and widely used drug in tuberculosis treatment. The administration of toxic amounts of INH causes recurrent seizures, profound metabolic acidosis, coma and even death but therapeutic dose of isoniazid is a very rare cause of seizures. We present a case of 44-year-old HIV positive African-American female who was recently started on a preventive dose of INH after being found purified protein derivative (PPD) positive. She developed status-epilepticus that did not respond to most of the antiepileptics. As soon as she received intravenous pyridoxine, the seizures terminated abruptly.

  7. The geographic distribution of tuberculosis and pyridoxine supply in Ontario.

    Science.gov (United States)

    McGuigan, M A; Yamada, J

    1995-12-01

    Acute poisoning with isoniazid causes generalized convulsions which should be treated with intravenous pyridoxine and a rapidly-acting anticonvulsant. The purpose of this study was to determine the correlation between the distribution of tuberculosis (as a proxy for isoniazid use) and acute care hospital supplies of intravenous pyridoxine (the antidote for isoniazid overdose). The distribution of tuberculosis was based on Ontario public health regions. The study was descriptive using simple linear regression to assess the degree of correlation. Only 15.6% of Ontario acute care hospitals have enough intravenous pyridoxine to treat an average isoniazid overdose. The distribution of tuberculosis and the number of hospitals in the region correlated best with hospital supplies of pyridoxine, although these variables explained only 22% and 23.7%, respectively, of the variation in supply. It does not appear that the distribution of tuberculosis is a major determinant of the availability of the isoniazid antidote, pyridoxine. Acute care hospitals in Ontario should re-evaluate their need for pyridoxine in light of the incidence of tuberculosis in their regions. Each hospital should stock at least 5 Gm of intravenous pyridoxine; additional amounts may be appropriate if there is an increased incidence in the area.

  8. Pyridoxine responsive epilepsy caused by a novel homozygous PNPO mutation

    Directory of Open Access Journals (Sweden)

    B. Jaeger

    2016-03-01

    Full Text Available We report a patient with anti-epileptic treatment refractory neonatal seizures responsive to pyridoxine. Biochemical analysis revealed normal markers for antiquitin deficiency and also mutation analysis of the ALDH7A1 (Antiquitin gene was negative. Mutation analysis of the PNPO gene revealed a novel, homozygous, presumed pathogenic mutation (c.481C>T; p.(Arg161Cys. Measurements of B6 vitamers in a CSF sample after pyridoxine administration revealed elevated pyridoxamine as the only metabolic marker for PNPO deficiency. With pyridoxine monotherapy the patient is seizure free and neurodevelopmental outcome at the age of 14 months is normal.

  9. Pyridoxine responsive epilepsy caused by a novel homozygous PNPO mutation☆

    Science.gov (United States)

    Jaeger, B.; Abeling, N.G.; Salomons, G.S.; Struys, E.A.; Simas-Mendes, M.; Geukers, V.G.; Poll-The, B.T.

    2016-01-01

    We report a patient with anti-epileptic treatment refractory neonatal seizures responsive to pyridoxine. Biochemical analysis revealed normal markers for antiquitin deficiency and also mutation analysis of the ALDH7A1 (Antiquitin) gene was negative. Mutation analysis of the PNPO gene revealed a novel, homozygous, presumed pathogenic mutation (c.481C > T; p.(Arg161Cys)). Measurements of B6 vitamers in a CSF sample after pyridoxine administration revealed elevated pyridoxamine as the only metabolic marker for PNPO deficiency. With pyridoxine monotherapy the patient is seizure free and neurodevelopmental outcome at the age of 14 months is normal. PMID:27014579

  10. Exacerbation of isoniazid induced peripheral neuropathy by pyridoxine.

    Science.gov (United States)

    Nisar, M; Watkin, S W; Bucknall, R C; Agnew, R A

    1990-05-01

    Mycobacterium kansasii was isolated from an area of cavitating pneumonia in a man with rheumatoid arthritis. Standard antituberculosis treatment, including isoniazid 300 mg daily, had to be stopped because of peripheral neuropathy. The patient, a slow acetylator, subjectively deteriorated despite withdrawal of isoniazid and treatment with pyridoxine 150 mg daily. Improvement occurred only after the pyridoxine had also been withdrawn. Pyridoxine may cause peripheral neuropathy and this case illustrates the need for caution in the use of this vitamin in the prevention and treatment of isoniazid induced peripheral neuropathy.

  11. Pyridoxine-dependent seizures: a review.

    Science.gov (United States)

    Rajesh, R; Girija, A S

    2003-07-01

    Pyridoxine-dependent seizure is a rare autosomal recessive disorder that usually presents with neonatal intractable seizures. This syndrome results from an inborn abnormality of the enzyme glutamic acid decarboxylase, which results in reduced pyridazine-dependent synthesis of the inhibitory neurotransmitter gamma amino butyric acid. The full range of symptomatology is unknown; but can be associated with autism, breath holding and severe mental retardation, bilious vomiting, transient visual agnosia, severe articulatory apraxia motor dyspraxia, microcephaly and intrauterine seizures. Parenteral pyridine injection test is a highly effective and reproducible test in confirming the diagnosis. Pyridoxine should be administered as a diagnostic test in all cases of convulsive disorders of infancy in which no other diagnosis is evident. Epileptic seizure discharges subside within 2-6 minutes after the intravenous injection of 50-100 mg of pyridaoxine. Once the diagnosis is confirmed, maintenance therapy should be continued indefinitely and doses increased with age or intercurrent illnesses. The maintenance dose of Bg needed is still not clear. There is a relatively wide range for the daily B6 dose necessary to control the seizure i.e., 10-200 mg/day.

  12. Thiamin and pyridoxine requirements during intravenous hyperalimentation.

    Science.gov (United States)

    Kishi, H; Nishii, S; Ono, T; Yamaji, A; Kasahara, N; Hiraoka, E; Okada, A; Itakura, T; Takagi, Y

    1979-02-01

    Studies were undertaken to determine rational dosages of vitamin B1 and B6 during long-term intravenous hyperalimentation, using more sensitive techniques than formerly used to evaluate B1 and B6 status. A standard vitamin combination, type A, (usually commercially available products) has been used up to now because of convenience, disregarding the effects of long-term administration. This combination lacks biotin, folic acid, and vitamin E and contains from 10 to 100 times the dietary allowances of such vitamins as B1, B2, B6, B12, and C. In response to the possibility of vitamin overdose, two new vitamin combinations, type B (from commercial products) and type C (a convenient and easily administered combination produced at the hospital) were developed in order to provide the normal dietary allowances and at the same time eliminate any harmful side-effects. From the results obtained, 5 mg/day for thiamin HCl and 3 mg/day for pyridoxine HCl in type B and type C were found to be a sufficient and safe level as opposed to 55 mg/day for thiamin HCl and 102 mg/day for pyridoxine HCl in type A.

  13. Pyridoxine hydroxamic acids as novel HIV-integrase inhibitors.

    Science.gov (United States)

    Stranix, Brent R; Wu, Jinzi J; Milot, Guy; Beaulieu, Françis; Bouchard, Jean-Emanuel; Gouveia, Kristine; Forte, André; Garde, Seema; Wang, Zhigang; Mouscadet, Jean-François; Delelis, Olivier; Xiao, Yong

    2016-02-15

    A series of pyridoxine hydroxamic acid analog bearing a 5-aryl-spacers were synthesized. Evaluation of these novel HIV integrase complex inhibitors revealed compounds with high potency against wild-type HIV virus.

  14. Congenital cataract in a child with pyridoxine-dependent epilepsy.

    Science.gov (United States)

    Yusuf, Imran H; Sandford, Victoria; Hildebrand, Göran Darius

    2013-06-01

    Pyridoxine-dependent epilepsy (PDE) is a cause of neonatal epileptic encephalopathy not previously known to cause ophthalmic disease. We describe the novel observation of a 5-year-old girl with pyridoxine-dependent epilepsy and bilateral cataracts. PDE is the result of mutations in the ALDH7A1 gene encoding antiquitin, an enzyme protective against cellular dehydration and osmotic stress. Accumulating metabolic precursors in PDE have been shown to be cataractogenic in vitro, and experimental pyridoxine deficiency has been associated with lenticular opacities in vivo. The association of ALDH7A1 haploinsufficiency in PDE and congenital cataract may offer insight into the relationship between osmotic stress and fetal cataract development. Bilateral progression of cataracts in this child suggests ongoing metabolic dysregulation within the crystalline lens despite pyridoxine supplementation at doses sufficient to control seizure activity.

  15. Assessment of pyridoxine and folate intake in migraine patients

    Directory of Open Access Journals (Sweden)

    Omid Sadeghi

    2016-01-01

    Conclusion: Migraine patients had lower dietary intake of folate, compared with non-migraine group subjects. There was no significant association between folate and pyridoxine intake with the frequency of migraine attacks. Further studies are needed to confirm our findings.

  16. Motor and sensory neuropathy secondary to excessive pyridoxine ingestion.

    Science.gov (United States)

    Foca, F J

    1985-09-01

    This report documents a case of mixed motor and sensory neuropathy that resulted from ingestion of excessive amounts of pyridoxine. An 81-year-old woman was admitted to the hospital because of difficulty in walking and frequent falls. History revealed that she had been taking large doses of pyridoxine daily for several months as treatment for carpal tunnel syndrome. Diagnostic work-up failed to suggest a cause for her symptoms. Nerve conduction studies revealed slowing of motor conduction velocities, prolonged F wave latencies, and prolonged sensory latencies in both lower extremities. We believe the patient's complaints and the results of nerve conduction studies were secondary to pyridoxine neurotoxicity. Since the bases for this neurotoxicity are unknown, we suggest that treatment of carpal tunnel syndrome with oral pyridoxine be carefully monitored and that dosage limits not be exceeded.

  17. Non-compliance in pyridoxine-dependent seizures and a way out.

    Science.gov (United States)

    Kumar, Praveen; Gupta, Vijay K; Mishra, Devendra

    2007-01-01

    Pyridoxine dependency is a rare autosomal-recessive disorder causing intractable seizures in neonates and infants. Life-long therapy with pyridoxine is required for prevention of seizure recurrence and for an optimum intellectual outcome. With the availability of newer biochemical confirmatory tests, the conventional pyridoxine-withdrawal test is being used less frequently for diagnosis. This report describes an infant whose parents were non-compliant with pyridoxine therapy and proposes that pyridoxine-withdrawal test may be useful in demonstrating to parents the need for life-long pyridoxine therapy, thereby reducing non-compliance.

  18. Pyridoxine induced neuropathy by subcutaneous administration in dogs

    OpenAIRE

    2008-01-01

    To construct a sensory neuropathy model, excess pyridoxine (150 mg/kg s.i.d.) was injected subcutaneously in dogs over a period of 7 days. During the administrations period, the dogs experienced body weight reduction and proprioceptive loss involving the hindquarters. After pyridoxine administration was completed, electrophysiological recordings showed that the M wave remained at a normal state, but the H-reflex of the treated dogs disappeared at 7 days. The dorsal funiculus of L4 was disrupt...

  19. Pyridoxine induced rosacea-like dermatitis.

    Science.gov (United States)

    Rezaković, Saida; Mokos, Zrinka Bukvić; Paštar, Zrinjka

    2015-03-01

    Rosacea is a common chronic inflammatory cutaneous disease of unknown etiology, characterized by remissions and exacerbations, presenting with centrofacial erythema and telangiectasias. It affects mainly adults around the age of 30 years and classically predominates in females. The pathophysiology of rosacea has not yet been fully understood. Risk factors are positive family history, very light skin phototype, sun exposure and consumption of spicy food or alcohol. Recently, there has been some evidence that some drugs or vitamins could be potential factors that can aggravate rosacea or induce rosacea-like symptoms. In this context, we present a 53-year-old female developing rosacea-like dermatitis due to a fixed combination of isoniazid and pyridoxine, which she was receiving along with rifampicin for the treatment of pulmonary tuberculosis.

  20. Status epilepticus in a neonate treated with pyridoxine because of a familial recurrence risk for antiquitin deficiency: pyridoxine toxicity?

    Science.gov (United States)

    Hartmann, Hans; Fingerhut, Michael; Jakobs, Cornelis; Plecko, Barbara

    2011-12-01

    Pyridoxine-dependent epilepsy (PDE) is a treatable inborn error of metabolism with autosomal recessive inheritance. Antenatal and postnatal prophylactic administration of pyridoxine has been recommended to improve the developmental outcome in possible future pregnancies. We report on a male offspring of a second pregnancy at risk for PDE. While on prophylactic treatment with oral pyridoxine, the newborn developed encephalopathy and status epilepticus at age 14 days. Seizures did not respond to parenteral pyridoxine and additional treatment with folinic acid. After treatment was changed to pyridoxal 5'-phosphate, the infant's condition improved. Antiquitin deficiency was excluded by biochemical and molecular genetic testing, and cofactor treatment was stopped on day 26. He has since remained seizure-free with normal psychomotor development. In healthy newborns, high-dose treatment with pyridoxine may result in increased rather than decreased neuroexcitability. Postnatal prophylactic pyridoxine treatment of fetuses and neonates at risk for PDE should be limited to the shortest possible time, by either prenatal diagnosis or immediate postnatal biochemical and genetic testing.

  1. Antenatal treatment in two Dutch families with pyridoxine-dependent seizures.

    NARCIS (Netherlands)

    Bok, L.A.; Been, J.V.; Struys, E.A.; Jakobs, C.; Rijper, E.A.; Willemsen, M.A.A.P.

    2010-01-01

    Incidental reports suggest that antenatal treatment of pyridoxine dependent seizures (PDS) may improve neurodevelopmental outcome of affected patients. Two families with PDS are reported, both with two affected siblings. Antenatal treatment with pyridoxine was instituted during the second pregnancy

  2. Antenatal treatment in two Dutch families with pyridoxine-dependent seizures.

    NARCIS (Netherlands)

    Bok, L.A.; Been, J.V.; Struys, E.A.; Jakobs, C.; Rijper, E.A.; Willemsen, M.A.A.P.

    2010-01-01

    Incidental reports suggest that antenatal treatment of pyridoxine dependent seizures (PDS) may improve neurodevelopmental outcome of affected patients. Two families with PDS are reported, both with two affected siblings. Antenatal treatment with pyridoxine was instituted during the second pregnancy

  3. Long-term outcome in pyridoxine-responsive infantile epilepsy.

    Science.gov (United States)

    Riikonen, R; Mankinen, K; Gaily, E

    2015-11-01

    Dose regimens of pyridoxine (vitamin B6) for treatment of infantile spasms have varied from 200 mg/d to 300 mg/kg/d. Only two long-term outcome studies of the treated patients are available. We asked all pediatric neurologists treating pediatric epilepsy in Finland if they had seen patients with pyridoxine-responsive infantile epilepsy. Five children with infantile spasms and hypsarrhythmia and one with focal epilepsy were reported as pyridoxine responders. Data on clinical presentation and outcome were collected from patient charts. All B6 responders had un-known aetiology. Two patients were studied for pyridoxal 5'-phosphate oxidase (PNPO) deficiency and showed negative results. Ages at seizure onset ranged from 4 to 7 months. The maintenance dose of oral pyridoxine was 150 mg/day. Response occurred within 1-to 14 days (mean 5 days). Two patients were treated with concomitant antiepileptic drugs. Duration of pyridoxine therapy varied from 6 weeks to 4 years (mean 26 months). Four patients had later seizure recurrence: one at 15 months with motor seizures (stopped by valproate), another two in adolescence with focal epilepsy and one at 20 years with unclassified epilepsy. Intelligence was normal in five patients and one had a mild mental deficiency. Follow-up ranged from 8.5 to 24 years. Rare patients with infantile epilepsy but not pyridoxine dependency may respond to smaller doses of pyridoxine than reported before. Long-term cognitive outcome appears to be good but late seizure recurrence (in adolescence or in adulthood) occur. So far it is unknown if the response was determined by genetic traits or disease-related factors. Copyright © 2015. Published by Elsevier Ltd.

  4. Pyridoxine deficiency and peripheral neuropathy associated with long-term phenelzine therapy.

    Science.gov (United States)

    Heller, C A; Friedman, P A

    1983-11-01

    A 51-year-old, nonalcoholic, nondiabetic woman with sensorimotor peripheral neuropathy and pyridoxine deficiency associated with long-term phenelzine therapy is described. Since phenelzine, like hydralazine and isoniazid, is a hydrazine capable of reducing pyridoxine levels in the rat, it is suggested that phenelzine, like hydralazine and isoniazid, may cause a pyridoxine-responsive peripheral neuropathy in humans.

  5. Pyridoxine-dependent seizures: a clinical and biochemical conundrum.

    Science.gov (United States)

    Baxter, Peter

    2003-04-11

    Pyridoxine-dependent seizures have been recognised for 40 years, but the clinical and biochemical features are still not understood. It is a rare recessively inherited condition where classically a baby starts convulsing in utero and continues to do so after birth, until given pyridoxine. Many of these early onset cases also have an acute encephalopathy and other clinical features. Late onset cases are now recognised with a less severe form of the condition. Seizures can break through with intercurrent illness but otherwise remain controlled on pharmacologic doses of pyridoxine. The long-term outcome is affected by several factors including whether onset is early or late and how soon pyridoxine is given. Biochemical studies have been sparse, on very small numbers. There does not appear to be any defect in the uptake or metabolism of pyridoxine or pyridoxal phosphate (PLP). For a long time glutamic acid decarboxylase (GAD), a pyridoxal-dependent enzyme, has been suspected to be the abnormal gene product, but glutamate and gamma-aminobutyric acid (GABA) studies on the cerebrospinal fluid (CSF) have been contradictory and recent genetic studies have not found any linkage to the two brain isoforms. A recent report describes raised pipecolic acid levels in patients but how this ties in is unexplained.

  6. Impairment of memorization by high doses of pyridoxine in man.

    Science.gov (United States)

    Molimard, R; Marillaud, A; Paille, A; Le Devehat, C; Lemoine, A; Dougny, M

    1980-05-01

    Two controlled trials were performed successively to evaluate the effect of high doses of oral pyridoxine on brain performance in man. In trial I, medical students volunteered to take 100 mg, 500 mg of pyridoxine a day or placebo for 10 days. A digit coding test was performed before, and at the end of the treatment period and a third 15 days later. The improvement of performance from the first to the third test (learning effect) was significantly better in the placebo group than in the B6 treated groups. This could be attributed to memorization of skills. Trial II was performed in obese patients starting a low calorie diet in whom vitamins are routinely prescribed. Performance in a work recognition test and in a visual retention test was lower for the group receiving 1 g of pyridoxine a day. Thus, high doses of oral pyridoxine are likely to impair memorization in man. Disturbances of neuro-transmitter metabolism such as increase of GABA production might explain the effect. As the benefit of high doses of pyridoxine has not been well-documented and as the study has suggested that undesired effects may indeed exist, the widespread use of such doses is questionable.

  7. High-dose pyridoxine as an 'anti-stress' strategy.

    Science.gov (United States)

    McCarty, M F

    2000-05-01

    Pyridoxine nutritional status has a significant and selective modulatory impact on central production of both serotonin and GABA - neurotransmitters which control depression, pain perception, and anxiety - owing to the fact that the decarboxylases which produce these neurotransmitters have a relatively low affinity for pyridoxal phosphate (PLP). Pyridoxine deficiency leads to increased sympathetic outflow and hypertension in rodents, possibly reflecting decreased central production of these neurotransmitters; conversely, supplemental pyridoxine lowers blood pressure in many animal models of hypertension, and there is preliminary evidence for antihypertensive activity in humans as well. Additionally, physiological levels of PLP interact with glucocorticoid receptors to down-regulate their activity. Thus, high-dose pyridoxine, by amplifying tissue levels of PLP, may be expected to have a favorable impact on certain dysphoric mental states, while diminishing sympathetic output and acting peripherally to blunt the physiological impact of corticosteroids. In light of growing evidence that chronic dysphoria, particularly when accompanied by hopelessness or cynicism, has a major negative impact on morbidity and mortality from a wide range of disorders, high intakes of pyridoxine may have the potential to improve prognosis in many individuals. With respect to cardiovascular health, reduction of homocysteine levels should contribute to this benefit. These predictions are consistent with recent epidemiology correlating plasma PLP levels with risk for vascular events and overall survival.

  8. Effects of pyridoxine on male fertility.

    Science.gov (United States)

    Tsutsumi, S; Tanaka, T; Gotoh, K; Akaike, M

    1995-08-01

    Pyridoxine (PN) was intraperitoneally given at 250 and 500 mg/kg to male rats for 2, 4, or 6 weeks, and its effects on male fertility evaluated in terms of the optimal treatment period and detection parameters. Animals of all PN groups showed depression of body weight gains from week I of treatment onwards, significant at all but the 250 mg/kg 2 week administration I week time point. After 2 weeks treatment, the testes demonstrated only very slight histopathological changes. The 4- and 6-week treatments caused decreased spermatozoal motility and some histopathological changes in the testes including degeneration of germinal epithelial cells with both doses and also decreases in the fertility index and mean velocity of sperm, reduction in the testes and epididymides weights, and changes in testicular proteins. In the animals undergoing a 4-week recovery period following 4 or 6 weeks exposure, changes disappeared with the 250 mg/kg dose, but still remained with 500 mg/kg. From these findings, it is concluded that a treatment period of 4 weeks is sufficient for evaluation of drug effects on male fertility and that histopathology can detect the slightest toxic effects on the testis.

  9. Characteristics of pyridoxine overdose neuropathy syndrome.

    Science.gov (United States)

    Dalton, K; Dalton, M J

    1987-07-01

    A newly recognised neurotoxic syndrome due to pyridoxine (B6) overdose is described. It is the largest series of B6 intoxication hitherto reported. A raised serum B6 level was present in 172 women of whom 60% had neurological symptoms, which disappeared when B6 was withdrawn and reappeared in 4 cases when B6 was restarted. The mean dose of B6 in the 103 women with neurological symptoms was 117 +/- 92 mgs, compared with 116.2 +/- 66 mgs in the control group. There was a significant difference (P less than 0.01) in the average duration of ingestion of B6 in the neurotoxic group of 2.9 +/- 1.9 years compared with 1.6 +/- 2.1 years in controls. The symptoms were paraesthesia, hyperaesthesia, bone pains, muscle weakness, numbness and fasciculation, most marked on the extremities and predominantly bilateral unless there was a history of previous trauma to the limb. These women were taking a lower dose of B6 than previously described (1,2), which may account for the complete recovery within 6 months of stopping B6.

  10. Impact of the Increased Recommended Dosage of Isoniazid on Pyridoxine Levels in Children and Adolescents.

    Science.gov (United States)

    Rodà, Diana; Rozas, Librada; Fortuny, Clàudia; Sierra, Cristina; Noguera-Julian, Antoni

    2016-05-01

    Isoniazid exposure causes dose-dependent pyridoxine deficiency. Recently, the recommended dosage of isoniazid in children was increased from 5 (4-6) to 10 (10-15) mg/kg/day. We aimed to analyze longitudinally pyridoxine levels in a cohort of previously healthy children and adolescents treated with isoniazid. Mild symptom-free pyridoxine deficiency was observed in 4/75 (5.6%) and 3/40 (7.5%) at baseline and at 3-month follow-up, respectively. Classical age-related risk factors identified patients at risk of pyridoxine deficiency. Our preliminary results support current recommendations regarding pyridoxine supplementation in healthy children.

  11. Synthesis and Antibacterial Activity of Novel Quaternary Ammonium Pyridoxine Derivatives.

    Science.gov (United States)

    Shtyrlin, Nikita V; Sapozhnikov, Sergey V; Koshkin, Sergey A; Iksanova, Alfiya G; Sabirov, Arthur H; Kayumov, Airat R; Nureeva, Aliya A; Zeldi, Marina I; Shtyrlin, Yurii G

    2015-01-01

    A series of 26 quaternary ammonium pyridoxine derivatives were synthesized and their cytotoxicity and antibacterial activities against clinically relevant bacterial strains were tested in vitro. The antibacterial activity of mono-ammonium salts increased with the rise of the lipophilicity and compound 3,3,5-trimethyl-8,8-dioctyl-1,7,8,9-tetrahydro-[1,3]dioxino[5,4-d]pyrrolo[3,4-b]pyridin-8-ium chloride (2d) reaches a maximum among them. Bis-ammonium salt of pyridoxine 4 with two dimethyloctylamine groups also demonstrated high antibacterial activity despite lower lipophilicity. The results of MTT assay indicated that HEK 293 cells were more sensitive than HSF to quaternary ammonium pyridoxine derivatives. Compounds 2d and 4 did not induce the damage of the DNA and might be of interest in the development of new antimicrobials.

  12. The influence of pyridoxine in diabetic peripheral neuropathy.

    Science.gov (United States)

    Levin, E R; Hanscom, T A; Fisher, M; Lauvstad, W A; Lui, A; Ryan, A; Glockner, D; Levin, S R

    1981-01-01

    To determine the role of pyridoxine in the treatment of diabetic peripheral neuropathy, 18 symptomatic diabetic patients were treated with vitamin B6 or placebo in a double-blind controlled study. Only one patient had a low plasma pyridoxal phosphate level at the start of the study. After 4 mo of treatment with pyridoxine hydrochloride (50 mg three times daily) 6 of 9 pyridoxine-treated and 4 of 9 placebo-treated patients noted significant relief from their neuropathic symptoms. There was no difference between the two groups with regard to fasting plasma glucose, motor nerve conduction velocity, or ophthalmologic examination at the beginning or at the conclusion of the study. Our results suggest that vitamin B6 deficiency is not a factor in the etiology of diabetic peripheral neuropathy. Furthermore, treating diabetic peripheral neuropathy with high dose vitamin B6 or placebo results in a similar frequency of symptomatic improvement.

  13. Dose-dependent expression of neuronopathy after experimental pyridoxine intoxication.

    Science.gov (United States)

    Xu, Y; Sladky, J T; Brown, M J

    1989-08-01

    We examined the sequence of nervous system abnormalities that resulted when rats were given excess amounts of vitamin B6 (pyridoxine). High doses of pyridoxine (1,200 or 600 mg/kg/d) for 6 to 10 days caused a neuronopathy with necrosis of dorsal root ganglion (DRG) sensory neurons, accompanied by centrifugal axonal atrophy and breakdown of peripheral and central sensory axons. Large diameter neurons with long processes and large cytoplasmic volumes were especially affected. Smaller doses (300 to 150 mg/kg/d) for up to 12 weeks had minor effects on DRG neurons, but produced a neuropathy with axonal atrophy and degeneration. Guinea pigs given 1,800 mg/kg/d developed sensory neuronopathy, whereas mice given similar or higher doses did not have neuropathologic abnormalities. Multiple factors including rate of administration, differential neuronal vulnerability, and species susceptibility have bearing on the final expression of pyridoxine neurotoxicity.

  14. Pyridoxine induced neuropathy by subcutaneous administration in dogs.

    Science.gov (United States)

    Chung, Jin-Young; Choi, Jung-Hoon; Hwang, Cheol-Yong; Youn, Hwa-Young

    2008-06-01

    To construct a sensory neuropathy model, excess pyridoxine (150 mg/kg s.i.d.) was injected subcutaneously in dogs over a period of 7 days. During the administrations period, the dogs experienced body weight reduction and proprioceptive loss involving the hindquarters. After pyridoxine administration was completed, electrophysiological recordings showed that the M wave remained at a normal state, but the H-reflex of the treated dogs disappeared at 7 days. The dorsal funiculus of L(4) was disrupted irregularly in the axons and myelin with vacuolation. The dorsal root ganglia of L(4), and sciatic and tibial nerves showed degenerative changes and vacuolation. However, the lateral and ventral funiculi of L(4) showed a normal histopathologic pattern. Although this subcutaneous administration method did not cause systemic toxicity and effectively induced sensory neuropathy, this study confirmed the possibility of producing a pyridoxine-induced sensory neuropathy model in dogs with short-term administration.

  15. Effects of pyridoxine on the intestinal absorption and pharmacokinetics of isoniazid in rats.

    Science.gov (United States)

    Zhou, Yan; Jiao, Yang; Wei, Yu-Hui; Zhang, Guo-Rong; Zhang, Jian-Ping; Ren, Jiang-Xia; Zhang, Fan; Zhang, Guo-Qiang; Duan, Hao-Gang; Wu, Xin-An

    2013-03-01

    Pyridoxine is always simultaneously administered orally with isoniazid for tuberculosis patients in the clinic to prevent or treat the nervous system side effects induced by isoniazid. So the aim of this research was to investigate the effects of pyridoxine on the intestinal absorption and pharmacokinetics of isoniazid. The intestinal absorption of isoniazid with or without pyridoxine was investigated by the rat single-pass intestinal perfusion model in situ, and a high-performance liquid chromatographic method was applied to study the pharmacokinetics of isoniazid with or without pyridoxine. The results suggested that the intestinal apparent permeability (P app) and intestinal absorption rate constant (K a) for isoniazid (30 μg/ml) were decreased by 43.7 and 36.4 %, respectively, by co-perfused pyridoxine (40 μg/ml). In vivo, the effect of pyridoxine on isoniazid pharmacokinetic correlated with the doses of pyridoxine. The blood concentrations of isoniazid at the absorption phase were affected by co-administered pyridoxine, but the AUC and C max of isoniazid were not greatly affected by pyridoxine as expected from the inhibition by pyridoxine of the intestinal absorption of isoniazid, which could be caused by its rapid absorption phase. Therefore, although the intestinal absorption of isoniazid could be significantly inhibited by pyridoxine, the pharmacokinetics of isoniazid oral administration was not greatly affected by the decreased intestinal absorption of isoniazid due to its rapid absorption.

  16. Negligible effect of oral garlic oil on the oral absorption of pyridoxine in metadoxine in rats.

    Science.gov (United States)

    Lee, Dae Young; Kang, Hee Eun; Kim, Sang Geon; Lee, Myung Gull

    2010-07-01

    Metadoxine [an ion-pair between pyridoxine and pyrrolidone carboxylate (PCA)] plus garlic oil treatment synergistically reduces alcoholic steatosis compared to each agent alone. We evaluated the effect of garlic oil on the pharmacokinetics of pyridoxine. After the oral administration of metadoxine, the total area under the plasma concentration-time curve from time zero to time infinity (AUC) and the peak plasma concentration (C(max)) of pyridoxine were significantly greater (by 40.6%) and higher (by 63.9%), respectively, than after oral administration of pyridoxine plus PCA. Oral metadoxine plus garlic oil also gave larger AUC (31.8%) and higher C(max) (64.9%) than pyridoxine plus PCA. However, garlic oil did not change the AUC or C(max) of pyridoxine in metadoxine. Thus, garlic oil does not enhance the metadoxine activity by affecting the absorption of pyridoxine.

  17. Revisiting the evidence for neuropathy caused by pyridoxine deficiency and excess.

    Science.gov (United States)

    Ghavanini, Amer A; Kimpinski, Kurt

    2014-09-01

    Pyridoxine deficiency and excess have been implicated as a cause for peripheral neuropathy. As a result, unrelated neuropathies are often treated with pyridoxine based on questionable evidence. However, neurological practitioners frequently discourage patients from taking pyridoxine in excess of 50 mg/d given concerns around the development of a toxic sensory neuronopathy. There is no systematic review to support either of the 2 practices. To address this gap in knowledge, we reviewed the available literature on neuropathy attributed to pyridoxine deficiency and excess. Based on the current limited data, it can be concluded that very low doses of daily pyridoxine are required to prevent peripheral neuropathy. There is inadequate evidence to support routine pyridoxine supplementation in patients with disorders of peripheral nervous system. Supplementation with pyridoxine at doses greater than 50 mg/d for extended duration may be harmful and should be discouraged.

  18. PNPO deficiency: an under diagnosed inborn error of pyridoxine metabolism.

    Science.gov (United States)

    Khayat, Morad; Korman, Stanley H; Frankel, Pnina; Weintraub, Zalman; Hershckowitz, Sylvia; Sheffer, Vered Fleisher; Ben Elisha, Mordechai; Wevers, Ronald A; Falik-Zaccai, Tzipora C

    2008-08-01

    The rare autosomal recessive disorder pyridoxine 5'-phosphate oxidase (PNPO) deficiency is a recently described cause of neonatal and infantile seizures. Clinical evaluation, and biochemical and genetic testing, were performed on a neonate with intractable seizures who did not respond to anticonvulsant drugs and pyridoxine. Sequencing of the PNPO gene revealed a novel homozygous c.284G>A transition in exon 3, resulting in arginine to histidine substitution and reduced activity of the PNPO mutant to 18% relative to the wild type. This finding enabled molecular prenatal diagnosis in a subsequent pregnancy, accurate genetic counseling in the large inbred family, and population screening.

  19. Experimental model of pyridoxine (B6) deficiency-induced neuropathy.

    Science.gov (United States)

    Dellon, A L; Dellon, E S; Tassler, P L; Ellefson, R D; Hendrickson, M

    2001-08-01

    A pyridoxine (B6) dietary deficiency was studied in female adult Sprague-Dawley rats by hind-limb walking-track analysis. Serum levels of pyridoxine and three metabolites were quantified by high-pressure liquid chromatography with fluorescence measurement. Morphometric analysis of the sciatic and posterior tibial nerves (from within the tarsal tunnel) was performed after 1 year on a diet deficient in vitamin B6. The B6-deficient rats developed abnormal walking-track patterns by 8 months, and these track parameters were different from age- and sex-matched normal diet control rats at the p neuropathy.

  20. Sensory neuropathy from pyridoxine abuse. A new megavitamin syndrome.

    Science.gov (United States)

    Schaumburg, H; Kaplan, J; Windebank, A; Vick, N; Rasmus, S; Pleasure, D; Brown, M J

    1983-08-25

    We describe seven adults who had ataxia and severe sensory-nervous-system dysfunction after daily high-level pyridoxine (vitamin B6) consumption. Four were severely disabled; all improved after withdrawal. Weakness was not a feature of this condition, and the central nervous system was clinically spared. Although consumption of large doses of pyridoxine has gained wide public acceptance, this report indicates that it can cause sensory neuropathy or neuronopathy syndromes and that safe guidelines should be established for the use of this widely abused vitamin.

  1. Long-term outcome in pyridoxine-dependent epilepsy.

    NARCIS (Netherlands)

    Bok, L.A.; Halbertsma, F.J.; Houterman, S.; Wevers, R.A.; Vreeswijk, C.; Jakobs, C.; Struys, E.; Hoeven, J.H. van; Sival, D.A.; Willemsen, M.A.A.P.

    2012-01-01

    Aim The long-term outcome of the Dutch pyridoxine-dependent epilepsy cohort and correlations between patient characteristics and follow-up data were retrospectively studied. Method Fourteen patients recruited from a national reference laboratory were included (four males, 10 females, from 11 familie

  2. Long-term outcome in pyridoxine-dependent epilepsy

    NARCIS (Netherlands)

    Bok, Levinus A.; Halbertsma, Feico J.; Houterman, Saskia; Wevers, Ron A.; Vreeswijk, Charlotte; Jakobs, Cornelis; Struys, Eduard; Van der Hoeven, Johan H.; Sival, Deborah A.; Willemsen, Michel A.

    2012-01-01

    AIM: The long-term outcome of the Dutch pyridoxine-dependent epilepsy cohort and correlations between patient characteristics and follow-up data were retrospectively studied. METHOD: Fourteen patients recruited from a national reference laboratory were included (four males, 10 females, from 11 famil

  3. PNPO deficiency: an under diagnosed inborn error of pyridoxine metabolism.

    NARCIS (Netherlands)

    Khayat, M.; Korman, S.H.; Frankel, P.; Weintraub, Z.; Hershckowitz, S.; Sheffer, V.F.; Elisha, M. Ben; Wevers, R.A.; Falik-Zaccai, T.C.

    2008-01-01

    The rare autosomal recessive disorder pyridoxine 5'-phosphate oxidase (PNPO) deficiency is a recently described cause of neonatal and infantile seizures. Clinical evaluation, and biochemical and genetic testing, were performed on a neonate with intractable seizures who did not respond to anticonvuls

  4. Long-Term Outcome in Pyridoxine-Dependent Epilepsy

    Science.gov (United States)

    Bok, Levinus A.; Halbertsma, Feico J..; Houterman, Saskia; Wevers, Ron A.; Vreeswijk, Charlotte; Jakobs, Cornelis; Struys, Eduard; van der Hoeven, Johan H.; Sival, Deborah A.; Willemsen, Michel A.

    2012-01-01

    Aim: The long-term outcome of the Dutch pyridoxine-dependent epilepsy cohort and correlations between patient characteristics and follow-up data were retrospectively studied. Method: Fourteen patients recruited from a national reference laboratory were included (four males, 10 females, from 11 families; median age at assessment 6y; range 2y…

  5. Long-Term Outcome in Pyridoxine-Dependent Epilepsy

    Science.gov (United States)

    Bok, Levinus A.; Halbertsma, Feico J..; Houterman, Saskia; Wevers, Ron A.; Vreeswijk, Charlotte; Jakobs, Cornelis; Struys, Eduard; van der Hoeven, Johan H.; Sival, Deborah A.; Willemsen, Michel A.

    2012-01-01

    Aim: The long-term outcome of the Dutch pyridoxine-dependent epilepsy cohort and correlations between patient characteristics and follow-up data were retrospectively studied. Method: Fourteen patients recruited from a national reference laboratory were included (four males, 10 females, from 11 families; median age at assessment 6y; range 2y…

  6. Pyridoxine-dependent seizures associated with hypophosphatasia in a newborn.

    Science.gov (United States)

    Nunes, Magda Lahorgue; Mugnol, Fabiana; Bica, Igor; Fiori, Renato Machado

    2002-03-01

    Pyridoxine dependency and congenital hypophosphatasia are unusual metabolic disorders. We report a female infant born from healthy consanguineous parents with shortening of limbs, detected during pregnancy by ultrasonography. Immediately after delivery, the baby was admitted to the neonatal intensive care unit because of respiratory distress. A bone radiograph showed hypomineralization of all bones, and serum alkaline phosphatase was very low (10 U/L). Within the first day of life, seizures (focal clonic and tonic) started. The seizures were refractory to phenobarbital and other antiepileptic drugs. The first electroencephalogram (EEG) showed a burst-suppression pattern. Pyridoxine was administered (50 mg/kg) and completely controlled the seizures. Antiepileptic drugs were discontinued, and a maintenance dose of pyridoxine (10 mg/day) was established. A postpyridoxine EEG revealed the disappearance of the burst-suppression pattern. The patient died at age 26 days. Pyridoxine-dependent seizures, when recognized early and treated, have a more favorable prognosis. However, hypophosphatasia detected at birth almost always has a lethal outcome.

  7. PNPO deficiency: an under diagnosed inborn error of pyridoxine metabolism.

    NARCIS (Netherlands)

    Khayat, M.; Korman, S.H.; Frankel, P.; Weintraub, Z.; Hershckowitz, S.; Sheffer, V.F.; Elisha, M. Ben; Wevers, R.A.; Falik-Zaccai, T.C.

    2008-01-01

    The rare autosomal recessive disorder pyridoxine 5'-phosphate oxidase (PNPO) deficiency is a recently described cause of neonatal and infantile seizures. Clinical evaluation, and biochemical and genetic testing, were performed on a neonate with intractable seizures who did not respond to

  8. Mutations in antiquitin in individuals with pyridoxine-dependent seizures.

    NARCIS (Netherlands)

    Mills, P.B.; Struys, E.A.; Jakobs, C.; Plecko, B.; Baxter, P.; Baumgartner, M.; Willemsen, M.A.A.P.; Omran, H.; Tacke, U.; Uhlenberg, B.; Weschke, B.; Clayton, P.T.

    2006-01-01

    We show here that children with pyridoxine-dependent seizures (PDS) have mutations in the ALDH7A1 gene, which encodes antiquitin; these mutations abolish the activity of antiquitin as a delta1-piperideine-6-carboxylate (P6C)-alpha-aminoadipic semialdehyde (alpha-AASA) dehydrogenase. The accumulating

  9. [Depression, contraceptive pills and pyridoxine (vitamin B6)].

    Science.gov (United States)

    Bergsjo, P

    1974-05-20

    Women who use oral contraceptives experience depression and loss of libido in about 7% of the cases in various studies. This may be due to a lack of pyridoxine (Vitamin-B6). Dosage of Vitamin-B6 from 20-50 mg given daily to women suffering from depression helped in many cases.

  10. Acute isoniazid toxicity and the need for adequate pyridoxine supplies.

    Science.gov (United States)

    Morrow, Lee E; Wear, Robert E; Schuller, Dan; Malesker, Mark

    2006-10-01

    A 25-year-old, 54-kg Hispanic man who had recently started multidrug therapy for pulmonary tuberculosis presented in status epilepticus after ingesting 9 g of isoniazid in a suicide attempt. Successful management of this patient required collaboration between several institutions to provide the large amount of necessary intravenous pyridoxine. Ultimately, this single overdose depleted the supply of intravenous pyridoxine for a significant region of the state of Nebraska. Isoniazid is commonly used to treat tuberculosis, but it is encountered relatively infrequently as the cause of an acute overdose. Severe isoniazid overdoses may present as seizure activity that is refractory to conventional antiepileptic therapy. Although intravenous pyridoxine is an effective antidote for isoniazid overdoses in patients presenting with status epilepticus, this agent has few indications and is typically stocked in limited quantities. In regions with large populations of patients who receive antituberculosis therapy, collaborative networks must be created to ensure that adequate supplies of intravenous pyridoxine (> or = 20 g) are available for effective treatment of isoniazid poisonings.

  11. Pyridoxine-induced sensory ataxic neuronopathy and neuropathy: revisited.

    Science.gov (United States)

    Kulkantrakorn, Kongkiat

    2014-11-01

    High dose pyridoxine is neurotoxic. Previous case reports were sparse and little is known about the clinical and electrodiagnostic findings. Three patients with pyridoxine-induced sensory ataxic neuropathy were studied and a review of the involved literature was performed. Three patients, aged 80, 83 and 83 years old, presented with sensory ataxia for 3-8 months. Examination showed signs of polyneuropathy and sensory ataxia. Six hundred milligrams of pyridoxine was consumed each day for 3-10 years, in the form of vitamin B1-6-12 combination tablet. Investigations for other causes of neuropathy were unremarkable. Blood levels of vitamin B6 were markedly elevated at 104.6, 81.4 and 66.9 times of upper normal limits. Electrodiagnostic tests showed symmetric axonal sensory polyneuropathy in two patients. Two years after vitamin discontinuation, all patients showed no significant improvement in the neuropathy and gait. In conclusion, consumption of high dose pyridoxine can cause sensory neuronopathy and axonal sensorimotor polyneuropathy, leading to sensory ataxia which may not be reversible.

  12. Pyridoxine and pyridostigmine treatment in vincristine-induced neuropathy.

    Science.gov (United States)

    Ozyurek, Hamit; Turker, Hande; Akbalik, Mehtap; Bayrak, Ayse Oytun; Ince, Hulya; Duru, Feride

    2007-09-01

    Vincristine is a commonly used antineoplastic drug and frequently causes neurotoxicity. Here the authors report a 4-year-old boy with acute lymphoblastic leukemia in whom vincristine-induced peripheral and cranial neuropathy developed during remission induction therapy. The patient seemed to benefit from pyridoxine and pyridostigmine therapy greatly and this therapy is recommended in patients with severe vincristine-induced neuropathy.

  13. Amitriptyline-related peripheral neuropathy relieved during pyridoxine hydrochloride administration.

    Science.gov (United States)

    Meadows, G G; Huff, M R; Fredericks, S

    1982-11-01

    Tricyclic antidepressants rarely cause peripheral neuropathy. In fact, this class of drugs has been used to control the symptoms of pain and paresthesia that accompany peripheral neuropathy. We report peripheral paresthesias that occurred in a 39-year-old female during five years of amitriptyline administration. The patient's symptoms were relieved by oral pyridoxine hydrochloride, associated with elevated plasma pyridoxal phosphate.

  14. Triple therapy with pyridoxine, arginine supplementation and dietary lysine restriction in pyridoxine-dependent epilepsy: Neurodevelopmental outcome.

    Science.gov (United States)

    Coughlin, Curtis R; van Karnebeek, Clara D M; Al-Hertani, Walla; Shuen, Andrew Y; Jaggumantri, Sravan; Jack, Rhona M; Gaughan, Sommer; Burns, Casey; Mirsky, David M; Gallagher, Renata C; Van Hove, Johan L K

    2015-01-01

    Pyridoxine-dependent epilepsy (PDE) is an epileptic encephalopathy characterized by response to pharmacologic doses of pyridoxine. PDE is caused by deficiency of α-aminoadipic semialdehyde dehydrogenase resulting in impaired lysine degradation and subsequent accumulation of α-aminoadipic semialdehyde. Despite adequate seizure control with pyridoxine monotherapy, 75% of individuals with PDE have significant developmental delay and intellectual disability. We describe a new combined therapeutic approach to reduce putative toxic metabolites from impaired lysine metabolism. This approach utilizes pyridoxine, a lysine-restricted diet to limit the substrate that leads to neurotoxic metabolite accumulation and L-arginine to compete for brain lysine influx and liver mitochondrial import. We report the developmental and biochemical outcome of six subjects who were treated with this triple therapy. Triple therapy reduced CSF, plasma, and urine biomarkers associated with neurotoxicity in PDE. The addition of arginine supplementation to children already treated with dietary lysine restriction and pyridoxine further reduced toxic metabolites, and in some subjects appeared to improve neurodevelopmental outcome. Dietary lysine restriction was associated with improved seizure control in one subject, and the addition of arginine supplementation increased the objective motor outcome scale in two twin siblings, illustrating the contribution of each component of this treatment combination. Optimal results were noted in the individual treated with triple therapy early in the course of the disease. Residual disease symptoms could be related to early injury suggested by initial MR imaging prior to initiation of treatment or from severe epilepsy prior to diagnosis. This observational study reports the use of triple therapy, which combines three effective components in this rare condition, and suggests that early diagnosis and treatment with this new triple therapy may ameliorate the

  15. Pyridoxine-induced toxicity in rats: a stereological quantification of the sensory neuropathy.

    Science.gov (United States)

    Perry, Tracy Ann; Weerasuriya, Ananda; Mouton, Peter R; Holloway, Harold W; Greig, Nigel H

    2004-11-01

    Excess ingestion of pyridoxine (vitamin B6) causes a severe sensory neuropathy in humans. The mechanism of action has not been fully elucidated, and studies of pyridoxine neuropathy in experimental animals have yielded disparate results. Pyridoxine intoxication appears to produce a neuropathy characterized by necrosis of dorsal root ganglion (DRG) sensory neurons and degeneration of peripheral and central sensory projections, with large diameter neurons being particularly affected. The major determinants affecting the severity of the pyridoxine neuropathy appear to be duration and dose of pyridoxine administration, differential neuronal vulnerability, and species susceptibility. The present study used design-based stereological techniques in conjunction with electrophysiological measures to quantify the morphological and physiological changes that occur in the DRG and the distal myelinated axons of the sciatic nerve following pyridoxine intoxication. This combined stereological and electrophysiological method demonstrates a general approach that could be used for assessing the correlation between pathophysiological and functional parameters in animal models of toxic neuropathy.

  16. Effects of magnesium and high dietary intakes of pyridoxine on the chick.

    Science.gov (United States)

    Rogerson, G; Singsen, E P

    1976-05-01

    Day-old broiler-type male chicks were used to determine what effects magnesium and high dietary pyridoxine had on the chick's performance. The chicks were randomly assigned to 15 treatments of magnesium at 875, 1375 and 1875 mg/kg. diet and pyridoxine at 1, 4, 31, 301, and 3001 mg/kg. diet in a 3 x 5 factorial block design. A regression was used to study some of the criteria. The highest mortality of 20% occurred in chicks on the 1875 mg. magnesium-3001 mg. pyridoxine treatment. Magnesium and pyridoxine had highly significant effects on body moisture. Effects due to magnesium and pyridoxine and the interaction between the two were highly significant for weight gain and the efficiency of feed utilization (E.F.U.) At 1875 mg. magnesium/kg diet, maximum growth response and E.F.U. were predicted to occur on 10 and 39 mg pyridoxine/kg diet, respectively, Neither magnesium nor the interaction between magnesium and pyridoxine had any significant effect on carcass protein. Pyridoxine had a highly significant effect on carcass protein. Maximum response in carcass protein occurred at 31 mg. pyridoxine/kg diet irrespective of magnesium level. Serum aminotransferase activity (S.A) was significant for magnesium, pyridoxine and the interaction between the two. Pyridoxine requirement for maximum S.A. was 49 mg/kg diet at 1875 mg magnesium/kg diet. Pyridoxine requirement for maximum response was highest for S.A. and least for growth. But S.A. had the highest R2 whereas growth had the least.

  17. Seizures caused by pyridoxine (vitamin B6) deficiency in adults: A case report and literature review

    OpenAIRE

    2014-01-01

    Pyridoxine (vitamin B6) deficiency is a recognised cause of intractable seizures in neonates. However, pyridoxine deficiency related seizures in adults were rarely reported. This article reports a case of a 79 year old lady who suffered from new-onset seizures and was successfully treated with vitamin B6. The patient had chronic renal disease and weight loss due to anepithymia following a pelvic fracture. This article also reviews literatures of seizures caused by pyridoxine deficiency in adu...

  18. A randomised study evaluating the use of pyridoxine to avoid capecitabine dose modifications

    OpenAIRE

    2012-01-01

    Background: Pyridoxine is frequently used to treat capecitabine-induced hand–foot syndrome (HFS), although the evidence of benefit is lacking. We performed a randomised placebo-controlled trial to determine whether pyridoxine could avoid the need for capecitabine dose modifications and improve outcomes. Methods: A total of 106 patients planned for palliative single-agent capecitabine (53 in each arm, 65%/ 35% colorectal/breast cancer) were randomised to receive either concomitant pyridoxine (...

  19. Pyridoxine Dependent Seizures-Report Of A Case And Brief Review Of Literature

    OpenAIRE

    2002-01-01

    Pyridoxine-dependent seizure is a rare autosornal recessive disorder that usually presents as neonatal intractable seizures. This syndrome is due to an inborn abnormality of the enzyme glutamic acid decarboxylase, which results in reduced pyridoxine-dependent synthesis of the inhibitory neurotransmitter gamma amino butyric acid. We report a girl child who had seizures on the second post natal day which was controlled with oral pyridoxine. She had status epilepticus twice when the drug was ...

  20. Pyridoxine-dependent seizures: 10-year follow-up of eight cases.

    Science.gov (United States)

    Koul, Roshan

    2009-01-01

    Eight children with pyridoxine-dependent seizures (PDS) were seen over a period of 10 years. Of those children, 6 are on regular follow-up. Four of the children were seen in one family. All the patients presented with refractory seizures, mainly neonatal status epilepticus. Though PDS is a rare condition, it must be considered in all cases with refractory seizures, particularly in children younger than 3 years. When confirming a diagnosis, oral pyridoxine is as effective as intravenous pyridoxine.

  1. THE EFFECT OF A PYRIDOXINE DEFICIENCY ON COLD-ADJUSTED RATS

    Science.gov (United States)

    Ninety-one rats, of which 49 were kept at 25 C and 42 at 5 C, were fed a pyridoxine -free diet until growth ceased. Following this, graded levels of... pyridoxine were fed for 28 days at both temperatures. Food intake and growth were measured. The pyridoxine requirement, expressed as micrograms per...Food intake in the cold rats was characteristically depressed by the vitamin deficiency, while being simultaneously stimulated by the low environmental temperatures. (Author)

  2. Subepidermal vesicular dermatosis and sensory peripheral neuropathy caused by pyridoxine abuse.

    Science.gov (United States)

    Friedman, M A; Resnick, J S; Baer, R L

    1986-05-01

    A woman who had ingested 2 gm of pyridoxine (vitamin B6) daily for 2 years for menstrual water retention developed a subepidermal vesicular eruption on the dorsa of the hands and toes, as well as a sensory peripheral neuropathy. The cutaneous and neurologic manifestations subsided about 2 months after discontinuation of the pyridoxine. The possible relationship of subepidermal vesicular eruptions caused by pyridoxine abuse to epidermolysis bullosa acquisita is discussed.

  3. Glutamate Carboxypeptidase II Inhibition Behaviorally and Physiologically Improves Pyridoxine-Induced Neuropathy in Rats

    OpenAIRE

    2014-01-01

    Pyridoxine is used as a supplement for treating conditions such as vitamin deficiency as well as neurological disorders such as depression, epilepsy and autism. A significant neurologic complication of pyridoxine therapy is peripheral neuropathy thought to be a result of long-term and high dose usage. Although pyridoxine-induced neuropathy is transient and can remit after its withdrawal, the process of complete recovery can be slow. Glutamate carboxypeptidase II (GCP II) inhibition has been s...

  4. Simultaneous determination of melatonin and pyridoxine in tablets by gas chromatography-mass spectrometry.

    Science.gov (United States)

    Nùñez-Vergara, L J; Squella, J A; Sturm, J C; Baez, H; Camargo, C

    2001-12-01

    A gas chromatographic-mass spectrometric (GC-MS) method for the qualitative and quantitative determination of melatonin plus pyridoxine commercial tablets is described. Melatonin and pyridoxine were simultaneously determined by GC-MS after extraction from ground tablets with methanol and derivatization with N-methyl-N-N-trimethlylsilyltrifluoroacetamide (MSTFA). The mass chromatograms were generated using 232 m/z ion for melatonin and 280 m/z ion for pyridoxine, respectively. Splitless injection offers good reproducibility with a standard deviation of 2%. The developed method was applied to analyze the melatonin and pyridoxine content from two different tablet formulations. Also, recovery, detection and quantification limits are reported.

  5. Ultrasonic study of pyridoxine solutions at different temperatures and concentrations

    Science.gov (United States)

    Naik, Ritesh R.; Bawankar, S. V.; Tekade, P. V.; Mahodaya, Om A.

    2015-01-01

    In the present study ultrasonic velocity ( U), density (ρ), and viscosity (η) have been measured at frequency 1 MHz in the binary mixtures of pyridoxine hydrochloride with water in the concentration range (0.1 to 0.0125 M) at 303, 308, 313 K using multifrequency ultrasonic interferometer. The measured value of density, ultrasonic velocity, and viscosity have been used to estimate the acoustical parameters namely adiabatic compressibility (β a), relaxation time (τ), acoustic impedance ( z), free length ( L f), free volume ( V f), and internal pressure ( P i), Wada's constant to investigate the nature and strength of molecular interaction in the binary mixture of pyridoxine hydrochloride with water. The obtained result support the complex formation, molecular association by intermolecular hydrogen bonding in the binary liquid mixtures.

  6. Letter: supplementary pyridoxine given to women using oral contraceptives.

    Science.gov (United States)

    Winston, F

    1975-07-15

    This letter is a response to an article describing the efficacy of administering large doses of tryptophan to depressive patients taking oral contraceptives. This letter-writer argues that the salient action of mood elevation is a result of the supplemental pyridoxine (vitamin B) which ameliorates the deficiency induced by oral contraceptive use that leads to depression resulting from inhibition of synthesis of biogenic amines in the central nervous system. Instead of large doses of tryptophan, which may cause dangerous accumulations of possibly carcinogenic and diabetogenic metabolites when therapy for depression is indicated, pyridoxine should be administered together with the tryptophan; the tryptophan should be discontinued once the deficiency is corrected, although the vitamin therapy should continue throughout oral contraceptive use.

  7. Two successful pregnancies in pyridoxine-nonresponsive homocystinuria.

    Science.gov (United States)

    Vilaseca, M A; Cuartero, M L; Martinez de Salinas, M; Lambruschini, N; Pintó, X; Urreizti, R; Balcells, S; Grinberg, D

    2004-01-01

    Two successful pregnancies are reported in a pyridoxine-nonresponsive woman who was also homozygous for the MTHFR 677C>T polymorphism. Two healthy children were delivered, although there had also been an early miscarriage of an apparently normal fetus in another pregnancy. Management of the patient's homocystine and methionine levels was maintained throughout pregnancy and, in view of the increased thromboembolic risk, anticoagulation therapy was also included in management.

  8. Pyridoxine induces non-specific EEG alterations in infants with therapy resistant seizures

    NARCIS (Netherlands)

    Teune, L. K.; Van der Hoeven, J. H.; Maurits, N. M.; Bos, A. F.; Alffenaar, J. W. C.; Reijngoud, D. J.; Brouwer, O. F.; Sival, D.A.

    2007-01-01

    Purpose: In infants with frequent therapy resistant seizures (TRS-infants), clinical detection of pyridoxine-dependency (PD) or -responsiveness (PR) occurs by empirical intravenous (IV) pyridoxine administration during recording of the EEG. However, in undiagnosed TRS-infants it is stilt unclear to

  9. High-dosage pyridoxine-induced auditory neuropathy and protection with coffee in mice.

    Science.gov (United States)

    Hong, Bin Na; Yi, Tae Hoo; Kim, Sun Yeou; Kang, Tong Ho

    2009-04-01

    Auditory neuropathy (AN) is a hearing disorder characterized by an abnormal auditory brainstem response (ABR). This study examined experimental AN model induced in mice following increased dosages of pyridoxine. Induced AN was examined for pyridoxine treatment. To assess AN, we evaluated the ABR, auditory middle latency response (AMLR), otoacoustic emission (OAE), and histochemical morphology of the auditory nerve. Pyridoxine-treated mice exhibited an increase in the hearing threshold shift and delayed latency of both ABR and AMLR in proportion to pyridoxine dosage. Additionally, the extent of auditory nerve fiber loss increased in a dose-dependent manner following pyridoxine intoxication. Coffee or trigonelline treatment ameliorated the hearing threshold shift, delayed latency of the auditory evoked potential, and improved sensory fiber loss induced by pyridoxine intoxication. The present findings demonstrate that high-dose pyridoxine administration can be used to produce a new mouse model for AN, and coffee or trigonelline as a main active compound of coffee extract can potentially facilitate recovery from pyridoxine-induced auditory neuropathy.

  10. Pyridoxine as an adjunct in the treatment of carpal tunnel syndrome.

    Science.gov (United States)

    Amadio, P C

    1985-03-01

    Nineteen consecutive patients with carpal tunnel syndrome were treated with pyridoxine. Two thirds of the patients who specifically presented symptoms of median neuropathy eventually required surgical release. Although pyridoxine may have a place alongside other nonsurgical modalities in the treatment of carpal tunnel syndrome, surgical release continues to be indicated in many patients with carpal tunnel syndrome.

  11. Pyridoxine-dependent seizures: a case report and a critical review of the literature.

    Science.gov (United States)

    Gupta, V K; Mishra, D; Mathur, I; Singh, K K

    2001-12-01

    Pyridoxine-dependent seizures are a recognized, although rare, cause of intractable seizures in neonates. Patients with this autosomal recessive disorder have recurrent seizures that are resistant to conventional anticonvulsants but respond dramatically to intravenous administration of pyridoxine. Life-long supplementation with pyridoxine is required to prevent seizure recurrence. In the absence of a biological marker for the disease, clinical diagnosis is often delayed and severe neurological sequelae are common. Herein, we report on the clinical course of a neonate with pyridoxine-dependent seizures. Delayed normalization of the electroencephalogram and a normal developmental outcome (at 15 months of age) on a dose of 10 mg/kg pyridoxine are distinctive features of the present case. We also review recent clinical observations and neurochemical studies that have added to our knowledge of this disorder.

  12. A case of extreme prematurity and delayed diagnosis of pyridoxine-dependent epilepsy.

    Science.gov (United States)

    Al-Saman, Abdulaziz S; Rizk, Tamer M

    2012-10-01

    Pyridoxine-dependent epilepsy presents early in life, even in utero. It is usually refractory to conventional antiepileptic medications and responds only to lifelong pyridoxine supplementation. Seizures are usually generalized tonic clonic. We report a 3-year-old child that was born prematurely at 25 weeks of gestation. He presented with abnormal movements in the second month of life. At 10 months of age he presented with status epilepticus, which was refractory to multiple antiepileptic medications and was controlled with intravenous pyridoxine. An elevated level of a-aminoadipic semialdehyde excretion in the urine supported the diagnosis of pyridoxine-dependent epilepsy. Subsequently, a c.1195G>C homozygous mutation in the 5q31 aldehyde dehydrogenase 7A1 gene was confirmed. This case calls for considering pyridoxine-dependent epilepsy and its early management in cases with resistant seizures; even in the presence of extreme prematurity with its neurological consequences.

  13. Diagnosis of pyridoxine-dependent seizures in a nineteen-year-old patient.

    Science.gov (United States)

    Russell, Kate E; Mulligan, Sarah R; Mallory, Leah A

    2012-08-01

    Although a diagnosis of pyridoxine-dependent seizures may commonly be delayed, this case involves an extremely late diagnosis with associated morbidity. Our patient received pyridoxine during the neonatal period, in conjunction with other antiepileptic drugs that masked its effect. This patient also underwent ventriculoperitoneal shunting, which complicated the diagnosis. Pyridoxine was continued with other antiepileptic drugs, without definite recognition of its therapeutic relationship. Pyridoxine-dependent seizures were finally recognized at age 19 years when the patient manifested refractory status epilepticus, several days after wisdom tooth removal (and discontinuing oral medications including pyridoxine and phenobarbital before surgery). The diagnosis was only established via genetic testing. Our patient highlights the difficulty in diagnosing this rare seizure type and its potential importance in refractory epilepsy.

  14. Effects of pyridoxine on rat testes by means of Sertoli-germ cell co-culture system in vitro

    Institute of Scientific and Technical Information of China (English)

    Huang Houjin

    2001-01-01

    Objective To investigate the effects of pyridoxine on rat testis in vitro. Method an in vitro systen of Sertoligem cell co-culture was applied, the toxic effects of pyridoxine at different concentrations an exposed duration were olserved. Results The detachment of germ cells from sertoli cells showed marked dose-response and time response relafionships with the exposure of pyridoxine. Meanwhile, the characteristic of loosing and ratracting skeletun in the Sertoli cells was found. Conclusions The effects induced by pyridoxine in vitro may reflect damage to Sertoli cells, and testicular cells co-culture could be of value for the study of underlying mechanisms of toxic effects of pyridoxine on rat testis.

  15. Pyridoxine responsiveness in novel mutations of the PNPO gene

    OpenAIRE

    2014-01-01

    OBJECTIVE: To determine whether patients with pyridoxine-responsive seizures but normal biomarkers for antiquitin deficiency and normal sequencing of the ALDH7A1 gene may have PNPO mutations. METHODS: We sequenced the PNPO gene in 31 patients who fulfilled the above-mentioned criteria. RESULTS: We were able to identify 11 patients carrying 3 novel mutations of the PNPO gene. In 6 families, a homozygous missense mutation p.Arg225His in exon 7 was identified, while 1 family was compound h...

  16. Pyridoxine neuropathy in rats: specific degeneration of sensory axons.

    Science.gov (United States)

    Windebank, A J; Low, P A; Blexrud, M D; Schmelzer, J D; Schaumburg, H H

    1985-11-01

    When rats received pyridoxine in doses large enough to cause neuropathy in humans, the animals developed gait ataxia that subsided after the toxin was withdrawn. By using quantitative histologic techniques, we found axonal degeneration of sensory system fibers and that the fibers derived from the ventral root were spared. Although the degeneration approached the dorsal root ganglion, neurons in the ganglion did not degenerate. We found no early decrease in oxygen consumption of nerve, suggesting that impaired oxidative metabolism was not the primary event.

  17. Pyridoxine-dependent epilepsy with elevated urinary α-amino adipic semialdehyde in molybdenum cofactor deficiency.

    Science.gov (United States)

    Struys, Eduard Alexander; Nota, Benjamin; Bakkali, Abdellatif; Al Shahwan, Saad; Salomons, Gajja Sophi; Tabarki, Brahim

    2012-12-01

    α-Amino adipic semialdehyde (α-AASA) accumulates in body fluids from patients with pyridoxine-dependent epilepsy because of mutations in antiquitin (ALDH7A1) and serves as the biomarker for this condition. We have recently found that the urinary excretion of α-AASA was also increased in molybdenum cofactor and sulfite oxidase deficiencies. The seizures in pyridoxine-dependent epilepsy are caused by lowered cerebral levels of pyridoxal-5-phosphate (PLP), the bioactive form of pyridoxine (vitamin B(6)), which can be corrected by the supplementation of pyridoxine. The nonenzymatic trapping of PLP by the cyclic form of α-AASA is causative for the lowered cerebral PLP levels. We describe 2 siblings with clinically evident pyridoxine-responsive seizures associated with increased urinary excretion of α-AASA. Subsequent metabolic investigations revealed several metabolic abnormities, all indicative for molybdenum cofactor deficiency. Molecular investigations indeed revealed a known homozygous mutation in the MOCS2 gene. Based upon the clinically evident pyridoxine-responsive seizures in these 2 siblings, we recommend considering pyridoxine supplementation to patients affected with molybdenum cofactor or sulfite oxidase deficiencies.

  18. Immune-dependent antineoplastic effects of cisplatin plus pyridoxine in non-small-cell lung cancer.

    Science.gov (United States)

    Aranda, F; Bloy, N; Pesquet, J; Petit, B; Chaba, K; Sauvat, A; Kepp, O; Khadra, N; Enot, D; Pfirschke, C; Pittet, M; Zitvogel, L; Kroemer, G; Senovilla, L

    2015-06-04

    cis-Diamminedichloroplatinum(II) (CDDP), which is mostly referred to as cisplatin, is a widely used antineoplastic. The efficacy of cisplatin can be improved by combining it with the vitamin B6 precursor pyridoxine. Here, we evaluated the putative synergistic interaction of CDDP with pyridoxine in the treatment of an orthotopic mouse model of non-small-cell lung cancer (NSCLC). CDDP and pyridoxine exhibited hyperadditive therapeutic effects. However, this synergy was only observed in the context of an intact immune system and disappeared when the otherwise successful drug combination was applied to the same NSCLC cancer implanted in the lungs of athymic mice (which lack T lymphocytes). Immunocompetent mice that had been cured from NSCLC by the combined regimen of CDDP plus pyridoxine became resistant against subcutaneous rechallenge with the same (but not with an unrelated) cancer cell line. In vitro, CDDP and pyridoxine did not only cause synergistic killing of NSCLC cells but also elicited signs of immunogenic cell death including an endoplasmic reticulum stress response and exposure of calreticulin at the surface of the NSCLC cells. NSCLC cells treated with CDDP plus pyridoxine in vitro elicited a protective anticancer immune response upon their injection into immunocompetent mice. Altogether, these results suggest that the combined regimen of cisplatin plus pyridoxine mediates immune-dependent antineoplastic effects against NSCLC.

  19. High-yield recombinant xylanase production by Aspergillus nidulans under pyridoxine limitation.

    Science.gov (United States)

    Müller, Michael; Segato, Fernando; Prade, Rolf A; Wilkins, Mark R

    2014-10-01

    The present study investigated the limitation of pyridoxine on an Aspergillus nidulans culture that produces xylanase B (XynB) as a client enzyme and was unable to synthesize pyridoxine. This technique was used to limit cell growth and divert substrate to product formation for a surface grown culture that could be used in trickle bed reactors. It was observed that growth was limited when pyridoxine was absent, while enzyme production was unaffected. Enzyme production was 1,026 U after 480 h of continuous fermentation, which was similar to a culture that grew on medium with pyridoxine. Furthermore, the present study investigated the growth rate of A. nidulans with pyridoxine in the medium and determined the productivity of XynB production with and without pyridoxine. A maximum growth rate of 0.311/h was observed. The maximum XynB productivity of 21.14 U/g h was achieved when pyridoxine was not added to the medium.

  20. Clinical features and the management of pyridoxine-dependent and pyridoxine-responsive seizures: review of 63 North American cases submitted to a patient registry.

    Science.gov (United States)

    Basura, Gregory J; Hagland, Shawn P; Wiltse, Anna M; Gospe, Sidney M

    2009-06-01

    To facilitate clinical research on pyridoxine-dependent seizures (PDS), a rare disease registry was established for affected patients in the United States and Canada. From 1999 to 2007, 63 cases, ranging in age from 11 months to 40 years, were registered. All registered cases were diagnosed with PDS by their physicians using clinical criteria. Seventy percent of the cases presented with neonatal seizures, and the mean lag time between presentation and diagnosis was 313 days. Pyridoxine treatment regimens were varied, ranging from 50 to 2,500 mg per day (1.4 to 67.8 mg/kg/day). While 47 of the cases were seizure-free on pyridoxine monotherapy, over time, eight other cases also required the concomitant use of anticonvulsants for effective seizure control, while the remainder continued to have recurrent seizures, despite the use of pyridoxine and multiple anticonvulsants. Our review of this collection of cases suggests that, for some registered individuals, either pyridoxine may be acting as an adjunctive anticonvulsant or the patient may have developed a secondary etiology for seizures. In addition, some of these cases may have pyridoxine-responsive seizures (PRS) rather than pyridoxine-dependency. Four adult and seven school-aged cases were described as developmentally normal, while the other cases had a variety of neurodevelopmental handicaps. Twenty-five percent of the cases required the pharmacologic treatment of behavioral symptoms. Clinicians caring for neonates and other young patients with intractable seizures do not necessarily consider PDS as an etiology; therefore, certain cases may be undiagnosed or diagnosed late in the course of their evaluation and treatment. As the diagnosis of PDS can now be confirmed by genetic and biochemical testing, formal screening protocols for this disorder should be developed. Patients previously diagnosed with PDS by clinical criteria should also receive confirmatory testing.

  1. Pyridoxine-dependent seizures: findings from recent studies pose new questions.

    Science.gov (United States)

    Gospe, Sidney M

    2002-03-01

    Pyridoxine-dependent seizures, although a rare clinical entity, have been recognized as an etiology of intractable seizures in neonates and infants for more than 45 years. Recent research has focused on the molecular and neurochemical aspects of this disorder, as well as the optimal treatment of the condition. This review discusses the clinical features and management of patients with pyridoxine-dependent seizures together with a new hypothesis suggesting that an abnormality of pyridoxine transport may underlie the pathophysiology of this autosomal-recessive disorder.

  2. Pyridoxine-dependent seizures: 10-year follow-up of eight cases

    Directory of Open Access Journals (Sweden)

    Koul Roshan

    2009-01-01

    Full Text Available Eight children with pyridoxine-dependent seizures (PDS were seen over a period of 10 years. Of those children, 6 are on regular follow-up. Four of the children were seen in one family. All the patients presented with refractory seizures, mainly neonatal status epilepticus. Though PDS is a rare condition, it must be considered in all cases with refractory seizures, particularly in childrens younger than 3 years. When confirming a diagnosis, oral pyridoxine is as effective as intravenous pyridoxine.

  3. Pyridoxine neuropathy. A four-year electrophysiological and clinical follow-up of a severe case.

    Science.gov (United States)

    Santoro, L; Ragno, M; Nucciotti, R; Barbieri, F; Caruso, G

    1991-02-01

    In a 54-year-old male a severe sensory neuropathy was observed during treatment for pulmonary tuberculosis with isoniazid (400 mg/day) and pyridoxine (600 mg/day). Eight months after withdrawal from isoniazid the sensory symptomatology was still progressing, although muscle strength was never reduced. A sural nerve biopsy revealed marked loss of large myelinated fibres. Only when pyridoxine treatment was interrupted did a slow improvement begin. A clinical and electrophysiologic follow-up showed a very slow and still incomplete recovery after four years. The possibility of an unusual individual susceptibility to toxic effects of pyridoxine is considered.

  4. Pyridoxine-dependent seizures: long-term follow-up of two cases with clinical and MRI findings, and pyridoxine treatment.

    Science.gov (United States)

    Ulvi, Hizir; Müngen, Bülent; Yakinci, Cengiz; Yoldaş, Tahir

    2002-10-01

    Pyridoxine-dependency is a rare autosomal recessive disorder causing a severe seizure disorder of neonatal onset. There are a few reports including neuroimaging studies, such as cranial CT and MRI, and one report with longitudinal MRI findings in two cases with pyridoxine-dependent seizures (PDS). We report long-term follow-up of two siblngs with PDS in the light of clinical, EEG, CT and MRI findings, and pyridoxine treatment. The first patient, an 8-year-old female who had neonatal seizures, has sequential cranial CT and MRIs which are normal except for mega cistema magna thus far. She still has mild mental retardation, although the accurate diagnosis was made when she was 6 years old and pyridoxine treatment was initiated. The second patient, a 1-year-old female, who is the younger sibling of the first patient, presented with neonatal seizures and PDS was diagnosed immediately, with resulting pyridoxine treatment (10 mg/kg/day). She is now neurologically normal, seizure-free, and has sequential normal CT and MRIs. These patients show rather benign clinical courses.

  5. Clinical, Biochemical, and Molecular Studies and Treatment of Pyridoxine-Dependent Epilepsy

    Directory of Open Access Journals (Sweden)

    J. Gordon Millichap

    2013-03-01

    Full Text Available Researchers at Autonomous University of Madrid, and other centers in Spain studied the clinical, biochemical, and genetic spectrum of pyridoxine-dependent epilepsy (PDE in 12 patients with the clinically proven diagnosis.

  6. Focal status epilepticus as atypical presentation of pyridoxine-dependent epilepsy.

    Science.gov (United States)

    Yoshii, Akira; Takeoka, Masanori; Kelly, Peter J; Krishnamoorthy, Kalpahty S

    2005-08-01

    Pyridoxine-dependent epilepsy usually presents in the neonatal period or even in utero, is refractory to antiepileptic medications, and is treatable with lifelong administration of pyridoxine. The seizures are typically generalized tonic-clonic, although myoclonic seizures or infantile spasms have been described. We report an infant who presented at 5 months of age with a right-sided clonic seizure with fever. Subsequently, she had recurrent right focal or generalized seizures despite sequential treatment with various antiepileptic medications. At 7 months, she was hospitalized with status epilepticus, which was finally controlled with pyridoxine. After she became seizure free, she continued to have a strong left arm preference with mild weakness of the right arm and delayed language skill. Eventually, she outgrew these symptoms. This case illustrates that pyridoxine-dependent epilepsy, although rare, must be included in the differential diagnosis of focal seizures, especially when the seizures are refractory to traditional antiepileptic drugs.

  7. Pyridoxine Dependent Seizures-Report Of A Case And Brief Review Of Literature

    Directory of Open Access Journals (Sweden)

    Rajesh R

    2002-01-01

    Full Text Available Pyridoxine-dependent seizure is a rare autosornal recessive disorder that usually presents as neonatal intractable seizures. This syndrome is due to an inborn abnormality of the enzyme glutamic acid decarboxylase, which results in reduced pyridoxine-dependent synthesis of the inhibitory neurotransmitter gamma amino butyric acid. We report a girl child who had seizures on the second post natal day which was controlled with oral pyridoxine. She had status epilepticus twice when the drug was stopped at the age of 3 months and 21 months. The neurological development was normal. There was normalization of EEG abnormalities on intravenous administration of 100 mg pyridoxine. A brief review of the literature is also included.

  8. Depression of jejunal dipeptide transport by pyridoxine deficiency in the rat.

    Science.gov (United States)

    Gupta, V J; Edwards, K D; Asatoor, A M

    1975-02-01

    Three dipeptides (L-alanyl-L-alanine, beta-alanyl-L-histidine and L-prolylglycine), representative of distinctly different transport groups, and a dicarboxylic acid dipeptide (L-glutamyl-L-glutamic acid) showed a quantitatively equivalent decrease of absorption (mean difference, 12% disappearance 15 min-1 5 cm-1) from jejunal loops in vivo in pyridoxine deficient rats, compared with pyridoxine-repleted controls. Analysis of results for seven dipeptides, including three studied previously, indicated that pyridoxine deficiency caused a general or non-specific reduction in dipeptide transport, similar for all dipeptides. Decrease in dipeptide transport in vitamin deficiency ran parallel to, but was significantly less than, the decrease in amino acid transport, suggesting in theory involvement of pyridoxine in a common cellular efflux mechanism or, less likely, in the energetics of active transport.

  9. Variations in the lipid profile of patients with chronic renal failure treated with pyridoxine

    OpenAIRE

    2003-01-01

    Abstract Background Hyperhomocysteinemia and lipid abnormalities are commonly found in patients with chronic renal failure; both are recognized as risk factors for atherosclerosis. The homocysteine-lowering effect of pyridoxine is controversial. This study was performed to determine the effect of a high dose of pyridoxine (300 mg i.v. three times a week) on plasma and red blood cell lipid profile and plasma homocysteine concentration in twelve chronic renal failure patients on regular hemodia...

  10. Lipid profiles of rats fed with diets supplemented with vitamins niacin and pyridoxine

    OpenAIRE

    2012-01-01

    Hypercholesterolemia is a major risk factor for cardiovascular disease. Supplements containing the vitamins niacin (B3) and pyridoxine (B6) can promote the reduction of total cholesterol and an increase in HDL cholesterol. In this study, the effects of diets supplemented with niacin (B3) and pyridoxine (B6) on the hepatic and serum lipid profiles of Wistar rats were assessed. The diets were prepared with combinations of three concentrations of niacin (3, 4 and 5 g/kg) ...

  11. Pyridoxine-dependent seizures: 10-year follow-up of eight cases

    OpenAIRE

    2009-01-01

    Eight children with pyridoxine-dependent seizures (PDS) were seen over a period of 10 years. Of those children, 6 are on regular follow-up. Four of the children were seen in one family. All the patients presented with refractory seizures, mainly neonatal status epilepticus. Though PDS is a rare condition, it must be considered in all cases with refractory seizures, particularly in childrens younger than 3 years. When confirming a diagnosis, oral pyridoxine is as effective as intravenous pyrid...

  12. Continuous xylanase production with Aspergillus nidulans under pyridoxine limitation using a trickle bed reactor.

    Science.gov (United States)

    Müller, Michael; Prade, Rolf A; Segato, Fernando; Atiyeh, Hasan K; Wilkins, Mark R

    2015-01-01

    A trickle bed reactor (TBR) with recycle was designed and tested using Aspergillus nidulans with a pyridoxine marker and over-expressing/secreting recombinant client xylanase B (XynB). The pyridoxine marker prevented the fungus from synthesizing its own pyridoxine and fungus was unable to grow when no pyridoxine was present in the medium; however, enzyme production was unaffected. Uncontrolled mycelia growth that led to clogging of the TBR was observed when fungus without a pyridoxine marker was used for XynB production. Using the fungus with pyridoxine marker, the TBR was operated continuously for 18 days and achieved a XynB output of 41 U/ml with an influent and effluent flow rate of 0.5 ml/min and a recycle flow rate of 56 ml/min. Production yields in the TBR were 1.4 times greater than a static tray culture and between 1.1 and 67 times greater than yields for SSF enzyme production stated in the literature.

  13. Pyridoxine-dependent epilepsy due to antiquitin deficiency: achieving a favourable outcome.

    Science.gov (United States)

    Oliveira, Renata; Pereira, Cristina; Rodrigues, Fidjy; Alfaite, Claudia; Garcia, Paula; Robalo, Conceição; Fineza, Isabel; Gonçalves, Olavo; Struys, Eduard; Salomons, Gajja; Jakobs, Cornelis; Diogo, Luísa

    2013-12-01

    We report 4 pyridoxine-dependent epilepsy patients in which good outcome was determined in three. The 4 patients were male and aged from 7 to 24 years old (from three unrelated Caucasian families). A clinical diagnosis of neonatal pyridoxine-dependent epilepsy was confirmed by biochemical and genetic studies. Clinical evaluation was performed and medical records were reviewed for therapy implementation and management, neurodevelopment outcome, magnetic resonance imaging, and electroencephalography. All were taking pyridoxine treatment and were seizure-free. Elevated urinary alpha-aminoadipic semialdehyde excretion was found in all patients. Antiquitin gene analysis identified a large homozygous deletion in one patient and two heterozygous mutations in the others. Treatment with pyridoxine should be attempted for all cases of infantile and childhood refractory epilepsy, as has been the case over the last 20 years. Currently, urinary alpha-aminoadipic semialdehyde is a reliable biomarker of pyridoxine-dependent epilepsy, even under pyridoxine treatment. Detection of mutations in the antiquitin gene, encoding alpha-aminoadipic semialdehyde dehydrogenase, establishes the diagnosis and allows for adequate genetic counselling.

  14. Antenatal treatment in two Dutch families with pyridoxine-dependent seizures.

    Science.gov (United States)

    Bok, Levinus A; Been, Jasper V; Struys, Eduard A; Jakobs, Cornelis; Rijper, Elisabeth A M; Willemsen, Michèl A

    2010-03-01

    Incidental reports suggest that antenatal treatment of pyridoxine dependent seizures (PDS) may improve neurodevelopmental outcome of affected patients. Two families with PDS are reported, both with two affected siblings. Antenatal treatment with pyridoxine was instituted during the second pregnancy in each family (50 and 60 mg daily from 3 and 10 weeks of gestation, respectively). Perinatal characteristics and neurodevelopmental outcome at 4 (Family A) and 12 (Family B) years of age were compared between the untreated and treated child within each family. Meconium-stained amniotic fluid was present in both first pregnancies and abnormal foetal movements were noticed in one. In the treated infants, pregnancy and birth were uncomplicated. In family A, postnatal pyridoxine supplementation prevented neonatal seizures. Both children in family A were hypotonic and started walking after 2 years of age; both had white matter changes on MRI, and the first child was treated for squint. IQ was 73 and 98 in the antenatally untreated and treated child, respectively. The second child in family B developed seizures on the seventh day, because pyridoxine maintenance therapy had not been instituted after birth. Seizures responded rapidly to pyridoxine supplementation. MRI showed large ventricles and a mega cisterna magna. IQ was 80 and 106 in the antenatally untreated and treated child respectively. Both children had normal motor development. These results suggest that antenatal pyridoxine supplementation may be effective in preventing intrauterine seizures, decreasing the risk of complicated birth and improving neurodevelopmental outcome in PDS.

  15. Molecular Basis of Reduced Pyridoxine 5′-Phosphate Oxidase Catalytic Activity in Neonatal Epileptic Encephalopathy Disorder*

    OpenAIRE

    2009-01-01

    Mutations in pyridoxine 5′-phosphate oxidase are known to cause neonatal epileptic encephalopathy. This disorder has no cure or effective treatment and is often fatal. Pyridoxine 5′-phosphate oxidase catalyzes the oxidation of pyridoxine 5′-phosphate to pyridoxal 5′-phosphate, the active cofactor form of vitamin B6 required by more than 140 different catalytic activities, including enzymes involved in amino acid metabolism and biosynthesis of neurotransmitters. Our aim is to elucidate the mec...

  16. Lack of efficacy of pyridoxine (vitamin B6) treatment in acquired idiopathic sideroblastic anaemia, including refractory anaemia with ring sideroblasts.

    Science.gov (United States)

    Baumann Kreuziger, Lisa M; Wolanskyj, Alexandra P; Hanson, Curtis A; Steensma, David P

    2011-06-01

    Pyridoxine, or vitamin B6, is commonly used to treat acquired idiopathic sideroblastic anaemia (AISA, including refractory anaemia with ring sideroblasts), but the efficacy of this therapy in an unselected AISA population (i.e. patients without confirmed ALAS2 or other pyridoxine-responsive germline mutations) has not been established. We reviewed clinical data from 231 patients with AISA and found that 42% of 203 evaluable patients had been treated with pyridoxine. Only 6.8% of pyridoxine-treated patients experienced a haemoglobin improvement (≥ 1.5 g/dL) meeting 2006 International Working Group for Myelodysplastic Syndromes standardised response criteria. As some patients received combination therapy with erythropoietin or other agents, improvement could be attributed to pyridoxine monotherapy in only one patient (1.4%). Smaller, less meaningful increments in haemoglobin levels of 0.5 g/dL were observed in 13.5% of patients. Response to therapy did not correlate with International Prognostic Scoring System (IPSS) risk group or multilineage vs unilineage dysplasia. New symptomatic peripheral neuropathy was noted in 2.3% of patients treated with pyridoxine. In this large series of unselected patients with sideroblastic anaemia, pyridoxine therapy was ineffective and was associated with a risk of adverse effects. Pyridoxine therapy should be reserved for patients with known or suspected pyridoxine-responsive mutations.

  17. Multiple mechanisms of action of pyridoxine in primary hyperoxaluria type 1.

    Science.gov (United States)

    Fargue, Sonia; Rumsby, Gill; Danpure, Christopher J

    2013-10-01

    Primary hyperoxaluria type 1 (PH1) is a rare hereditary calcium oxalate kidney stone disease caused by a deficiency of the liver-specific pyridoxal-phosphate-dependent peroxisomal enzyme alanine:glyoxylate aminotransferase (AGT). About one third of patients are responsive to pharmacological doses of pyridoxine (vitamin B6), but its mechanism of action is unknown. Using stably transformed Chinese Hamster Ovary (CHO) cells expressing various normal and mutant forms of AGT, we have shown that pyridoxine increases the net expression, catalytic activity and peroxisomal import of the most common mistargeted mutant form of AGT (i.e. Gly170Arg on the background of the polymorphic minor allele). These multiple effects explain for the first time the action of pyridoxine in the most common group of responsive patients. Partial effects of pyridoxine were also observed for two other common AGT mutants on the minor allele (i.e. Phe152Ile and Ile244Thr) but not for the minor allele mutant AGT containing a Gly41Arg replacement. These findings demonstrate that pyridoxine, which is metabolised to pyridoxal phosphate, the essential cofactor of AGT, achieves its effects both as a prosthetic group (increasing enzyme catalytic activity) and a chemical chaperone (increasing peroxisome targeting and net expression). This new understanding should aid the development of pharmacological treatments that attempt to enhance efficacy of pyridoxine in PH1, as well as encouraging a re-evaluation of the extent of pyridoxine responsiveness in PH1, as more patients than previously thought might benefit from such treatment.

  18. Pyridoxine for prevention of hand-foot syndrome caused by chemotherapy: a systematic review.

    Directory of Open Access Journals (Sweden)

    Min Chen

    Full Text Available BACKGROUND: Hand-foot syndrome (HFS is a relatively frequent dermatologic toxic reaction to certain anti-cancer chemotherapies. The syndrome can evolve into a distressing condition that limits function and affects quality of life. Pyridoxine (vitamin B6 has been used empirically for the prevention of HFS caused by anti-cancer therapy. However, evidence of its efficacy remains controversial. METHODOLOGY//PRINCIPAL FINDINGS: Systematic literature searches were conducted on the Cochrane Library, PUBMED, EMBASE, LILACS, CBM, CNKI, VIP, WANFANG and the U.S. ClinicalTrials.gov website. We included all related randomized controlled trials (RCTs irrespective of language. Reviewers from different professions independently assessed all potential studies and extracted data. Subgroup analysis was planned according to dose of pyridoxine. 5 RCTs involving 607 patients were contributed to the meta-analysis. No significant differences were found between patients receiving pyridoxine and placebo for prevention of incidence of HFS and grade 2 or worse HFS (relative risk (RR 0.96, 95%confidence interval (CI 0.86-1.06; RR0.95, 95%CI 0.73-1.24, respectively. Similarly, no significant improvement in quality of life was detected among patients. However, significant difference was found for prevention of grade 2 or worse HFS with pyridoxine 400 mg daily compared to 200 mg (RR0.55, 95%CI 0.33-0.92. CONCLUSIONS/SIGNIFICANCE: There is inadequate evidence to make any recommendation about using pyridoxine for prevention of HFS caused by chemotherapy. However, pyridoxine 400 mg may have some efficacy. Further studies of large sample sizes are needed to evaluate the efficacy and safety of pyridoxine, especially at high dose, in comparison with placebo.

  19. Glutamate carboxypeptidase II inhibition behaviorally and physiologically improves pyridoxine-induced neuropathy in rats.

    Directory of Open Access Journals (Sweden)

    Michelle C Potter

    Full Text Available Pyridoxine is used as a supplement for treating conditions such as vitamin deficiency as well as neurological disorders such as depression, epilepsy and autism. A significant neurologic complication of pyridoxine therapy is peripheral neuropathy thought to be a result of long-term and high dose usage. Although pyridoxine-induced neuropathy is transient and can remit after its withdrawal, the process of complete recovery can be slow. Glutamate carboxypeptidase II (GCP II inhibition has been shown to improve symptoms of both chemotherapy- and diabetic-induced neuropathy. This study evaluated if GCP II inhibition could behaviorally and physiologically improve pyridoxine-induced neuropathy. In the current study, high doses of pyridoxine (400 mg/kg, twice a day for seven days were used to induce neuropathy in rats. An orally bioavailable GCP II inhibitor, 2-(3-mercaptopropyl pentanedioic acid (2-MPPA, was administered daily at a dose of 30 mg/kg starting from the onset of pyridoxine injections. Body weight, motor coordination, heat sensitivity, electromyographical (EMG parameters and nerve morphological features were monitored. The results show beneficial effects of GCP II inhibition including normalization of hot plate reaction time, foot fault improvements and increased open field distance travelled. H wave frequency, amplitude and latency as well as sensory nerve conduction velocity (SNCV were also significantly improved by 2-MPPA. Lastly, GCP II inhibition resulted in morphological protection in the spinal cord and sensory fibers in the lumbar region dorsal root ganglia (DRG. In conclusion, inhibition of GCP II may be beneficial against the peripheral sensory neuropathy caused by pyridoxine.

  20. Glutamate carboxypeptidase II inhibition behaviorally and physiologically improves pyridoxine-induced neuropathy in rats.

    Science.gov (United States)

    Potter, Michelle C; Wozniak, Krystyna M; Callizot, Noelle; Slusher, Barbara S

    2014-01-01

    Pyridoxine is used as a supplement for treating conditions such as vitamin deficiency as well as neurological disorders such as depression, epilepsy and autism. A significant neurologic complication of pyridoxine therapy is peripheral neuropathy thought to be a result of long-term and high dose usage. Although pyridoxine-induced neuropathy is transient and can remit after its withdrawal, the process of complete recovery can be slow. Glutamate carboxypeptidase II (GCP II) inhibition has been shown to improve symptoms of both chemotherapy- and diabetic-induced neuropathy. This study evaluated if GCP II inhibition could behaviorally and physiologically improve pyridoxine-induced neuropathy. In the current study, high doses of pyridoxine (400 mg/kg, twice a day for seven days) were used to induce neuropathy in rats. An orally bioavailable GCP II inhibitor, 2-(3-mercaptopropyl) pentanedioic acid (2-MPPA), was administered daily at a dose of 30 mg/kg starting from the onset of pyridoxine injections. Body weight, motor coordination, heat sensitivity, electromyographical (EMG) parameters and nerve morphological features were monitored. The results show beneficial effects of GCP II inhibition including normalization of hot plate reaction time, foot fault improvements and increased open field distance travelled. H wave frequency, amplitude and latency as well as sensory nerve conduction velocity (SNCV) were also significantly improved by 2-MPPA. Lastly, GCP II inhibition resulted in morphological protection in the spinal cord and sensory fibers in the lumbar region dorsal root ganglia (DRG). In conclusion, inhibition of GCP II may be beneficial against the peripheral sensory neuropathy caused by pyridoxine.

  1. Lack of Response in an Autistic Population to a Low Dose Clinical Trial of Pyridoxine Plus Magnesium.

    Science.gov (United States)

    Tolbert, Lelland; And Others

    1993-01-01

    As some therapeutic benefits for autistic persons have been reported from combined high doses of pyridoxine and magnesium, this study evaluated long-term administration of low doses (to minimize adverse effects) to 15 subjects with autism. Findings indicated that, at this dosage level, pyridoxine and magnesium had no effect on the severity of…

  2. Pyridoxine-Dependent Seizures: A Family Phenotype that Leads to Severe Cognitive Deficits, Regardless of Treatment Regime

    Science.gov (United States)

    Rankin, Peter M; Harrison, Sue; Chong, W. K.; Boyd, Stewart; Aylett, Sarah E.

    2007-01-01

    The neuropsychological and clinical histories of three male siblings affected by pyridoxine-dependent seizures with known homozygous antiquitin mutations are presented. Neuropsychological evaluation is reported from when the siblings were 11, 9, and 7 years of age. Two of the siblings had received early pyridoxine treatment (antenatal, 2-4 wks…

  3. Effectiveness of Pyridoxine and Pyridostigmine in the Treatment of Vincristine-Induced Bilateral Ptosis and External Ophthalmoplegia: A Case Report

    Directory of Open Access Journals (Sweden)

    Osman Okan Olcaysu

    2014-08-01

    Full Text Available In this manuscript, we present the case of a patient with acute lymphoblastic leukemia who developed vincristine-induced bilateral ptosis and external ophthalmoplegia and who was treated successfully with pyridoxine and pyridostigmine. Pyridostigmine and pyridoxine are promising treatment option in cases of vincristine-induced neuropathy. (Turk J Ophthalmol 2014; 44: 330-1

  4. Effectiveness of Pyridoxine and Pyridostigmine in the Treatment of Vincristine-Induced Bilateral Ptosis and External Ophthalmoplegia: A Case Report

    OpenAIRE

    2014-01-01

    In this manuscript, we present the case of a patient with acute lymphoblastic leukemia who developed vincristine-induced bilateral ptosis and external ophthalmoplegia and who was treated successfully with pyridoxine and pyridostigmine. Pyridostigmine and pyridoxine are promising treatment option in cases of vincristine-induced neuropathy. (Turk J Ophthalmol 2014; 44: 330-1)

  5. Genotypic and phenotypic spectrum of pyridoxine-dependent epilepsy (ALDH7A1 deficiency)

    DEFF Research Database (Denmark)

    Mills, Philippa B; Footitt, Emma J; Mills, Kevin A

    2010-01-01

    Pyridoxine-dependent epilepsy was recently shown to be due to mutations in the ALDH7A1 gene, which encodes antiquitin, an enzyme that catalyses the nicotinamide adenine dinucleotide-dependent dehydrogenation of l-alpha-aminoadipic semialdehyde/L-Delta1-piperideine 6-carboxylate. However, whilst t...... to pyridoxine. These findings support the use of biochemical and DNA tests for antiquitin deficiency and a clinical trial of pyridoxine in infants and children with epilepsy across a broad range of clinical scenarios.......Pyridoxine-dependent epilepsy was recently shown to be due to mutations in the ALDH7A1 gene, which encodes antiquitin, an enzyme that catalyses the nicotinamide adenine dinucleotide-dependent dehydrogenation of l-alpha-aminoadipic semialdehyde/L-Delta1-piperideine 6-carboxylate. However, whilst...... with suspected or clinically proven pyridoxine-dependent epilepsy and to characterize further the phenotypic spectrum of antiquitin deficiency. Urinary L-alpha-aminoadipic semialdehyde concentration was determined by liquid chromatography tandem mass spectrometry. When this was above the normal range, DNA...

  6. Sustained pyridoxine response in primary hyperoxaluria type 1 recipients of kidney alone transplant.

    Science.gov (United States)

    Lorenz, E C; Lieske, J C; Seide, B M; Meek, A M; Olson, J B; Bergstralh, E J; Milliner, D S

    2014-06-01

    Combined liver kidney transplant is the preferred transplant option for most patients with primary hyperoxaluria type 1 (PH1) given that it removes the hepatic source of oxalate production and improves renal allograft survival. However, PH1 patients homozygous for the G170R mutation can develop normal urine oxalate levels with pyridoxine therapy and may be candidates for kidney alone transplant (KTx). We examined the efficacy of pyridoxine therapy following KTx in five patients homozygous for G170R transplanted between September 1999 and July 2013. All patients were maintained on pyridoxine posttransplant. Median age at transplant was 39 years (range 33-67 years). Median follow-up posttransplant was 8.5 years (range 0.2-13.9 years). At the end of follow-up, four grafts were functioning. One graft failed 13.9 years posttransplant due to recurrent oxalate nephropathy following an acute medical illness. After tissue oxalate stores had cleared, posttransplant urine oxalate levels were pyridoxine therapy following KTx. Therefore, pyridoxine combined with KTx should be considered for PH1 patients with a homozygous G170R mutation.

  7. Teratogenic effects of pyridoxine on the spinal cord and dorsal root ganglia of embryonic chickens.

    Science.gov (United States)

    Sharp, A A; Fedorovich, Y

    2015-03-19

    Our understanding of the role of somatosensory feedback in regulating motility during chicken embryogenesis and fetal development in general has been hampered by the lack of an approach to selectively alter specific sensory modalities. In adult mammals, pyridoxine overdose has been shown to cause a peripheral sensory neuropathy characterized by a loss of both muscle and cutaneous afferents, but predominated by a loss of proprioception. We have begun to explore the sensitivity of the nervous system in chicken embryos to the application of pyridoxine on embryonic days 7 and 8, after sensory neurons in the lumbosacral region become post-mitotic. Upon examination of the spinal cord, dorsal root ganglion and peripheral nerves, we find that pyridoxine causes a loss of neurotrophic tyrosine kinase receptor type 3-positive neurons, a decrease in the diameter of the muscle innervating nerve tibialis, and a reduction in the number of large diameter axons in this nerve. However, we found no change in the number of Substance P or calcitonin gene-related peptide-positive neurons, the number of motor neurons or the diameter or axonal composition of the femoral cutaneous nerve. Therefore, pyridoxine causes a peripheral sensory neuropathy in embryonic chickens largely consistent with its effects in adult mammals. However, the lesion may be more restricted to proprioception in the chicken embryo. Therefore, pyridoxine lesion induced during embryogenesis in the chicken embryo can be used to assess how the loss of sensation, largely proprioception, alters spontaneous embryonic motility and subsequent motor development.

  8. Dose-dependent effects of glutamate in pyridoxine-induced neuropathy.

    Science.gov (United States)

    Arkaravichien, Tarinee; Sattayasai, Nison; Daduang, Sakda; Sattayasai, Jintana

    2003-10-01

    In order to explore the effects of glutamate in a pyridoxine megadose-induced neuropathy, rats were received glutamate either 0.5 or 1 g/kg/day orally with or without pyridoxine 0.8 g/kg/day intraperitoneally for 14 days. The animal's motor coordination, the muscle power and the thermal threshold were observed daily. The nerve conduction velocity was measured at day 0 and day 15 of the treatment. Glutamate either 0.5 or 1 g/kg/day appeared to have no effect on motor coordination, the nerve conduction velocity and the muscle power score compared with control. However, the thermal response latency was significantly decreased (from day 9) in animals treated with 1 g/kg/day glutamate. In pyridoxine-induced neuropathy rats, glutamate 0.5 g/kg/day significantly decreased the effects of pyridoxine on the sciatic nerve conduction velocity, the muscle power score and the motor coordination. Interestingly, glutamate at a dose of 1 g/kg/day worsened the neurotoxic effects cause by pyridoxine.

  9. Pyridoxine metabolism in carpal tunnel syndrome with and without peripheral neuropathy.

    Science.gov (United States)

    Byers, C M; DeLisa, J A; Frankel, D L; Kraft, G H

    1984-11-01

    The role of insufficient pyridoxine as an etiologic factor in the development of carpal tunnel syndrome (CTS) has been reported and has led to the empirical use of pyridoxine to treat CTS. Previous studies have not employed standardized electrodiagnostic criteria to objectively determine the presence of CTS or to rule out peripheral neuropathy (PN). The present study categorized subjects with symptoms suggestive of CTS into four groups by standardized electrodiagnostic criteria: (1) CTS, (2) PN, (3) CTS and PN, (4) normal. At least seven subjects were in each group. Erythrocyte glutamine oxaloacetic acid transaminase (EGOT) activity with and without in vitro enhancement with pyridoxal phosphate was used as a means of identifying subjects with and without pyridoxine metabolic abnormalities. A significant difference in pyridoxine metabolic activity (PMA) was found between groups by both chi square (p less than 0.05) and analysis of variance (p less than 0.05). Further evaluation showed that this difference was associated with the presence or absence of PN (p less than 0.05). There was no difference in PMA when groups were separated on the basis of CTS. Results showed that a PMA abnormality was a factor highly correlated with the presence of PN but not CTS. This finding suggested that the positive response reported previously in subjects with CTS taking supplemental pyridoxine may actually be related to an unrecognized PN, which was compounding the symptomatology.

  10. Nonparallel changes in brain monoamines of pyridoxine-deficient growing rats.

    Science.gov (United States)

    Dakshinamurti, K; LeBlancq, W D; Herchl, R; Havlicek, V

    1976-11-23

    The effects of a large number of neurotropic drugs have been attributed to changes in the metabolism of 5-hydroxytryptamine. The aromatic amino acid decarboxylase considered to decarboxylate both dihydroxyphenylalanine and 5-hydroxytryptophan requires pyridoxal phosphate as coenzyme. Thus, in pyridoxine deficiency one would expect a decrease of serotonin as well as the catecholamines of the brain. In the present study we have found a very significant decrease in brain serotonin of the pyridoxine-deficient growing rat. However, the brain levels of norepinephrine and dopamine were not altered. This decrease in serotonin does not result from a decrease either in the brain level of trytophan or the activity of tryptophan hydroxylase. Increased degradation of serotonin measured by the levels of its metabolite, 5-hydroxyindoleacetic acid is also excluded, thus suggesting the possibility that the decarboxylation of 5-hydroxytryptophan is decreased in pyridoxine deficiency.

  11. Genotypic and phenotypic spectrum of pyridoxine-dependent epilepsy (ALDH7A1 deficiency)

    DEFF Research Database (Denmark)

    Mills, Philippa B; Footitt, Emma J; Mills, Kevin A

    2010-01-01

    Pyridoxine-dependent epilepsy was recently shown to be due to mutations in the ALDH7A1 gene, which encodes antiquitin, an enzyme that catalyses the nicotinamide adenine dinucleotide-dependent dehydrogenation of l-alpha-aminoadipic semialdehyde/L-Delta1-piperideine 6-carboxylate. However, whilst...... with suspected or clinically proven pyridoxine-dependent epilepsy and to characterize further the phenotypic spectrum of antiquitin deficiency. Urinary L-alpha-aminoadipic semialdehyde concentration was determined by liquid chromatography tandem mass spectrometry. When this was above the normal range, DNA......, through abnormal foetal movements and a multisystem neonatal disorder, to the onset of seizures and autistic features after the first year of life. Our relatively large series suggested that clinical diagnosis of pyridoxine dependent epilepsy can be challenging because: (i) there may be some response...

  12. Two novel ALDH7A1 (antiquitin) splicing mutations associated with pyridoxine-dependent seizures.

    Science.gov (United States)

    Striano, Pasquale; Battaglia, Silvia; Giordano, Lucio; Capovilla, Giuseppe; Beccaria, Francesca; Struys, Eduard A; Salomons, Gajja S; Jakobs, Cornelis

    2009-04-01

    Pyridoxine-dependent seizures (PDS) is a rare autosomal recessive disorder causing intractable seizures in neonates and infants. Patients are typically resistant to conventional anticonvulsants but respond well to the administration of pyridoxine. We report two unrelated patients affected with PDS as a result of alpha-aminoadipic semialdehyde (alpha-AASA) dehydrogenase deficiency caused by pathogenic ALDH7A1/antiquitin mutations. Two of the three reported mutations are novel and result in erroneous splicing, as showed by messenger RNA (mRNA) studies. So far, the vast majority of the patients clinically diagnosed as PDS show alpha-AASA dehydrogenase deficiency, caused by mutations in the ALDH7A1 gene. However, despite the availability of reliable biomarkers, early consideration of a pyridoxine trial is still the most important issue in a child with therapy-resistant seizures.

  13. Seizures caused by pyridoxine (vitamin B6) deficiency in adults: A case report and literature review.

    Science.gov (United States)

    Tong, Yisha

    2014-05-01

    Pyridoxine (vitamin B6) deficiency is a recognised cause of intractable seizures in neonates. However, pyridoxine deficiency related seizures in adults were rarely reported. This article reports a case of a 79 year old lady who suffered from new-onset seizures and was successfully treated with vitamin B6. The patient had chronic renal disease and weight loss due to anepithymia following a pelvic fracture. This article also reviews literatures of seizures caused by pyridoxine deficiency in adults. Seizures caused by vitamin B6 deficiency in adults may result from dietary deficiency, liver disease, pregnancy and certain medications and can be easily treated by vitamin B6 with excellent outcome. Clinicians should consider vitamin B6 deficiency as a potential aetiology of seizures, even in patients who suffer from other underlying diseases which can cause seizures.

  14. Early diagnosis of pyridoxine-dependent epilepsy: video-EEG monitoring and biochemical and genetic investigation.

    Science.gov (United States)

    Ville, Dorothée; Ginguene, Carole; Marignier, Stéphanie; des Portes, Vincent; de Bellescize, Jullita

    2013-11-01

    Pyridoxine-dependent epilepsy (PDE) is a rare autosomal recessive metabolic disease. A delay of treatment may affect outcome and early initiation of pyridoxine based on effective diagnosis is crucial to ensure good cognitive outcome in neonates. A consensus for the diagnosis of PDE is based on refractive seizures and responsiveness to pyridoxine, however, a growing body of evidence suggests that additional elements should be considered which include biochemical data, genetic screening, and EEG monitoring. We present a case study of a neonate with PDE, who presented with misleading clinical presentation and a novel mutation in the antiquitin (ALDH7A1) gene (A294V), and highlight important aspects in order to consider the definition of diagnosis and management of PDE in the light of more recent data.

  15. Pyridoxine-dependent epilepsy: an under-recognised cause of intractable seizures.

    Science.gov (United States)

    Yeghiazaryan, Nune S; Zara, Federico; Capovilla, Giuseppe; Brigati, Giorgia; Falsaperla, Raffaele; Striano, Pasquale

    2012-03-01

    Pyridoxine-dependent epilepsy (PDE) is a rare autosomal recessive disorder causing intractable seizures in neonates and infants. PDE patients are typically resistant to anti-epileptic treatment but respond to the administration of pyridoxine. Different seizure types have been reported in PDE, and episodes of status epilepticus are common. Electroencephalographic or neuroimaging abnormalities are not pathognomonic for this disorder. Intellectual disability is frequent at the follow-up. Recently, elevated urinary α-aminoadipic semialdehyde has been shown to be a reliable biomarker of this disorder, and mutations in the ALDH7A1 gene, encoding α-aminoadipic semialdehyde dehydrogenase, have been demonstrated in the large majority of PDE patients. However, early consideration of a pyridoxine trial remains the most important issue in a neonate or in an infant with intractable early onset seizures.

  16. Pyridoxine in the treatment of premenstrual syndrome: a retrospective survey in 630 patients.

    Science.gov (United States)

    Brush, M G; Bennett, T; Hansen, K

    1988-11-01

    We present a survey summarising the retrospective reports of the therapeutic effect of pyridoxine (vitamin B6) in 630 women suffering from premenstrual syndrome (PMS) who attended a PMS clinic during the period 1976-1983. The daily doses of pyridoxine hydrochloride varied from 40 to 100 mg early in the study and from 120 to 200 mg in the later period of the investigations. The response to treatment was recorded as good (no significant residual complaints) in 40 per cent or more of patients taking 100-150 mg pyridoxine daily and in 60 per cent of patients treated with 160-200 mg daily. Together with partial response (useful benefit but still some significant complaints), the positive effect of the treatment increased to 65-68 per cent and 70-88 per cent respectively. No symptoms consistent with a diagnosis of peripheral neuropathy were reported.

  17. Genotypic and phenotypic spectrum of pyridoxine-dependent epilepsy (ALDH7A1 deficiency).

    Science.gov (United States)

    Mills, Philippa B; Footitt, Emma J; Mills, Kevin A; Tuschl, Karin; Aylett, Sarah; Varadkar, Sophia; Hemingway, Cheryl; Marlow, Neil; Rennie, Janet; Baxter, Peter; Dulac, Olivier; Nabbout, Rima; Craigen, William J; Schmitt, Bernhard; Feillet, François; Christensen, Ernst; De Lonlay, Pascale; Pike, Mike G; Hughes, M Imelda; Struys, Eduard A; Jakobs, Cornelis; Zuberi, Sameer M; Clayton, Peter T

    2010-07-01

    Pyridoxine-dependent epilepsy was recently shown to be due to mutations in the ALDH7A1 gene, which encodes antiquitin, an enzyme that catalyses the nicotinamide adenine dinucleotide-dependent dehydrogenation of l-alpha-aminoadipic semialdehyde/L-Delta1-piperideine 6-carboxylate. However, whilst this is a highly treatable disorder, there is general uncertainty about when to consider this diagnosis and how to test for it. This study aimed to evaluate the use of measurement of urine L-alpha-aminoadipic semialdehyde/creatinine ratio and mutation analysis of ALDH7A1 (antiquitin) in investigation of patients with suspected or clinically proven pyridoxine-dependent epilepsy and to characterize further the phenotypic spectrum of antiquitin deficiency. Urinary L-alpha-aminoadipic semialdehyde concentration was determined by liquid chromatography tandem mass spectrometry. When this was above the normal range, DNA sequencing of the ALDH7A1 gene was performed. Clinicians were asked to complete questionnaires on clinical, biochemical, magnetic resonance imaging and electroencephalography features of patients. The clinical spectrum of antiquitin deficiency extended from ventriculomegaly detected on foetal ultrasound, through abnormal foetal movements and a multisystem neonatal disorder, to the onset of seizures and autistic features after the first year of life. Our relatively large series suggested that clinical diagnosis of pyridoxine dependent epilepsy can be challenging because: (i) there may be some response to antiepileptic drugs; (ii) in infants with multisystem pathology, the response to pyridoxine may not be instant and obvious; and (iii) structural brain abnormalities may co-exist and be considered sufficient cause of epilepsy, whereas the fits may be a consequence of antiquitin deficiency and are then responsive to pyridoxine. These findings support the use of biochemical and DNA tests for antiquitin deficiency and a clinical trial of pyridoxine in infants and

  18. Lipid profiles of rats fed with diets supplemented with vitamins niacin and pyridoxine

    Directory of Open Access Journals (Sweden)

    Magna da Glória Lameiro

    2012-04-01

    Full Text Available Hypercholesterolemia is a major risk factor for cardiovascular disease. Supplements containing the vitamins niacin (B3 and pyridoxine (B6 can promote the reduction of total cholesterol and an increase in HDL cholesterol. In this study, the effects of diets supplemented with niacin (B3 and pyridoxine (B6 on the hepatic and serum lipid profiles of Wistar rats were assessed. The diets were prepared with combinations of three concentrations of niacin (3, 4 and 5 g/kg and pyridoxine (6, 12 and 18 mg/kg and one with neither vitamin. The animals were divided into eleven experimental groups of six animals per group, and nine groups were fed on a standard diet with 7.5% fat and vitamin supplementation. Another group was fed with 7.5% fat without vitamin supplements. A control group received the standard diet (AIN-93M without modifications (4% fat. The weight gain, food intake, serum and hepatic total cholesterol, serum cholesterol fractions (HDL, LDL, and VLDL, serum and hepatic triacylglycerols and hepatic and fecal lipid contents were measured after 30 days. The diet with the highest concentration of niacin and lowest concentration of pyridoxine had the lowest level of total hepatic cholesterol. Hepatic triacylglycerols were reduced by the highest concentration of niacin (5 g/kg, and this reduction was enhanced by increasing the pyridoxine concentration. The diets supplemented with niacin and pyridoxine reduced the levels of serum total cholesterol, LDL, VLDL, triacylglycerols and hepatic lipids. These effects on the lipid profile varied with the concentrations of the two vitamins and the interactions between them.

  19. Pyridoxine-dependent seizures caused by alpha amino adipic semialdehyde dehydrogenase deficiency: the first polish case with confirmed biochemical and molecular pathology.

    Science.gov (United States)

    Kaczorowska, Magdalena; Kmiec, Tomasz; Jakobs, Cornelis; Kacinski, Marek; Kroczka, Slawomir; Salomons, Gajja S; Struys, Eduard A; Jozwiak, Sergiusz

    2008-12-01

    Pyridoxine-dependent seizures are a rare condition recognized when numerous seizures respond to pyridoxine treatment and recur on pyridoxine withdrawal. For decades the diagnosis was confirmed only with pyridoxine treatment withdrawal trial. Recently described biochemical and molecular pathology improved the diagnostic process for those cases in which seizures are caused by alpha amino adipic semialdehyde dehydrogenase deficiency. This article presents a girl with recurrent status epilepticus episodes resistant to phenobarbital and phenytoin and partly responding to midazolam. Eventually the seizures were completely controlled with pyridoxine; however, due to the severe condition of this child when seizing, no trial of withdrawal has been performed. The diagnosis of pyridoxine-dependent seizures was confirmed with biochemical and molecular testing revealing elevated alpha-AASA excretion and the presence of 2 different mutations in the antiquitin ( ALDH7A1) gene. Due to the availability of reliable laboratory testing, confirmation of the diagnosis was made without the life-threatening trial of pyridoxine withdrawal.

  20. Infantile hypophosphatasia without bone deformities presenting with severe pyridoxine-resistant seizures.

    Science.gov (United States)

    de Roo, Marieke G A; Abeling, Nico G G M; Majoie, Charles B; Bosch, Annet M; Koelman, Johannes H T M; Cobben, Jan M; Duran, Marinus; Poll-The, Bwee Tien

    2014-03-01

    An infant carrying a heterozygous c.43_46delACTA and a heterozygous c.668 G>A mutation in the ALPL gene with hypophosphatasia in the absence of bone deformities presented with therapy-resistant seizures. Pyridoxal phosphate was extremely high in CSF and plasma. Pyridoxine treatment had only a transient effect and the severe encephalopathy was fatal. Repeated brain MRIs showed progressive cerebral damage. The precise metabolic cause of the seizures remains unknown and pyridoxine treatment apparently does not cure the epilepsy.

  1. 8-Way Randomized Controlled Trial of Doxylamine, Pyridoxine and Dicyclomine for Nausea and Vomiting during Pregnancy: Restoration of Unpublished Information

    Science.gov (United States)

    Zhang, Rujun; Persaud, Navindra

    2017-01-01

    Objectives We report information about an unpublished 1970s study (“8-way” Bendectin Study) that aimed to evaluate the relative therapeutic efficacy of doxylamine, pyridoxine, and dicyclomine in the management of nausea and vomiting during pregnancy. We are publishing the trial's findings according to the restoring invisible and abandoned trials (RIAT) initiative because the trial was never published. Design Double blinded, multi-centred, randomized placebo-controlled study. Setting 14 clinics in the United States. Participants 2308 patients in the first 12 weeks of pregnancy with complaints of nausea or vomiting were enrolled. Interventions Each patient was randomized to one of eight arms: placebo, doxylamine/pyridoxine/dicylcomine, doxylamine/pyridoxine, dicylomine/pyridoxine, doxylamine, dicyclomine/pyridoxine, pyridoxine and dicyclomine. Each patient was instructed to take 2 tablets at bedtime and 1 additional tablet in the afternoon or morning if needed, for 7 nights. Outcomes Reported outcomes included the number of hours of nausea reported by patients, the frequency of vomiting reported by patients and the overall efficacy of medication as judged by physicians. Results Data from 1599 (69% of those randomized) participants were analyzed. Based on the available summary data of physician evaluation of symptoms and ignoring missing data and data integrity issues, the proportion of participants who were “evaluated moderate or excellent” was greater in each of the seven active treatment groups when compared with placebo (57%): doxylamine/pyridoxine/dicylcomine (14% absolute difference versus placebo; 95% CI: 4 to 24), doxylamine/pyridoxine (21; 95% CI 11 to 30), dicylomine/pyridoxine (21; 95% CI 11 to 30), doxylamine (20; 95% CI 10 to 29), dicyclomine/pyridoxine (4; 95% CI -6 to 14), pyridoxine (9; 95% CI -1 to 19) and dicyclomine (4; 95% CI -6 to 14). Based on incomplete information, the most common adverse events were apparently drowsiness and fatigue

  2. Effect of pyridoxine on the reproduction of the mulberry silkworm, Bombyx mori L.

    Directory of Open Access Journals (Sweden)

    SI Faruki

    2005-03-01

    Full Text Available The present investigation reports the effects of vitamin B6, also known as pyridoxine supplementedfeed on the reproductive potential of Bombyx mori L. All the concentrations of the vitamin significantlyreduced the fecundity. Egg-viability was also reduced at all the concentrations, but the differences werenot significant in comparison to control.

  3. Gene expression of porcine blastocysts from gilts fed organic or inorganic selenium and pyridoxine.

    Science.gov (United States)

    Dalto, B D; Tsoi, S; Audet, I; Dyck, M K; Foxcroft, G R; Matte, J J

    2015-01-01

    In this study, we determined how maternal dietary supplementation with pyridoxine combined with different sources of selenium (Se) affected global gene expression of porcine expanded blastocysts (PEB) during pregnancy. Eighteen gilts were randomly assigned to one of the three experimental diets (n=6 per treatment): i) basal diet without supplemental Se or pyridoxine (CONT); ii) CONT+0.3 mg/kg of Na-selenite and 10 mg/kg of HCl-pyridoxine (MSeB610); and iii) CONT+0.3 mg/kg of Se-enriched yeast and 10 mg/kg of HCl-pyridoxine (OSeB610). All gilts were inseminated at their fifth post-pubertal estrus and killed 5 days later for embryo harvesting. A porcine embryo-specific microarray was used to detect differentially gene expression between MSeB610 vs CONT, OSeB610 vs CONT, and OSeB610 vs MSeB610. CONT gilts had lower whole blood Se and erythrocyte pyridoxal-5-P concentrations than supplemented gilts (Ppyridoxine influenced the Se-glutathione peroxidase metabolic pathway in the PEB, but OSeB610 selectively stimulated genes involved with antioxidant defense.

  4. Simultaneous chemometric determination of pyridoxine hydrochloride and isoniazid in tablets by multivariate regression methods.

    Science.gov (United States)

    Dinç, Erdal; Ustündağ, Ozgür; Baleanu, Dumitru

    2010-08-01

    The sole use of pyridoxine hydrochloride during treatment of tuberculosis gives rise to pyridoxine deficiency. Therefore, a combination of pyridoxine hydrochloride and isoniazid is used in pharmaceutical dosage form in tuberculosis treatment to reduce this side effect. In this study, two chemometric methods, partial least squares (PLS) and principal component regression (PCR), were applied to the simultaneous determination of pyridoxine (PYR) and isoniazid (ISO) in their tablets. A concentration training set comprising binary mixtures of PYR and ISO consisting of 20 different combinations were randomly prepared in 0.1 M HCl. Both multivariate calibration models were constructed using the relationships between the concentration data set (concentration data matrix) and absorbance data matrix in the spectral region 200-330 nm. The accuracy and the precision of the proposed chemometric methods were validated by analyzing synthetic mixtures containing the investigated drugs. The recovery results obtained by applying PCR and PLS calibrations to the artificial mixtures were found between 100.0 and 100.7%. Satisfactory results obtained by applying the PLS and PCR methods to both artificial and commercial samples were obtained. The results obtained in this manuscript strongly encourage us to use them for the quality control and the routine analysis of the marketing tablets containing PYR and ISO drugs.

  5. Turning pyridoxine into a catalytic chain-breaking and hydroperoxide-decomposing antioxidant.

    Science.gov (United States)

    Singh, Vijay P; Poon, Jia-fei; Engman, Lars

    2013-02-15

    Vitamin B6 is involved in a variety of enzymatic transformations. Some recent findings also indicate an antioxidant role of the vitamin in biological systems. We set out to turn pyridoxine (1a) into a catalytic chain-breaking and hydroperoxide-decomposing antioxidant by replacing the 2-methyl substituent with an alkyltelluro group. Target molecules 12 and derivatives 14, 17, 18, and 20 thereof were accessed by subjecting suitably substituted 2-halopyridin-3-ols to aromatic substitution using sodium alkanetellurolates as nucleophiles and then LAH-reduction of ester groups. The novel pyridoxine compounds were found to inhibit azo-initiated peroxidation of linoleic acid an order of magnitude more efficiently than α-tocopherol in a water/chlorobenzene two-phase system containing N-acetylcysteine as a reducing agent in the aqueous phase. The most lipid-soluble pyridoxine derivative 20c was regenerable and could inhibit peroxidation for substantially longer time (>410 min) than α-tocopherol (87 min). The chalcogen-containing pyridoxines could also mimic the action of the glutathione peroxidase enzymes. Thus, compound 20a catalyzed reduction of hydrogen peroxide three times more efficiently than Ebselen in the presence of glutathione as a stoichiometric reducing agent.

  6. Characterization of pyridoxine auxotrophs of Escherichia coli: chromosomal position of linkage group I.

    Science.gov (United States)

    Dempsey, W B

    1969-10-01

    The chromosomal location of Group I pyridoxine mutations in Escherichia coli is shown to be adjacent to dsdA,aroC, and purF (old purC) in E. coli B x K-12 hybrids. All mutants previously classified into Group I by nutrition tests and transduction frequency tests are shown to be linked to dsdA.

  7. Studying the antiemetic effect of vitamin B6 for morning sickness: pyridoxine and pyridoxal are prodrugs.

    Science.gov (United States)

    Matok, Ilan; Clark, Shannon; Caritis, Steve; Miodovnik, Menachem; Umans, Jason G; Hankins, Gary; Mattison, Donald R; Koren, Gideon

    2014-12-01

    Vitamin B6 has been known to possess antiemetic effects since 1942. This water soluble compound has several forms in the circulation including pyridoxine, pyridoxal, and pyridoxal phosphate. The active antiemetic form of vitamin B6 is unknown. This was a pre-specified substudy of a randomized, placebo-controlled trial comparing the antiemetic effect of the doxylamine-vitamin B6 combination (Diclectin®) (n = 131) to placebo (n = 126) in women with nausea and vomiting of pregnancy. Serum concentrations of pyridoxine, pyridoxal, and pyridoxal 5' phosphate (PLP) and doxylamine were measured on Days 4, 8, and 15. With Diclectin® exhibiting a significant antiemetic effect in pregnancy, serum concentrations of pyridoxine were unmeasurable in almost all patients and those of pyridoxal were undetectable in half of patients. In contrast, PLP was measurable at sustained, stable steady-state levels in all patients. Our data suggest that there is a correlation between PLP levels and PUQE score of morning sickness symptoms when pyridoxine and pyridoxal levels are undetectable, and hence they might be prodrugs of PLP, which may be the active antiemetic form of vitamin B6.

  8. Variations in the lipid profile of patients with chronic renal failure treated with pyridoxine

    Directory of Open Access Journals (Sweden)

    Touceda Luis A

    2003-09-01

    Full Text Available Abstract Background Hyperhomocysteinemia and lipid abnormalities are commonly found in patients with chronic renal failure; both are recognized as risk factors for atherosclerosis. The homocysteine-lowering effect of pyridoxine is controversial. This study was performed to determine the effect of a high dose of pyridoxine (300 mg i.v. three times a week on plasma and red blood cell lipid profile and plasma homocysteine concentration in twelve chronic renal failure patients on regular hemodialysis. Fasting blood samples were taken at the beginning of the study (basal 1, after 30 and 60 days of treatment and 4 months after withdrawal (basal 2. Results Pyridoxine supplementation induced a significant decrease in total plasma homocysteine level and also a lowering effect in plasma total cholesterol and triglycerides. These biochemical data increased when the samples were taken at basal 2, reaching the levels obtained at the beginning of the experiment. LDL cholesterol increased whereas HDL cholesterol was reduced during the treatment. In erythrocyte membranes vitamin B6 therapy enhanced the cholesterol/phospholipid ratio as well as the fluorescence anisotropy of diphenyl-hexatriene. Conclusions We conclude that high doses of pyridoxine represent an effective strategy to ameliorate both plasma homocysteine levels and lipid profiles in chronic renal failure patients, protecting them from atherosclerosis. Further research using a long-term treatment would be necessary in an attempt to restore the fatty acid pattern and the fluidity of red cell membranes.

  9. Hyperhomocysteinemia is associated with low plasma pyridoxine levels in children with sickle cell disease.

    Science.gov (United States)

    Balasa, Vinod V; Kalinyak, Karen A; Bean, Judy A; Stroop, Davis; Gruppo, Ralph A

    2002-01-01

    Elevated plasma homocysteine levels have been shown to be a risk factor for endothelial cell damage and thrombosis, which are implicated in sickle cell disease (SCD)-related vaso-occlusion. The aim of this study was to determine the prevalence of hyperhomocysteinemia in SCD. Fasting and postmethionine load (PML) homocysteine, red cell folate, and the MTHFR C677T mutation were determined in 77 patients with SCD and 110 African-American controls. Plasma methylmalonic acid and pyridoxine levels were determined in 54 patients and all controls. For analysis, the subjects were divided into two age groups (2-10 years and 10.1-21 years). In both age groups, median PML homocysteine levels were significantly elevated in patients with SCD compared with controls. Fasting homocysteine levels were elevated in patients with SCD versus controls only in those older than 10 years. Hyperhomocysteinemia was noted in 38% of patients versus 7% in controls. Folate levels were higher among patients than controls and showed a significant negative correlation with PML homocysteine levels in patients with SCD. Pyridoxine levels in patients with SCD were significantly lower than in controls and showed a negative correlation with PML homocysteine levels. Among patients with SCD, pyridoxine deficiency was more common (62%) among those with hyperhomocysteinemia compared with those with normal homocysteine levels (30%). Homozygosity for the MTHFR C677T mutation was rare. These data suggest that children with SCD have significant hyperhomocysteinemia, associated with pyridoxine and relative folate deficiencies.

  10. Regioselective acylation of pyridoxine catalyzed by immobilized lipase in ionic liquid

    Institute of Scientific and Technical Information of China (English)

    Shu BAI; Mengyuan REN; Lele WANG; Yan SUN

    2008-01-01

    The regioselective acylation of pyridoxine cat-alyzed by immobilized lipase (Candida Antarctica) in 1-butyl-3-methylimidazolium hexafluorophosphate ([BMIM]PF6) has been investigated,and compared with that in acetonitrile (ACN).The acetylation of pyridox-ine using acetic anhydride in [BMIM]PF6 gave compar-able conversion of pyridoxine to 5-monoacetyl pyridoxine with considerably higher regioselectivity (93%-95%) than that in ACN (70%-73%).Among the tested parameters,water activity (aw) and temperature have profound effects on the reaction performances in either [BMIM]PF6 or ACN.For the reaction in [BMIM] PF6,higher temperature (50℃-55℃) and lower aw (<0.01) are preferable conditions to obtain better con-version and regioselectivity.Mass transfer limitation and intrinsic kinetic from the ionic nature of ionic liquids (ILs) may account for a different rate-temper-ature profile and a lower velocity at lower temperature in [BMIM]PF6-mediated reaction.Moreover,consec-utive batch reactions for enzyme reuse also show that lipase exhibited a much higher thermal stability and bet-ter reusability in [BMIM]PF6 than in ACN,which repre-sents another advantage of ILs as an alternative to traditional solvents beyond green technology.

  11. Neurotrophin-3 administration attenuates deficits of pyridoxine-induced large-fiber sensory neuropathy.

    Science.gov (United States)

    Helgren, M E; Cliffer, K D; Torrento, K; Cavnor, C; Curtis, R; DiStefano, P S; Wiegand, S J; Lindsay, R M

    1997-01-01

    Chronic treatment of adult rats for 2-3 weeks with high doses of pyridoxine (vitamin B6) produced a profound proprioceptive loss, similar to that found in humans overdosed with this vitamin or treated with the chemotherapeutic agent cisplatin. Pyridoxine toxicity was manifest as deficits in simple and precise locomotion and sensory nerve function and as degeneration of large-diameter/large-fiber spinal sensory neurons. As assessed quantitatively in a beam-walking task and by EMG recording of H waves evoked by peripheral nerve stimulation, coadministration of the neurotrophic factor neurotrophin-3 (NT-3; 5-20 mg . kg-1 . d-1, s.c.) during chronic pyridoxine treatment largely attenuated the behavioral and electrophysiological sequelae associated with pyridoxine toxicity. Furthermore, NT-3 administration prevented degeneration of sensory fibers in the dorsal column of the spinal cord. These data are consistent with the evidence that NT-3 is a target-derived neurotrophic factor for muscle sensory afferents and suggest that pharmacological doses of NT-3 may be beneficial in the treatment of large-fiber sensory neuropathies.

  12. Plasma and urine riboflavin and pyridoxine concentrations in enterally fed very-low-birth-weight neonates.

    Science.gov (United States)

    Porcelli, P J; Adcock, E W; DelPaggio, D; Swift, L L; Greene, H L

    1996-08-01

    Preterm infant formulas (PIFs) for very-low-birth-weight (VLBW) infants (birth weight, pyridoxine at levels up to five-fold greater than in term infant formula and 18-fold greater than in human milk. We evaluated plasma riboflavin and pyridoxine concentrations in VLBW infants who received PIF during their first postnatal month. Eighty-eight plasma and 124 urine samples were collected for riboflavin- and pyridoxine-concentration measurements from 57 clinically healthy VLBW infants weekly during their first postnatal month. Concentrations were measured using high-performance liquid chromatography. At the time of the sample, patients were receiving > or = 80% of their total calories via enteral feedings. Plasma riboflavin concentrations rose from 45.3 +/- 7.3 ng/ml at baseline (mean +/- SEM) to 173.5 +/- 20.3 ng/ml by 1 week of age and remained at 177.3-199.7 ng/ml during the following three weekly measurements; values were up to 14-fold above baseline concentration. Urine riboflavin concentration increased from 534 +/- 137 ng/ml at baseline to 3,521 +/- 423 ng/ml by 1 week of age and remained at 4,451-5,216 ng/ml during the next 3 weeks. In a similar pattern, baseline plasma (69.4 +/- 10.4 ng/ml) and urine (145 +/- 30 ng/ml) pyridoxine concentrations were significantly increased by 1 week postnatal age; they remained at 163-248 ng/ml (plasma) and 1,573-2,394 ng/ml (urine) through the first postnatal month. Plasma and urine riboflavin and pyridoxine concentrations in enterally fed VLBW infants increased from baseline concentrations by 1 week of postnatal age and remained elevated for the first postnatal month. High daily intake and immature renal development are probable contributing causes of the elevated plasma riboflavin and pyridoxine concentrations. We suggest that lower daily enteral administration of riboflavin and pyridoxine should maintain adequate blood concentrations and minimize potential toxicity.

  13. Effects of pyridoxine on growth performance and plasma aminotransferases and homocysteine of white pekin ducks.

    Science.gov (United States)

    Xie, Ming; Tang, Jing; Wen, Zhiguo; Huang, Wei; Hou, Shuisheng

    2014-12-01

    A dose-response experiment with seven supplemental pyridoxine levels (0, 0.66, 1.32, 1.98, 2.64, 3.30, and 3.96 mg/kg) was conducted to investigate the effects of pyridoxine on growth performance and plasma aminotransferases and homocysteine of White Pekin ducks and to estimate pyridoxine requirement for these birds. A total of 336 one-day-old male White Pekin ducks were divided to 7 experimental treatments and each treatment contained 8 replicate pens with 6 birds per pen. Ducks were reared in raised wire-floor pens from hatch to 28 d of age. At 28 d of age, the weight gain, feed intake, feed/gain, and the aspartate aminotransferase, alanine aminotransferase, and homocysteine in plasma of ducks from each pen were all measured. In our study, the pyridoxine deficiency of ducks was characterized by growth depression, decreasing plasma aspartate aminotransferase activity and increasing plasma homocysteine. The ducks fed vitamin B6-deficient basal diets had the worst weight gain and feed/gain among all birds and this growth depression was alleviated (ppyridoxine was supplemented to basal diets. On the other hand, plasma aspartate aminotransferase and homocysteine may be the sensitive indicators for vitamin B6 status of ducks. The ducks fed basal diets had much lower aspartate aminotransferase activity and higher homocysteine level in plasma compared with other birds fed pyridoxine-supplemented diets (ppyridoxine requirements of Pekin ducks from hatch to 28 days of age was 2.44 mg/kg for feed/gain and 2.08 mg/kg for plasma aspartate aminotransferase and the corresponding total requirements of this vitamin for these two criteria were 4.37 and 4.01 mg/kg when the pyridoxine concentration of basal diets was included, respectively. All data suggested that pyridoxine deficiency could cause growth retardation in ducks and the deficiency of this vitamin could be indicated by decreasing plasma aspartate aminotransferase activity and increasing plasma homocysteine.

  14. Infantile hypophosphatasia secondary to a novel compound heterozygous mutation presenting with pyridoxine-responsive seizures.

    Science.gov (United States)

    Belachew, Dina; Kazmerski, Traci; Libman, Ingrid; Goldstein, Amy C; Stevens, Susan T; Deward, Stephanie; Vockley, Jerry; Sperling, Mark A; Balest, Arcangela L

    2013-01-01

    Hypophosphatasia (HPP) is a rare metabolic disease with the hallmark finding of deficient serum tissue nonspecific alkaline phosphatase (TNSALP) activity. TNSALP is primarily known for its role in mineralization; hence, HPP is characterized by defective mineralization of bone and/or teeth. TNSALP is also necessary for proper vitamin B6 metabolism and its participation as a cofactor for neurotransmitters in the central nervous system. Defective TNSALP activity in the brain can result in intractable seizures responsive to pyridoxine. The pathophysiology of pyridoxine-responsive seizures (PRS) in severe HPP remains to be clearly defined. We review the case of a 2-month-old Caucasian boy presenting with seizures refractory to conventional antiepileptic medications. Empiric treatment with favorable response to pyridoxine in conjunction with severe metabolic bone disease, extremely low serum alkaline phosphatase, elevated phosphoethanolamine, hypercalcemia, hypercalciuria, and nephrocalcinosis led to a clinical diagnosis of infantile HPP. Sequence analysis revealed compound heterozygosity of the TNSALP gene with a novel mutation in exon 9 and a previously reported mutation in exon 12. This case reminds the physician that severe infantile HPP can present with PRS as its major initial manifestation and should alert clinicians to consider HPP in their differential of PRS. In addition, despite this severe genotype, the clinical diagnosis of our patient was delayed because of minimal phenotypic features initially. This highlights that the phenotype-genotype correlation could be variable even in severe disease. This case also demonstrates that HPP should be classified as PRS and not a form of pyridoxine-dependent epilepsy (PDE) as our patient was able to stop the pyridoxine supplementation without seizure recurrence once enzyme replacement was initiated. With the advent of enzyme replacement therapy, this once fatal disease may have improved morbidity and mortality.

  15. Clinical and genetic analysis of three Korean children with pyridoxine-dependent epilepsy.

    Science.gov (United States)

    Nam, Sook Hyun; Kwon, Min-Jung; Lee, Jeehun; Lee, Cha Gon; Yu, Hee Joon; Ki, Chang-Seok; Lee, Munhyang

    2012-01-01

    Pyridoxine-dependent epilepsy (PDE) is a rare autosomal recessive disorder that causes intractable seizures, especially in neonates and infants. Patients are typically resistant to typical antiepileptic drugs (AEDs) but respond dramatically to pyridoxine. Mutations in the ALDH7A1 gene are associated with the pathogenesis of PDE. Herein, we report the clinical phenotypes and disease-causative mutations in the ALDH7A1 gene in three Korean patients with PDE. We reviewed the medical records, electroencephalography (EEG), brain magnetic resonance imaging (MRI) findings, and the results of molecular genetic tests for the patients who were diagnosed with PDE in our institution between Jan. 1996 and Dec. 2010. In all patients, the first seizures began during the first week of life. The seizures were not fully controlled with multiple AEDs, but disappeared immediately after administration of pyridoxine and returned after it was transiently discontinued. Before the use of pyridoxine, interictal EEGs showed multifocal epileptiform discharges, which became normalized with pyridoxine. Direct sequencing analyses revealed two mutant alleles in all three patients. Patient 1 was compound heterozygous with two different missense mutations, c.1061A>G (p.Y354C) and c.1232C>T (p.P411L). Patient 2 was homozygous for a missense mutation, c.1279G>C (p.E427Q). Patient 3 was compound heterozygous for two different missense mutations, c.1061A>G (p.Y354C) and c.1279G>C (p.E427Q), and her parents and younger brother were heterozygous carriers of each one of the mutations. All three mutations had not previously been reported. Herein, we report three Korean patients with three novel mutations who presented with PDE.

  16. Molecular basis of reduced pyridoxine 5'-phosphate oxidase catalytic activity in neonatal epileptic encephalopathy disorder.

    Science.gov (United States)

    Musayev, Faik N; Di Salvo, Martino L; Saavedra, Mario A; Contestabile, Roberto; Ghatge, Mohini S; Haynes, Alexina; Schirch, Verne; Safo, Martin K

    2009-11-06

    Mutations in pyridoxine 5'-phosphate oxidase are known to cause neonatal epileptic encephalopathy. This disorder has no cure or effective treatment and is often fatal. Pyridoxine 5'-phosphate oxidase catalyzes the oxidation of pyridoxine 5'-phosphate to pyridoxal 5'-phosphate, the active cofactor form of vitamin B(6) required by more than 140 different catalytic activities, including enzymes involved in amino acid metabolism and biosynthesis of neurotransmitters. Our aim is to elucidate the mechanism by which a homozygous missense mutation (R229W) in the oxidase, linked to neonatal epileptic encephalopathy, leads to reduced oxidase activity. The R229W variant is approximately 850-fold less efficient than the wild-type enzyme due to an approximately 192-fold decrease in pyridoxine 5'-phosphate affinity and an approximately 4.5-fold decrease in catalytic activity. There is also an approximately 50-fold reduction in the affinity of the R229W variant for the FMN cofactor. A 2.5 A crystal structure of the R229W variant shows that the substitution of Arg-229 at the FMN binding site has led to a loss of hydrogen-bond and/or salt-bridge interactions between FMN and Arg-229 and Ser-175. Additionally, the mutation has led to an alteration of the configuration of a beta-strand-loop-beta-strand structure at the active site, resulting in loss of two critical hydrogen-bond interactions involving residues His-227 and Arg-225, which are important for substrate binding and orientation for catalysis. These results provide a molecular basis for the phenotype associated with the R229W mutation, as well as providing a foundation for understanding the pathophysiological consequences of pyridoxine 5'-phosphate oxidase mutations.

  17. Treatment of premenstrual tension syndrome with Vitex agnus castus controlled, double-blind study versus pyridoxine.

    Science.gov (United States)

    Lauritzen, C; Reuter, H D; Repges, R; Böhnert, K J; Schmidt, U

    1997-09-01

    The objective of the present study was to determine the efficacy and tolerability of a new solid formulation (capsules) of Agnolyt®(*)) in a randomized, controlled trial versus pyridoxine in women with PMTS over a period of three treatment cycles (Vitex agnus castus (VAC): 1 capsule + 1 placebo capsule/day, n = 90; pyridoxine (B6): 2 capsules day, n = 85). The therapeutic response was assessed using the premenstrual tension syndrome scale (PMTS scale), the recording of six characteristic complaints of the syndrome, and the clinical global impression scale (CGI scale). Upon completion of the trial, efficacy of the treatment was assessed by the physician as well as by the patient. On the PMTS scale, treatment with VAC and B6 produced a reduction in score points from 15.2 to 5.1 (-47,4%) and from 11.9 to 5.1 (-48%)(*), respectively. In comparison with pyridoxine, VAC caused a considerably more marked alleviation of typical PMTS complaints, such as breast tenderness, edema, inner tension, headache, constipation, and depression. Analogous results were obtained with the CGI scale. In both treatment groups, efficacy was rated as at least adequate by more than 80% of the investigators; however, VAC treatment was rated as excellent by 24.5% and pyridoxine treatment by 12.1% of the investigators. According to the patients' assessment, 36.1% of the cases in the VAC group and 21.3% in the pyridoxine group were free from complaints. Adverse events (gastrointestinal and lower abdominal complaints, skin manifestations and transitory headache) occurred in 5 patients under B6 and in 12 patients under VAC. Serious adverse events were not observed. The results of the present study confirm the efficacy and safety of Agnolyt® capsules in the treatment of PMTS.

  18. Evidence of GLP-1-mediated neuroprotection in an animal model of pyridoxine-induced peripheral sensory neuropathy

    OpenAIRE

    2006-01-01

    Pyridoxine (vitamin B6) intoxicated rodents develop a peripheral neuropathy characterized by sensory nerve conduction deficits associated with disturbances of nerve fiber geometry and axonal atrophy. To investigate the possibility that glucagon-like peptide-1 (7-36)-amide (GLP-1) receptor agonism may influence axonal structure and function through neuroprotection neurotrophic support, effects of GLP-1 and its long acting analog, Exendin-4 (Ex4) treatment on pyridoxine-induced peripheral neuro...

  19. Pyridoxine enhances cell proliferation and neuroblast differentiation by upregulating the GABAergic system in the mouse dentate gyrus.

    Science.gov (United States)

    Yoo, Dae Young; Kim, Woosuk; Kim, Dae Won; Yoo, Ki-Yeon; Chung, Jin Young; Youn, Hwa Young; Yoon, Yeo Sung; Choi, Soo Young; Won, Moo-Ho; Hwang, In Koo

    2011-05-01

    We investigated the effects of pyridoxine (vitamin B(6)) on cell death, cell proliferation, neuroblast differentiation, and the GABAergic system in the mouse dentate gyrus. We administered pyridoxine (350 mg/kg intraperitoneally) to 8 week old mice twice a day for 14 days and sacrificed them at 10 weeks of age. Pyridoxine treatment did not induce neuronal death or activate microglia in the dentate gyrus, while glial fibrillary acidic protein (GFAP)-positive cells were significantly increased in the subgranular zone of the dentate gyrus. The increase in GFAP-positive cells was confirmed to be due to proliferating cells based on double immunofluorescence staining. GFAP-positive cells, which were also labeled with Ki67, a marker for cell proliferation, and doublecortin, a marker for neuroblast differentiation, were significantly increased in the pyridoxine-treated group compared to those in the vehicle-treated group. Pyridoxine treatment also increased the protein levels of glutamic acid decarboxylase (GAD) 67, an enzyme for GABA synthesis, and pyridoxal 5'-phosphate (PNP) oxidase, an enzyme for pyridoxal phosphate synthesis, in the dentate gyrus. These results suggest that pyridoxine treatment distinctly increases cell proliferation, neuroblast differentiation, and upregulated the GABAergic system, as revealed by the increases of GAD67 and PNP oxidase in the mouse dentate gyrus.

  20. The role of pyridoxine as a countermeasure for in-flight loss of lean body mass

    Science.gov (United States)

    Gilbert, Joyce A.

    1992-01-01

    Ground based and in flight research has shown that humans, under conditions of microgravity, sustain a loss of lean body tissue (protein) and changes in several biological processes including, reductions in red blood cell mass, and neurotransmitters. The maintenance of muscle mass, the major component of lean body mass, is required to meet the needs of space station EVAs. Central to the biosynthesis of amino acids, the building blocks of protein, is pyridoxine (vitamin B-6). Muscle mass integrity requires the availability of vitamin B-6 for protein metabolism and neurotransmitter synthesis. Furthermore, the formation of red blood cells require pyridoxine as a cofactor in the biosynthesis of hemoglobin, a protein that carries oxygen to tissues. In its active form, pyridoxal-5'-phosphate (PLP), vitamin B-6 serves as a link between amino acid and carbohydrate metabolism through intermediates of glycolysis and the tricarboxylic acid cycle. In addition to its role in energy metabolism, PLP is involved in the biosynthesis of hemoglobin and neurotransmitter which are necessary for neurological functions. Alterations in pyridoxine metabolism may affect countermeasures designed to overcome some of these biochemical changes. The focus of this research is to determine the effects of microgravity on the metabolic utilization of vitamin B-6, integrating nutrition as an integral component of the countermeasure (exercise) to maintain lean body mass and muscle strength. The objectives are: 1) to determine whether microgravity effects the metabolic utilization of pyridoxine and 2) to quantitate changes in B-6 vitamer distribution in tissue and excreta relative to loss of lean body tissue. The rationale for this study encompasses the unique challenge to control biochemical mechanisms effected during space travel and the significance of pyridoxine to maintain and counter muscle integrity for EVA activities. This experiment will begin to elucidate the importance of biochemical

  1. Pyridoxine treatment alters embryonic motility in chicks: Implications for the role of proprioception.

    Science.gov (United States)

    Sharp, Andrew A; Bekoff, Anne

    2015-03-01

    Somatosensory feedback is important for the modulation of normal locomotion in adult animals, but we do not have a good understanding of when somatosensory information is first used to modulate motility during embryogenesis or how somatosensation is first used to regulate motor output. We used pyridoxine administration (vitamin B6 ), which is known to mostly kill proprioceptive neurons in adult mammals and embryonic chicks, to explore the role of proprioceptive feedback during early embryonic motility in the chick. Injection of pyridoxine on embryonic day 7 (E7) and E8 reduced the amplitude of leg movements recorded on E9 and the number of large, healthy neurons in the ventral-lateral portion of the DRGs. We conclude that proprioception is initially used during embryogenesis to modulate the strength of motor output, but that it is not incorporated into other aspects of pattern generation until later in development as poly-synaptic pathways develop.

  2. Rv2607 from Mycobacterium tuberculosis is a pyridoxine 5'-phosphate oxidase with unusual substrate specificity.

    Directory of Open Access Journals (Sweden)

    Ellene H Mashalidis

    Full Text Available Despite intensive effort, the majority of the annotated Mycobacterium tuberculosis genome consists of genes encoding proteins of unknown or poorly understood function. For example, there are seven conserved hypothetical proteins annotated as homologs of pyridoxine 5'-phosphate oxidase (PNPOx, an enzyme that oxidizes pyridoxine 5'-phosphate (PNP or pyridoxamine 5'-phosphate (PMP to form pyridoxal 5'-phosphate (PLP. We have characterized the function of Rv2607 from Mycobacterium tuberculosis H37Rv and shown that it encodes a PNPOx that oxidizes PNP to PLP. The k(cat and K(M for this reaction were 0.01 s(-1 and 360 µM, respectively. Unlike many PNPOx enzymes, Rv2607 does not recognize PMP as a substrate.

  3. Reversal of psychopathology in adult coeliac disease with the aid of pyridoxine (vitamin B6).

    Science.gov (United States)

    Hallert, C; Aström, J; Walan, A

    1983-03-01

    Signs of mental depression are typical in adults presenting with coeliac disease. The response to treatment was evaluated in 12 consecutive patients by means of the Minnesota Multiphasic Personality Inventory (MMPI), with surgical patients serving as controls. The coeliacs reported no change in depressive symptoms after 1 year's gluten withdrawal despite evidence of improvement in the small intestine. When retested after 3 years, however, after 6 months of 80 mg/day of oral pyridoxine (vitamin B6) therapy, they showed a fall in the score of scale 2 ('depression') from 70 to 56 (p less than 0.01), which became normalized like other pretreatment abnormalities in the MMPI. Cholecystectomy in the control subjects produced no alterations in the MMPI profile. The results indicate a causal relationship between adult coeliac disease and concomitant depressive symptoms which seems to implicate metabolic effects from pyridoxine deficiency influencing central mechanisms regulating mood.

  4. Pyridoxine megavitaminosis produces degeneration of peripheral sensory neurons (sensory neuronopathy) in the dog.

    Science.gov (United States)

    Krinke, G; Schaumburg, H H; Spencer, P S; Suter, J; Thomann, P; Hess, R

    1981-01-01

    Pyridoxine, a water-soluble vitamin, produces a sensory neuronopathy when administered in high doses to dogs. Beagles who received a daily oral dose of 300 mg/kg of pyridoxol hydrochloride developed a swaying gait within 9 days. They eventually became unable to walk, but were not weak. Animals were sacrificed at intervals up to 78 days. Morphological examination revealed widespread neuronal degeneration in the dorsal root ganglia and the Gasserian ganglia. Cytoplasmic changes were first observed after 8 days and consisted of small, electronlucent vacuoles that subsequently coalesced leading to death of the cells. Degeneration of sensory nerve fibers in peripheral nerves, dorsal columns of the spinal cord and the descending spinal tract of the trigeminal nerve was apparent. The pathogenesis of these changes is unclear, but may, in part, reflect the selective permeability of blood vessels in the peripheral ganglia. It is apparent that the peripheral neuropathy previously attributed to pyridoxine actually represents a toxic, peripheral sensory neuronopathy.

  5. Development of a molecularly imprinted polymer for pyridoxine using an ion-pair as template.

    Science.gov (United States)

    Alizadeh, Taher

    2008-08-01

    One of the main challenges in the molecularly imprinted polymers (MIP) field is the proper MIP design for water-soluble compounds because of appearance of serious drawbacks in polar solvents and insolubility of those compounds in non-polar solvents which are commonly used for MIP synthesis. In this work a novel and simple method for synthesis of molecularly imprinted polymers for a water-soluble compound was introduced. Pyridoxine was chosen as a target molecule and the ion-pair complex formed between pyridoxine ion (Py(+)) and dodecyl sulfate ion (DS(-)) was transferred into the chloroform via liquid-liquid extraction. Then polymerization was carried out in chloroform. The molecular mechanics and density functional theory were proposed to screen proper monomer. Binding energy, DeltaE, of a template and a monomer as a measure of their interaction was considered. Ion-pair [Py(+)-DS(-)] was supposed as a template molecule and acrylic acid, methacrylic acid, allyamine, vinylpridine and 2-hydroxy ethyl methacrylate were as tested monomers. The MIP synthesized using acrylic acid showed the highest selectivity to pyridoxine as predicted from the DeltaE calculation. The obtained MIP showed very high affinity against vitamin B6 in comparison to non-imprinted polymers (NIP). It was proved that the obtained MIP with introduced method was much better than that prepared in methanol as porogen. It was showed that the MIP prepared by this new method could be used as an adsorber for extraction and determination of pyridoxine in real and synthetic samples.

  6. Attention-deficit hyperactivity disorder (ADHD) as a pyridoxine-dependent condition: urinary diagnostic biomarkers.

    Science.gov (United States)

    Dolina, S; Margalit, D; Malitsky, S; Rabinkov, A

    2014-01-01

    The data obtained in children with different forms of epilepsy allowed us to consider epilepsy as an inborn error of pyridoxine (vitamin B6) metabolism (Dolina et al., 2012). Mutual interconnections between ADHD and epilepsy indicate that such an approach is reasonable for ADHD. To check such an assumption we analyzed in ADHD patients the same parameters of pyridoxal phosphate (PLP)-dependent tryptophan (TRP) degradation, which were analyzed in epileptic children. The level of TRP and concentrations of compounds formed or metabolized by TRP degradation, the ratios between some of them, and the level of 4-pyridoxic acid were HPLC detected in ADHD children and healthy controls. The data obtained, including low values of 4PA/TRP, IND/TRP and IND/KYN ratios, have evidenced dramatically impaired activity of pyridoxine-dependent enzymes in ADHD patients. Ritalin treatment did not change the general pattern of TRP degradation, but still created a kind of balance between some of detected metabolites. However, the 4PA/TRP, IND/TRP and IND/KYN ratios remained as low as in untreated patients, keeping the importance of diagnostic markers. Almost identical parameters of TRP degradation in untreated ADHD and epileptic patients allow to assume that inborn disorders of vitamin B6 metabolism are the common biochemical background of both diseases. The disturbed activity of PLP dependent enzymes apparently forms those profound disturbances of neurotransmitter systems, which are inherent in ADHD: low concentrations of monoamines and disordered amino acid metabolism. If vitamin B6 disorders are the core biochemical disturbances inherent in ADHD, then the long-term pyridoxine treatment is pathogenetically based replacement therapy of the disease. According to our data, multi-year pyridoxine treatment normalizes completely the pattern of ADHD behavior, without causing any serious side effects.

  7. Pyridoxine for Prevention of Hand-Foot Syndrome Caused by Chemotherapy: A Systematic Review

    OpenAIRE

    2013-01-01

    BACKGROUND: Hand-foot syndrome (HFS) is a relatively frequent dermatologic toxic reaction to certain anti-cancer chemotherapies. The syndrome can evolve into a distressing condition that limits function and affects quality of life. Pyridoxine (vitamin B6) has been used empirically for the prevention of HFS caused by anti-cancer therapy. However, evidence of its efficacy remains controversial. METHODOLOGY//PRINCIPAL FINDINGS: Systematic literature searches were conducted on the Cochrane Librar...

  8. Teratogenic Effects of Pyridoxine on the Spinal Cord and Dorsal Root Ganglia of Embryonic Chickens

    OpenAIRE

    2015-01-01

    Our understanding of the role of somatosensory feedback in regulating motility during chicken embryogenesis and fetal development in general has been hampered by the lack of an approach to selectively alter specific sensory modalities. In adult mammals, pyridoxine overdose has been shown to cause a peripheral sensory neuropathy characterized by a loss of both muscle and cutaneous afferents, but predominated by a loss of proprioception. We have begun to explore the sensitivity of the nervous s...

  9. New Derivatives of Pyridoxine Exhibit High Antibacterial Activity against Biofilm-Embedded Staphylococcus Cells.

    Science.gov (United States)

    Kayumov, Airat R; Nureeva, Aliya A; Trizna, Elena Yu; Gazizova, Guzel R; Bogachev, Mikhail I; Shtyrlin, Nikita V; Pugachev, Mikhail V; Sapozhnikov, Sergey V; Shtyrlin, Yurii G

    2015-01-01

    Opportunistic bacteria Staphylococcus aureus and Staphylococcus epidermidis often form rigid biofilms on tissues and inorganic surfaces. In the biofilm bacterial cells are embedded in a self-produced polysaccharide matrix and thereby are inaccessible to biocides, antibiotics, or host immune system. Here we show the antibacterial activity of newly synthesized cationic biocides, the quaternary ammonium, and bisphosphonium salts of pyridoxine (vitamin B6) against biofilm-embedded Staphylococci. The derivatives of 6-hydroxymethylpyridoxine were ineffective against biofilm-embedded S. aureus and S. epidermidis at concentrations up to 64 μg/mL, although all compounds tested exhibited low MICs (2 μg/mL) against planktonic cells. In contrast, the quaternary ammonium salt of pyridoxine (N,N-dimethyl-N-((2,2,8-trimethyl-4H-[1,3]dioxino[4,5-c]pyridin-5-yl)methyl)octadecan-1-aminium chloride (3)) demonstrated high biocidal activity against both planktonic and biofilm-embedded bacteria. Thus, the complete death of biofilm-embedded S. aureus and S. epidermidis cells was obtained at concentrations of 64 and 16 μg/mL, respectively. We suggest that the quaternary ammonium salts of pyridoxine are perspective to design new synthetic antibiotics and disinfectants for external application against biofilm-embedded cells.

  10. Recycling of pyridoxine (vitamin B6) by PUP1 in Arabidopsis.

    Science.gov (United States)

    Szydlowski, Nicolas; Bürkle, Lukas; Pourcel, Lucille; Moulin, Michael; Stolz, Jürgen; Fitzpatrick, Teresa B

    2013-07-01

    Vitamin B6 is a cofactor for more than 140 essential enzymatic reactions and was recently proposed as a potent antioxidant, playing a role in the photoprotection of plants. De novo biosynthesis of the vitamin has been described relatively recently and is derived from simple sugar precursors as well as glutamine. In addition, the vitamin can be taken up from exogenous sources in a broad range of organisms, including plants. However, specific transporters have been identified only in yeast. Here we assess the ability of the family of Arabidopsis purine permeases (PUPs) to transport vitamin B6. Several members of the family complement the growth phenotype of a Saccharomyces cerevisiae mutant strain impaired in both de novo biosynthesis of vitamin B6 as well as its uptake. The strongest activity was observed with PUP1 and was confirmed by direct measurement of uptake in yeast as well as in planta, defining PUP1 as a high affinity transporter for pyridoxine. At the tissue level the protein is localised to hydathodes and here we use confocal microscopy to illustrate that at the cellular level it is targeted to the plasma membrane. Interestingly, we observe alterations in pyridoxine recycling from the guttation sap upon overexpression of PUP1 and in a pup1 mutant, consistent with the role of the protein in retrieval of pyridoxine. Furthermore, combining the pup1 mutant with a vitamin B6 de novo biosynthesis mutant (pdx1.3) corroborates that PUP1 is involved in the uptake of the vitamin.

  11. Synthesis and crystal structure of the coordination compound of pyridoxine with manganese sulfate

    Science.gov (United States)

    Furmanova, N. G.; Verin, I. A.; Shyityeva, N.; Sulaimankulov, K. S.; Berdalieva, Zh.; Resnyanskii, V. F.; Duishenbaeva, A. T.

    2011-11-01

    The reaction of pyridoxine with manganese sulfate in an aqueous solution gave the coordination compound MnSO4 · 2C8H11O3N · 2H2O ( I). The structure of I was determined from single-crystal X-ray diffraction data. In the centrosymmetric complex (sp. gr. Pbar 1, Z = 1), the Mn atom is coordinated by two pyridoxine molecules and two water molecules, thus adopting an octahedral coordination. The sulfate anion is also at a center of symmetry and, consequently, is disordered. The pyridoxine molecules are coordinated to the metal atom through the oxygen atoms of the deprotonated hydroxyl group and the CH2OH group that retains the hydrogen atom. The nitrogen atom is protonated in such a way that the heterocycle assumes a pyridinium character. The crystal structure also contains six water molecules of crystallization. A thermogravimetric study showed that the decomposition of I occurs in several successive steps, such as dehydration, the combustion of organic ligands, and the formation of an inorganic residue.

  12. Pyridoxine-derived organoselenium compounds with glutathione peroxidase-like and chain-breaking antioxidant activity.

    Science.gov (United States)

    Singh, Vijay P; Poon, Jia-Fei; Butcher, Ray J; Engman, Lars

    2014-09-22

    One of the vitamin B6 vitamers, pyridoxine, was modified to incorporate selenium in various oxidation states in place of the methyl group in position 2. Such compounds were conveniently accessed by treatment of bis-4,5-(carboethoxy)-2-iodo-3-pyridinol with disodium diselenide and LiAlH4 -reduction. After work-up, selone 7 was isolated in good yield as an air-stable crystalline material. Hydrogen bonding to the neighboring hydroxyl group, as revealed by the short intramolecular Se⋅⋅⋅H distance in the crystal structure is likely to provide extra stabilization to the compound. Computational studies showed that selone 7 is more stable than the corresponding selenol tautomer by 12.2 kcal mol(-1) . Hydrogen peroxide oxidation of the selone 7 afforded diselenide 12, and, on further oxidation, seleninic acid 13. Treatment of the seleninic acid with thiophenol provided an isolable selenosulfide 14. The glutathione peroxidase-like properties of the pyridoxine-derived compounds were assessed by using the coupled reductase method. Seleninic acid 13 was found to be twofold more active than ebselen. The chain-breaking capacity of the pyridoxine compounds were studied in a water/chlorobenzene membrane model containing linoleic acid as an oxidizable substrate and N-acetylcysteine as a thiol reducing agent. Diselenide 15 could match α-tocopherol when it comes to reactivity towards peroxyl radicals and inhibition time.

  13. Profound neonatal hypoglycemia and lactic acidosis caused by pyridoxine-dependent epilepsy.

    Science.gov (United States)

    Mercimek-Mahmutoglu, Saadet; Horvath, Gabriella A; Coulter-Mackie, Marion; Nelson, Tanya; Waters, Paula J; Sargent, Michael; Struys, Eduard; Jakobs, Cornelis; Stockler-Ipsiroglu, Sylvia; Connolly, Mary B

    2012-05-01

    Pyridoxine-dependent epilepsy (PDE) was first described in 1954. The ALDH7A1 gene mutations resulting in α-aminoadipic semialdehyde dehydrogenase deficiency as a cause of PDE was identified only in 2005. Neonatal epileptic encephalopathy is the presenting feature in >50% of patients with classic PDE. We report the case of a 13-month-old girl with profound neonatal hypoglycemia (0.6 mmol/L; reference range >2.4), lactic acidosis (11 mmol/L; reference range pyridoxine. The diagnosis of α-aminoadipic semialdehyde dehydrogenase deficiency was confirmed based on the elevated urinary α-aminoadipic semialdehyde excretion, compound heterozygosity for a known splice mutation c.834G>A (p.Val278Val), and a novel putative pathogenic missense mutation c.1192G>C (p.Gly398Arg) in the ALDH7A1 gene. She has been seizure-free since 1.5 months of age on treatment with pyridoxine alone. She has motor delay and central hypotonia but normal language and social development at the age of 13 months. This case is the first description of a patient with PDE due to mutations in the ALDH7A1 gene who presented with profound neonatal hypoglycemia and lactic acidosis masquerading as a neonatal-onset gluconeogenesis defect. PDE should be included in the differential diagnosis of hypoglycemia and lactic acidosis in addition to medically refractory neonatal seizures.

  14. New Derivatives of Pyridoxine Exhibit High Antibacterial Activity against Biofilm-Embedded Staphylococcus Cells

    Directory of Open Access Journals (Sweden)

    Airat R. Kayumov

    2015-01-01

    Full Text Available Opportunistic bacteria Staphylococcus aureus and Staphylococcus epidermidis often form rigid biofilms on tissues and inorganic surfaces. In the biofilm bacterial cells are embedded in a self-produced polysaccharide matrix and thereby are inaccessible to biocides, antibiotics, or host immune system. Here we show the antibacterial activity of newly synthesized cationic biocides, the quaternary ammonium, and bisphosphonium salts of pyridoxine (vitamin B6 against biofilm-embedded Staphylococci. The derivatives of 6-hydroxymethylpyridoxine were ineffective against biofilm-embedded S. aureus and S. epidermidis at concentrations up to 64 μg/mL, although all compounds tested exhibited low MICs (2 μg/mL against planktonic cells. In contrast, the quaternary ammonium salt of pyridoxine (N,N-dimethyl-N-((2,2,8-trimethyl-4H-[1,3]dioxino[4,5-c]pyridin-5-ylmethyloctadecan-1-aminium chloride (3 demonstrated high biocidal activity against both planktonic and biofilm-embedded bacteria. Thus, the complete death of biofilm-embedded S. aureus and S. epidermidis cells was obtained at concentrations of 64 and 16 μg/mL, respectively. We suggest that the quaternary ammonium salts of pyridoxine are perspective to design new synthetic antibiotics and disinfectants for external application against biofilm-embedded cells.

  15. Doxylamine succinate–pyridoxine hydrochloride (Diclegis for the management of nausea and vomiting in pregnancy: an overview

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    Nuangchamnong N

    2014-04-01

    Full Text Available Nina Nuangchamnong, Jennifer Niebyl Department of Obstetrics and Gynecology, University of Iowa Hospitals and Clinics, Iowa, IA, USA Abstract: Nausea and vomiting in pregnancy (NVP is common and often undertreated, in part due to fears of adverse effects of medications on the fetus during early pregnancy. In April 2013, the US Food and Drug Administration (FDA approved doxylamine succinate 10 mg and pyridoxine hydrochloride (a vitamin B6 analog 10 mg as a delayed-release combination pill called Diclegis for the treatment of NVP. Diclegis is currently the only medication that is FDA-approved for the indication of NVP. This review addresses the historical context, safety, efficacy, pharmacology, and practical role of doxylamine and pyridoxine for the management of NVP. The reintroduction of this doxylamine–pyridoxine combination pill into the American market fills a therapeutic gap in the management of NVP left by the removal of the same active drugs marketed over 30 years ago in the form of Bendectin. The substantial amount of safety data accumulated over the years makes it one of the few drugs that qualify for FDA Pregnancy Category A status. In the hierarchical approach to pharmacological treatment of NVP, the combination of doxylamine and pyridoxine should thus be first-tier. Keywords: doxylamine, pyridoxine, vitamin B6, nausea, vomiting, pregnancy

  16. Dose response, coasting, and differential fiber vulnerability in human toxic neuropathy: a prospective study of pyridoxine neurotoxicity.

    Science.gov (United States)

    Berger, A R; Schaumburg, H H; Schroeder, C; Apfel, S; Reynolds, R

    1992-07-01

    We administered either 1 or 3 g/d of pyridoxine (vitamin B6) to five healthy volunteers and repeatedly followed serum pyridoxal phosphate levels, clinical symptoms and signs, quantitative sensory thresholds (QSTs), and sural nerve electrophysiology. Pyridoxine was discontinued at the first sign of either clinical or laboratory abnormality. In all subjects, sensory symptoms and QST abnormalities occurred concurrently. Subjects receiving higher doses became symptomatic earlier than low-dose subjects. Elevation of thermal QSTs preceded or exceeded that for vibration in the three low-dose subjects; vibration and thermal QST became abnormal simultaneously in the higher-dose subjects. A reduction in the amplitude of the sural sensory potential lagged behind QST changes in two of three subjects. Symptoms continued to progress ("coasting") for 2 to 3 weeks despite stopping pyridoxine administration and the return of serum pyridoxal phosphate levels to normal. This study suggests that (1) there is a clear dose-percent relationship for pyridoxine-induced neuropathy, (2) QST is a sensitive measurement for detecting early peripheral neuropathy; QST abnormalities may precede changes in nerve conduction studies, (3) coasting appears unrelated to persistently elevated blood levels of the toxin, and (4) a dose-dependent vulnerability may exist among nerve fibers of different caliber when exposed to an axonal toxin, such as pyridoxine.

  17. High dose dietary pyridoxine induces T-helper type 1 polarization and decreases contact hypersensitivity response to fluorescein isothiocyanate in mice.

    Science.gov (United States)

    Kobayashi, Chie; Kurohane, Kohta; Imai, Yasuyuki

    2012-01-01

    Pyridoxine (vitamin B(6)) is commonly used as a dietary supplement and beneficial effects of it are expected. However, excess ingestion of pyridoxine has been shown to cause a severe sensory neuropathy in humans and experimental animals. We have been studying the linkage between the nervous and immune systems using a fluorescein isothiocyanate (FITC)-induced contact hypersensitivity (CHS) mouse model. We have found that activation of transient receptor potential ankyrin 1 (TRPA1), which is expressed on sensory neurons, enhances skin sensitization to FITC. Another feature of FITC-induced CHS is its dependence on T helper 2 (Th2) type responses. We hypothesized that the excess intake of pyridoxine may affect sensitization to FITC and influence helper T-cell polarization. We examined FITC-induced CHS in BALB/c mice fed a diet containing excess pyridoxine (120 mg/kg diet) for 3 weeks. We found that mice fed on the excess-pyridoxine diet exhibited a lower response as to FITC-induced CHS compared with ones fed on a diet with a standard pyridoxine content (6.0 mg/kg diet). Moreover, the interferon (IFN)-γ/interleukin (IL)-4 ratio produced by draining lymph node cells was significantly higher with the excess-pyridoxine diet. This suggested that the cytokine balance was shifted toward Th1 with the excess-pyridoxine diet. Consistently, Th1-dependent oxazolone-induced CHS was enhanced with the excess-pyridoxine diet. These results suggested that an excess pyridoxine intake actively influences the immune system by altering helper T cell polarization.

  18. Effects of combined lipoic acid and pyridoxine on albuminuria, advanced glycation end-products, and blood pressure in diabetic nephropathy.

    Science.gov (United States)

    Noori, Nazanin; Tabibi, Hadi; Hosseinpanah, Farhad; Hedayati, Mehdi; Nafar, Mohsen

    2013-01-01

    This study was designed to investigate the effects of combined administration of lipoic acid and pyridoxine on albuminuria, oxidative stress, blood pressure, serum advanced glycation end-products, nitric oxide (NO), and endothelin-1 in patients with diabetic nephropathy. Thirty-four patients were randomly assigned to either a supplement group or a placebo group. The patients in the supplement group received 800 mg lipoic acid and 80 mg pyridoxine daily for 12 weeks, whereas the placebo group received corresponding placebos. Urinary albumin, serum malondialdehyde (MDA), and systolic blood pressure decreased significantly in the supplement group compared to the placebo group (p blood pressure. The present study indicates that combined administration of lipoic acid and pyridoxine improves albuminuria in patients with diabetic nephropathy by reducing oxidative stress, advanced glycation end-products, and systolic blood pressure. The reduction in microalbuminuria may be of benefit in retarding the progression of diabetic nephropathy.

  19. The Problem of the Mechanism of Action of Pyridoxine (Vitamin B6) in Acute Radiation Injury USSR.

    Science.gov (United States)

    2007-11-02

    eantradietory. Sossa autho?» «ässiday pyridoxin ® th« bait tharapauiie agast ie radiation «ie&nag« (27, 30); othare assert that thi« pffep&rstioa... pyridoxin « an« dlssadrel <ha?iag.th« aoute period of radiation •iQletM«» i»r«**«l th* aurrt val «ta öf tha rat« to 71 .3 par««* (*f tha 80 rate 57...IB the irradiated rabbit« which ha* ba«ss givan pyridoxine or bistamin« for a vaak befer® tha irradiation tha’■ eastajst of Mstasisa*« iß the bleed

  20. MexiB 6 AS A RESULT OF FORTIFICATION OF ETHYLMETHYLHYDROXYPYRIDINE SUCCINATE WITH MAGNESIUM AND PYRIDOXINE: PROTEOME EFFECTS

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    O. A. Gromova

    2016-01-01

    Full Text Available The efficacy of ethylmethylhydroxypyridine succinate (EMHPS  depends on the concentration and activity of proteomic proteins. To provide the body with magnesium and pyridoxine is an important condition for the efficacy of EMHPS because these micronutrients are essential for maintaining neuronal function.Objective: to analyze the biological effects of pyridoxineand magnesium-dependent proteins providing the molecular mechanisms of multi-targeted action of EMHPS,  pyridoxine, and magnesium.Material and methods. Proteins that interact with both pyridoxine and magnesium were found in the genomic and proteomic databases. A list of 78 vitamin B6-dependent proteins, which is based on the available human genome records in NCBIPROTEIN, EMBL,  UNIPROT,  and HumanProteomeMap databases, was analyzed using a functional binding assay. The same assay was also applied to analyze a list 720 magnesium-dependent proteins.Results. The analysis has shown that 78 pyridoxine-dependent proteomic proteins are necessary for: 1 the synthesis and processing of amino acids; 2 cell energy metabolism (ATP synthesis, and 3 the synthesis of neurotransmitters and neuronal membranes. MexiB 6 has numerous synergistic interactions between the molecules of EMHPS,  pyridoxine, and magnesium. The combination of the components of EMHPS,  pyridoxine and magnesium in MexiB 6 (triple synergism allows prediction that the drug has more pronounced clinical effects than the molecules of EMHPS,  which emerges in its antihypoxic and antioxidant activities, the improvement of synaptic transmission of a signal, the neutralization of homocysteine, and the regulation of lipid and carbohydrate metabolism (restoration of cell sensitivity to insulin and carbohydrates in patients with atherosclerosis and in those at risk for diabetes mellitus or obesity. Pyridoxineand magnesium-induced potentiation of the effects of EMHPS may enhance its activity.

  1. Effect of pyridoxine treatment of a homocystinuric patient on the urinary excretion of some sulfur-containing amino acids

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    Kodama,H.

    1974-08-01

    Full Text Available The effect of pyridoxine treatment of a homocystinuric patient on the urinary excretion of some sulfur-containing amino acids was studied and the following results were obtained. As a result of pyridoxine treatment, urinary homocystine decreased to a fairly great extent, and its unusual metabolites S.(3-hydroxy-3-carboxyn- propylthio homocysteine (HCPTHC and S-C8-carboxyethylthio homocysteine (j3-CETHC increased to some extent. But its oxidation product (homocysteic acid showed a tendency to decrease slightly. Urinary methionine and cystine increased to some extent, but cysteinehomocysteine mixed disulfide showed no remarkable change.

  2. A nutritional conditional lethal mutant due to pyridoxine 5'-phosphate oxidase deficiency in Drosophila melanogaster.

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    Chi, Wanhao; Zhang, Li; Du, Wei; Zhuang, Xiaoxi

    2014-04-16

    The concept of auxotrophic complementation has been proposed as an approach to identify genes in essential metabolic pathways in Drosophila melanogaster. However, it has achieved limited success to date, possibly due to the low probability of finding mutations fit with the chemically defined profile. Instead of using the chemically defined culture media lacking specific nutrients, we used bare minimum culture medium, i.e., 4% sucrose, for adult Drosophila. We identified a nutritional conditional lethal mutant and localized a c.95C > A mutation in the Drosophila pyridoxine 5'-phosphate oxidase gene [dPNPO or sugarlethal (sgll)] using meiotic recombination mapping, deficiency mapping, and whole genome sequencing. PNPO converts dietary vitamin B6 such as pyridoxine to its active form pyridoxal 5'-phosphate (PLP). The missense mutation (sgll(95)) results in the substitution of alanine to aspartate (p.Ala32Asp). The sgll(95) flies survive well on complete medium but all die within 6 d on 4% sucrose only diet, which can be rescued by pyridoxine or PLP supplement, suggesting that the mutation does not cause the complete loss of PNPO activity. The sgll knockdown further confirms its function as the Drosophila PNPO. Because better tools for positional cloning and cheaper whole genome sequencing have made the identification of point mutations much easier than before, alleviating the necessity to pinpoint specific metabolic pathways before gene identification, we propose that nutritional conditional screens based on bare minimum growth media like ours represent promising approaches for discovering important genes and mutations in metabolic pathways, thereby accelerating the establishment of in vivo models that recapitulate human metabolic diseases.

  3. Ru(III)-catalyzed oxidation of pyridoxine and albuterol in pharmaceuticals

    Science.gov (United States)

    Ashok, More; Prasad, Adapa V. S. S.; Reddy, P. Muralidhar; Ravinder, Vadde

    2009-02-01

    Ru(III) complexes with coordinated amide were synthesized and characterized by elemental, IR, mass, electronic, ESR spectral analysis, magnetic and conductance measurements and octahedral structures have been proposed. These complexes were used as catalysts for the oxidation of pyridoxine and albuterol in pharmaceuticals in presence of hydrogen peroxide. The role of co-oxidant and the effect of reaction time on the yields of oxidation products which were spectrophotometrically determined by condensing them with sulfanilic acid in acid medium were investigated. Structures of the oxidation products were established with the help of IR and NMR spectral analysis.

  4. Dynamic NMR study of dinitrophenyl derivatives of seven-membered cyclic ketals of pyridoxine.

    Science.gov (United States)

    Rakhmatullin, Ilfat Z; Galiullina, Leisan F; Garipov, Marsel' R; Strel'nik, Alexey D; Shtyrlin, Yurii G; Klochkov, Vladimir V

    2015-10-01

    Two pyridoxine derivatives containing a dinitrophenyl moiety were investigated by (1)H NMR spectroscopy. Conformational dynamics in solution were studied for each compound using dynamic NMR experiments. It was shown that both compounds studied are involved into two conformational exchange processes. The first process is a transformation of the seven-membered cycle conformation between the enantiomeric P-twist and M-twist forms, and the second is a rotation of the dinitrophenyl fragment of the molecules around the C-O bond. Energy barriers of both conformational transitions were determined.

  5. [Vitamin B6 (Pyridoxine)--excessive dosage in food supplements and OTC medications].

    Science.gov (United States)

    Barak, Nir; Huminer, David; Stahl, Bracha

    2004-12-01

    Vitamin B6 (Pyridoxine) is sold in Israel as a supplement and is available over-the-counter (OTC) without regulation. High intake of this vitamin is found in patients with premenstrual syndrome, carpal tunnel syndrome, pregnancy associated nausea and vomiting, decreasing homocysteine levels and improving cognitive function. Mega-doses of this vitamin may result in intoxication. In this review we will outline vitamin B6 function, daily recommended intake, deficiency signs and patients in deficiency risk, and the clinical spectrum of vitamin B6 intoxication.

  6. [Effect of pyridoxine on the psychopathology and pathochemistry of involutional depressions].

    Science.gov (United States)

    Bukreev, V I

    1978-01-01

    In agreement with the catecholamine hypotheses of affective disorders the main role in the pathogenesis of depressive states is allocated to the central "noradrenergic insufficiency". The author thinks it feasible to use pyridoxine (vit. B6) in the treatment of depressive states, inasmuch as it is involved in the process of catecholamine synthesis as a cofactor of DOPA-decarboxylase. The author examined 48 patients among which 31 were with involutional melancholia and 17 with manic-depressive psychoses, manifesting after 40 years. Along with a positive therapeutical effect there was an increase in the noradrenaline excretion and a drop in the relative adrenaline content.

  7. [Pyridoxine for severe metabolic acidosis and seizures due to isoniazid overdose].

    Science.gov (United States)

    Adler, M; Girsh-Solomonovich, Z; Raikhlin-Eisenkraft, B

    1993-05-16

    A 15-year-old girl took 3 g of isoniazid (15 tablets) in a suicide attempt and was brought unconscious to the emergency room. She was in respiratory failure, with seizures that could not be stopped with diazepam. Severe metabolic acidosis with normal serum lactate developed (pH 6.85), but did not improve after infusion of bicarbonate. Intravenous administration of pyridoxine led to prompt cessation of the seizures and to gradual improvement of acid-base status. She recovered consciousness after several hours and was discharged a week later.

  8. Use of pyridoxine and pyridostigmine in children with vincristine-induced neuropathy.

    Science.gov (United States)

    Akbayram, Sinan; Akgun, Cihangir; Doğan, Murat; Sayin, Refah; Caksen, Huseyin; Oner, Ahmet Faik

    2010-06-01

    Four children with vincristine (VCR)-induced neuropathy are being reported. All cases were followed with the diagnosis of acute lymphoblastic leukemia. Two were boys aged between 2 and 13 year. Electromyographic examination consisted of sensoriomotor polyneuropathy with axonal involvement in three patients. In another patient, it consisted of motor axonal polyneuropathy. In all patients, pyridoxine and pyridostigmine were successfully used in the treatment of VCR-induced neuropathy. They recovered completely with this drug combination. Recovering period of symptoms was between 1-2 week.

  9. Radiolysis of pyridoxine (vitamin B 6) in aqueous solution under different conditions

    Science.gov (United States)

    Albarrán, Guadalupe; Ramírez-Cahero, Fernando; Aliev, Roustam

    2008-05-01

    Aqueous solutions of pyridoxine (1 mM) without or with additive of K 3[Fe(CN) 6] (2.5 mM) were gamma-irradiated at different doses and dose rate of 2.16 kGy/h in the absence of air, in the presence of air or by their saturation with N 2O. The radiolytic products were analyzed with HPLC, mass spectrometry and UV spectroscopy. 2,4,5-Trihydroxymethyl-3-pyridinol, pyridoxal, isopyridoxal and 6-hydroxypyridoxine were formed by radiolysis in the absence of K 3[Fe(CN) 6], and their concentrations were much higher in samples saturated with N 2O. Pyridoxi-3,6-quinone was found by radiolysis under all the above-mentioned conditions but only in the presence of K 3[Fe(CN) 6]. Besides, the pyridoxal formation increased in the presence of this oxidizing agent. G values of pyridoxal formation and pyridoxine degradation were quantified. Some details of the radiolytic product formation were discussed.

  10. Analysis of Water Soluble Vitamins (Thiamine, Nicotinamide and Pyridoxine in Fortified Infant Food Products by Hplc

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    Narjis Naz

    2016-05-01

    Full Text Available The present study provides information about the levels of fortification of three water soluble vitamins i.e. thiamine (B1, nicotinamide (B3 and pyridoxine (B6 in a variety of foodstuffs include milk products and cereals for young children. Food fortification is key implement for improving health of the growing children. Twenty food samples were chosen for analysis because of their common utilization in the local area. The vitamin concentrations were determined by high performance liquid chromatography with C18 column with a gradient of mobile phase made of water and acetonitrile and a diode array detector set at 280 nm. The thiamine content investigated in the samples ranging from 268 µg/mL to 3 µg/ml, nicotinamide content was from 41 µg/ml to 1 µg/mL while the pyridoxine level was in between 412 µg/mL to 20 µg/mL. Detection and Quantification of compounds were attained by comparing their retention times with standard reference materials and on the basis the off peak area match against those of a standard. The method used, offer excellent linearity with r2 ≥ 0.994, detection limits, reproducibility, and analyte recovery.

  11. Epilepsy due to 20q13.33 subtelomere deletion masquerading as pyridoxine-dependent epilepsy.

    Science.gov (United States)

    Mefford, Heather C; Cook, Joseph; Gospe, Sidney M

    2012-12-01

    A cause of antiepileptic medication resistant seizures presenting in neonates and young infants is pyridoxine-dependent epilepsy (PDE), an organic aciduria, which is due to recessive mutations in the ALDH7A1 gene, resulting in deficiency of antiquitin. Since the discovery of molecular basis of this disorder, a few patients have been reported with a similar clinical phenotype but without evidence of antiqutin dysfunction. We report on a patient who had carried a clinical diagnosis of PDE for 7 years, but who was than shown to have normal ALDH7A1 sequencing and the absence of biomarkers characteristic of this familial epilepsy. Array comparative genomic hybridization (CGH) demonstrated a 1.5-Mb terminal deletion of the long arm of chromosome 20, which included deletion of the KCNQ2 and CHRNA4 genes, both of which have been associated with specific epilepsy syndromes. We suggest that this boy's neonatal epilepsy and neurodevelopmental disabilities are secondary to this deletion and that his clinical response to pyridoxine was coincidental. This patient's history emphasizes the utility of array CGH in the evaluation of children with epilepsy of unknown etiology.

  12. Fetal onset ventriculomegaly and subependymal cysts in a pyridoxine dependent epilepsy patient.

    Science.gov (United States)

    Jain-Ghai, Shailly; Mishra, Navin; Hahn, Cecil; Blaser, Susan; Mercimek-Mahmutoglu, Saadet

    2014-04-01

    Pyridoxine dependent epilepsy (PDE) is caused by mutations in the ALDH7A1 gene encoding α-aminoadipic semialdehyde dehydrogenase. The classic clinical presentation is neonatal seizures responsive only to pyridoxine therapy. White matter abnormalities, corpus callosum agenesis or hypoplasia, megacisterna magna, cortical dysplasia, neuronal heterotopias, intracerebral hemorrhage, and hydrocephalus in neuroimaging have been reported in patients with PDE. We report a new patient with asymmetric progressive ventriculomegaly noted on fetal sonography at 22 weeks' gestation. Postnatal brain sonography on day 1 and MRI on day 5 confirmed bilateral asymmetric ventriculomegaly caused by bilateral subependymal cysts. Intractable seizures at age 7 days initially responded to phenobarbital. Markedly elevated urinary α-aminoadipic acid semialdehyde levels and compound heterozygous mutations in the ALDH7A1 gene (c.446C>A/c.919C>T) confirmed the diagnosis of PDE caused by ALDH7A1 genetic defect. Despite the presence of structural brain malformations and subependymal cysts, PDE should always be included in the differential diagnosis of neonatal seizures that are refractory to treatment with antiepileptic drugs.

  13. Simultaneous derivative spectrophotometric analysis of doxylamine succinate, pyridoxine hydrochloride and folic Acid in combined dosage forms.

    Science.gov (United States)

    Pathak, A; Rajput, S J

    2008-01-01

    Two UV spectrophotometric methods have been developed, based on first derivative spectrophotometry for simultaneous estimation of doxylamine succinate, pyridoxine hydrochloride, and folic acid in tablet formulations. In method I, the concentrations of these drugs were determined by using linear regression equation. Method II is also based on first derivative spectrophotometry however simultaneous equations (Vierdot's method) were derived on derivative spectra. The first derivative amplitudes at 270.0, 332.8 and 309.2 nm were utilized for simultaneous estimation of these drugs respectively by both methods. In both the methods, linearity was obtained in the concentration range 2.5-50 mug/ml, 1-40 mug/ml and 1-30 mug/ml for doxylamine succinate, pyridoxine hydrochloride, and folic acid respectively. The developed methods show best results in terms of linearity, accuracy, precision, LOD, LOQ and ruggedness for standard laboratory mixtures of pure drugs and marketed formulations. The common excipients and additives did not interfere in their determinations.

  14. Simultaneous derivative spectrophotometric analysis of doxylamine succinate, pyridoxine hydrochloride and folic acid in combined dosage forms

    Directory of Open Access Journals (Sweden)

    Pathak A

    2008-01-01

    Full Text Available Two UV spectrophotometric methods have been developed, based on first derivative spectrophotometry for simultaneous estimation of doxylamine succinate, pyridoxine hydrochloride, and folic acid in tablet formulations. In method I, the concentrations of these drugs were determined by using linear regression equation. Method II is also based on first derivative spectrophotometry however simultaneous equations (Vierdot′s method were derived on derivative spectra. The first derivative amplitudes at 270.0, 332.8 and 309.2 nm were utilized for simultaneous estimation of these drugs respectively by both methods. In both the methods, linearity was obtained in the concentration range 2.5-50 µg/ml, 1-40 µg/ml and 1-30 µg/ml for doxylamine succinate, pyridoxine hydrochloride, and folic acid respectively. The developed methods show best results in terms of linearity, accuracy, precision, LOD, LOQ and ruggedness for standard laboratory mixtures of pure drugs and marketed formulations. The common excipients and additives did not interfere in their determinations.

  15. Fate of dietary pyridoxine-beta-glucoside in the lactating rat

    Energy Technology Data Exchange (ETDEWEB)

    Trumbo, P.R.; Gregory, J.F. III

    1989-01-01

    (/sup 3/H)5'-O-(beta-D-glucopyranosyl) pyridoxine (PN-glucoside) and (/sup 14/C)pyridoxine (PN) were orally administered to lactating rats. Milk was collected from the dam, and the stomach contents and liver were collected from the suckling pups 24 and 48 h after administration. Analysis of the isotopic ratio (/sup 3/H//sup 14/C) in the milk and stomach contents indicated that the secretion of /sup 3/H in the milk was 20-25% as great as the secretion of /sup 14/C. The only labeled form of /sup 3/H and /sup 14/C in the stomach contents was pyridoxal phosphate (PLP), indicating that PN-glucoside was hydrolyzed to PN and subsequently metabolized prior to secretion by the mammary gland. The isotopic ratio in the livers of the pups was similar to that of the stomach contents. Furthermore, the relative distribution of the two isotopes among the hepatic metabolites of the pups was similar. The results of this study indicate that intact PN-glucoside is not secreted in milk, although vitamin B-6 derived from the limited hydrolysis and metabolism of PN-glucoside is delivered to the mammary gland for secretion.

  16. Pyridoxine (vitamin B6) and the premenstrual syndrome: a randomized crossover trial.

    Science.gov (United States)

    Doll, H; Brown, S; Thurston, A; Vessey, M

    1989-09-01

    A randomized double-blind crossover trial was conducted to study the effects of pyridoxine (vitamin B6) at a dose of 50 mg per day on symptoms characteristic of the premenstrual syndrome. Sixty three women aged 18-49 years, identified by means of a general practice based survey of menstrual patterns in the community, entered the trial. All of the women had noticed moderate to severe premenstrual symptoms during the previous year. The women kept a daily menstrual diary which graded the severity of nine individual symptoms from zero to three. After completing a diary for an initial month the women were randomized to receive either drug or placebo for three months, after which the treatments were crossed over for a further three months. Thirty two women completed the full seven months of the study. In these women a significant beneficial effect (P less than 0.05) of pyridoxine was observed on emotional type symptoms (depression, irritability and tiredness). No significant effect was observed on premenstrual symptoms of any other type.

  17. Fenugreek seed extract treats peripheral neuropathy in pyridoxine induced neuropathic mice.

    Science.gov (United States)

    Moghadam, Farshad Homayouni; Vakili-Zarch, Behzad; Shafiee, Mohammad; Mirjalili, Azam

    2013-01-01

    Trigonella foenum graecum commonly known as Fenugreek exerts normoglycemic and insulinotropic effects in humans by compounds from its seed and leaf extracts. Some studies reported that treating pregnant mice with fenugreek seed could cause toxic effects on the nervous system of its pubs during developmental growth, while in some other studies neuroprotective properties were considered for it. Safety of anti-diabetic drugs for nervous system is very important because peripheral neuropathy is a common complication of diabetes and hazardous drugs could worsen it. In this study, the effect of treatment with fenugreek seed extract on the function of sciatic nerves of neuropathic mice was evaluated. Neuropathy was induced in male mice by pyridoxine intoxication. After that, animals were treated with 0.2, 2 and 20 mg/kg of hydro-alcoholic extract of fenugreek seeds for 10 days, tail flick, electrophysiological and histological assays were performed to evaluate the effect of fenugreek seed extract on function of the peripheral nerves. Our data showed that fenugreek has anti neuropathic effect and restores the function of nerve fibers. Results of electrophysiological recordings stated that the highest rate of healing was occurred in 20 mg/kg fenugreek extract treated animals. In conclusion, findings of the present study demonstrate that treatment with fenugreek seed extract can potentially facilitate healing from pyridoxine induced peripheral neuropathy in mice.

  18. Evaluation of the efficacy of thiamine and pyridoxine in the treatment of symptomatic diabetic peripheral neuropathy.

    Science.gov (United States)

    Abbas, Z G; Swai, A B

    1997-12-01

    The clinical response to therapeutic doses of two vitamins were determined in diabetic patients with symptomatic peripheral neuropathy. Of 200 consecutive patients, 100 were randomly allocated to treatment with both thiamine (25 mg/day) and pyridoxine (50 mg/day) group A and the rest group B to treatment with an identical tablet containing 1 mg/day each of thiamine and pyridoxine. Pain, numbness, paraesthesia and impairment of sensation and ankle in the legs were graded into none, mild, moderate or severe. Blood thiamine levels were measured using HPLC fluorimetry. Four weeks after starting treatment the grade was less than on the first visit in 88.9%, 82.5% and 89.7% of those whose worst symptoms were pain, numbness and paraesthesia respectively for group A compared with 11.1%, 40.5% and 39.4% respectively for group B. The severity of signs of peripheral neuropathy decreased in 48.9% of patients in group A compared with 11.4% in group B. The mean (s.e.) pre-treatment whole blood thiamine levels decreased with increasing severity of symptoms: 64.2 (2.81), 57.7 (3.25) and 52.2 (2.14) micrograms/l for those with mild, moderate and severe symptoms respectively (analysis of variance, p = 0.03). Diabetic peripheral neuropathy in Dar es Salaam is associated with thiamine deficiency. Dietary guidelines for diabetic patients should emphasize a balanced diet.

  19. Pyridoxine-induced neuropathy in rats: a sensory neuropathy that responds to 4-methylcatechol.

    Science.gov (United States)

    Callizot, N; Warter, J M; Poindron, P

    2001-08-01

    Sensory neuropathies are frequently associated with diabetes or with antimitotic treatments in humans suffering from cancer, and are in this case the most important limitation to the use of antimitotic drugs. For this reason, there is a need to establish and validate animal models of sensory neuropathies that could be routinely used, together with the already known models, for studying and evaluating the effects of putative neuroprotective compounds. In the present study, we prove by behavioral and electromyographical analyses that (a) it is possible to induce a nonlethal, exclusively sensory, reversible neuropathy by intoxicating rats with large amounts of pyridoxine, using a new schedule of intoxication; (b) 4-methylcatechol, a drug known to induce nerve growth factor synthesis, improves the clinical status of pyridoxine-intoxicated animals, shortens the duration of the disease, and restores the morphological integrity of the sensory fibers. Owing to its mode of installation and its clinical features, we propose that this model be used as an additional model for preclinical studies of neuroprotective drugs.

  20. Influence of concentration on the radiolytic decomposition of thiamine, riboflavin, and pyridoxine in aqueous solution

    Directory of Open Access Journals (Sweden)

    Guadalupe Albarrán

    2014-10-01

    Full Text Available Vitamin loss during irradiation has been claimed as a critical area in food irradiation technology, especially that of thiamine (B1, which has been considered as the most sensitive to radiation. Although it has been suggested that no vitamin deficiency could result from consuming irradiated food, a long debate on the loss of vitamins and other nutrients during food irradiation has been maintained by the lack of experimental studies monitoring decomposition rates at different concentrations and doses. Since thiamine, riboflavin, and pyridoxine are labile vitamins, this study has focused on their radiolytic decomposition in dilute aqueous solutions in the presence of air. The decomposition process was followed by HPLC and UV-spectroscopy. The results obtained in aqueous solutions showed a dependence of the decomposition as a nonlinear function of the dose. Of these three compounds, the decomposition was higher for thiamine than for riboflavin and even less in pyridoxine.

  1. Simultaneous Determination of Pyridoxine and Riboflavin in Energy Drinks by High-Performance Liquid Chromatography with Fluorescence Detection

    Science.gov (United States)

    Martí-Andre´s, P.; Escuder-Gilabert, L.; Martín-Biosca, Y.; Sagrado, S.; Medina-Herna´ndez, M.J.

    2015-01-01

    Energy drinks, as familiar consumer products, have been widely used in laboratory courses to help promote student interest, as well as to connect lecture concepts with laboratory work. Energy drinks contain B vitamins: pyridoxine (vitamin B6) and riboflavin (vitamin B2) of which amounts are high enough to be of concern. In this work, a fast and…

  2. Pyridoxine-dependent epilepsy: normal outcome in a patient with late diagnosis after prolonged status epilepticus causing cortical blindness.

    Science.gov (United States)

    Kluger, G; Blank, R; Paul, K; Paschke, E; Jansen, E; Jakobs, C; Wörle, H; Plecko, B

    2008-10-01

    We report on a male proband with pyridoxine-dependent epilepsy (PDE) and neonatal seizure onset. At the age of 31 months, a prolonged status epilepticus led to severe neurological regression with cortical blindness, loss of speech and muscular hypotonia with slow recovery over the following 3 months. At 33 months of age pyridoxine therapy was initiated with excellent response and the boy remained seizure-free on pyridoxine monotherapy, except for two occasions with seizure recurrence 10 days after accidental pyridoxine withdrawal. alpha-aminoadipic semialdehyde dehydrogenase (antiquitin) deficiency was indicated by elevated pipecolic acid concentrations in plasma and alpha-aminoadipic semialdehyde excretion in urine. Molecular analysis of the antiquitin gene revealed a novel missense mutation c.57insA, while the mutation of the other allele remained unidentified so far. Despite the delay in diagnosis and prolonged status epilepticus, neuropsychological evaluations at the ages of 11 and 18 years demonstrated full-scale IQ of 93 and 92, respectively, with better verbal IQ (103 and 101) than performance IQ (85 and 82).

  3. Doxylamine succinate-pyridoxine hydrochloride (Diclegis) for the management of nausea and vomiting in pregnancy: an overview.

    Science.gov (United States)

    Nuangchamnong, Nina; Niebyl, Jennifer

    2014-01-01

    Nausea and vomiting in pregnancy (NVP) is common and often undertreated, in part due to fears of adverse effects of medications on the fetus during early pregnancy. In April 2013, the US Food and Drug Administration (FDA) approved doxylamine succinate 10 mg and pyridoxine hydrochloride (a vitamin B6 analog) 10 mg as a delayed-release combination pill called Diclegis for the treatment of NVP. Diclegis is currently the only medication that is FDA-approved for the indication of NVP. This review addresses the historical context, safety, efficacy, pharmacology, and practical role of doxylamine and pyridoxine for the management of NVP. The reintroduction of this doxylamine-pyridoxine combination pill into the American market fills a therapeutic gap in the management of NVP left by the removal of the same active drugs marketed over 30 years ago in the form of Bendectin. The substantial amount of safety data accumulated over the years makes it one of the few drugs that qualify for FDA Pregnancy Category A status. In the hierarchical approach to pharmacological treatment of NVP, the combination of doxylamine and pyridoxine should thus be first-tier.

  4. Epilepsy as a pyridoxine-dependent condition: quantified urinary biomarkers for status evaluation and monitoring antiepileptic treatment.

    Science.gov (United States)

    Dolina, Svetlana; Margalit, Dov; Malitsky, Sergey; Pressman, Eugeny; Rabinkov, Aharon

    2012-08-01

    The study testifies an assumption on epilepsy as an inborn error of pyridoxine metabolism and suggests non-invasive quantitative biomarkers for clarified evaluation of clinical status and monitoring an individual treatment by antiepileptic drugs. Urinary parameters of pyridoxal-phosphate (PLP)-dependent tryptophan degradation and the level of 4-pyridoxic acid, the end product of pyridoxine metabolism, were measured by HPLC method with simultaneous ultraviolet and fluorimetric detection in children with different forms of epilepsy and matched healthy controls. The concentrations of compounds formed or metabolized in the course of tryptophan degradation (kynurenines, indoxyl-sulfate) along with correlations between them turned out to be quantitative biomarkers useful for both clarifying patient's clinical state and monitoring antiepileptic treatment. In particular, the value of the ratio of 4-pyridoxic acid to kynurenine appears to be an index of an experienced seizure attack, while the ratio of 3-hydroxyanthranilic acid to 3-hydroxykynurenine reflects activity of kynureninase, the enzyme of critical sensitivity to PLP supply. Growing progressively worse, epilepsy is accompanied by aggravation of PLP-dependent disturbances of tryptophan metabolism and expanding inhibition of kynureninase. The affected pyridoxine metabolism is discussed as an inborn genetic trait in epilepsy in general, rather than a specific sign of pyridoxine-dependent epilepsy solely.

  5. Functional modeling of vitamin responsiveness in yeast: a common pyridoxine-responsive cystathionine beta-synthase mutation in homocystinuria.

    Science.gov (United States)

    Kim, C E; Gallagher, P M; Guttormsen, A B; Refsum, H; Ueland, P M; Ose, L; Folling, I; Whitehead, A S; Tsai, M Y; Kruger, W D

    1997-12-01

    Cystathionine beta-synthase (CBS) deficiency is an autosomal recessive disorder which results in extremely elevated levels of total plasma homocysteine (tHcy) and high risk of thromboembolic events. About half of all patients diagnosed with CBS deficiency respond to pyridoxine treatment with a significant lowering of tHcy levels. We examined 12 CBS-deficient patients from 10 Norwegian families for mutations in the CBS gene and identified mutations in 18 of the 20 CBS alleles. Five of the seven patients classified as pyridoxine-responsive contain the newly identified point mutation, G797A (R266K). This point mutation is tightly linked with a previously identified 'benign' 68 bp duplication of the intron 7-exon 8 boundary within the CBS gene. We tested the effect of all of the mutations identified on human CBS function utilizing a yeast system. Five of the six mutations had a distinguishable phenotype in yeast, indicating that they were in fact pathogenic. Interestingly, the G797A allele had no phenotype when the yeast were grown in high concentrations of pyridoxine, but a severe phenotype when grown in low concentrations, thus mirroring the behavior in humans. These studies show that the G797A mutation is an important cause of pyridoxine-responsive CBS deficiency and demonstrate the utility of yeast functional assays in the analysis of human mutations.

  6. Comparative study of the effects of pyridoxine, rifampin, and renal function on hematological adverse events induced by linezolid.

    Science.gov (United States)

    Soriano, Alex; Ortega, Mar; García, Sebastián; Peñarroja, Georgina; Bové, Albert; Marcos, Miguel; Martínez, Juan C; Martínez, José A; Mensa, Josep

    2007-07-01

    Hematological disturbances that develop during linezolid treatment are a major concern when linezolid is administered for prolonged periods of time. The aim of this study was to evaluate the influences of pyridoxine, rifampin, and renal function on hematological adverse events. From January 2002 to April 2006, 52 patients received a long-term course of linezolid. Blood cell counts were monitored weekly. Thrombocytopenia was defined as a decrease to or =2 g/liter from the baseline value. Twenty-four patients received linezolid alone, and 28 patients received linezolid plus 200 mg of pyridoxine. The Kaplan-Meier survival method, followed by the log-rank test, was used to estimate the cumulative probability of adverse events, and Cox regression analysis was performed to evaluate the independent predictors of toxicity. The baseline characteristics of the patients in both groups were similar. The cumulative probability of thrombocytopenia and anemia in patients who received pyridoxine was not different from that in patients who did not receive it. Hematological adverse events were less frequent in patients taking rifampin and were more frequent in patients with renal failure. However; the Cox regression analysis showed that rifampin was the only independent predictor associated with a lower risk of thrombocytopenia (hazard ratio, 0.37; 95% confidence interval, 0.14 to 0.98; P = 0.045). In conclusion, pyridoxine did not prevent linezolid-related hematological adverse events, and the coadministration of rifampin was associated with a lower risk of thrombocytopenia.

  7. Simultaneous Determination of Pyridoxine and Riboflavin in Energy Drinks by High-Performance Liquid Chromatography with Fluorescence Detection

    Science.gov (United States)

    Martí-Andre´s, P.; Escuder-Gilabert, L.; Martín-Biosca, Y.; Sagrado, S.; Medina-Herna´ndez, M.J.

    2015-01-01

    Energy drinks, as familiar consumer products, have been widely used in laboratory courses to help promote student interest, as well as to connect lecture concepts with laboratory work. Energy drinks contain B vitamins: pyridoxine (vitamin B6) and riboflavin (vitamin B2) of which amounts are high enough to be of concern. In this work, a fast and…

  8. Clinical diagnosis, treatment, and ALDH7A1 mutations in pyridoxine-dependent epilepsy in three Chinese infants.

    Science.gov (United States)

    Yang, Zhixian; Yang, Xiaoling; Wu, Ye; Wang, Jingmin; Zhang, Yuehua; Xiong, Hui; Jiang, Yuwu; Qin, Jiong

    2014-01-01

    Pyridoxine-dependent epilepsy (PDE) is a rare autosomal recessive disorder that causes seizures in neonates and infants. Mutations of the ALDH7A1 gene are now recognized as the molecular basis PDE and help to define this disease. Three Chinese children with PDE were clinically analyzed, followed by treatment and examination of the ALDH7A1 mutations. The seizures of the 3 patients were all resistant to multiple anticonvulsants (2 to 7 types). For case 1, onset of seizures was at the age of 2 months. His seizures were well controlled by intravenous pyridoxine for several days at the age of 3 months 20 days and recurred at intervals of 13, 14 and 38 days after pyridoxine withdrawn for 3 times. At the age of 7 months, symptoms of PDE appeared and uninterrupted oral pyridoxine started. For case 2, her seizures occurred at 8 days after birth. After administration of multiple antiepileptic drugs observed ineffective, high-dose pyridoxine continuous therapy was taken at the age of 10 months and the significant treatment effect induced a diagnostic PDE. Seizure onset in case 3 was at the first day of birth. He experienced inadvertently pyridoxine therapy several times (first time at 2 days after birth) and achieved good therapeutic effect, which was confirmed by physicians until 4 months 10 days. The treatment process in our 3 patients suggested that pyridoxine should be early and purposefully used in patients with early onset seizures. ALDH7A1 gene mutation analysis revealed compound heterozygous mutations in each case: heterozygous c.410G>A (p.G137E) and IVS11+1G>A in case 1, heterozygous c.952G>C (p.A318P) and heterozygous c.965C>T (p.A322V) in case 2, and heterozygous c.902A>T (p.N301I) and IVS11+1G>A in case 3. Only p.N301I was reported previously, all other mutations were novel. This is the first time to report cases of Chinese patients diagnosed with PDE by molecular genetic analysis.

  9. Clinical diagnosis, treatment, and ALDH7A1 mutations in pyridoxine-dependent epilepsy in three Chinese infants.

    Directory of Open Access Journals (Sweden)

    Zhixian Yang

    Full Text Available Pyridoxine-dependent epilepsy (PDE is a rare autosomal recessive disorder that causes seizures in neonates and infants. Mutations of the ALDH7A1 gene are now recognized as the molecular basis PDE and help to define this disease. Three Chinese children with PDE were clinically analyzed, followed by treatment and examination of the ALDH7A1 mutations. The seizures of the 3 patients were all resistant to multiple anticonvulsants (2 to 7 types. For case 1, onset of seizures was at the age of 2 months. His seizures were well controlled by intravenous pyridoxine for several days at the age of 3 months 20 days and recurred at intervals of 13, 14 and 38 days after pyridoxine withdrawn for 3 times. At the age of 7 months, symptoms of PDE appeared and uninterrupted oral pyridoxine started. For case 2, her seizures occurred at 8 days after birth. After administration of multiple antiepileptic drugs observed ineffective, high-dose pyridoxine continuous therapy was taken at the age of 10 months and the significant treatment effect induced a diagnostic PDE. Seizure onset in case 3 was at the first day of birth. He experienced inadvertently pyridoxine therapy several times (first time at 2 days after birth and achieved good therapeutic effect, which was confirmed by physicians until 4 months 10 days. The treatment process in our 3 patients suggested that pyridoxine should be early and purposefully used in patients with early onset seizures. ALDH7A1 gene mutation analysis revealed compound heterozygous mutations in each case: heterozygous c.410G>A (p.G137E and IVS11+1G>A in case 1, heterozygous c.952G>C (p.A318P and heterozygous c.965C>T (p.A322V in case 2, and heterozygous c.902A>T (p.N301I and IVS11+1G>A in case 3. Only p.N301I was reported previously, all other mutations were novel. This is the first time to report cases of Chinese patients diagnosed with PDE by molecular genetic analysis.

  10. Analytical Method Validation and Determination of Pyridoxine, Nicotinamide, and Caffeine in Energy Drinks Using Thin Layer Chromatography-Densitometry

    Directory of Open Access Journals (Sweden)

    Florentinus Dika Octa Riswanto

    2015-03-01

    Full Text Available Food supplement which contains vitamins and stimulants such as caffeine were classified as energy drink. TLC-densitometry method was chosen to determine the pyridoxine, nicotinamide, and caffeine in the energy drink sample. TLC plates of silica gel 60 F254 was used as the stationary phase and methanol : ethyl acetate : ammonia 25% (134:77:10 was used as the mobile phase. The correlation coefficient for each pyridoxine, nicotinamide, and caffeine were 0.9982, 0.9997, and 0.9966, respectively. Detection and quantitation limits of from the three analytes were 4.05 and 13.51 µg/mL; 13.15 and 43.83 µg/mL; 5.43 and 18.11 µg/mL, respectively. The recovery of pyridoxine, nicotinamide, and caffeine were within the required limit range of 95-105%. The percent of RSD were below the limit value of 5.7% for caffeine and nicotinamide and 8% for pyridoxine. The content amount of pyridoxine in the sample 1 and 2 were 33.59 ± 0.981 and 30.29 ± 2.061 µg/mL, respectively. The content amount of nicotinamide in the sample 1 and 2 were 106.53 ± 3.521 and 98.20 ± 3.648 µg/mL, respectively. The content amount of caffeine in the sample 1 and 2 were 249.50 ± 5.080 and 252.80 ± 2.640 µg/mL, respectively. Robustness test results showed that the most optimal method conditions should be applied for the analysis.

  11. Identification, characterization, and quantification of an anti-pyridoxine factor from flaxseed using ultrahigh-performance liquid chromatography-mass spectrometry.

    Science.gov (United States)

    Mayengbam, Shyamchand; Yang, Haifeng; Barthet, Veronique; Aliani, Michel; House, James D

    2014-01-15

    In the present study, the anti-pyridoxine compounds linatine (1-[(n-γ-L-glutamyl)amino]-D-proline) and 1-amino-D-proline (1ADP) were quantified following extraction from defatted flaxseed using aqueous isopropanol as a solvent, with extraction variables including time, temperature, and the solid/solvent ratio. Both linatine and 1ADP were identified, characterized, and quantified via UPLC/ESI-MS using authentic standards. To optimize the extraction conditions for these anti-pyridoxine compounds, a response surface methodology was applied using a second-order polynomial to describe the experimental data. The predicted model for the optimal extraction was significant (P pyridoxine present in flaxseed ranged from 177 to 437 μg 1ADPE/g of whole seed. The current study establishes the content of specific anti-pyridoxine factors in flaxseed and positions the data for use in subsequent risk assessment modeling.

  12. Long-term treatment outcome of two patients with pyridoxine-dependent epilepsy caused by ALDH7A1 mutations: normal neurocognitive outcome.

    Science.gov (United States)

    Nasr, Enas; Mamak, Eva; Feigenbaum, Anette; Donner, Elizabeth J; Mercimek-Mahmutoglu, Saadet

    2015-04-01

    Pyridoxine-dependent epilepsy is an autosomal recessively inherited disorder of lysine catabolism caused by mutations in the ALDH7A1 gene. We report 2 patients with normal neurocognitive outcome (full-scale IQ of 108 and 74) and their more than 10 years' treatment outcome on pyridoxine monotherapy. Both patients had specific borderline impairments in visual processing speed. More long-term treatment outcome reports will increase our knowledge about the natural history of the disease.

  13. Overexpression of a non-native deoxyxylulose-dependent vitamin B6 pathway in Bacillus subtilis for the production of pyridoxine.

    Science.gov (United States)

    Commichau, Fabian M; Alzinger, Ariane; Sande, Rafael; Bretzel, Werner; Meyer, Frederik M; Chevreux, Bastien; Wyss, Markus; Hohmann, Hans-Peter; Prágai, Zoltán

    2014-09-01

    Vitamin B6 is a designation for the vitamers pyridoxine, pyridoxal, pyridoxamine, and their respective 5'-phosphates. Pyridoxal 5'-phosphate, the biologically most-important vitamer, serves as a cofactor for many enzymes, mainly active in amino acid metabolism. While microorganisms and plants are capable of synthesizing vitamin B6, other organisms have to ingest it. The vitamer pyridoxine, which is used as a dietary supplement for animals and humans is commercially produced by chemical processes. The development of potentially more cost-effective and more sustainable fermentation processes for pyridoxine production is of interest for the biotech industry. We describe the generation and characterization of a Bacillus subtilis pyridoxine production strain overexpressing five genes of a non-native deoxyxylulose 5'-phosphate-dependent vitamin B6 pathway. The genes, derived from Escherichia coli and Sinorhizobium meliloti, were assembled to two expression cassettes and introduced into the B. subtilis chromosome. in vivo complementation assays revealed that the enzymes of this pathway were functionally expressed and active. The resulting strain produced 14mg/l pyridoxine in a small-scale production assay. By optimizing the growth conditions and co-feeding of 4-hydroxy-threonine and deoxyxylulose the productivity was increased to 54mg/l. Although relative protein quantification revealed bottlenecks in the heterologous pathway that remain to be eliminated, the final strain provides a promising basis to further enhance the production of pyridoxine using B. subtilis.

  14. Synergistic effects of sodium butyrate, a histone deacetylase inhibitor, on increase of neurogenesis induced by pyridoxine and increase of neural proliferation in the mouse dentate gyrus.

    Science.gov (United States)

    Yoo, Dae Young; Kim, Woosuk; Nam, Sung Min; Kim, Dae Won; Chung, Jin Young; Choi, Soo Young; Yoon, Yeo Sung; Won, Moo-Ho; Hwang, In Koo

    2011-10-01

    We previously observed that pyridoxine (vitamin B(6)) significantly increased cell proliferation and neuroblast differentiation without any neuronal damage in the hippocampus. In this study, we investigated the effects of sodium butyrate, a histone deacetylase (HDAC) inhibitor which serves as an epigenetic regulator of gene expression, on pyridoxine-induced neural proliferation and neurogenesis induced by the increase of neural proliferation in the mouse dentate gyrus. Sodium butyrate (300 mg/kg, subcutaneously), pyridoxine (350 mg/kg, intraperitoneally), or combination with sodium butyrate were administered to 8-week-old mice twice a day and once a day, respectively, for 14 days. The administration of sodium butyrate significantly increased acetyl-histone H3 levels in the dentate gyrus. Sodium butyrate alone did not show the significant increase of cell proliferation in the dentate gyrus. But, pyridoxine alone significantly increased cell proliferation. Sodium butyrate in combination with pyridoxine robustly enhanced cell proliferation and neurogenesis induced by the increase of neural proliferation in the dentate gyrus, showing that sodium butyrate treatment distinctively enhanced development of neuroblast dendrites. These results indicate that an inhibition of HDAC synergistically promotes neurogenesis induced by a pyridoxine and increase of neural proliferation.

  15. Effect of the Ascorbic Acid, Pyridoxine and Hydrogen Peroxide Treatments on Germination, Catalase Activity, Protein and Malondialdehyde Content of Three Oil Seeds

    Directory of Open Access Journals (Sweden)

    Aria DOLATABADIAN

    2008-08-01

    Full Text Available Oil seed production has an important role in human nutrition and industry. Success in oil plant cultivation is related to seed production with high viability and rapid germination, because these seeds rapidly loose their viability by fats oxidation. Thus, in this work we studied the effects of ascorbic acid, pyridoxine and hydrogen peroxide solutions on germination quantitative traits, catalase activity, protein and malondialdehyde content of three old oil seeds (sunflower, rape seed and safflower. The results showed that ascorbic acid and pyridoxine stimulated significantly the sunflower and rape seed germination. These vitamins, however, didn't have any effect on safflower germination. Hydrogen peroxide strongly increased safflower germination. Ascorbic acid and pyridoxine decreased catalase activity in sunflower and rape seed, whereas hydrogen peroxide increased it. Ascorbic acid and pyridoxine prevented protein degradation and lipid peroxidation in germinated seeds. Consequently, we understand that ascorbic acid and pyridoxine can increase sunflower and rape seed germination and stimulate rate of growth. Also safflower germination increased due to germination inhibitor oxidation by hydrogen peroxide. In conclusion, this report shows that oil seeds treated with ascorbic acid, pyridoxine and hydrogen peroxide remarkably increase the capacity of germination. We suggest that treatments with such substances can improve the old oil seed germination during storage.

  16. Rapid determination of thiamine, riboflavin, pyridoxine, and niacinamide in infant formulas by liquid chromatography.

    Science.gov (United States)

    Woollard, David C; Indyk, Harvey E

    2002-01-01

    A simplified, simultaneous determination of vitamins B1, B2, B3, and B6 in supplemented infant formulas was developed from a single deproteinized sample extract, with analysis by reversed-phase, ion-pair chromatography with an acidified methanol-water mobile phase. The dioctylsulfosuccinate counter-ion facilitates unique retention of the pyridine-based vitamins (niacinamide and pyridoxine) and allows for concurrent measurement of both the pyridoxal and riboflavin 5'-phosphate endogenous components of milk. Other naturally occurring undetected vitamin congeners have minimal analytical significance. UV detection is used for niacinamide, and programmed fluorescence detection is used for riboflavin and the B6 vitamins. Thiamine is routinely determined sequentially under modified elution conditions.

  17. Synthesis and crystal structures of coordination compounds of pyridoxine with zinc and cadmium sulfates

    Science.gov (United States)

    Furmanova, N. G.; Berdalieva, Zh. I.; Chernaya, T. S.; Resnyanskiĭ, V. F.; Shiitieva, N. K.; Sulaĭmankulov, K. S.

    2009-03-01

    The pyridoxine complexes with zinc and cadmium sulfates are synthesized. The IR absorption spectra and thermal behavior of the synthesized compounds are described. Crystals of the [ M(C8H11O3N)2(H2O)2]SO4 · 3H2O ( M = Zn, Cd) compounds are investigated using X-ray diffraction. In the structures of both compounds, the M atoms are coordinated by the oxygen atoms of the deprotonated OH group and the CH2OH group retaining its own hydrogen atom, as well as by two H2O molecules, and have an octahedral coordination. The nitrogen atom of the heterocycle is protonated, so that the heterocycle acquires a pyridinium character. The cationic complexes form layers separated by the anions and crystallization water molecules located in between. The structural units of the crystals are joined together by a complex system of hydrogen bonds.

  18. Sensory denervation of the plantar lumbrical muscle spindles in pyridoxine neuropathy.

    Science.gov (United States)

    Krinke, G; Heid, J; Bittiger, H; Hess, R

    1978-09-15

    Male albino rats treated with excessive amounts of pyridoxine developed an impairment of neuromuscular function. The equatorial region of the plantar lumbrical intrafusal muscle fibres was studied in the electron microscope and the calibre of the nerve fibres was determined in semi-thin sections of the posterior tibial nerves. Degeneration of the primary sensory endings coincided with the onset of ataxia, and in more advanced stages of the neuropathy as well as after a 2-month treatment-free period the equatorial region was denervated. There was a corresponding decrease in the number of large nerve fibres. It is considered essential that primary sensory endings of lumbrical muscle spindles should be included in studies of distally accentuated sensory neuropathies.

  19. Simultaneous determination of riboflavin and pyridoxine by UHPLC/LC-MS in UK commercial infant meal food products.

    Science.gov (United States)

    Zand, Nazanin; Chowdhry, Babur Z; Pullen, Frank S; Snowden, Martin J; Tetteh, John

    2012-12-15

    An assay for the simultaneous quantitative determination of riboflavin and pyridoxine in eight different complementary infant meal products has been developed in order to (1) estimate the daily intake of these vitamins from commercial infant food consumption, and (2) ascertain their nutritional suitability relative to dietary guidelines for the 6-9 months age group. The method involves mild hydrolysis of the foods, an extraction of the supernatant by centrifugation followed by quantitative determination using ultra-high performance liquid chromatography. Separation of the two water soluble vitamins is achieved within one minute and the resultant sample is also LC-MS compatible. Despite wide individual differences between brands (p=6.5e-12), no significant differences were observed in the level of pyridoxine between the meat and vegetable-based varieties (p=0.7) per 100g of commercial infant food. Riboflavin was not detected in any of the samples where the detection limit was below 0.07 μg/mL. In terms of the Reference Nutrient Intake (RNI) of pyridoxine for 6-9 months old infants, the complementary infant meal products analysed herein provided less than 15% of the RNI values with mean (SD) values of 12.87 (± 4.46)% and 13.88 (± 4.97)% for the meat- and vegetable-based recipes, respectively. The estimated total daily intake of riboflavin and pyridoxine from the consumption of commercial complementary food was found to be satisfactory and in accordance with the Dietary Reference Values (DRVs). The intake of both riboflavin and pyridoxine was estimated to be mainly derived from the consumption of formula milk which could be a cause of concern if the quality of an infant's milk diet is compromised by an inadequate or lack of supplemented milk intake. The results of this study suggest that the selected commercial complementary infant foods in the UK market may not contain the minimum levels of riboflavin and pyridoxine required for the labelling declaration of the

  20. Pyridoxine dependent epilepsy and antiquitin deficiency: clinical and molecular characteristics and recommendations for diagnosis, treatment and follow-up.

    Science.gov (United States)

    Stockler, Sylvia; Plecko, Barbara; Gospe, Sidney M; Coulter-Mackie, Marion; Connolly, Mary; van Karnebeek, Clara; Mercimek-Mahmutoglu, Saadet; Hartmann, Hans; Scharer, Gunter; Struijs, Eduard; Tein, Ingrid; Jakobs, Cornelis; Clayton, Peter; Van Hove, Johan L K

    2011-01-01

    Antiquitin (ATQ) deficiency is the main cause of pyridoxine dependent epilepsy characterized by early onset epileptic encephalopathy responsive to large dosages of pyridoxine. Despite seizure control most patients have intellectual disability. Folinic acid responsive seizures (FARS) are genetically identical to ATQ deficiency. ATQ functions as an aldehyde dehydrogenase (ALDH7A1) in the lysine degradation pathway. Its deficiency results in accumulation of α-aminoadipic semialdehyde (AASA), piperideine-6-carboxylate (P6C) and pipecolic acid, which serve as diagnostic markers in urine, plasma, and CSF. To interrupt seizures a dose of 100 mg of pyridoxine-HCl is given intravenously, or orally/enterally with 30 mg/kg/day. First administration may result in respiratory arrest in responders, and thus treatment should be performed with support of respiratory management. To make sure that late and masked response is not missed, treatment with oral/enteral pyridoxine should be continued until ATQ deficiency is excluded by negative biochemical or genetic testing. Long-term treatment dosages vary between 15 and 30 mg/kg/day in infants or up to 200 mg/day in neonates, and 500 mg/day in adults. Oral or enteral pyridoxal phosphate (PLP), up to 30 mg/kg/day can be given alternatively. Prenatal treatment with maternal pyridoxine supplementation possibly improves outcome. PDE is an organic aciduria caused by a deficiency in the catabolic breakdown of lysine. A lysine restricted diet might address the potential toxicity of accumulating αAASA, P6C and pipecolic acid. A multicenter study on long term outcomes is needed to document potential benefits of this additional treatment. The differential diagnosis of pyridoxine or PLP responsive seizure disorders includes PLP-responsive epileptic encephalopathy due to PNPO deficiency, neonatal/infantile hypophosphatasia (TNSALP deficiency), familial hyperphosphatasia (PIGV deficiency), as well as yet unidentified conditions and nutritional

  1. Engineering Bacillus subtilis for the conversion of the antimetabolite 4-hydroxy-l-threonine to pyridoxine.

    Science.gov (United States)

    Commichau, Fabian M; Alzinger, Ariane; Sande, Rafael; Bretzel, Werner; Reuß, Daniel R; Dormeyer, Miriam; Chevreux, Bastien; Schuldes, Jörg; Daniel, Rolf; Akeroyd, Michiel; Wyss, Markus; Hohmann, Hans-Peter; Prágai, Zoltán

    2015-05-01

    Until now, pyridoxine (PN), the most commonly supplemented B6 vitamer for animals and humans, is chemically synthesized for commercial purposes. Thus, the development of a microbial fermentation process is of great interest for the biotech industry. Recently, we constructed a Bacillus subtilis strain that formed significant amounts of PN via a non-native deoxyxylulose 5'-phosphate-(DXP)-dependent vitamin B6 pathway. Here we report the optimization of the condensing reaction of this pathway that consists of the 4-hydroxy-l-threonine-phosphate dehydrogenase PdxA, the pyridoxine 5'-phosphate synthase PdxJ and the native DXP synthase, Dxs. To allow feeding of high amounts of 4-hydroxy-threonine (4-HO-Thr) that can be converted to PN by B. subtilis overexpressing PdxA and PdxJ, we first adapted the bacteria to tolerate the antimetabolite 4-HO-Thr. The adapted bacteria produced 28-34mg/l PN from 4-HO-Thr while the wild-type parent produced only 12mg/l PN. Moreover, by expressing different pdxA and pdxJ alleles in the adapted strain we identified a better combination of PdxA and PdxJ enzymes than reported previously, and the resulting strain produced 65mg/l PN. To further enhance productivity mutants were isolated that efficiently take up and convert deoxyxylulose (DX) to DXP, which is incorporated into PN. Although these mutants were very efficient to convert low amount of exogenous DX, at higher DX levels they performed only slightly better. The present study uncovered several enzymes with promiscuous activity and it revealed that host metabolic pathways compete with the heterologous pathway for 4-HO-Thr. Moreover, the study revealed that the B. subtilis genome is quite flexible with respect to adaptive mutations, a property, which is very important for strain engineering.

  2. Bis-phosphonium salts of pyridoxine: the relationship between structure and antibacterial activity.

    Science.gov (United States)

    Pugachev, Mikhail V; Shtyrlin, Nikita V; Sapozhnikov, Sergey V; Sysoeva, Lubov P; Iksanova, Alfiya G; Nikitina, Elena V; Musin, Rashid Z; Lodochnikova, Olga A; Berdnikov, Eugeny A; Shtyrlin, Yurii G

    2013-12-01

    A series of 23 novel bis-phosphonium salts based on pyridoxine were synthesized and their antibacterial activities were evaluated in vitro. All compounds were inactive against gram-negative bacteria and exhibited the structure-dependent activity against gram-positive bacteria. The antibacterial activity enhanced with the increase in chain length at acetal carbon atom in the order n-Pr>Et>Me. Further increasing of length and branching of alkyl chain leads to the reduction of antibacterial activity. Replacement of the phenyl substituents at the phosphorus atoms in 5,6-bis(triphenylphosphonio(methyl))-2,2,8-trimethyl-4H-[1,3]-dioxino[4,5-c]pyridine dichloride (compound 1) with n-butyl, m-tolyl or p-tolyl as well as chloride anions in the compound 1 with bromides (compound 14a) increased the activity against Staphylococcus aureus and Staphylococcus epidermidis up to 5 times (MICs=1-1.25 μg/ml). But in practically all cases chemical modifications of compound 1 led to the increase of its toxicity for HEK-293 cells. The only exception is compound 5,6-bis[tributylphosphonio(methyl)]-2,2,8-trimethyl-4H-[1,3]dioxino[4,5-c]pyridine dichloride (10a) which demonstrated lower MIC values against S. aureus and S. epidermidis (1 μg/ml) and lower cytotoxicity on HEK-293 cells (CC(50)=200 μg/ml). Compound 10a had no significant mutagenic and genotoxic effects and was selected for further evaluation. It should be noted that all bis-phosphonium salt based on pyridoxine were much more toxic than vancomycin.

  3. Pyridoxine-dependent convulsions among children with refractory seizures: A 3-year follow-up study

    Directory of Open Access Journals (Sweden)

    Sadanandavalli Retnaswami Chandra

    2016-01-01

    Full Text Available Introduction: Epilepsy accounts for 1% of the global disease burden and about 8–10 million epilepsy patients live in India. About 30–40% of these patients become drug-resistant and land up with palliative or disease-modifying surgeries. This is a situation causing great concern in view of the psychosocial and economic burden on the patient and the family apart from severe cognitive and motor consequences, especially in children. Therefore, it is mandatory to have an insight into the wide spectrum of causes with reference to refractoriness to antiepileptic medications in children with epilepsy. Patients and Methods: Children admitted under our team with refractory epilepsy as per the International League Against Epilepsy (ILAE criteria in the last 3 years were included in the study. Results: Refractory epilepsy constituted 13.3% of inpatients in the pediatric group. Males dominated with 68.9% of these patients. Nearly 34.4% of these patients were found to suffer from various neurometabolic diseases. Almost 3.5% were due to pyridoxine-dependent convulsions. This group of patients showed an excellent response to dietary manipulation, disease-modifying treatment for the metabolic disorder, and supportive small-dose anticonvulsants. During follow-up, they showed very good response with reference to global development and seizure control. Conclusion: Pyridoxine-dependent convulsions are relatively rare forming about 3.5% of refractory epilepsies in this series. With initiation of appropriate therapy, results with reference to seizure control as well as neurodevelopment became evident within 2 weeks, and at 1-year follow-up, complete independence for majority of the needed activities is achieved with minimum cost, almost zero side effects, and absolute elimination of the need for palliative surgery.

  4. First cases of pyridoxine-dependent epilepsy in Bulgaria: novel mutation in the ALDH7A1 gene.

    Science.gov (United States)

    Tincheva, Savina; Todorov, Tihomir; Todorova, Albena; Georgieva, Ralica; Stamatov, Dimitar; Yordanova, Iglika; Kadiyska, Tanya; Georgieva, Bilyana; Bojidarova, Maria; Tacheva, Genoveva; Litvinenko, Ivan; Mitev, Vanyo

    2015-12-01

    Pyridoxine-dependent epilepsy (PDE) is a rare autosomal recessive disorder characterized by intractable seizures in neonates and infants. The seizures cannot be controlled with antiepileptic medications but respond both clinically and electrographically to large daily supplements of pyridoxine (vitamin B6). PDE is caused by mutations in the ALDH7A1 gene. Molecular genetic analysis of the ALDH7A1 gene was performed in seven patients, referred with clinical diagnosis of PDE. Mutations were detected in a dizygotic twin pair and a non-related boy with classical form of PDE. Direct sequencing of the ALDH7A1 gene revealed one novel (c.297delG, p.Trp99*) and two already reported (c.328C>T, p.Arg110*; c.584A>G, p.Asn195Ser) mutations. Here, we report the first genetically proven cases of PDE in Bulgaria.

  5. Allelic and non-allelic heterogeneities in pyridoxine dependent seizures revealed by ALDH7A1 mutational analysis.

    Science.gov (United States)

    Kanno, Junko; Kure, Shigeo; Narisawa, Ayumi; Kamada, Fumiaki; Takayanagi, Masaru; Yamamoto, Katsuya; Hoshino, Hisao; Goto, Tomohide; Takahashi, Takao; Haginoya, Kazuhiro; Tsuchiya, Shigeru; Baumeister, Fritz A M; Hasegawa, Yuki; Aoki, Yoko; Yamaguchi, Seiji; Matsubara, Yoichi

    2007-08-01

    Pyridoxine dependent seizure (PDS) is a disorder of neonates or infants with autosomal recessive inheritance characterized by seizures, which responds to pharmacological dose of pyridoxine. Recently, mutations have been identified in the ALDH7A1 gene in Caucasian families with PDS. To elucidate further the genetic background of PDS, we screened for ALDH7A1 mutations in five PDS families (patients 1-5) that included four Orientals. Diagnosis as having PDS was confirmed by pyridoxine-withdrawal test. Exon sequencing analysis of patients 1-4 revealed eight ALDH7A1 mutations in compound heterozygous forms: five missense mutations, one nonsense mutation, one point mutation at the splicing donor site in intron 1, and a 1937-bp genomic deletion. The deletion included the entire exon 17, which was flanked by two Alu elements in introns 16 and 17. None of the mutations was found in 100 control chromosomes. In patient 5, no mutation was found by the exon sequencing analysis. Furthermore, expression level or nucleotide sequences of ALDH7A1 mRNA in lymphoblasts were normal. Plasma pipecolic acid concentration was not elevated in patient 5. These observations suggest that ALDH7A1 mutation is unlikely to be responsible for patient 5. Abnormal metabolism of GABA/glutamate in brain has long been suggested as the underlying pathophysiology of PDS. CSF glutamate concentration was elevated during the off-pyridoxine period in patient 3, but not in patient 2 or 5. These results suggest allelic and non-allelic heterogeneities of PDS, and that the CSF glutamate elevation does not directly correlate with the presence of ALDH7A1 mutations.

  6. Doxylamine succinate–pyridoxine hydrochloride (Diclegis) for the management of nausea and vomiting in pregnancy: an overview

    OpenAIRE

    Nuangchamnong N; Niebyl J

    2014-01-01

    Nina Nuangchamnong, Jennifer Niebyl Department of Obstetrics and Gynecology, University of Iowa Hospitals and Clinics, Iowa, IA, USA Abstract: Nausea and vomiting in pregnancy (NVP) is common and often undertreated, in part due to fears of adverse effects of medications on the fetus during early pregnancy. In April 2013, the US Food and Drug Administration (FDA) approved doxylamine succinate 10 mg and pyridoxine hydrochloride (a vitamin B6 analog) 10 mg as a delayed-release combination pill ...

  7. 8-Way Randomized Controlled Trial of Doxylamine, Pyridoxine and Dicyclomine for Nausea and Vomiting during Pregnancy: Restoration of Unpublished Information

    OpenAIRE

    Zhang, Rujun; Persaud, Navindra

    2017-01-01

    Objectives We report information about an unpublished 1970s study (“8-way” Bendectin Study) that aimed to evaluate the relative therapeutic efficacy of doxylamine, pyridoxine, and dicyclomine in the management of nausea and vomiting during pregnancy. We are publishing the trial's findings according to the restoring invisible and abandoned trials (RIAT) initiative because the trial was never published. Design Double blinded, multi-centred, randomized placebo-controlled study. Setting 14 clinic...

  8. Comparative Study of the Effects of Pyridoxine, Rifampin, and Renal Function on Hematological Adverse Events Induced by Linezolid▿

    OpenAIRE

    2007-01-01

    Hematological disturbances that develop during linezolid treatment are a major concern when linezolid is administered for prolonged periods of time. The aim of this study was to evaluate the influences of pyridoxine, rifampin, and renal function on hematological adverse events. From January 2002 to April 2006, 52 patients received a long-term course of linezolid. Blood cell counts were monitored weekly. Thrombocytopenia was defined as a decrease to

  9. Long-term folic acid (but not pyridoxine) supplementation lowers elevated plasma homocysteine level in chronic renal failure.

    Science.gov (United States)

    Chauveau, P; Chadefaux, B; Coudé, M; Aupetit, J; Kamoun, P; Jungers, P

    1996-01-01

    Moderate hyperhomocysteinemia, a risk factor for premature atherosclerosis, is present in chronic uremic patients. We prospectively evaluated the effects of sequential supplementation with pyridoxine (70 mg/day) and folic acid (10 mg/day) for two 3-month periods in 37 nondialyzed patients (29 males) with creatinine clearance (CCr) ranging from 10 to 80 ml/min, whose plasma vitamin B12 and folate level was in the normal range. Mean (+/- SD) baseline plasma total homocysteine (Hcy) was 14.9 +/- 5.2, 16.5 +/- 5.1 and 26.1 +/- 12.1 mumol/l (upper limit in 45 healthy controls 14.1 mumol/l) in patients with CCr 40-80, 20-40 and pyridoxine Hcy did not significantly decrease whereas following folic acid Hcy decreased significantly to 9.9 +/- 2.9 (-33% vs. baseline), 10.3 +/- 3.4 (-37%) and 15.4 +/- 5.5 (-40%), respectively (Student's paired t test, p pyridoxine) pharmacologic supplementation is effective in lowering elevated plasma Hcy in chronic renal failure patients, thus suggesting that enhancing the Hcy remethylation pathway may overcome hyperhomocysteinemia in such patients. In view of the potential atherogenic effects of hyperhomocysteinemia, long-term folate supplementation should be considered in uremic patients.

  10. Polyneuropathy, anti-tuberculosis treatment and the role of pyridoxine in the HIV/AIDS era: a systematic review.

    Science.gov (United States)

    van der Watt, J J; Harrison, T B; Benatar, M; Heckmann, J M

    2011-06-01

    Tuberculosis (TB) is increasing in incidence in certain parts of the world, particularly where there is a co-epidemic of human immunodeficiency virus/acquired immune-deficiency syndrome (HIV/AIDS), and it is associated with a significant degree of morbidity and mortality. One of the most common complications of anti-tuberculosis treatment is the development of a painful isoniazid (INH) associated polyneuropathy (PN), which is preventable with adequate pyridoxine supplementation. As PN is also the most frequent neurological complication associated with HIV infection, subjects who are HIV and TB co-infected may be at increased risk of developing PN. In this review, we explore current knowledge of anti-tuberculosis drug associated PN focusing on INH and its relationship to pyridoxine, as well as the additional impact of antiretroviral treatment and TB-HIV co-infection. It is evident that guidelines established for the prevention and treatment of this problem differ between industrialised and developing countries, and that further research is needed to define the optimum dosing of pyridoxine supplementation in populations where there is a significant burden of TB and HIV.

  11. Spectrophotometric determination of meclizine hydrochloride and pyridoxine hydrochloride in laboratory prepared mixtures and in their pharmaceutical preparation

    Science.gov (United States)

    Ibrahim, Maha M.; Elzanfaly, Eman S.; El-Zeiny, Mohamed B.; Ramadan, Nesreen K.; Kelani, Khadiga M.

    2017-05-01

    In this paper, three rapid, simple, accurate and precise spectrophotometric methods were developed for the determination of meclizine hydrochloride in the presence of pyridoxine hydrochloride without previous separation. The methods under study are dual wavelength (DWL), ratio difference (RD) and continuous wavelet transform (CWT). On the other hand, pyridoxine hydrochloride (PYH) was determined directly at 291 nm. The methods obey Beer's law in the range of (5-50 μg/mL) for both compounds. All the methods were validated according to the ICH guidelines where the accuracy was found to be 98.29, 99.59, 100.42 and 100.62% for DWL, RD, CWT and PYH; respectively. Moreover the precision of the methods were calculated in terms of %RSD and it was found to be 0.545, 0.372, 1.287 and 0.759 for DWL, RD,CWT and PYH; respectively. The selectivity of the proposed methods was tested using laboratory prepared mixtures and assessed by applying the standard addition technique. So, they can be used for the routine analysis of pyridoxine hydrochloride and meclizine hydrochloride in quality-control laboratories.

  12. Direct and indirect effects of RNA interference against pyridoxal kinase and pyridoxine 5'-phosphate oxidase genes in Bombyx mori.

    Science.gov (United States)

    Huang, ShuoHao; Yao, LiLi; Zhang, JianYun; Huang, LongQuan

    2016-08-01

    Vitamin B6 comprises six interconvertible pyridine compounds (vitamers), among which pyridoxal 5'-phosphate is a coenzyme involved in a high diversity of biochemical reactions. Humans and animals obtain B6 vitamers from diet, and synthesize pyridoxal 5'-phosphate by pyridoxal kinase and pyridoxine 5'-phosphate oxidase. Currently, little is known on how pyridoxal 5'-phosphate biosynthesis is regulated, and pyridoxal 5'-phosphate is supplied to meet their requirement in terms of cofactor. Bombyx mori is a large silk-secreting insect, in which protein metabolism is most active, and the vitamin B6 demand is high. In this study, we successfully down-regulated the gene expression of pyridoxal kinase and pyridoxine 5'-phosphate oxidase by body cavity injection of synthesized double-stranded small interfering RNA to 5th instar larvae of Bombyx mori, and analyzed the gene transcription levels of pyridoxal 5'-phosphate dependent enzymes, phosphoserine aminotransferase and glutamic-oxaloacetic transaminase. Results show that the gene expression of pyridoxal kinase and pyridoxine 5'-phosphate oxidase has a greater impact on the gene transcription of enzymes using pyridoxal 5'-phosphate as a cofactor in Bombyx mori. Our study suggests that pyridoxal 5'-phosphate biosynthesis and dynamic balance may be regulated by genetic networks.

  13. Evidence of GLP-1-mediated neuroprotection in an animal model of pyridoxine-induced peripheral sensory neuropathy.

    Science.gov (United States)

    Perry, TracyAnn; Holloway, Harold W; Weerasuriya, Ananda; Mouton, Peter R; Duffy, Kara; Mattison, Julie A; Greig, Nigel H

    2007-02-01

    Pyridoxine (vitamin B6) intoxicated rodents develop a peripheral neuropathy characterized by sensory nerve conduction deficits associated with disturbances of nerve fiber geometry and axonal atrophy. To investigate the possibility that glucagon-like peptide-1 (7-36)-amide (GLP-1) receptor agonism may influence axonal structure and function through neuroprotection neurotrophic support, effects of GLP-1 and its long acting analog, Exendin-4 (Ex4) treatment on pyridoxine-induced peripheral neuropathy were examined in rats using behavioral and morphometric techniques. GLP-1 is an endogenous insulinotropic peptide secreted from the gut in response to the presence of food. GLP-1 receptors (GLP-1R) are coupled to the cAMP second messenger pathway, and are expressed widely throughout neural tissues of humans and rodents. Recent studies have established that GLP-1 and Ex4, have multiple synergistic effects on glucose-dependent insulin secretion pathways of pancreatic beta-cells and on neural plasticity. Data reported here suggest that clinically relevant doses of GLP-1 and Ex4 may offer some protection against the sensory peripheral neuropathy induced by pyridoxine. Our findings suggest a potential role for these peptides in the treatment of neuropathies, including that associated with type II diabetes mellitus.

  14. Efficacy of pyridoxine to ameliorate the cutaneous toxicity associated with doxorubicin containing pegylated (Stealth) liposomes: a randomized, double-blind clinical trial using a canine model.

    Science.gov (United States)

    Vail, D M; Chun, R; Thamm, D H; Garrett, L D; Cooley, A J; Obradovich, J E

    1998-06-01

    A cutaneous reaction termed palmar-plantar erythrodysesthesia (PPES) or hand-foot syndrome can be dose limiting for Doxil, a doxorubicin containing pegylated (Stealth) liposome. The objective of this study was to determine the ability of concomitant pyridoxine therapy to prevent the development of PPES during Doxil therapy. Forty-one dogs with non-Hodgkin's lymphoma were randomized in a double-blind fashion to receive either oral pyridoxine or placebo daily during Doxil chemotherapy (1.0 mg/kg, i.v., every 3 weeks for a total of five treatments). Cutaneous toxicity was determined by clinical and histological scoring. No difference was observed in remission rates (71.4 versus 75%) achieved between groups. The likelihood of developing serious PPES and having to decrease or discontinue Doxil therapy was 4.2 times (relative risk) greater in placebo group dogs than in pyridoxine group dogs (P = 0.032). Pyridoxine did not completely abrogate PPES; however, it occurred later and less dramatically than in placebo-treated dogs and resulted in fewer treatment delays or discontinuations, allowing a higher cumulative dose of Doxil to be received. Compared to the 5.0 mg/kg cumulative target dose, pyridoxine-treated dogs received a median cumulative dose of 4.7 mg/kg (mean, 4.1 mg/kg), and the placebo-treated dogs received a median of 2.75 mg/kg (mean, 2.9 mg/kg; P pyridoxine, which was likely attributable to their ability to receive more Doxil without delay or discontinuation. We conclude that pyridoxine is effective in delaying the onset and severity of PPES in this canine model.

  15. Enzymatic conversion from pyridoxal to pyridoxine caused by microorganisms within tobacco phyllosphere.

    Science.gov (United States)

    Huang, ShuoHao; Zhang, JianYun; Tao, Zhen; Lei, Liang; Yu, YongHui; Huang, LongQuan

    2014-12-01

    Vitamin B6 (VB6) comprises six interconvertible pyridine compounds (vitamers), among which pyridoxal 5'-phosphate (PLP) is a coenzyme involved in a high diversity of biochemical reactions. In plants, PLP is de novo synthesized, and pyridoxine (PN) is usually maintained as the predominant B6 vitamer. Although the conversion from pyridoxal (PL) to PN catalyzed by PL reductase in plants has been confirmed, the enzyme itself remains largely unknown. We previously found pre-incubation at 35 °C dramatically enhanced PL reductase activity in tobacco leaf homogenate. In this study, we demonstrated that the increase in the reductase activity was a consequence of phyllosphere microbial proliferation. VB6 was detected from tobacco phyllosphere, and PL level was the highest among three non-phosphorylated B6 vitamers. When the sterile tobacco rich in PL were kept in an open, warm and humid environment to promote microorganism proliferation, a significant change from PL to PN was observed. Our results suggest that there may be a plant-microbe interaction in the conversion from PL to PN within tobacco phyllosphere.

  16. Preparation and Identification of Major Impurity A in Pyridoxine Hydrochloride%维生素B6中关键杂质A的制备与分析

    Institute of Scientific and Technical Information of China (English)

    徐勇智; 范卫东; 章根宝; 党登峰

    2011-01-01

    Impurity A in European pharmacopoeia for pyridoxine hydrochloride was synthesized from pyridoxine hydrochloride with the presence of sulfuric acid, and its structure was characterized by lH NMR, MS, FT-IR, HPLC. This study provides a convenient method to prepare impurity A reference substance, which can be used for quality control of pyridoxine hydrochloride.%以维生素B6为起始原料,在硫酸存在下合成了欧洲药典中的维生素B6杂质A,并通过1H NMR、MS、FT-IR、HPLC方法对其结构进行鉴定,为生产维生素B6质量控制提供了一种简便的杂质标准物制备方法.

  17. Modified Eu-doped Y2 O3 nanoparticles as turn-off luminescent probes for the sensitive detection of pyridoxine.

    Science.gov (United States)

    Zobeiri, Eshagh; Bayandori Moghaddam, Abdolmajid; Gudarzy, Forugh; Mohammadi, Hadi; Mozaffari, Shahla; Ganjkhanlou, Yadolah

    2015-05-01

    Europium-doped yttrium oxide nanoparticles (Y2 O3 :Eu NPs) modified by captopril were prepared in aqueous solution. In this study, we report the effect of pyridoxine hydrochloride on the photoluminescence intensity of Y2 O3 :Eu NPs in pH 7.2 buffer solution. By increasing the pyridoxine concentration, the luminescence intensity of Y2 O3 :Eu NPs is quenched. The results show that this method demonstrates high sensitivity for pyridoxine determination. A linear relationship is observed between 0.0 and 62.0 μM with a correlation coefficient of 0.995 and a detection limit of 0.023 μM.

  18. High-performance column liquid chromatographic method for the simultaneous determination of buclizine, tryptophan, pyridoxine, and cyanocobalamin in tablets and oral suspension.

    Science.gov (United States)

    Kuminek, Gislaine; Stulzer, Hellen K; Tagliari, Monika P; Oliveira, Paulo R; Bernardi, Larissa S; Rauber, Gabriela S; Cardoso, Simone G

    2011-01-01

    An HPLC method was developed and validated for the simultaneous determination of buclizine, tryptophan, pyridoxine, and cyanocobalamin in pharmaceutical formulations. The chromatographic separation was carried out on an RP-C18 column using a mobile phase gradient of methanol, 0.015 M phosphate buffer (pH 3.0), and 0.03 M phosphoric acid at a flow rate of 1.0 mL/min and UV detection at 230, 280, and 360 nm, respectively, for buclizine, tryptophan, pyridoxine, and cyanocobalamin. The method validation yielded good results with respect to linearity (r>0.999), specificity, precision, accuracy, and robustness. The RSD values for intraday and interday precision were below 1.82 and 0.63%, respectively, and recoveries ranged from 98.11 to 101.95%. The method was successfully applied for the QC analysis of buclizine, tryptophan, pyridoxine, and cyanocobalamin in tablets and oral suspension.

  19. The effect of high-dose pyridoxine and folic acid supplementation on serum lipid and plasma homocysteine concentrations in dialysis patients.

    Science.gov (United States)

    Arnadottir, M; Brattström, L; Simonsen, O; Thysell, H; Hultberg, B; Andersson, A; Nilsson-Ehle, P

    1993-10-01

    Pyridoxine and folic acid supplementation in dialysis patients is a matter of debate. This study was performed to estimate the effects of pharmacologic doses of these vitamins on serum lipid and plasma homocysteine concentrations, which are known to be high in dialysis patients. Both hemodialysis and continuous ambulatory peritoneal dialysis patients were included in the study. Pyridoxine supplementation had a mild but significant cholesterol-lowering effect (7%). Folic acid supplementation significantly lowered plasma homocysteine concentrations by a mean of 30%. There was a strong, inverse correlation between blood folate and plasma homocysteine concentrations. These results indicate that daily supplementation with pyridoxine 300 mg and folic acid 5 mg has a beneficial effect on the cardiovascular risk profile in dialysis patients.

  20. Hydrolytic activity toward pyridoxine-5'-beta-D-glucoside in rat intestinal mucosa is not increased by vitamin B-6 deficiency: effect of basal diet composition and pyridoxine intake.

    Science.gov (United States)

    Mackey, Amy D; Lieu, Siam O; Carman, Catherine; Gregory, Jesse F

    2003-05-01

    Pyridoxine-5'-beta-D-glucoside (PNG), a glycosylated form of dietary vitamin B-6, is partially hydrolyzed in the small intestine by the cytosolic enzyme pyridoxine-5'-beta-D-glucoside hydrolase (PNG hydrolase) and by the brush border enzyme lactase phlorizin hydrolase (LPH) to release free pyridoxine (PN). This laboratory has previously shown that PNG hydrolase activity is inversely related to dietary vitamin B-6 in rats and guinea pigs. The current investigation was done to examine the effect of dietary PN on PNG hydrolytic activity and its distribution. Nutrient compositional differences between the AIN-76A and AIN-93G purified diets that were unrelated to vitamin B-6 were also examined in relation to PNG hydrolysis in rat small intestinal mucosa. Study one included rats (n = 29) that were fed the AIN-93G diet providing a range of PN concentrations for 5 wk. Rats (n = 49) in study two were fed either AIN-76A or AIN-93G each with graded concentrations of PN. In both studies, rat growth and plasma and liver pyridoxal 5'-phosphate (PLP) concentrations increased (P < 0.05) with increasing concentrations of dietary PN. PNG hydrolytic activity localized to the brush border membrane was five times that measured in the cytosol. Cytosolic PNG hydrolytic activity increased significantly with increasing dietary PN concentration in rats fed the AIN-76A, but not AIN-93G diet. Activity in the mucosal total membrane fraction did not increase in proportion to dietary PN concentration for either diet. Regardless of dietary PN concentration, the basal nutrient composition of the diets affected growth and PNG hydrolytic activity in intestinal mucosa. In contrast to previous results from this laboratory, intestinal hydrolytic activity toward PNG did not increase in vitamin B-6-deficient rats.

  1. Biochemical and molecular characterization of 18 patients with pyridoxine-dependent epilepsy and mutations of the antiquitin (ALDH7A1) gene.

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    Plecko, Barbara; Paul, Karl; Paschke, Eduard; Stoeckler-Ipsiroglu, Sylvia; Struys, Eduard; Jakobs, Cornelis; Hartmann, Hans; Luecke, Thomas; di Capua, Matteo; Korenke, Christoph; Hikel, Christiane; Reutershahn, Elke; Freilinger, Michael; Baumeister, Fritz; Bosch, Friedrich; Erwa, Wolfgang

    2007-01-01

    Patients with pyridoxine dependent epilepsy (PDE) present with early-onset seizures resistant to common anticonvulsants. According to the benefit of pyridoxine (vitamin B(6)) and recurrence of seizures on pyridoxine withdrawal, patients so far have been classified as having definite, probable, or possible PDE. Recently, PDE has been shown to be caused by a defect of alpha-amino adipic semialdehyde (AASA) dehydrogenase (antiquitin) in the cerebral lysine degradation pathway. The accumulating compound piperideine-6-carboxylic acid (P6C) was shown to inactivate pyridoxalphosphate (PLP) by a Knoevenagel condensation. Pipecolic acid (PA) and AASA are markedly elevated in urine, plasma, and cerebrospinal fluid (CSF) and thus can be used as biomarkers of the disease. We have investigated 18 patients with neonatal seizure onset, who have been classified as having definite (11), probable (four), or possible (three) PDE. All patients had elevated PA and AASA in plasma (and urine) while on treatment with individual dosages of pyridoxine. Within this cohort, molecular analysis identified 10 novel mutations (six missense mutations, one nonsense mutation, two splice site mutations) within highly conserved regions of the antiquitin gene. Seven mutations were located in exonic sequences and two in introns 7 and 17. Furthermore, a novel deletion of exon 7 was identified. Two of the 36 alleles investigated require further investigation. A known mutation (p.Glu399Gln) was found with marked prevalence, accounting for 12 out of 36 alleles (33%) within our cohort. Pyridoxine withdrawal is no longer needed to establish the diagnosis of "definite" PDE. Administration of pyridoxine in PDE may not only correct secondary PLP deficiency, but may also lead to a reduction of AASA (and P6C) as presumably toxic compounds.

  2. Identification of a novel missense mutation in the ALDH7A1 gene in two unrelated Tunisian families with pyridoxine-dependent epilepsy.

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    Tlili, Abdelaziz; Hamida Hentati, Nadia; Gargouri, Abdellatif; Fakhfakh, Faiza

    2013-01-01

    Pyridoxine-dependent Epilepsy (PDE) is a rare autosomal recessive disorder causing intractable seizures in neonates and infants. It is characterized by seizures that are resistant to common anticonvulsants, but patients respond well to the administration of pyridoxine. PDE is caused by ALDH7A1 genetic defect. Here, we report the disease-causative variant in the ALDH7A1 gene in two affected Tunisian families. Direct sequencing analysis revealed a novel missense mutation c.1364T>C (p.Leu455Pro). Using bioinformatic tools we suggested that this variant may have deleterious effects on ALDH7A1 protein structure and function.

  3. Pyridoxine-dependent epilepsy initially responsive to phenobarbital Epilepsia por dependência de piridoxina inicialmente responsiva ao fenobarbital

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    Jaime Lin

    2007-12-01

    Full Text Available Pyridoxine-dependent epilepsy is a rare autossomal recessive disorder characterized by recurrent seizures that are not controlled by anticonvulsant medications but remits after administration of pyridoxine. We report on a 30 day-old girl who presented with seizures during the first day of life, initially responsive to anticonvulsant therapy, which remitted within two weeks. Seizures were characterized as multifocal myoclonic jerks of upper and lower limbs associated with buccal-lingual oral movements and eyelid blinking. Laboratory and neuroimaging studies were normal. Electroencephalographic record demonstrated a abnormal background activity with high-voltage epileptic discharges and a burst-suppression pattern. The seizures ceased after oral administration of pyridoxine, but recurred after withdrawal, confirming the diagnosis.A epilepsia por dependência de piridoxina é uma doença autossômica recessiva rara caracterizada por crises recorrentes refratárias a tratamento medicamentoso, mas que remitem após a administração de piridoxina. Relatamos o caso de menina de 30 dias de vida que iniciou crises convulsivas desde o primeiro dia de vida, inicialmente responsivas a tratamento com drogas anticonvulsivantes, mas que reiniciaram após a segunda semana de vida. As crises eram caracterizadas por movimentos clônicos erráticos de membros superiores e inferiores associados a movimentos oromandibulares e piscamentos. Exames laboratoriais e de neuroimagem foram normais. O exame eletrencefalográfico evidenciou atividade de base desorganizada com descargas epilépticas de alta voltagem associadas a um padrão de surto-supressão. As crises cessaram após a administração de piridoxina e recorreram após a sua retirada, confirmando o diagnóstico.

  4. Molecular genetic analysis of pyridoxine-nonresponsive homocystinuric siblings with different blood methionine levels during the neonatal period

    OpenAIRE

    1999-01-01

    Two mutations in the cystathionine β-synthase (CBS) gene were found in two Japanese siblings with pyridoxine non-responsive homocystinuria who had different methionine levels in their blood during the neonatal period. Both patients were com-pound heterozygotes of two mutant alleles:one had an A-to-G transition at nucleotide194 (A194G) that caused a histidine-to-arginine substitution at position 65 of the protein (H65R), while the other had a G-to-A transition at nucleotide346 (G346A) which re...

  5. The distribution of thiamin and pyridoxine in the western tropical North Atlantic Amazon River plume

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    Laila Pualani Barada

    2013-03-01

    Full Text Available B-vitamins are recognized as essential organic growth factors for many organisms, although little is known about their abundance and distribution in marine ecosystems. Despite their metabolic functions regulating important enzymatic reactions, the methodology to directly measure different B-vitamins in aquatic environments has only recently been developed. Here, we present the first direct measurements of two B-vitamins, thiamin (B1 and pyridoxine (B6, in the Amazon River plume-influenced Western Tropical North Atlantic (WTNA Ocean, an area known to have high productivity, carbon (C and dinitrogen (N2 fixation, and C sequestration. The vitamins B1 and B6 ranged in concentrations from undetectable to 230 pM and 40 pM, respectively. Significantly higher concentrations were measured in the surface plume water at some stations and variation with salinity was observed, suggesting a possible riverine influence on those B-vitamins. The influences of vitamins B1 and B6 on biogeochemical processes such as C and N2 fixation were investigated using a linear-regression model that indicated that the availability of those organic factors could affect these rates in the WTNA. In fact, significant increases in C fixation and N2 fixation were observed with increasing vitamin B1 concentrations at some low and mesohaline stations (stations 9.1 and 1; p value <0.017 and <0.03, respectively. N2 fixation was also found to have a significant positive correlation with B1 concentrations at station 1 (p value = 0.029, as well as vitamin B6 at station 9.1 (p value <0.017. This work suggests that there can be a dynamic interplay between essential biogeochemical rates (C and N2 fixation and B-vitamins, drawing attention to potential roles of B-vitamins in ecosystem dynamics, community structure, and global biogeochemistry.

  6. Effects of pyridoxine on a high-fat diet-induced reduction of cell proliferation and neuroblast differentiation depend on cyclic adenosine monophosphate response element binding protein in the mouse dentate gyrus.

    Science.gov (United States)

    Yoo, Dae Young; Kim, Woosuk; Yoo, Ki-Yeon; Nam, Sung Min; Chung, Jin Young; Yoon, Yeo Sung; Won, Moo-Ho; Hwang, In Koo

    2012-08-01

    In this study, we challenged pyridoxine to mice fed a high-fat diet (HFD) and investigated the effects of pyridoxine on HFD-induced phenotypes such as blood glucose, reduction of cell proliferation and neuroblast differentiation in the dentate gyrus using Ki67 and doublecortin (DCX), respectively. Mice were fed a commercially available low-fat diet (LFD) as control diet or HFD (60% fat) for 8 weeks. After 5 weeks of LFD or HFD treatment, 350 mg/kg pyridoxine was administered for 3 weeks. The administration of pyridoxine significantly decreased body weight in the HFD-treated group. In addition, there were no significant differences in hepatic histology and pancreatic insulin-immunoreactive (-ir) and glucagon-ir cells of the HFD-treated group after pyridoxine treatment. In the HFD-fed group, Ki67-positive nuclei and DCX-ir neuroblasts were significantly decreased in the dentate gyrus compared with those in the LFD-fed mice. However, the administration of pyridoxine significantly increased Ki67-positive nuclei and DCX-ir neuroblasts in the dentate gyrus in both LFD- and HFD-fed mice. In addition, the administration of pyridoxine significantly increased the protein levels of glutamic acid decarboxylase 67 (GAD67) and brain-derived neurotrophic factor (BDNF) and the immunoreactivity of phosphorylated cyclic AMP response element binding protein (pCREB) compared with the vehicle-treated LFD- and HFD-fed mice. In contrast, the administration of pyridoxine significantly decreased HFD-induced malondialdehyde (MDA) levels in the hippocampus. These results showed that pyridoxine supplement reduced the HFD-induced reduction of cell proliferation and neuroblast differentiation in the dentate gyrus via controlling the levels of GAD67, pCREB, BDNF, and MDA.

  7. Nanosized silver (II) pyridoxine complex to cause greater inflammatory response and less cytotoxicity to RAW264.7 macrophage cells

    Science.gov (United States)

    Paul, Avijit; Ju, Hee; Rangasamy, Sabarinathan; Shim, Yumi; Song, Joon Myong

    2015-03-01

    With advancements in nanotechnology, silver has been engineered into a nanometre size and has attracted great research interest for use in the treatment of wounds. Silver nanoparticles (AgNPs) have emerged as a potential alternative to conventional antibiotics because of their potential antimicrobial property. However, AgNPs also induce cytotoxicity, generate reactive oxygen species (ROS), and cause mitochondrial damage to human cells. Pyridoxine possesses antioxidant and cell proliferation activity. Therefore, in the present investigation, a nanosilver-pyridoxine complex (AgPyNP) was synthesized, and its cytotoxicity and immune response was compared with AgNPs in macrophage RAW264.7 cells. Results revealed that AgPyNPs showed less cytotoxicity compared with AgNPs by producing a smaller amount of ROS in RAW264.7 cells. Surprisingly, however, AgPyNPs caused macrophage RAW264.7 cells to secrete a larger amount of interleukin-8 (IL-8) and generate a more active inflammatory response compared to AgNPs. It activated TNF-α, NF-κB p65, and NF-κB p50 to generate a more vigorous immune protection that produces a greater amount of IL-8 compared to AgNPs. Overall findings indicate that AgPyNPs exhibited less cytotoxicity and evoked a greater immune response in macrophage RAW264.7 cells. Thus, it can be used as a better wound-healing agent than AgNPs.

  8. Bifunctional Therapeutic High-Valence Silver-Pyridoxine Nanoparticles with Proliferative and Antibacterial Wound-Healing Activities.

    Science.gov (United States)

    Rangasamy, Sabarinathan; Tak, Yu Kyung; Kim, Sunhee; Paul, Avijit; Song, Joon Myong

    2016-01-01

    The antibacterial and moisturizing effects inherent to silver nanoparticles contribute greatly to their use as a topical antibacterial agent. The antibacterial property of silver nanoparticles provides topical wounds with an indirect environment for healing through the prevention of pathogenic infection. However, the direct wound-healing effects of silver nanoparticles have not been previously explored. In this work, we report a bimodal therapeutic silver nanoparticle that possesses both direct wound-healing and antibacterial properties. The nanoparticles consist of high-valence silver-pyridoxine complexes. The wound-healing efficacy was verified in diabetic mice, as well as in vitro assays. A MAPK pathway study demonstrated that silver-pyridoxine nanoparticles induced the proliferation and migration of keratinocyte and fibroblast cells. Antibacterial activities in 8 different pathogenic bacteria responsible for the infection of burn wounds were tested. The rapid wound healing occurring on skin wounds of diabetic mice attests to the utility of bimodal therapeutic silver nanoparticles as a next-generation topical therapeutic agent.

  9. Pyridoxine Supplementation Improves the Activity of Recombinant Glutamate Decarboxylase and the Enzymatic Production of Gama-Aminobutyric Acid.

    Directory of Open Access Journals (Sweden)

    Yan Huang

    Full Text Available Glutamate decarboxylase (GAD catalyzes the irreversible decarboxylation of L-glutamate to the valuable food supplement γ-aminobutyric acid (GABA. In this study, GAD from Escherichia coli K12, a pyridoxal phosphate (PLP-dependent enzyme, was overexpressed in E. coli. The GAD produced in media supplemented with 0.05 mM soluble vitamin B6 analog pyridoxine hydrochloride (GAD-V activity was 154.8 U mL-1, 1.8-fold higher than that of GAD obtained without supplementation (GAD-C. Purified GAD-V exhibited increased activity (193.4 U mg-1, 1.5-fold higher than that of GAD-C, superior thermostability (2.8-fold greater than that of GAD-C, and higher kcat/Km (1.6-fold higher than that of GAD-C. Under optimal conditions in reactions mixtures lacking added PLP, crude GAD-V converted 500 g L-1 monosodium glutamate (MSG to GABA with a yield of 100%, and 750 g L-1 MSG with a yield of 88.7%. These results establish the utility of pyridoxine supplementation and lay the foundation for large-scale enzymatic production of GABA.

  10. High-Dose Pyridoxine and Magnesium Administration in Children with Autistic Disorder: An Absence of Salutary Effects in a Double-Blind, Placebo-Controlled Study.

    Science.gov (United States)

    Findling, Robert L.; Maxwell, Kathleen; Scotese-Wojtila, Lynette; Huang, Jie; Yamashita, Toyoko; Wiznitzer, Max

    1997-01-01

    Evaluation of high doses of pyridoxine and magnesium in a 10-week double-blind placebo-controlled trial with 10 patients (mean age 6 years) having autism concluded that the high doses used were ineffective in ameliorating autistic behaviors. (DB)

  11. Effect of pyridoxine on vitamin B6 concentrations and glutamic-oxaloacetic transaminase activity in whole blood of tuberculous patients receiving high-dosage isoniazid.

    Science.gov (United States)

    Krishnamurthy, D V; Selkon, J B; Ramachandran, K; Devadatta, S; Mitchison, D A; Radhakrishna, S; Stott, H

    1967-01-01

    An earlier report from the Tuberculosis Chemotherapy Centre, Madras, showed that, in tuberculous patients receiving high-dosage isoniazid (12.5-15.6 mg/kg body-weight), the concomitant administration of 6 mg of pyridoxine prevented peripheral neuropathy. In that study, biochemical determinations of B(6) concentrations and GOT activity in whole blood had been routinely undertaken on all patients on admission to treatment, and at 6, 12, 24 and 52 weeks thereafter; in addition, extra determinations were undertaken for patients who developed peripheral neuropathy. The present paper reports the findings of these investigations, which are: (a) peripheral neuropathy developed predominantly among slow inactivators of isoniazid, and was associated with a substantial reduction in GOT activity but no apparent change in B(6) concentration; (b) the reduction in GOT activity appeared to be due to deficiency of both the coenzyme (pyridoxal phosphate) and the apoenzyme; (c) the concomitant administration of pyridoxine (6 mg or 48 mg) with high-dosage isoniazid to 3 patients with peripheral neuropathy, 1 of whom had convulsions also, resulted in increased B(6) concentrations and GOT activity, and no further convulsions; and (d) the concomitant administration of pyridoxine 6 mg daily, as a prophylactic, resulted in a significant increase in B(6) concentrations and GOT activity and prevention of the neuropathy.These findings establish the existence of a definite association between the occurrence of isoniazid-induced toxicity and diminished pyridoxine function.

  12. Striatal dopamine receptors modulate the expression of insulin receptor, IGF-1 and GLUT-3 in diabetic rats: effect of pyridoxine treatment.

    Science.gov (United States)

    Anitha, M; Abraham, Pretty Mary; Paulose, C S

    2012-12-05

    The incidence of type 2 diabetes mellitus is rising at alarming proportions. Central nervous system plays an important part in orchestrating glucose metabolism, with accumulating evidence linking dysregulated central nervous system circuits to the failure of normal glucoregulatory mechanisms. Pyridoxine is a water soluble vitamin and it has important role in brain function. This study aims to evaluate the role of pyridoxine in striatal glucose regulation through dopaminergic receptor expressions in streptozotocin induced diabetic rats. Radio receptor binding assays for dopamine D(1), D(2) receptors were done using [(3)H] 7-chloro-3-methyl-1-phenyl-1,2,4,5-tetrahydro-3-benzazepin-8-ol and [(3)H] 5-chloro-2-methoxy-4-methylamino-N-[-2-methyl-1-(phenylmethyl)pyrrolidin-3-yl]benzamide. Gene expressions were done using fluorescently labeled Taqman probes of dopamine D(1), D(2) receptor, Insulin receptor, Insulin like growth factor-1(IGF-1) and Glucose transporter-3 (GLUT-3). Bmax of dopamine D(1) receptor is decreased and B(max) of dopamine D(2) was increased in diabetic rats compared to control. Gene expression of dopamine D(1) receptor was down regulated and dopamine D(2) receptor was up regulated in diabetic rats. Our results showed decreased gene expression of Insulin receptor, IGF-1 and increased gene expression of GLUT-3 in diabetic rats compared to control. Pyridoxine treatment restored diabetes induced alterations in dopamine D(1), D(2) receptors, Insulin receptor, IGF-1, GLUT-3 gene expressions in striatum compared to diabetic rats. Insulin treatment reversed dopamine D(1), D(2) receptor, GLUT-3 mRNA expression, D(2) receptor binding parameters in the striatum compared to diabetic group. Our results suggest the potential role of pyridoxine supplementation in ameliorating diabetes mediated dysfunctions in striatal dopaminergic receptor expressions and insulin signaling. Thus pyridoxine has therapeutic significance in diabetes management.

  13. Effects of pyridoxine supplementation on severity, frequency and duration of migraine attacks in migraine patients with aura: A double-blind randomized clinical trial study in Iran.

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    Omid Sadeghi

    2015-06-01

    Full Text Available Migraine is a chronic disease that affects nearly 6% of men and 18% of women worldwide. There are various drugs, which can successfully decrease migraine symptoms and frequency of migraine attacks, but these drugs usually are expensive. Hence, this study aimed to assess the effects of pyridoxine supplementation on severity, frequency and duration of migraine attacks as well as headache diary results (HDR.This double-blind randomized clinical trial study was conducted on 66 patients with migraine with aura (MA in Khorshid and Emam Mosa Sadr clinics of Isfahan University of Medical Sciences, Iran, in 2013. Patients were randomly allocated to receive either pyridoxine supplements (80 mg pyridoxine per day or placebo. Severity, frequency and duration of migraine attacks and HDR were measured at baseline and at the end of the study.Mean age of patients was 34.24 ± 9.44 years old. Pyridoxine supplementation led to a significant decrease in headache severity (-2.20 ± 1.70 compared with -1 ± 1.50; P = 0.007, attacks duration (-8.30 ± 12.60 compared with -1.70 ± 9.60; P = 0.030 and HDR (-89.70 ± 134.60 compared with -6.10 ± 155.50; P = 0.040 compared with placebo, but was not effective on the frequency of migraine attacks (-2.30 ± 4 compared with -1.20 ± 7.80; P = 0.510.Pyridoxine supplementation in patients with MA was effective on headache severity, attacks duration and HDR, but did not affect the frequency of migraine attacks.

  14. Experimental and theoretical studies of vibrational spectrum and molecular structure and related properties of pyridoxine (vitamin B6).

    Science.gov (United States)

    Srivastava, Mayuri; Rani, P; Singh, N P; Yadav, R A

    2014-01-01

    Vibrational spectrum of pyridoxine has been investigated using experimental IR and Raman spectroscopic and density functional theory (DFT) methods. Vibrational assignments of the observed IR and Raman bands have been proposed in light of the results obtained from computations. In order to assign the observed IR and Raman frequencies the potential energy distributions (PEDs) have also been computed. Optimized geometrical parameters suggest that if the OH groups of the two methyl groups are replaced by H atoms the resulting molecule has Cs point group symmetry. To investigate molecular stability and bond strength we have used natural bond orbital analysis (NBO). Charge transfer occurs in the molecule have been shown by the calculated highest occupied molecular orbital-lowest unoccupied molecular orbital (HOMO-LUMO) energies. The mapping of electron density iso-surface with electrostatic potential (ESP), has been carried out to get the information about the size, shape, charge density distribution and site of chemical reactivity of the molecule.

  15. Evaluation of the effect of triterpenes on urinary risk factors of stone formation in pyridoxine deficient hyperoxaluric rats.

    Science.gov (United States)

    Vidya, Lakshminarasimhan; Lenin, Mahimainathan; Varalakshmi, Palaninathan

    2002-09-01

    Investigations were carried out to evaluate the efficacy of the pentacyclic triterpene, lupeol and its ester, lupeol linoleate, against calcium oxalate urolithiasis in rats. Administration of a pyridoxine deficient diet containing 3% glycollic acid for 21 days led to increased excretion of stone forming constituents such as calcium, oxalate and uric acid. Crystal deposition and subsequent renal tubular damage resulted in increased excretion of the tubular enzymes alkaline phosphatase, lactate dehydrogenase, gamma glutamyl transferase, beta glucuronidase and N-acetyl glucosaminidase along with reduced fibrinolytic enzymes. A reduction in the urinary inhibitory factors magnesium and glycosaminoglycans was also observed. Treatment with lupeol and lupeol linoleate reduced the extent of tubular damage as evidenced from reduced enzymuria and minimized the excretion of stone forming constituents.

  16. In vivo gene therapy for pyridoxine-induced neuropathy by herpes simplex virus-mediated gene transfer of neurotrophin-3.

    Science.gov (United States)

    Chattopadhyay, Munmun; Wolfe, Darren; Huang, Shaohua; Goss, James; Glorioso, Joseph C; Mata, Marina; Fink, David J

    2002-01-01

    Neurotrophic factors have been demonstrated to prevent the development of peripheral neuropathy in animal models, but the therapeutic use of these factors in human disease has been limited by the short serum half-life and dose-limiting side effects of these potent peptides. We used peripheral subcutaneous inoculation with a replication-incompetent, genomic herpes simplex virus-based vector containing the coding sequence for neurotrophin-3 to transduce sensory neurons of the rat dorsal root ganglion in vivo, and found that expression of neurotrophin-3 from the vector protected peripheral sensory axons from neuropathy induced by intoxication with pyridoxine assessed by electrophysiological (foot sensory response amplitude, and conduction velocity, and H-wave), histological (nerve morphology and morphometry), and behavioral measures of proprioceptive function. In vivo gene transfer using herpes simplex virus vectors provides a unique option for treatment of diseases of the sensory peripheral nervous system.

  17. Oral exposure to the anti-pyridoxine compound 1-amino D-proline further perturbs homocysteine metabolism through the transsulfuration pathway in moderately vitamin B₆ deficient rats.

    Science.gov (United States)

    Mayengbam, Shyamchand; Raposo, Sara; Aliani, Michel; House, James D

    2015-03-01

    Pyridoxal 5'-phosphate (PLP; a B₆ vitamer) serves as an important cofactor in a myriad of metabolic reactions, including the transsulfuration (TS) pathway, which converts homocysteine (Hcy) to cysteine. While overt vitamin B₆ deficiency is rare, moderate deficiency is common and may be exacerbated by anti-pyridoxine factors in the food supply. To this end, we developed a model of moderate B₆ deficiency and a study was conducted to examine the in vivo effect of 1-amino D-proline (1ADP), an anti-pyridoxine factor found in flaxseed, on indices of Hcy metabolism through the TS pathway in moderately B₆ deficient rats. Male weaning rats received a semi-purified diet containing either 7 mg/kg (control; CD) or 0.7 mg/kg (moderately deficient; MD) diet of pyridoxine·hydrochloride (PN∙HCl), each with 1 of 4 levels of 1ADP, viz. 0, 0.1, 1 and 10 mg/kg diet for 5 weeks. Perturbations in vitamin B₆ biomarkers were more pronounced in the MD group. Plasma PLP was significantly reduced, while plasma Hcy (8-fold) and cystathionine (11-fold) were increased in rats consuming the highest amount of 1ADP in the MD group. The activities of hepatic cystathionine β-synthase and cystathionine γ-lyase enzymes were significantly reduced in rats consuming the highest 1ADP compared to the lowest, for both levels of PN∙HCl. Dilation of hepatic central veins and sinusoids, mild steatosis and increased liver triglycerides were present in MD rats consuming the highest 1ADP level. The current data provide evidence that the consumption of an anti-pyridoxine factor linked to flaxseed may pose a risk for subjects who are moderate/severe vitamin B₆ deficient.

  18. Pyridoxine hydrochloride attenuate and decrease the depressant effects of meclizine on human psychomotor performance: Randomized clinical trial, cross-over study.

    Directory of Open Access Journals (Sweden)

    Hayder M. Al-kuraishy

    2011-12-01

    Full Text Available The present study was conducted to assess and compare the cognitive and psychomotor effects of Pyridoxine HCl 50mg and meclizine 25mg or both in 30healthy adult volunteers in a single blind, randomized cross over study. Following single dose of each drug, the volunteers were subjected to perform a series of tests of cognitive and psychomotor performance at 2 hours post dose. The Leeds Battery Psychomotor Instrument test consisted of both subjective and objective tests which were further grouped into Instrumental tests which included Simple reaction time (SRT, Choice Reaction Time Task (CRT and Critical Flicker Fusion frequency threshold (CFFT. Meclizine at dose of 25mg was significantly different from placebo (p0.05. The dual and combined effects of pyridoxine HCl 50mg plus meclizine 25mg attenuate and remove the depressant effects that mediated via meclizine. These results allow the conclusion that pyridoxine at its recommended therapeutic dose of 50mg is needed to be mixed with meclizine or others antihistamine to eliminate psychomotor and cognitive impairment as usual adverse effect of meclizine

  19. Alterations in hippocampal serotonergic and INSR function in streptozotocin induced diabetic rats exposed to stress: neuroprotective role of pyridoxine and Aegle marmelose.

    Science.gov (United States)

    Abraham, Pretty Mary; Kuruvilla, Korah P; Mathew, Jobin; Malat, Anitha; Joy, Shilpa; Paulose, C S

    2010-09-25

    Diabetes and stress stimulate hippocampal 5-HT synthesis, metabolism and release. The present study was carried out to find the effects of insulin, Aegle marmelose alone and in combination with pyridoxine on the hippocampal 5-HT, 5-HT(2A) receptor subtype, gene expression studies on 5-HT(2A), 5-HTT, INSR, immunohistochemical studies and elevated plus maze in streptozotocin induced diabetic rats. 5-HT content showed a significant decrease (p Pyridoxine treated in combination with insulin and A. marmelose to diabetic rats reversed the 5-HT content, B(max), Kd of 5-HT, 5-HT(2A) and gene expression of 5-HT(2A), 5-HTT and INSR in hippocampus to near control. The gene expression of 5-HT(2A) and 5-HTT were confirmed by immunohistochemical studies. Behavioural studies using elevated plus maze showed that serotonin through its transporter significantly increased (p anxiety-related traits in diabetic rats which were corrected by combination therapy. Our results suggest that pyridoxine treated in combination with insulin and A. marmelose has a role in the regulation of insulin synthesis and release, normalising diabetic related stress and anxiety through hippocampal serotonergic function. This has clinical significance in the management of diabetes.

  20. Antibacterial effects of quaternary bis-phosphonium and ammonium salts of pyridoxine on Staphylococcus aureus cells: A single base hitting two distinct targets?

    Science.gov (United States)

    Nikitina, Elena V; Zeldi, Marina I; Pugachev, Mikhail V; Sapozhnikov, Sergey V; Shtyrlin, Nikita V; Kuznetsova, Svetlana V; Evtygin, Vladimir E; Bogachev, Mikhail I; Kayumov, Airat R; Shtyrlin, Yurii G

    2016-01-01

    We studied the effects of quaternary bis-phosphonium and bis-ammonium salts of pyridoxine with lipophilic substituents on the survival and morphology of Staphylococcus aureus cells. We found that, while originating from the same base, they exhibit considerably different antimicrobial mechanisms. In the presence of Ca(2+) ions the MIC and MBC values of ammonium salt increased 100-fold, suggesting that Ca(2+) ions can successfully impede the membrane Ca(2+) ions exchange required for ammonium salt incorporation. In contrast, in the presence of quaternary phosphonium salt, the artificial capsular-like material was formed around the cells and the filamentous and chain-like growth of the cells was observed suggesting the disruption of the cell division mechanisms. Altogether, both pyridoxine derivatives successfully inhibited the growth of gram-positive bacteria (Staphylococcus aureus, Staphylococcus epidermidis, Bacillus subtilis) and Escherichia coli considerably, while demonstrated nearly no effect against Klebsiella pneumoniae and Pseudomonas aeruginosa. We suggest that due to their effects on distinct and likely complementary targets the derivatives of pyridoxine represent potentially perspective antibacterials with complicated adaptation and thus with lower risk of drug resistance development.

  1. Contents of all forms of vitamin B6, pyridoxine-β-glucoside and 4-pyridoxic acid in mature milk of Japanese women according to 4-pyridoxolactone-conversion high performance liquid chromatography.

    Science.gov (United States)

    Yagi, Toshiharu; Iwamoto, Saya; Mizuseki, Rie; Furuya, Michi; Nakayama, Kazuko

    2013-01-01

    The contents of six vitamin B6 forms, pyridoxine-β-glucoside, and 4-pyridoxic acid in mature milk of 20 Japanese lactating women consuming ordinary Japanese foods were determined by a 4-pyridoxolactone-conversion HPLC method. These compounds were determined with the average recovery rate of 83.9% or more. The average total content of vitamin B6 forms was 1.01 ± 0.32 (µmol/L). Pyridoxal and pyridoxal 5'-phosphate were found in all of the samples, and their average contents were 0.71 ± 0.28 (µmol/L) and 0.16 ± 0.07 (µmol/L), respectively. Pyridoxamine, pyridoxine, pyridoxamine 5'-phosphate, pyridoxine 5'-phosphate, and pyridoxine-β-glucoside were found in 15, 14, 13, 9, and 7 samples, respectively. The presence of pyridoxine 5'-phosphate was for the first time found in human milk. A method for the determination of 4-pyridoxic acid, which is the excretion form of vitamin B6, was modified to quantitate it by isocratic HPLC. 4-Pyridoxic acid was found in all samples, and its average content was 0.094 ± 0.040 (µmol/L), which was only 12% of its content in cow (Holstein) milk. The total content of vitamin B6 forms, and predominant presence of pyridoxal among other vitamin B6 forms in the Japanese women's milk samples shared similar characteristics with American women's milk samples.

  2. Four new mutations in the erythroid-specific 5-aminolevulinate synthase (ALAS2) gene causing X-linked sideroblastic anemia: increased pyridoxine responsiveness after removal of iron overload by phlebotomy and coinheritance of hereditary hemochromatosis.

    Science.gov (United States)

    Cotter, P D; May, A; Li, L; Al-Sabah, A I; Fitzsimons, E J; Cazzola, M; Bishop, D F

    1999-03-01

    X-linked sideroblastic anemia (XLSA) in four unrelated male probands was caused by missense mutations in the erythroid-specific 5-aminolevulinate synthase gene (ALAS2). All were new mutations: T647C, C1283T, G1395A, and C1406T predicting amino acid substitutions Y199H, R411C, R448Q, and R452C. All probands were clinically pyridoxine-responsive. The mutation Y199H was shown to be the first de novo XLSA mutation and occurred in a gamete of the proband's maternal grandfather. There was a significantly higher frequency of coinheritance of the hereditary hemochromatosis (HH) HFE mutant allele C282Y in 18 unrelated XLSA hemizygotes than found in the normal population, indicating a role for coinheritance of HFE alleles in the expression of this disorder. One proband (Y199H) with severe and early iron loading coinherited HH as a C282Y homozygote. The clinical and hematologic histories of two XLSA probands suggest that iron overload suppresses pyridoxine responsiveness. Notably, reversal of the iron overload in the Y199H proband by phlebotomy resulted in higher hemoglobin concentrations during pyridoxine supplementation. The proband with the R452C mutation was symptom-free on occasional phlebotomy and daily pyridoxine. These studies indicate the value of combined phlebotomy and pyridoxine supplementation in the management of XLSA probands in order to prevent a downward spiral of iron toxicity and refractory anemia.

  3. Enhanced production of recombinant Escherichia coli glutamate decarboxylase through optimization of induction strategy and addition of pyridoxine.

    Science.gov (United States)

    Su, Lingqia; Huang, Yan; Wu, Jing

    2015-12-01

    This report describes the optimization of recombinant Escherichia coli glutamate decarboxylase (GAD) production from engineered E. coli BL21(DE3) in a 3-L fermentor. Investigation of different induction strategies revealed that induction was optimal when the temperature was maintained at 30°C, the inducer (lactose) was fed at a rate of 0.2 g L(-1)h(-1), and protein expression was induced when the cell density (OD600) reached 50. Under these conditions, the GAD activity of 1273.8 U mL(-1) was achieved. Because GAD is a pyridoxal 5'-phosphate (PLP)-dependent enzyme, the effect of supplementing the medium with pyridoxine hydrochloride (PN), a cheap and stable PLP precursor, on GAD production was also investigated. When the culture medium was supplemented with PN to a concentration of 2mM at the initiation of protein expression, and then again 10h later, the GAD activity reached 3193.4 U mL(-1), which represented the highest GAD production ever reported.

  4. Vitamin B-6 status of breast-fed neonates: influence of pyridoxine supplementation on mothers and neonates.

    Science.gov (United States)

    Kang-Yoon, S A; Kirksey, A; Giacoia, G; West, K

    1992-09-01

    Vitamin B-6 concentrations in human milk are known to respond rapidly to changes in maternal vitamin B-6 intake. In this study, mothers were supplemented during the first 28 d of lactation with 2 or 27 mg pyridoxine (PN)-HCl/d and a subgroup of breast-fed infants of the 2-mg/d-supplemented mothers were supplemented with 0.4 mg PN-HCl/d. Vitamin B-6 intakes of breast-fed infants reflected the amount of their mother's supplement; intakes were highest for the vitamin-supplemented infants. Vitamin B-6 intake of mothers was a strong indicator of infant vitamin B-6 status. Vitamin intake of infants correlated significantly with five measures of vitamin B-6 status. Plasma pyridoxal-5'-phosphate (PLP) concentrations and birth weight were the strongest predictors of infant growth that were examined. Alkaline phosphatase activity in the mother's milk and infant plasma reflected pyridoxal-PLP ratios in these fluids, suggesting that the enzyme acts in regulating circulating vitamer concentrations.

  5. Sensitivity to 4-aminopyridine observed in mammalian sciatic nerves during acute pyridoxine-induced sensory neuropathy and recovery.

    Science.gov (United States)

    Bowe, C M; Veale, K

    1988-06-01

    In vitro physiologic properties of rat sciatic nerve were examined during pyridoxine-induced sensory neuropathy and following recovery. Compound action potential waveform characteristics, recovery cycle properties during paired stimulation, and ability to follow stimuli presented at high frequencies were examined. All parameters were assessed before and after potassium channel blockade with 4-aminopyridine in nerves from acutely toxic, recovered, and age-matched control rats. Compound action potential waveforms recorded from acutely toxic nerves were less affected by application of 4-aminopyridine than were those recorded from control nerves. Recovery cycles were less prolonged and frequency-following abilities less compromised a 3-month recovery period, experimental nerves demonstrated a more pronounced sensitivity to 4-aminopyridine than did age-matched control nerves. It is proposed that these differences in the physiological effects of 4-aminopyridine reflect the selective loss of large-caliber sensory fibers during the acute toxic phase and the increased sensitivity to the drug of regenerated sensory fibers following recovery.

  6. OPTIMAL DIETARY PYRIDOXINE REQUIREMENT OF JUVENILE BLUNT SNOUT BREAM, MEGALOBRAMA AMBLYCEPHALA%团头鲂幼鱼吡哆醇适宜需求量的研究

    Institute of Scientific and Technical Information of China (English)

    王莹; 李向飞; 张微微; 徐维娜; 刘文斌

    2013-01-01

    试验采用单因素试验设计,以饲料中吡哆醇浓度为影响因素,研究了团头鲂幼鱼的适宜吡哆醇需求量。试验共配置了7组等氮等能的半纯化饲料,其吡哆醇的实际含量分别为0、1.04、1.99、4.07、5.91、7.96和9.22 mg/kg。选用840尾[均重:(6.81±0.17) g]团头鲂幼鱼,随机分为7组,每组4重复,每重复30尾鱼,日投饵3次,养殖期为8周。结果表明,当饲料中吡哆醇含量由0升高至5.91 mg/kg时,团头鲂的增重率、特定生长率、饲料利用率、成活率、蛋白效率比和氮保留率均得到显著改善(P0.05)。饲料中的吡哆醇含量显著影响团头鲂的肝体比(P0.05)。当饲料吡哆醇含量由0升高至5.91 mg/kg时,肝脏谷草转氨酶和谷丙转氨酶活性以及吡哆醇含量均显著升高(P0.05)。以肝脏中的谷丙和谷草转氨酶活性以及吡哆醇含量为评价指标,拟合折线模型得到团头鲂幼鱼的适宜吡哆醇的需求量为4.17-5.02 mg/kg。%This study was conducted to determine the optimal dietary pyridoxine requirement of juvenile blunt snout bream Megalobrama amblycephala. Eight hundred and forty fishes [average initial weight:(6.81±0.17) g] were fed with seven isonitrogenous and isoenergetic diets containing different pyridoxine levels (0, 1.04, 1.99, 4.07, 5.91, 7.96 and 9.22 mg/kg) 3 times daily for 8 weeks, respectively. Each diet was tested in four replicates, and each replicate had 30 fishes. Weight gain (WG), specific growth rate (SGR), feed conversion ratio (FCR), survival rate, protein efficiency ratio (PER) and nitrogen retention efficiency (NRE) were all increased significantly (P0.05). No significant difference (P>0.05) was observed both in condition factor and dressout percentage among all the treatments, while hepatosomatic index was significantly (P0.05) with further increase of pyridoxine levels. On the basis of the broken-line analysis of hepatic GOT and GPT activities and liver

  7. The importance of pyridoxine for the impact of the dietary selenium sources on redox balance, embryo development, and reproductive performance in gilts.

    Science.gov (United States)

    Dalto, Danyel Bueno; Audet, Isabelle; Lapointe, Jérôme; Matte, J Jacques

    2016-03-01

    This study aimed to determine the effects of dietary pyridoxine and selenium (Se) on embryo development, reproductive performance and redox system in gilts. Eighty-four gilts were fed one of five diets: CONT) basal diet; MSeB60) CONT+0.3mg/kg of Na-selenite; MSeB610) diet 2+10mg/kg of HCl-pyridoxine; OSeB60) CONT+0.3mg/kg of Se-enriched yeast; and OSeB610) diet 4+10mg/kg of HCl-pyridoxine. Blood samples were collected for long-term (each estrus and slaughter) and peri-estrus (fourth estrus d -4 to d +3) profiles. At slaughter (gestation d 30), organs and embryos were collected. For long-term and peri-estrus profiles, Se level and source affected (P<0.01) blood Se concentration whereas B6 level increased (P<0.01) erythrocyte pyridoxal-5-phosphate concentration. A B6 level (P<0.05) effect was observed on long-term plasma Se-dependent glutathione peroxidase (Se-GPX) activity whereas peri-estrus Se-GPX was minimum on d -1 (P<0.01). Selenium level increased sows' organs and embryo Se concentration (P<0.01). Selenium source tended to enhance embryo Se content (P=0.06). Within-litter embryo Se content was increased by B6 level (P<0.01). Selenium level tended to affect Se-GPX and total GPX activities in organs mitochondria (P=0.09 and 0.07, respectively). Selenium source affected kidney ATP synthesis (P=0.05). In conclusion, B6 level affected the Se-GPX activity on a long-term basis, whereas the basal level of Se was adequate during the peri-estrus period. Embryo quality was not improved by dietary Se, and B6 impaired within-litter homogeneity.

  8. Folic acid, pyridoxine, and cyanocobalamin combination treatment and age-related macular degeneration in women: the Women's Antioxidant and Folic Acid Cardiovascular Study.

    Science.gov (United States)

    Christen, William G; Glynn, Robert J; Chew, Emily Y; Albert, Christine M; Manson, Joann E

    2009-02-23

    Observational epidemiologic studies indicate a direct association between homocysteine concentration in the blood and the risk of age-related macular degeneration (AMD), but randomized trial data to examine the effect of therapy to lower homocysteine levels in AMD are lacking. Our objective was to examine the incidence of AMD in a trial of combined folic acid, pyridoxine hydrochloride (vitamin B(6)), and cyanocobalamin (vitamin B(12)) therapy. We conducted a randomized, double-blind, placebo-controlled trial including 5442 female health care professionals 40 years or older with preexisting cardiovascular disease or 3 or more cardiovascular disease risk factors. A total of 5205 of these women did not have a diagnosis of AMD at baseline and were included in this analysis. Participants were randomly assigned to receive a combination of folic acid (2.5 mg/d), pyridoxine hydrochloride (50 mg/d), and cyanocobalamin (1 mg/d) or placebo. Our main outcome measures included total AMD, defined as a self-report documented by medical record evidence of an initial diagnosis after randomization, and visually significant AMD, defined as confirmed incident AMD with visual acuity of 20/30 or worse attributable to this condition. After an average of 7.3 years of treatment and follow-up, there were 55 cases of AMD in the combination treatment group and 82 in the placebo group (relative risk, 0.66; 95% confidence interval, 0.47-0.93 [P = .02]). For visually significant AMD, there were 26 cases in the combination treatment group and 44 in the placebo group (relative risk, 0.59; 95% confidence interval, 0.36-0.95 [P = .03]). These randomized trial data from a large cohort of women at high risk of cardiovascular disease indicate that daily supplementation with folic acid, pyridoxine, and cyanocobalamin may reduce the risk of AMD.

  9. Sex differences in the pharmacokinetics and bioequivalence of the delayed-release combination of doxylamine succinate-pyridoxine hydrochloride; implications for pharmacotherapy in pregnancy.

    Science.gov (United States)

    Koren, Gideon; Vranderick, Manon; Gill, Simerpal K; Macleod, Stuart

    2013-12-01

    Most bioequivalence (BE) studies are conducted in males with the assumption that variability in pharmacokinetics is similar between the sexes. The purpose of this single-center, reference replicate study was to determine the effect of sex on the pharmacokinetics and BE of doxylamine-pyridoxine 10 mg-10 mg delayed-release tablets. Healthy males (n = 12) and non-pregnant females (n = 12) were administered two tablets, and blood sampling was conducted from 1 hour pre-dose until 72 hours post-dose. After 21 days, dose administration and blood sampling were re-conducted. All analytes were measured using liquid chromatography-tandem mass-spectrometry. Pharmacokinetic parameters were calculated for each study period using standard, non-compartmental methods, and differences were assessed using ANOVA. BE testing was conducted using the relative 90% confidence interval for the AUC0-t for each analyte. Females had significantly larger AUC0-t for doxylamine, 1,550 ng h/mL (coefficient of variance [CV = 19%]) versus 1,272 ng h/mL (CV = 21%; P ≤ .05), and pyridoxine, 35 ng h/mL, (CV = 43%) versus 25 ng h/mL (CV = 31%; P ≤ .05) compared to males. A higher Cmax for doxylamine was observed in females, 107 ng/mL (CV = 16%), compared to males, 86 ng/mL (CV = 15%) (P ≤ .05). BE testing did not demonstrate bioequivalence between males and females. Pharmacokinetic differences observed between the sexes have implications for future BE studies using doxylamine-pyridoxine.

  10. THE PREVENTION AND TREATMENT OF ISONIAZID TOXICITY IN THE THERAPY OF PULMONARY TUBERCULOSIS. 2. AN ASSESSMENT OF THE PROPHYLACTIC EFFECT OF PYRIDOXINE IN LOW DOSAGE.

    Science.gov (United States)

    ZILBER, L A; BAJDAKOVA, Z L; GARDASJAN, A N; KONOVALOV, N V; BUNINA, T L; BARABADZE, E M

    1963-01-01

    A recent report from the Tuberculosis Chemotherapy Centre, Madras, showed that a vitamin-B-complex preparation containing a small amount of pyridoxine (as well as aneurine hydrochloride, riboflavine, nicotinamide, panthenol and cyanocobalamin) was effective in the treatment of peripheral neuropathy caused by daily high-dosage (12.5-15.2 mg/kg body-weight) isoniazid therapy of pulmonary tuberculosis. The present report gives results which show that the B-complex preparation is fully effective in preventing peripheral neuropathy in patients receiving the same high dosage of isoniazid, and that this is due to the small pyridoxine content of only 6 mg daily, and not to any of its other constituents. The low cost of this small dose of pyridoxine makes high-dosage isoniazid therapy, given in combination with other drugs or alone, a possible proposition in developing countries.Studies in the Centre have produced clear evidence that there is an increase in the frequency of peripheral neuropathy when the dosage of isoniazid is increased from 7.8-9.6 mg/kg body-weight to 12.5-15.6 mg/kg daily, and that its incidence is higher among slow than among rapid inactivators of isoniazid.The studies also show that increasing the dosage of isoniazid when given alone from a moderate daily dosage of 7.8-9.6 mg/kg to the high daily dosage of 12.5-15.6 mg/kg has not materially altered the radiographic or the bacteriological response to treatment.

  11. Net analyte signal standard addition method (NASSAM) as a novel spectrofluorimetric and spectrophotometric technique for simultaneous determination, application to assay of melatonin and pyridoxine

    Science.gov (United States)

    Asadpour-Zeynali, Karim; Bastami, Mohammad

    2010-02-01

    In this work a new modification of the standard addition method called "net analyte signal standard addition method (NASSAM)" is presented for the simultaneous spectrofluorimetric and spectrophotometric analysis. The proposed method combines the advantages of standard addition method with those of net analyte signal concept. The method can be applied for the determination of analyte in the presence of known interferents. The accuracy of the predictions against H-point standard addition method is not dependent on the shape of the analyte and interferent spectra. The method was successfully applied to simultaneous spectrofluorimetric and spectrophotometric determination of pyridoxine (PY) and melatonin (MT) in synthetic mixtures and in a pharmaceutical formulation.

  12. The return to the USA of doxylamine-pyridoxine delayed release combination (Diclegis®) for morning sickness--a new morning for American women.

    Science.gov (United States)

    Koren, Gideon

    2013-01-01

    The US FDA approval in April 2013 of Diclegis®, the doxylamine-pyridoxine combination for morning sickness, is a major milestone, particularly since it is indicated for use in pregnancy and the FDA has labeled it a pregnancy category A drug the strongest evidence of fetal safety. After thirty years of being orphaned from an FDA-labeled drug for the most common medical condition in pregnancy, American women and their health care providers have a therapeutic solution that is likely to positively impact millions of women each year. This review highlights the milestones of this antiemetic agent over the last 40 years.

  13. Lysine-restricted diet and mild cerebral serotonin deficiency in a patient with pyridoxine-dependent epilepsy caused by ALDH7A1 genetic defect

    OpenAIRE

    2014-01-01

    Pyridoxine dependent epilepsy (PDE) is caused by mutations in the ALDH7A1 gene (PDE-ALDH7A1) encoding α-aminoadipic-semialdehyde-dehydrogenase enzyme in the lysine catabolic pathway resulting in an accumulation of α-aminoadipic-acid-semialdehyde (α-AASA). We present the one-year treatment outcome of a patient on a lysine-restricted diet. Serial cerebral-spinal-fluid (CSF) α-AASA and CSF pipecolic-acid levels showed decreased levels but did not normalize. He had a normal neurodevelopmental ...

  14. Prenatal high-dose pyridoxine may prevent hypertension and syndrome X in-utero by protecting the fetus from excess glucocorticoid activity.

    Science.gov (United States)

    McCarty, M F

    2000-05-01

    The increased risk for hypertension, insulin resistance syndrome, and coronary events associated with small-for-gestational-age birth, has plausibly been attributed to excessive prenatal exposure to glucocorticoids; this may up-regulate glucocorticoid activity throughout life by permanently decreasing expression of hippocampal glucocorticoid receptors crucial for feedback control of cortisol secretion. Since pyridoxal phosphate is a safe physiological antagonist of glucocorticoid activity, it is proposed that prenatal supplementation with high-dose pyridoxine may counteract the adverse impact of glucocorticoids on fetal growth, as well as on subsequent cardiovascular risk.

  15. Inactive mutants of human pyridoxine 5′‐phosphate oxidase: a possible role for a noncatalytic pyridoxal 5′‐phosphate tight binding site

    OpenAIRE

    2016-01-01

    Pyridoxal 5′‐phosphate (PLP) is a cofactor for many vitamin B6‐requiring enzymes that are important for the synthesis of neurotransmitters. Pyridoxine 5′‐phosphate oxidase (PNPO) is one of two enzymes that produce PLP. Some 16 known mutations in human PNPO (hPNPO), including R95C and R229W, lead to deficiency of PLP in the cell and have been shown to cause neonatal epileptic encephalopathy (NEE). This disorder has no effective treatment, and is often fatal unless treated with PLP. In this stu...

  16. The safety of higher than standard dose of doxylamine-pyridoxine (Diclectin) for nausea and vomiting of pregnancy.

    Science.gov (United States)

    Atanackovic, G; Navioz, Y; Moretti, M E; Koren, G

    2001-08-01

    A delayed-release combination of doxylamine-pyridoxine (D-P) (Diclectin) is the only approved antiemetic medication for use in pregnancy in Canada. The standard recommended dose is up to 4 tablets a day, regardless of body weight or severity of symptoms. The objective of this study was to determine the incidence of adverse maternal and fetal effects and pregnancy outcome in 225 women taking Diclectin at the recommended (n = 123) or higher than recommended (n = 102) doses. In this observational, prospective study, one-third (33.6%) of women reported having adverse effects (sleepiness, tiredness, and/or drowsiness) temporally related to the medication. There was no association between the dose per kg and rates of reported maternal adverse effects with doses ranging from 0.1 mg/kg to 2.0 mg/kg (1-12 tablets). Nausea and vomiting of pregnancy (NVP) was reported as severe by the majority (75.8%) of women. Mean birth weight (BW) was 3,400 g and gestational age (GA) 39 weeks. Multivariate analysis revealed that only prepregnancy weight and GA predicted lower BW, not the dose of D-P or the severity of NVP. There were two pregnancies with major malformation, a finding that is consistent with the rates of birth defects in the general population. It was concluded that the higher than standard dose of Diclectin, when calculated per kg of body weight, does not affect either the incidence of maternal adverse effects or pregnancy outcome. If needed, Diclectin can be given at doses higher than 4 tablets/day to normalize for body weight or optimize efficacy.

  17. Molecular genetic analysis of pyridoxine-nonresponsive homocystinuric siblings with different blood methionine levels during the neonatal period.

    Science.gov (United States)

    Chen, S; Ito, M; Saijo, T; Naito, E; Kuroda, Y

    1999-08-01

    Two mutations in the cystathionine beta-synthase (CBS) gene were found in two Japanese siblings with pyridoxine non-responsive homocystinuria who had different methionine levels in their blood during the neonatal period. Both patients were compound heterozygotes of two mutant alleles: one had an A-to-G transition at nucleotide 194 (A194 G) that caused a histidine-to-arginine substitution at position 65 of the protein (H65R), while the other had a G-to-A transition at nucleotide 346 (G346A) which resulted in a glycine-to-arginine substitution at position 116 of the protein (G116R). The two mutant proteins were separately expressed in Escherichia coli, and they completely lacked catalytic activity. Despite their identical genotypes and almost equal protein intake, these siblings showed different levels of blood methionine during the neonatal period, suggesting that the level of methionine in blood is determined not only by the defect in the CBS gene and protein intake, but also by the activity of other enzymes involved in methionine and homocysteine metabolism, especially during the neonatal period. Therefore, high-risk newborns who have siblings with homocystinuria, even if the level of methionine in their blood is normal in a neonatal mass screening, should be followed up and diagnosed by an assay of enzyme activity or a gene analysis so that treatment can be begun as soon as possible to prevent the development of clinical symptoms. In addition, a new, more sensitive method for the mass screening of CBS deficiency in neonates should be developed.

  18. Inactive mutants of human pyridoxine 5'-phosphate oxidase: a possible role for a noncatalytic pyridoxal 5'-phosphate tight binding site.

    Science.gov (United States)

    Ghatge, Mohini S; Karve, Sayali S; David, Tanya M S; Ahmed, Mostafa H; Musayev, Faik N; Cunningham, Kendra; Schirch, Verne; Safo, Martin K

    2016-05-01

    Pyridoxal 5'-phosphate (PLP) is a cofactor for many vitamin B6-requiring enzymes that are important for the synthesis of neurotransmitters. Pyridoxine 5'-phosphate oxidase (PNPO) is one of two enzymes that produce PLP. Some 16 known mutations in human PNPO (hPNPO), including R95C and R229W, lead to deficiency of PLP in the cell and have been shown to cause neonatal epileptic encephalopathy (NEE). This disorder has no effective treatment, and is often fatal unless treated with PLP. In this study, we show that R95C hPNPO exhibits a 15-fold reduction in affinity for the FMN cofactor, a 71-fold decrease in affinity for the substrate PNP, a 4.9-fold decrease in specific activity, and a 343-fold reduction in catalytic activity, compared to the wild-type enzyme. We have reported similar findings for R229W hPNPO. This report also shows that wild-type, R95C and R229W hPNPO bind PLP tightly at a noncatalytic site and transfer it to activate an apo-B6 enzyme into the catalytically active holo-form. We also show for the first time that hPNPO forms specific interactions with several B6 enzymes with dissociation constants ranging from 0.3 to 12.3 μm. Our results suggest a possible in vivo role for the tight binding of PLP in hPNPO, whether wild-type or variant, by protecting the very reactive PLP, and transferring this PLP directly to activate apo-B6 enzymes.

  19. Solvation behavior and sweetness response of carbohydrates, their derivatives and sugar alcohols in thiamine HCl (vitamin B1) and pyridoxine HCl (vitamin B6) at different temperatures.

    Science.gov (United States)

    Banipal, Parampaul K; Sharma, Mousmee; Banipal, Tarlok S

    2017-12-15

    Volumetric properties are important tools to study the solvation behavior of solutes and reveal valuable information about solute-solute/cosolute interactions. Therefore, standard partial molar volumes at infinite dilution have been calculated from density measurements for monosaccharides, their methoxy and deoxy derivatives, disaccharides and sugar alcohols in (0.05, 0.15, 0.25 and 0.35)molkg(-1) thiamine HCl(aq) and pyridoxine HCl(aq) solutions over temperature range (288.15-318.15)K at pressure, p=0.1MPa. The corresponding transfer volumes, expansibilities and apparent massic volumes have been evaluated to examine the solvation behavior and the basic taste quality of studied solutes. UV-Vis absorption study of these solutes has also been carried out in 1.0×10(-4)molkg(-1) thiamine HCl and pyridoxine HCl solutions. Results have been compared with our previously reported studies carried out in l-ascorbic acid (vitamin C). Stereochemical effects on hydration controlled by dominant conformations of studied solutes have also been discussed. Copyright © 2017 Elsevier Ltd. All rights reserved.

  20. Adequacy of maternal pyridoxine supplementation during pregnancy in relation to the vitamin B6 status and growth of neonates at birth.

    Science.gov (United States)

    Chang, S J

    1999-08-01

    To evaluate the adequacy of maternal pyridoxine supplementation during pregnancy for both maternal and neonatal status at birth, vitamin B6 status, assessed by plasma pyridoxal phosphate (PLP), pyridoxal (PL) and total aldehyde vitamer (PLP + PL) concentrations, and the growth of neonates, including weight, length, head and chest circumferences, were examined for 209 neonates whose mothers were supplemented with 0, 1, 2 or 3 mg pyridoxine.HCl (PN.HCl)/d during pregnancy. Maternal PN.HCl supplementations were positively correlated to both maternal (r = 0.62) and cord (r = 0.78) plasma PLP concentrations (p neonates whose mothers had maternal and cord plasma PLP concentrations > or = 40 nM was revealed by the maternal supplementation of 2 mg PN.HCl/d during pregnancy. Thus, in healthy pregnant women, according to our study, a daily supplement of 2 mg PN.HCl provides the adequacy of maternal and neonatal vitamin B6 status and the satisfactory growth of neonates at birth.

  1. Comparing the pharmacokinetics of doxylamine/pyridoxine delayed-release combination in nonpregnant women of reproductive age and women in the first trimester of pregnancy.

    Science.gov (United States)

    Matok, Ilan; Clark, Shannon; Caritis, Steve; Miodovnik, Menachem; Umans, Jason; Hankins, Gary; Koren, Gideon

    2013-03-01

    Although Diclectin (doxylamine/pyridoxine delayed-released combination) is widely used in Canada, its pharmacokinetics (PK) during pregnancy has never been described. The objective of this study was to compare the PK of doxylamine/pyridoxine delayed-released combination in pregnant versus nonpregnant women. The apparent clearances (CL) of doxylamine and pyridoxal 5'-phosphate (PLP; the active metabolite of vitamin B(6) ) during the first-trimester pregnancy in women who participated in a Diclectin randomized trial were compared with those of healthy, adult, nonpregnant women who participated in a voluntary PK trial. Eighteen nonpregnant women were compared with 50 pregnant women who were treated with Diclectin. There was no difference in the apparent CL of doxylamine in women in their first trimester of pregnancy when compared with nonpregnant women on day 4 (median = 196.7 vs 249.5 mL/h/kg, respectively, P = .065), day 8 (median = 248.4 vs 249.5 mL/h/kg, respectively, P = .82), and day 15 (median = 200.9 vs 249.5 mL/h/kg, respectively, P = .55). No difference was found in the apparent CL of PLP on day 15 (median = 342.3 vs 314.7 mL/h/kg, respectively, P = .92). There was no pregnancy-induced effect in the apparent CL of either doxylamine or PLP in women during the first trimester of pregnancy despite the existence of morning sickness.

  2. The delayed-release combination of doxylamine and pyridoxine (Diclegis®/Diclectin ®) for the treatment of nausea and vomiting of pregnancy.

    Science.gov (United States)

    Madjunkova, Svetlana; Maltepe, Caroline; Koren, Gideon

    2014-06-01

    Nausea and vomiting of pregnancy (NVP) affects up to 85 % of all pregnancies. Effective treatment can greatly improve a woman's quality of life, reduce the risk for maternal and fetal complications, and reduce healthcare costs. Unfortunately, many women receive either no pharmacological treatment or are recommended therapies for which fetal safety and efficacy have not been established. First-line treatment of NVP, as recommended by several leading healthcare and professional organizations, is the combination of doxylamine and pyridoxine. This combination, formulated as a 10 mg/10 mg delayed-release tablet, was approved by the US Food and Drug Administration (FDA) for the treatment of NVP in April 2013 under the brand name Diclegis(®), and has been on the Canadian market since 1979, currently under the brand name Diclectin(®). The efficacy of Diclegis(®)/Diclectin(®) has been demonstrated in several clinical trials, and, more importantly, studies on more than 200,000 women exposed to doxylamine and pyridoxine in the first trimester of pregnancy have demonstrated no increased fetal risk for congenital malformations and other adverse pregnancy outcomes. The present review aims to present the scientific evidence on the effectiveness and fetal safety of Diclegis(®)/Diclectin(®) for the treatment of NVP to justify its use as first-line treatment for NVP.

  3. Combination of low-dose folic acid and pyridoxine for treatment of hyperhomocysteinaemia in patients with premature arterial disease and their relatives.

    Science.gov (United States)

    van der Griend, R; Haas, F J; Biesma, D H; Duran, M; Meuwissen, O J; Banga, J D

    1999-03-01

    Hyperhomocysteinaemia is an independent risk factor for atherosclerotic disease and venous thrombosis. The optimal homocysteine-lowering vitamin dose and target total homocysteine (tHcy) concentration are currently unknown. We prospectively studied the homocysteine-lowering effect after 8 weeks low-dose combination of folic acid (0.5 mg) and pyridoxine (100 mg) in 49 hyperhomocysteinaemic persons (33 patients with documented premature arterial disease and 16 of their first-degree relatives). Hyperhomocysteinaemia was in both sexes defined as fasting tHcy concentration > 12 micromol/l and/or post-methionine load tHcy concentration > 38 micromol/l. Low-dose vitamin therapy significantly reduced fasting tHcy concentration (median 13.9 to 9.3 micromol/l, reduction 32% (95% CI: 27-37%)) and post-load tHcy concentration (median 55.2 to 36.5 micromol/l, reduction 30% (95% CI: 25-35%)). Fasting tHcy reduction was similar in women and men, as well as in patients and relatives. Post-load tHcy reduction was significantly less in men compared to women (P = 0.04) and in relatives compared to patients (P = 0.03). Although low-dose combination of folic acid and pyridoxine results in a substantial reduction of tHcy concentrations (30-32%) in subjects with hyperhomocysteinaemia, the normalisation percentage to predefined criteria was less impressive (49%).

  4. Pyridoxine and pyridoxamine inhibits superoxide radicals and prevents lipid peroxidation, protein glycosylation, and (Na+ + K+)-ATPase activity reduction in high glucose-treated human erythrocytes.

    Science.gov (United States)

    Jain, S K; Lim, G

    2001-02-01

    Vitamin B(6) (pyridoxine) supplementation has been found beneficial in preventing diabetic neuropathy and retinopathy, and the glycosylation of proteins. Oxygen radicals and oxidative damage have been implicated in the cellular dysfunction and complications of diabetes. This study was undertaken to test the hypothesis that pyridoxine (P) and pyridoxamine (PM) inhibit superoxide radical production, reduce lipid peroxidation and glycosylation, and increase the (Na+ + K+)-ATPase activity in high glucose-exposed red blood cells (RBC). Superoxide radical production was assessed by the reduction of cytochrome C by glucose in the presence and absence of P or PM in a cell-free buffered solution. To examine cellular effects, washed normal human RBC were treated with control and high glucose concentrations with and without P or PM. Both P and PM significantly lowered lipid peroxidation and glycated hemoglobin (HbA(1)) formation in high glucose-exposed RBC. P and PM significantly prevented the reduction in (Na+ + K+)-ATPase activity in high glucose-treated RBC. Thus, P or PM can inhibit oxygen radical production, which in turn prevents the lipid peroxidation, protein glycosylation, and (Na+ + K+)-ATPase activity reduction induced by the hyperglycemia. This study describes a new biochemical mechanism by which P or PM supplementation may delay or inhibit the development of complications in diabetes.

  5. Effects of a leucine and pyridoxine-containing nutraceutical on body weight and composition in obese subjects

    Directory of Open Access Journals (Sweden)

    Zemel MB

    2013-08-01

    Full Text Available Michael B Zemel,1,2 Antje Bruckbauer11NuSirt Sciences Inc, 2Nutrition Department, The University of Tennessee, Knoxville, TN, USABackground: We recently demonstrated leucine to modulate energy partitioning between adipose tissue and muscle. Further, leucine exhibits a synergy with B6, resulting in reduced adipocyte lipid storage coupled with increased muscle fat oxidation. Accordingly, a nutraceutical (NuShape™ containing 2.25 g leucine and 30 mg B6 increased fat oxidation by > 30 g/day in a 28-day randomized controlled trial. The present study evaluated the long-term efficacy of this combination in modulating body weight and composition.Methods: Two 24-week, placebo-controlled, randomized trials, one with weight maintenance (n = 20 and one hypocaloric (-500 kcal/day; n = 24, were conducted using the nutraceutical Nushape in obese subjects.Results: The supplement resulted in fat loss in the maintenance study (-1.12 ± 0.36 and -1.82 ± 0.70 kg at 12 and 24 weeks, P < 0.01 versus placebo while no change was found in the placebo group. In the hypocaloric study, the supplement group lost up to twice as much weight (6.18 ± 1.02 versus 3.40 ± 0.81 kg at 12 weeks and 8.15 ± 1.33 versus 5.25 ± 1.13 kg at 24 weeks, P < 0.01 and fat (4.96 ± 0.61 versus 2.31 ± 0.53 kg at 12 weeks and 7.00 ± 0.95 versus 4.22 ± 0.74 kg at 24 weeks, P < 0.01 than the placebo group.Conclusion: This nutraceutical combination results in significant fat loss in the absence of caloric restriction and markedly enhances weight and fat loss by 50%–80% over a 24-week period.Keywords: leucine, vitamin B6, pyridoxine, fat loss, weight loss, caloric restriction, adiposity, body composition

  6. [Pathologic processes of lumbar primary sensory neurons produced by high doses of pyridoxine in rats--morphometric and electron microscopic studies].

    Science.gov (United States)

    Yamamoto, T

    1991-06-01

    The morphologic effects of the toxicity of high doses of pyridoxine hydrochloride (vitamin B6) on the lumbar primary sensory neurons in rats were studied. The test rats were treated with 1,200 mg/kg of pyridoxine hydrochloride by intraperitoneal injection once a day, and were sacrificed by perfusion at periods ranging from one to seven days after the injection, together with the control rats. Initial lesions consisted of eccentricity and crenation of the nucleus and vacuole formation in the cytoplasm of large dorsal root ganglion neurons, 2 days after the injection. These lesions were followed by segregation of the nucleolus, axon reaction-like changes in the cytoplasm and axonal degeneration of both peripheral axons in the sural nerve and central axons in the fasciculus gracilis. The frequency of teased myelinated fibers showing axonal degeneration during tests was significantly greater than in control 3 to 7 days after the injection. No significant difference of such frequency was found between the proximal and distal sural nerve during tests. The number of large myelinated fibers per nerve in the sural nerve, when compared with control, was preferentially decreased during tests. In the fasciculus gracilis, the decrease of the density of myelinated fibers was more pronounced in the third cervical segment than in the fifth thoracic segment. Because both peripheral and central axons were similarly affected and the initial lesions were found in the neuronal cell body, the mode of degeneration of axons in this study was regarded as "neuronopathy". By both light and electron microscopy, accumulation of mitochondria, vesicles, multilamellar and dense bodies were found in the nodal and distal paranodal axons of myelinated fibers in the sixth dorsal root ganglion on the 2nd day after the injection, which preceded the degeneration of both peripheral and central axons. Such accumulation, revealed for the first time in this study, may reflect the presence of a blockade of

  7. EFSA Panel on Dietetic Products, Nutrition and Allergies (NDA); Scientific Opinion on the substantiation of a health claim related to a combination of thiamin, riboflavin, niacin, pantothenic acid, pyridoxine, D-biotin and pumpkin seed oil and maintenance of normal hair pursuant to Article 13

    DEFF Research Database (Denmark)

    Tetens, Inge

    claim related to a combination of thiamin, riboflavin, niacin, pantothenic acid, pyridoxine, D-biotin and pumpkin seed oil (Cucurbita pepo L.) and maintenance of normal hair. The Panel considers that the specified combination is sufficiently characterised. The claimed effects are “contributes to reduce......, riboflavin, niacin, pantothenic acid, pyridoxine, D-biotin and pumpkin seed oil (Cucurbita pepo L.) and maintenance of normal hair....

  8. Pyridoxine responsive hereditary sideroblastic erythropoiesis and iron overload: two microcytic subpopulations in the affected male, one normocytic and one microcytic subpopulation in the obligate female carrier.

    Science.gov (United States)

    Harris, J W; Danish, E H; Brittenham, G M; McLaren, C E

    1993-04-01

    Mild hepatic iron overload has been demonstrated by magnetic susceptibility measurements in a 22-year-old man with hereditary sideroblastic erythropoiesis despite hemoglobin levels in the normal range and a normal erythropoietin level. His grandfather's sideroblastic anemia has been found to be responsive to pyridoxine; his mother's hemoglobin has persisted in the normal range but red cell volume distribution analysis demonstrated two subpopulations; 30% with estimated geometric mean of 68 fl and 70% an estimated mean of 93 fl. Red cell distribution analysis of the grandson demonstrated two microcytic subpopulations; 46% with an estimated geometric mean of 45 fl and 54% an estimated mean of 70 fl. A therapeutic regimen is outlined to reduce to normal his iron stores and to prevent the future development of excessive iron overload.

  9. Homocysteine, fibrinogen, and lipoprotein(a) levels are simultaneously reduced in patients with chronic renal failure treated with folic acid, pyridoxine, and cyanocobalamin.

    Science.gov (United States)

    Naruszewicz, M; Klinke, M; Dziewanowski, K; Staniewicz, A; Bukowska, H

    2001-02-01

    Ischemic heart disease and other complications of atherosclerosis are the usual cause of death in patients with chronic renal failure. Important factors associated with early onset of atherosclerosis in these patients are hyperhomocysteinemia, hyperfibrinogenemia, and elevated levels of lipoprotein(a) (Lp(a)). Folic acid (15 mg/d), pyridoxine (150 mg/d), and cyanocobalamin (1 mg/wk) were administered for 4 weeks in 21 patients receiving dialysis, and a simultaneous, statistically significant reduction in the concentration of homocysteine, fibrinogen, and Lp(a) was found. A positive correlation between decreasing homocysteine and fibrinogen levels was also noted. The parameters studied approached presupplementation values 6 months after vitamins were discontinued. The results suggest that vitamin supplementation has a favorable effect on risk factors of atherosclerosis in patients with renal failure and that interactions may exist between homocysteine, fibrinogen, and Lp(a).

  10. Cloning, expression, purification, crystallization and preliminary X-ray studies of a pyridoxine 5′-phosphate oxidase from Mycobacterium smegmatis

    Energy Technology Data Exchange (ETDEWEB)

    Jackson, Colin J., E-mail: colin.jackson@csiro.au; Taylor, Matthew C.; Tattersall, David B.; French, Nigel G. [CSIRO Entomology, Black Mountain, ACT 2601 (Australia); Carr, Paul D.; Ollis, David L. [Research School of Chemistry, Australian National University, ACT 0200 (Australia); Russell, Robyn J.; Oakeshott, John G. [CSIRO Entomology, Black Mountain, ACT 2601 (Australia)

    2008-05-01

    Good-quality crystals of selenomethionine-substituted Msmeg-3380 were obtained by the hanging-drop vapour-diffusion technique and diffracted to 1.2 Å using synchrotron radiation. Pyridoxine 5′-phosphate oxidases (PNPOxs) are known to catalyse the terminal step in pyridoxal 5′-phosphate biosynthesis in a flavin mononucleotide-dependent manner in humans and Escherichia coli. Recent reports of a putative PNPOx from Mycobacterium tuberculosis, Rv1155, suggest that the cofactor or catalytic mechanism may differ in Mycobacterium species. To investigate this, a putative PNPOx from M. smegmatis, Msmeg-3380, has been cloned. This enzyme has been recombinantly expressed in E. coli and purified to homogeneity. Good-quality crystals of selenomethionine-substituted Msmeg-3380 were obtained by the hanging-drop vapour-diffusion technique and diffracted to 1.2 Å using synchrotron radiation.

  11. Pyridoxine (Vitamin B6)

    Science.gov (United States)

    ... product (NicAzel, Elorac Inc., Vernon Hills, IL), containing nicotinamide, azelaic acid, zinc, vitamin B6, copper, and folic ... children with asthma is unclear. Itchy and inflamed skin (atopic dermatitis (eczema)). Early research suggests that taking ...

  12. Development and Validation of a Rapid Chemometrics Assisted RP-HPLC with PDA Detection Method for the Simultaneous Estimation of Pyridoxine HCl and Doxylamine Succinate in Bulk and Pharmaceutical Dosage Form

    Directory of Open Access Journals (Sweden)

    P. Giriraj

    2014-01-01

    Full Text Available Simple, rapid, precise, and accurate RP-HPLC method was developed and optimized with the help of chemometric tool for the simultaneous estimation of pyridoxine HCl and doxylamine succinate in bulk and pharmaceutical dosage form. Optimization was done by central composite design in response surface methodology. Based on the trial and error, percentage of organic phase (methanol in mobile phase, flow rate, and molarity of the buffer were selected as factors. Resolution and retention time were used for the estimation of system response during the optimization procedure. The optimized condition was used and the separation was carried out on phenomenex C18 column (150 × 4.6 mm; i.d, 5 μ particle size using the mobile phase containing 49.37% of methanol and 50.63% of phosphate buffer (45.14 mM at a flow rate of 1 mL/min. Retention time was found to be 1.884 minutes for pyridoxine HCl and 3.959 minutes for doxylamine succinate. The calibration curves were found to be linear from 10 to 70 μg/mL and 10 to 90 μg/mL for pyridoxine HCl and doxylamine succinate with their correlation coefficient values 0.9995 and 0.9997. LOD and LOQ were found to be 23.5 ng/mL and 71.1 ng/mL for pyridoxine HCl and 99.9 ng/mL and 302.6 ng/mL for doxylamine succinate.

  13. Terahertz Spectroscopy of Biotin and Pyridoxine%生物素和吡哆素的太赫兹光谱特性研究

    Institute of Scientific and Technical Information of China (English)

    蒋玲; 李淼; 李春; 孙海军; 徐莉; 刘云飞

    2015-01-01

    Terahertz (THz) absorption spectra of the biotin and pyridoxine were studied using Fourier trans‐form infrared spectroscopy (FTIR) at room temperature .These spectra exhibit enhanced absorption in THz range because of strong intramolecular and intermolecular vibration modes .In the experiment ,the samples were mixed with high density polyethylene powder ,which was used as spectrophotometric grid .The absorp‐tion spectra show worse consistency at higher frequencies for the high ratio of the samples to polyethylene .It indicates that the absorbance of the biotin and pyridoxine increased with frequency .Molecular vibrational spec‐tral calculations based on density functional theory (DFT ) show strong correlation with the experiment .We investigated the absorption spectra of isolated molecules (single molecule ,two molecules ,three molecules) and unit cell of crystal to clarify the mechanism of the spectra change due to intramolecular and intermolecular vibration and rotation .%采用傅里叶变换红外光谱技术(FTIR)和密度泛函理论(DFT)研究了常温环境下生物素和吡哆素两种维生素的太赫兹光谱特性,测量和理论分析的结果显示在太赫兹范围内,维生素分子内存在较强的分子内和分子间相互作用力。实验中样品与聚乙烯粉末按照不同的比例进行混合,结果表明样品所含比例越大,其在高频段的吸收谱重复性越差,这证实了维生素样品的吸收率随着频率升高逐渐增加。采用密度泛函理论(DFT )分析了生物素和吡哆素的单分子、二分子、三分子、以及晶胞分子的太赫兹光谱,指证了对应的吸收峰,阐明了分子内和分子间相互作用力的振动和转动机制。

  14. Determination of Pyridoxine Hydrochloride in Luojijiangya Tablets by HPLC%HPLC法检测罗己降压片中盐酸吡哆辛含量

    Institute of Scientific and Technical Information of China (English)

    刘信奎

    2015-01-01

    目的:建立HPLC法测定罗己降压片中盐酸吡哆辛含量。方法:使用十八烷基硅烷键合硅胶为填充剂,以0.04%戊烷磺酸钠溶液(用冰醋酸调节p H至3.0)-甲醇(85:15)为流动相,检测波长为291n m进行测定。流速1.0m L•m i n-1,柱温35℃。结果:平均加样回收率盐酸吡哆辛为99.04%,RSD=0.17%(n=9)。盐酸吡哆辛在0.4000~1.600μg范围内,进样量与峰面积值呈良好的线性关系(r=0.9999)。结论:方法简便、结果准确、重现性好,可为罗己降压片的质量控制提供依据。%ObjectiveHPLC method was established for the determination of Pyridoxine Hydrochloride in Luojijiangya Tablets. Methods ODS C18 column was used. The mobile phase was 0.04% sodium pentanesulfonate(adjusted to pH 3.0 with acetic acid)-methanol(85:15). The detection wavelength was 291nm. The flow rate was 1.0 mL•min-1 with the column temperature at 35℃. Results The average recoveries were 99.04%,RSD=0.17%(n=9). The linear range of Pyridoxine was within 0.4000~1.600µg (r=0.9999). Conclusion T he method is simple, accurate, stableand reliable. It can be used for quality control of Luojijiangya tablets.

  15. Cubane-type Cu(II)4 and Mn(II)2Mn(III)2 complexes based on pyridoxine: a versatile ligand for metal assembling.

    Science.gov (United States)

    Marino, Nadia; Armentano, Donatella; Mastropietro, Teresa F; Julve, Miguel; De Munno, Giovanni; Martínez-Lillo, José

    2013-10-21

    By using Vitamin B6 in its monodeprotonated pyridoxine form (PN-H) [PN = 3-hydroxy-4,5-bis(hydroxymethyl)-2-methylpyridine], two tetranuclear compounds of formula [Mn4(PN-H)4(CH3CO2)3Cl2]Cl·2CH3OH·2H2O (1) and [Cu4(PN-H)4Cl2(H2O)2]Cl2 (2) have been synthesized and magneto-structurally characterized. 1 crystallizes in the triclinic system with space group P1 whereas 2 crystallizes in the orthorhombic system with Fdd2 as space group. They exhibit Mn(II)2Mn(III)2 (1) and Cu(II)4 (2) cubane cores containing four monodeprotonated pyridoxine groups simultaneously acting as chelating and bridging ligands (1 and 2), three bridging acetate ligands in the syn-syn conformation (1), and two terminally bound chloride anions (1 and 2) plus two coordinated water molecules (2). The electroneutrality is achieved by the presence of chloride counterions in both compounds. Tri- [Mn(1) and Mn(3)] and divalent [Mn(2) and Mn(4)] manganese centers coexist in 1, all being six-coordinate with distorted Mn(1/3)O6 and Mn(2/4)O5Cl octahedral surroundings, respectively, the equatorial Mn-O bonds being about 0.2 Å shorter at the former ones. The two crystallographically independent copper(II) ions in 2 are five-coordinate in somewhat distorted CuO5 [Cu(1)] and CuO4Cl [Cu(2)] square pyramidal geometries. The values of the intracore metal-metal separation cover the ranges 3.144(1)-3.535(1) (1) and 2.922(6)-3.376(1) Å (2). The magnetic properties of 1 and 2 were investigated in the temperature range 1.9-300 K, and they correspond to an overall antiferromagnetic behavior with susceptibility maxima at 5.0 (1) and 65.0 K (2). The analysis of the magnetic susceptibility data showed the coexistence of intracore antiferro- and ferromagnetic interactions in the two compounds. Their values compare well with those existing in the literature for the parent systems.

  16. Alterations in hippocampal serotonergic and INSR function in streptozotocin induced diabetic rats exposed to stress: neuroprotective role of pyridoxine and Aegle marmelose

    Directory of Open Access Journals (Sweden)

    Joy Shilpa

    2010-09-01

    Full Text Available Abstract Diabetes and stress stimulate hippocampal 5-HT synthesis, metabolism and release. The present study was carried out to find the effects of insulin, Aegle marmelose alone and in combination with pyridoxine on the hippocampal 5-HT, 5-HT2A receptor subtype, gene expression studies on 5-HT2A, 5-HTT, INSR, immunohistochemical studies and elevated plus maze in streptozotocin induced diabetic rats. 5-HT content showed a significant decrease (p p max and Kd showed a significant decrease (p 2A receptor binding parameters Bmax showed a significant decrease (p p d in hippocampus of diabetic rats compared to control. Gene expression studies of 5-HT2A, 5-HTT and INSR in hippocampus showed a significant down regulation (p A. marmelose to diabetic rats reversed the 5-HT content, Bmax , Kd of 5-HT, 5-HT2A and gene expression of 5-HT2A, 5-HTT and INSR in hippocampus to near control. The gene expression of 5-HT2A and 5-HTT were confirmed by immunohistochemical studies. Behavioural studies using elevated plus maze showed that serotonin through its transporter significantly increased (p A. marmelose has a role in the regulation of insulin synthesis and release, normalising diabetic related stress and anxiety through hippocampal serotonergic function. This has clinical significance in the management of diabetes.

  17. Simultaneous determination of pyridoxine hydrochloride and doxylamine succinate from tablets by ion pair reversed-phase high-performance liquid chromatography (RP-HPLC).

    Science.gov (United States)

    Argekar, A P; Sawant, J G

    1999-08-01

    A new, simple, precise, and rapid ion pair reversed-phase high-performance liquid chromatography (RP-HPLC) method has been developed for the simultaneous determination of pyridoxine hydrochloride (PYR) and doxylamine succinate (DOX) in tablets. The stationary phase was a Microbondapak C18 column (10 mu, 300 mm x 3.9 mm i.d.). The mobile phase was water:methanol (60:40) containing 10 mM heptanesulfonic acid and 0.25% triethylamine and adjusted to pH 2.2 with orthophosphoric acid. Detection was carried out at 263 nm using an ultraviolet (UV) detector. The flow rate was 1.0 ml/min, and retention times were 3.65 min and 7.32 min for PYR and DOX, respectively. The linearity was obtained in the concentration range 0.5-500 micrograms/ml for PYR and DOX. Mean percentage recoveries were 100.20% and 101.20% for PYR and DOX, respectively.

  18. Feasibility of amlodipine besylate, chloroquine phosphate, dapsone, phenytoin, pyridoxine hydrochloride, sulfadiazine, sulfasalazine, tetracycline hydrochloride, trimethoprim and zonisamide in SyrSpend(®) SF PH4 oral suspensions.

    Science.gov (United States)

    Ferreira, Anderson O; Polonini, Hudson C; Silva, Sharlene L; Patrício, Fernando B; Brandão, Marcos Antônio F; Raposo, Nádia R B

    2016-01-25

    The objective of this study was to evaluate the feasibility of 10 commonly used active pharmaceutical ingredients (APIs) compounded in oral suspensions using an internationally used suspending vehicle (SyrSpend(®) SF PH4 liquid): (i) amlodipine, (as besylate) 1.0mg/mL; (ii) chloroquine phosphate,15.0 mg/mL; (iii) dapsone, 2.0 mg/mL; (iv) phenytoin, 15.0 mg/mL; (v) pyridoxine hydrochloride, 50.0 mg/mL; (vi) sulfadiazine, 100.0 mg/mL; (vii) sulfasalazine, 100.0 mg/mL; (viii) tetracycline hydrochloride, 25.0 mg/mL; (ix) trimethoprim, 10.0 mg/mL; and (x) zonisamide, 10.0 mg/mL. All suspensions were stored both at controlled refrigeration (2-8 °C) and controlled room temperature (20-25 °C). Feasibility was assessed by measuring the percent recovery at varying time points throughout a 90-day period. API quantification was performed by high-performance liquid chromatography (HPLC-UV), via a stability-indicating method. Given the percentage of recovery of the APIs within the suspensions, the expiration date of the final products (API+vehicle) was at least 90 days for all suspensions with regard to both the controlled temperatures. This suggests that the vehicle is stable for compounding APIs from different pharmacological classes.

  19. A Stability-Indicating High Performance Liquid Chromatographic Assay for the Simultaneous Determination of Pyridoxine, Ethionamide, and Moxifloxacin in Fixed Dose Combination Tablets

    Directory of Open Access Journals (Sweden)

    Munib-ur-Rehman

    2014-01-01

    Full Text Available Stability indicating reversed phase HPLC method was developed and validated for the simultaneous quantitation of antitubercular drugs, ethionamide (ETH, and moxifloxacin (MOX with commonly coprescribed vitamin, pyridoxine (PYR in tablet dosage form. The method was found rapid, precise and accurate. The separation was performed in Hibar 150-4.6, Purospher STAR, RP-18e (5 μm column, using mobile phase A (0.03 M sodium citrate adjusted to pH 5 with glacial acetic acid and mobile phase B (100% methanol, ran at variable proportions at flow rate of 1.0 mL/min. The detection was carried out at 320 nm. The method was observed linearly in the range of 2.5–17.5 μg/mL for PYR, 25–175 μg/mL for ETH, and 40–280 μg/mL for MOX with respective limits of detection/quantitation of 0.125 μg/mL/1.28 μg/mL, 0.25 μg/mL/2.56 μg/mL, and 0.35 μg/mL/3.65 μg/mL. The drugs were also subjected to oxidative, hydrolytic, photolytic, and thermal degradation; the degradation products showed interference with the detection of PYR, ETH, and MOX. The proposed method was observed to be effective to quantitate MOX (400 mg, ETH (250 mg, and PYR (25 mg in fixed dose combination tablet formulation.

  20. Misfolding caused by the pathogenic mutation G47R on the minor allele of alanine:glyoxylate aminotransferase and chaperoning activity of pyridoxine.

    Science.gov (United States)

    Montioli, Riccardo; Oppici, Elisa; Dindo, Mirco; Roncador, Alessandro; Gotte, Giovanni; Cellini, Barbara; Borri Voltattorni, Carla

    2015-10-01

    Liver peroxisomal alanine:glyoxylate aminotransferase (AGT), a pyridoxal 5'-phosphate (PLP) enzyme, exists as two polymorphic forms, the major (AGT-Ma) and the minor (AGT-Mi) haplotype. Deficit of AGT causes Primary Hyperoxaluria Type 1 (PH1), an autosomal recessive rare disease. Although ~one-third of the 79 disease-causing missense mutations segregates on AGT-Mi, only few of them are well characterized. Here for the first time the molecular and cellular defects of G47R-Mi are reported. When expressed in Escherichia coli, the recombinant purified G47R-Mi variant exhibits only a 2.5-fold reduction of its kcat, and its apo form displays a remarkably decreased PLP binding affinity, increased dimer-monomer equilibrium dissociation constant value, susceptibility to thermal denaturation and to N-terminal region proteolytic cleavage, and aggregation propensity. When stably expressed in a mammalian cell line, we found ~95% of the intact form of the variant in the insoluble fraction, and proteolyzed (within the N-terminal region) and aggregated forms both in the soluble and insoluble fractions. Moreover, the intact and nicked forms have a peroxisomal and a mitochondrial localization, respectively. Unlike what already seen for G41R-Mi, exposure of G47R-Mi expressing cells to pyridoxine (PN) remarkably increases the expression level and the specific activity in a dose-dependent manner, reroutes all the protein to peroxisomes, and rescues its functionality. Although the mechanism of the different effect of PN on the variants G47R-Mi and G41R-Mi remains elusive, the chaperoning activity of PN may be of value in the therapy of patients bearing the G47R mutation.

  1. Effects of a Leucine and Pyridoxine-Containing Nutraceutical on Fat Oxidation, and Oxidative and Inflammatory Stress in Overweight and Obese Subjects

    Directory of Open Access Journals (Sweden)

    Antje Bruckbauer

    2012-06-01

    Full Text Available Leucine stimulates tissue protein synthesis and may also attenuate adiposity by increasing fatty acid oxidation and mitochondrial biogenesis in muscle and adipocytes. Accordingly, the effects of a nutraceutical containing 2.25 g leucine and 30 mg pyridoxine (Vitamin B6 (NuFit active blend were tested in cell culture and in a clinical trial. 3T3L1 adipocytes were treated with leucine (0.25 mM or 0.5 mM and/or Pyridoxal Phosphate (PLP (50 nM or 100 nM for 48 h. For the clinical trial, twenty overweight or obese subjects received the NuFit active blend or placebo three times/day for 4 weeks without energy restriction. Leucine decreased fatty acid synthase (FAS expression and triglyceride content in adipocytes, and PLP addition significantly augmented this effect. Administration of NuFit active blend in the clinical trial increased fat oxidation by 33.6 g/day (p < 0.04, decreased respiratory quotient, improved HOMAIR, reduced oxidative and inflammatory biomarkers (plasma MDA, 8-isoprostane-F, TNF-α, C-reactive protein, and increased the anti-inflammatory marker adiponectin. These data indicate that the NuFit active blend significantly increased fat oxidation and insulin sensitivity, and reduced oxidative and inflammatory stress. Therefore, the NuFit active blend appears to be a useful nutraceutical in the management of obesity and associated co-morbidities.

  2. Bioavailability of Cu, Zn and Mn from Mineral Chelates or Blends of Inorganic Salts in Growing Turkeys Fed with Supplemental Riboflavin and/or Pyridoxine.

    Science.gov (United States)

    Salami, S A; Oluwatosin, O O; Oso, A O; Fafiolu, A O; Sogunle, O M; Jegede, A V; Bello, F A; Pirgozliev, V

    2016-09-01

    An 84-day feeding trial was conducted in growing turkeys to measure the bioavailability of Cu, Zn and Mn from a commercial mineral chelate and corresponding inorganic salts in composite feeds containing supplemental riboflavin (B2) and/or pyridoxine (B6). A total of 320, 28-day-old British United Turkeys (BUT) were assigned to eight dietary treatments in a 2 × 4 factorial arrangement comprising two trace mineral sources: chelated trace mineral blend (CTMB) and its corresponding inorganic trace minerals blend (ITMB) fed solely or with supplements of vitamin B2 (8 ppm) or B6 (7 ppm) or 8 ppm B2 + 7 ppm B6. Each treatment was replicated four times with 10 turkeys each. It was observed that turkeys fed with diets supplemented solely with ITMB elicited higher (P < 0.05) Zn excretion than their counterparts fed with diets containing ITMB with supplements of vitamins B2 and/or B6. Manganese retention was lower (P < 0.05) in turkeys fed with diets supplemented solely with ITMB than those fed with diets containing vitamins B2 and/or B6 additives. Combination of CTMB or ITMB with B6 improved (P < 0.05) the concentration of Mn in the liver and Cu in the bone. It was concluded that the minerals in CTMB were more available to the animals than ITMB. Furthermore, vitamins B2 and/or B6 supplementation improved the bioavailability of the inorganic Cu, Zn and Mn in growing turkeys and tended to reduce the concentration of these trace elements in birds' excreta.

  3. Bimetallic magnetic nanoparticle as a new platform for fabrication of pyridoxine and pyridoxal-5'-phosphate imprinted polymer modified high throughput electrochemical sensor.

    Science.gov (United States)

    Patra, Santanu; Roy, Ekta; Das, Ranajit; Karfa, Paramita; Kumar, Sunil; Madhuri, Rashmi; Sharma, Prashant K

    2015-11-15

    The present work describes the fabrication of a selective and sensitive molecularly imprinted polymer (MIP)-based electrochemical sensor using a combination of surface imprinting and nanotechnology. The fabricated sensor was used for the detection of two major components of vitamin B6 i.e. pyridoxine (Py) and pyridoxal-5'-phosphate (PLP) using the same MIP format. Herein, acrylic acid modified zero valent iron nanoparticles were combined with the copper nanoparticle, resulting in vinyl groups modified bimetallic Fe/Cu magnetic nanoparticles (BMNPs). These BMNPs have high surface to volume ratios, higher electro-catalytic activity, and are therefore, a suitable platform to synthesize specific MIP cavities for Py and PLP. Herein, two different MIP formats (for Py and PLP) were synthesized on the surface of vinyl silane modified pencil graphite electrodes by activator regenerated by an electron transfer-atom transfer radical polymerization (ARGET-ATRP) method. The sensor shows a good analytical performance for the detection of Py and PLP by a square wave stripping voltammetric technique (SWSV). The limit of detection (LOD) was calculated to be 0.040 µg L(-1) and 0.043 µg L(-1) for Py and PLP, respectively, at signal to noise ratio of 3. The sensors are highly selective for the templates and can detect them from multivitamin tablets, corn flakes, energy drinks, cerebrospinal fluid (CSF) and blood samples (serum, plasma and whole blood) without any interfering effect, suggesting the clinical applicability of the fabricated sensor. The sensor can also be used as better alternative to the commercially available ELISA kits which are rather complex, less sensitive and difficult to handle.

  4. [Study of pharmacological activity of complex magnesium-containing preparation based on mineral bishofit and pyridoxine hydrochloride in a rat model of chronic alcoholic intoxication].

    Science.gov (United States)

    Spasov, A A; Petrov, V I; Iezhitsa, I N; Onishchenko, N V; Churbakova, N V; Parshev, V V

    2003-01-01

    Nervous disturbances accompanying alcoholic illness were studied in relation to the depletion of magnesium ion content in the organism. The possibility of correcting the development of psychic (behavioral) pathologies by treatment with a complex magnesium-containing preparation based on mineral bishofit and pyridoxine hydrochloride (below, Mg-containing preparation) was studied in rats upon three-month voluntary alcoholization. A decrease in the locomotor (number of crossed squares) and vertical (number of standings) activity as evaluated in the open-field test and an increase in the immobilization time in the forced swim test showed evidence of depressive state in animals after long-term ethanol administration. After treatment with the Mg-containing preparation (50 mg Mg/kg in 2.5 ml volume, p.o.), the immobilization time of alcohol-preferring rats decreased in comparison to that before treatment and showed no statistically significant differences from the value in the intact control group. A decrease in the immobilization time (the main sign of antidepressant action) allows the Mg-containing preparation to be considered as antidepressant. The level of magnesium in rat blood erythrocytes decreased upon three-month voluntary alcoholization by 40.95 +/- 2.41% relative to control (p < 0.05). After a 5-week treatment with Mg-containing preparation under conditions of free access to alcohol, the content of magnesium in the erythrocytes of alcohol-preferring rats restored on a normal level. Chronic alcoholism reduces the content of microelements and vitamins (in particular, B6), these changes being mutually related.

  5. In vitro and in vivo gene therapy with CMV vector-mediated presumed dog beta-nerve growth factor in pyridoxine-induced neuropathy dogs.

    Science.gov (United States)

    Chung, Jin Young; Choi, Jung Hoon; Shin, Il Seob; Choi, Eun Wha; Hwang, Cheol Yong; Lee, Sang Koo; Youn, Hwa Young

    2008-12-01

    Due to the therapeutic potential of gene therapy for neuronal injury, many studies of neurotrophic factors, vectors, and animal models have been performed. The presumed dog beta-nerve growth factor (pdbeta-NGF) was generated and cloned and its expression was confirmed in CHO cells. The recombinant pdbeta-NGF protein reacted with a human beta-NGF antibody and showed bioactivity in PC12 cells. The pdbeta-NGF was shown to have similar bioactivity to the dog beta-NGF. The recombinant pdbeta-NGF plasmid was administrated into the intrathecal space in the gene therapy group. Twenty-four hours after the vector inoculation, the gene therapy group and the positive control group were intoxicated with excess pyridoxine for seven days. Each morning throughout the test period, the dogs' body weight was taken and postural reaction assessments were made. Electrophysiological recordings were performed twice, once before the experiment and once after the test period. After the experimental period, histological analysis was performed. Dogs in the gene therapy group had no weight change and were normal in postural reaction assessments. Electrophysiological recordings were also normal for the gene therapy group. Histological analysis showed that neither the axons nor the myelin of the dorsal funiculus of L4 were severely damaged in the gene therapy group. In addition, the dorsal root ganglia of L4 and the peripheral nerves (sciatic nerve) did not experience severe degenerative changes in the gene therapy group. This study is the first to show the protective effect of NGF gene therapy in a dog model.

  6. Simultaneous determination of alpha-aminoadipic semialdehyde, piperideine-6-carboxylate and pipecolic acid by LC-MS/MS for pyridoxine-dependent seizures and folinic acid-responsive seizures.

    Science.gov (United States)

    Sadilkova, Katerina; Gospe, Sidney M; Hahn, Si Houn

    2009-10-30

    Pyridoxine-dependent seizures (PDS) is an autosomal recessive disorder characterized by seizures presenting in neonates or infants up to 3 years of age which respond to pharmacological doses of pyridoxine. Alpha-aminoadipic semialdehyde dehydrogenase (antiquitin) deficiency was identified as an underlying defect in PDS characterized by accumulation of alpha-aminoadipic semialdehyde (alpha-AASA) as a specific marker and recently folinic acid-responsive seizures (FRS) were found to be allelic to PDS as the putative mutations were identified in the antiquitin gene (ALDH7A1). alpha-AASA is known to be in reversible equilibrium with its cyclic Shiff base, delta(1)-piperideine-6-carboxylate (P6C). Pipecolic acid (PA) is another biomarker often elevated but is not specific to PDS. Here, we developed the liquid chromatography-mass spectrometry (LC-MS/MS) method to determine the analytes of alpha-AASA, P6C and PA simultaneously in plasma and validated the assay using samples from confirmed cases. This approach eliminates the extra time and expense of running multiple assays and provides valuable information for the rapid diagnosis and treatment of patients with PDS and FRS which potentially could lead to a better outcome with improved quality of life. The stability study showed that alpha-AASA and P6C were unstable even at -20 degrees C. A careful sample handling with immediate freezing and testing is required for reliable result.

  7. Protective effect of HSV-mediated gene transfer of nerve growth factor in pyridoxine neuropathy demonstrates functional activity of trkA receptors in large sensory neurons of adult animals.

    Science.gov (United States)

    Chattopadhyay, Munmun; Goss, James; Lacomis, David; Goins, William C; Glorioso, Joseph C; Mata, Marina; Fink, David J

    2003-02-01

    The distinct distribution of trkA receptors on small neurons and trkC receptors on large neurons in the dorsal root ganglion correlates with the dependence of these two classes of neurons on nerve growth factor and neurotrophin-3, respectively, for survival during development. In adult animals, the distribution of high affinity neurotrophin (trk) is complex and overlapping; neurotrophins are not required for cell survival, but may influence cell phenotype and the response to injury. In order to test the functional activity of trkA receptors in the sensory ganglia of adult animals in vivo, we examined the ability of a nerve growth factor-expressing recombinant replication-defective herpes simplex virus-based vector to prevent the selective degeneration of large sensory fibres caused by intoxication with pyridoxine. Transduction of dorsal root ganglion neurons in vivo by subcutaneous inoculation of the nerve growth factor-expressing vector prevented the development of pyridoxine-induced neuropathy measured by electrophysiological, morphological and behavioural measures. These results demonstrate a functional activity of trkA receptors expressed on large neurons in the dorsal root ganglion in mature animals; this observation has important implications for the choice of neurotrophic factors for treatment of peripheral nerve disease.

  8. 二氧化锰晶型对吡哆醇氧化反应的稳定性研究%The Effect of MnO2 Crystals on the Oxidation of Pyridoxine

    Institute of Scientific and Technical Information of China (English)

    施湘君; 陈巧巧

    2012-01-01

    Pyridoxal(1) was synthesized from pyridoxine(2) by manganese dioxide. The crystal form of different commercial MnO2 was characterized via X-ray diffraction. We found the different crystal form of MnO2 influenced the result of oxidizing reaction, and γα- MnO2 is the most effective form.%以吡哆醇(1)为起始原料,经二氧化锰选择性氧化反应制得吡哆醛(2),通过X射线衍射脚)分析不同市售二氧化锰的晶型,研究不同晶型对催化氧化能力的影响,发现较优的晶型为γα-MnO2(混铆。

  9. Doxylamine succinate/pyridoxine hydrochloride.

    Science.gov (United States)

    Cada, Dennis J; Demaris, Kendra; Levien, Terri L; Baker, Danial E

    2013-10-01

    Each month, subscribers to The Formulary Monograph Service receive 5 to 6 well-documented monographs on drugs that are newly released or are in late phase 3 trials. The monographs are targeted to Pharmacy & Therapeutics Committees. Subscribers also receive monthly 1-page summary monographs on agents that are useful for agendas and pharmacy/nursing in-services. A comprehensive target drug utilization evaluation/medication use evaluation (DUE/MUE) is also provided each month. With a subscription, the monographs are sent in print and are also available online. Monographs can be customized to meet the needs of a facility. A drug class review is now published monthly with The Formulary Monograph Service. Through the cooperation of The Formulary, Hospital Pharmacy publishes selected reviews in this column. For more information about The Formulary Monograph Service, call The Formulary at 800-322-4349. The October 2013 monograph topics are afatinib, ferric carboxymaltose, cangrelor, vedolizumab, and albiglutide. The DUE/MUE is on afatinib.

  10. 家蚕磷酸吡哆醇氧化酶基因的表达谱分析%Expression profiling of pyridoxine 5’-phosphate oxidase gene in Bombyx mori

    Institute of Scientific and Technical Information of China (English)

    葛俊楠; 张剑韵; 黄龙全

    2011-01-01

    [Aim] The expression profile of gene encoding pyridoxine phosphate oxidase (PNPO) , which is a key enzyme related to VB6 metabolism, was analyzed in different developmental stages and tissues of the 5th instar larvae of Bombyx mori. [ Methods ] The recombinant plasmid pET-22b ( + ) -PNPO was transformed to Escherichia coli Rosetta for induction, expression and purification of PNPO, and then the polyclonal antibody was prepared. The expression profile of PNPO gene was analyzed by Real-time PCR and Western blot, respectively. [ Results ] The highest translation level of PNPO gene was found in the 5th instar larvae. The transcription level in tissues of 5th instar larvae was in sequence of testis > head > tnidgut > Malpighian tubules > ovary > cuticle > fat body > silk glands. However, the highest translation level was found in testis, and then was in head, midgut, and malpighian tubules, respectively. [ Conclusion ] The expression profile PNPO gene in B. Mori has been defined by this study.%目的 了解家蚕Bombyx mori维生素B6关键代谢酶磷酸吡哆醇氧化酶(pyridoxine-5'-phosphate oxidase,PNPO)基因在家蚕不同发育阶段及5龄幼虫不同组织中的表达差异.方法 将家蚕PNPO基因的重组表达质粒pET-22b(+)-PNPO转化入大肠杆菌Escherichia coli Rosetta中诱导表达,纯化蛋白制备多克隆抗体.分别采用荧光定量PCR和Western blot方法对家蚕PNPO基因进行了转录水平和翻译水平的表达分析.结果 在家蚕发育水平上,5龄幼虫的PNPO翻译量为最高.PNPO基因在5龄幼虫各组织中的转录水平由高到低依次为精巢、头、中肠、马氏管、卵巢、表皮、脂肪体、丝腺;翻译量也以精巢为最高,其次是头、中肠和马氏管.结论 明确了PNPO在家蚕各发育阶段及5龄幼虫各组织中的表达情况.

  11. 反相高效液相色潽法测定罗己降压片中维生素B6含量%Determination of Pyridoxine Hydrochloride in Luojijiangya Tablets by RP-HPLC

    Institute of Scientific and Technical Information of China (English)

    尹艳华

    2015-01-01

    Objective: HPLC method was established for the determination of Pyridoxine Hydrochloride in Luojijiangya Tablets. Methods:ODS C18 column w as used. The mobile phase was 0.04%sodium pentanesulfonate(adjusted to pH 3.0 with acetic acid)-methanol(85:15). The detection wavelength was 291nm. The flow rate was 1.0 mL·min-1 with the column temperature at 35℃. Results:The average recoveries were 99.04%,RSD=0.17%(n=9). The linear range of Pyridoxine was within 0.4000~1.600μg (r=0.9999). Con-clusion:The method is simple, accurate, stableand reliable. It can be used for quality control of Luojijiangy a Tablets.%目的:建立RP-HPLC法测定罗己降压片中维生素B6含量。方法:使用十八烷基硅烷键合硅胶为填充剂,以0.04%戊烷磺酸钠溶液(用冰醋酸调节pH至3.0)-甲醇(85:15)为流动相,检测波长为291nm进行测定。流速1.0mL·min-1,柱温35℃。结果:平均加样回收率维生素B6为99.04%,RSD=0.17%(n=9)。维生素B6在0.4000~1.600µg范围内,进样量与峰面积值呈良好的线性关系(r=0.9999)。结论:方法简便、结果准确、重现性好,可为罗己降压片的质量控制提供依据。

  12. Comparative ANNs with Different Input Layers and GA-PLS Study for Simultaneous Spectrofluorimetric Determination of Melatonin and Pyridoxine HCl in the Presence of Melatonin’s Main Impurity

    Directory of Open Access Journals (Sweden)

    Amer M. Alanazi

    2013-01-01

    Full Text Available Melatonin (MLT has many health implications, therefore it is important to develop specific analytical methods for the determination of MLT in the presence of its main impurity, N-{2-[1-({3-[2-(acetylaminoethyl]-5-methoxy-1H-indol-2-yl}methyl-5-methoxy-1H-indol-3-yl]ethyl}acetaamide (DMLT and pyridoxine HCl (PNH as a co-formulated drug. This work describes simple, sensitive, and reliable four multivariate calibration methods, namely artificial neural network preceded by genetic algorithm (GA-ANN, principal component analysis (PCA-ANN and wavelet transform procedures (WT-ANN as well as partial least squares preceded by genetic algorithm (GA-PLS for the spectrofluorimetric determination of MLT and PNH in the presence of DMLT. Analytical performance of the proposed methods was statistically validated with respect to linearity, accuracy, precision and specificity. The proposed methods were successfully applied for the assay of MLT in laboratory prepared mixtures containing up to 15% of DMLT and in commercial MLT tablets with recoveries of no less than 99.00%. No interference was observed from common pharmaceutical additives and the results compared favorably with those obtained by a reference method.

  13. Expression of Bombyx mori Pyridoxine-5'-phosphate Oxidase in E. coli and Assay of Enzymological Characters%家蚕磷酸吡哆醇氧化酶在E.coli中的表达及酶学特征研究

    Institute of Scientific and Technical Information of China (English)

    王振; 张剑韵; 黄龙全

    2010-01-01

    磷酸吡哆醇氧化酶(pyridoxine-5′-phosphate oxidase, PNPO)是维生素B6(VB6)代谢的关键酶.采用重组质粒pET32a(+)-PNPO原核表达家蚕(Bombyx mori)PNPO,经Ni2+亲和层析纯化后对其基本酶学性质进行分析.结果表明,纯化后的家蚕重组PNPO经SDS-PAGE鉴定为单一条带,比活力为529.81 nmol/(min·mg)蛋白,纯化倍数为7.1倍;该酶的最适反应温度为40 ℃,在50 ℃以下稳定;在pH 8.0~9.0之间酶活力最高,pH 6.0~10.0之间活力保持稳定.该结果有助于进一步开展家蚕PNPO的催化作用和表达调控机制的研究.

  14. Rapid determination of thiamine, riboflavin, niacinamide, pantothenic acid, pyridoxine, folic acid and ascorbic acid in Vitamins with Minerals Tablets by high-performance liquid chromatography with diode array detector.

    Science.gov (United States)

    Jin, Pengfei; Xia, Lufeng; Li, Zheng; Che, Ning; Zou, Ding; Hu, Xin

    2012-11-01

    A simple, isocratic, and stability-indicating high-performance liquid chromatography (HPLC) method has been developed for the rapid determination of thiamine (VB(1)), niacinamide (VB(3)), pyridoxine (VB(6)), ascorbic acid (VC), pantothenic acid (VB(5)), riboflavin (VB(2)) and folic acid (VB(9)) in Vitamins with Minerals Tablets (VMT). An Alltima C(18) column (250 mm × 4.6 mm i.d., 5 μm) was used for the separation at ambient temperature, with 50mM ammonium dihydrogen phosphate (adjusting with phosphoric acid to pH 3.0) and acetonitrile as the mobile phase at the flow rate of 0.5 ml min(-1). VB(1), VB(3), VB(6), VC and VB(5) were extracted with a solution containing 0.05% phosphoric acid (v/v) and 0.3% sodium thiosulfate (w/v), and were then simultaneously analyzed by using the mobile phase of phosphate buffer-acetonitrile (95:5, v/v), while VB(2) and VB(9) were extracted with a solution containing 0.5% ammonium hydroxide solution (v/v), and were then simultaneously analyzed by using the mobile phase of phosphate buffer-acetonitrile (85:15, v/v). The detection wavelengths were 275 nm for VB(1), VB(3), VB(6), VC, 210 nm for VB(5), and 282 nm for VB(2) and VB(9). The method showed good system suitability, sensitivity, linearity, specificity, precision, stability and accuracy. All the seven water-soluble vitamins were well separated from other ingredients and degradation products. Method comparison indicated good concordance between the developed method and the USP method. The developed method was reliable and convenient for the rapid determination of VB(1), VB(3), VB(6), VC, VB(5), VB(2) and VB(9) in VMT.

  15. Simultaneous determination of a ternary mixture of doxylamine succinate, pyridoxine hydrochloride, and folic acid by the ratio spectra-zero-crossing, double divisor-ratio spectra derivative, and column high-performance liquid chromatographic methods.

    Science.gov (United States)

    Pathak, Ashutosh; Rajput, Sadhana J

    2008-01-01

    Three simple, rapid, and accurate methods, i.e., the derivative ratio spectra-zero-crossing method (method I), double divisor-ratio spectra derivative method (method II), and column reversed-phase high-performance liquid chromatographic (RP-HPLC) method (method III) were developed for the simultaneous determination of doxylamine succinate (DOX), pyridoxine hydrochloride (PYR), and folic acid (FA) in their ternary mixtures and in tablets. In methods I and II, the calibration graphs were linear in the range of 2.5-80, 1.0-40, and 1.0-30 microg/mL for DOX, PYR, and FA, respectively. In the HPLC method, the separation of these compounds was performed using mobile phase consisting of 0.05 M phosphate buffer (pH 6.3)-methanol-acetonitrile (50 + 20 + 30, v/v/v), and UV detection was performed at 263 nm. Linearity was observed between the concentrations of the analytes and peak areas [correlation coefficient (r) > or =0.9998] in the concentration range of 1.0-200, 4.0-600, and 4.0-600 microg/mL for DOX, PYR, and FA, respectively. The standard deviation of retention time in method III was 0.011, 0.015, and 0.016 for DOX, PYR, and FA, respectively. The precision studies for all of the methods gave relative standard deviation values of <2%. The results obtained from the methods were statistically compared by means of Student's t-test and the variance ratio F-test. It was concluded that all of the developed methods were equally accurate, sensitive, and precise. These methods could be applied to determine DOX, PYR, and FA in their combined dosage forms.

  16. Scientific Opinion on the substantiation of a health claim related to a combination of thiamin, riboflavin, niacin, pantothenic acid, pyridoxine, D-biotin and pumpkin seed oil and maintenance of normal hair pursuant to Article 13(5 of Regulation (EC No 1924/2006

    Directory of Open Access Journals (Sweden)

    EFSA Panel on Dietetic Products, Nutrition and Allergies

    2012-07-01

    Full Text Available

    Following two applications from Nutrilinks Sarl, submitted pursuant to Article 13(5 of Regulation (EC No 1924/2006 via the Competent Authority of Belgium, the Panel on Dietetic Products, Nutrition and Allergies (NDA was asked to deliver an opinion on the scientific substantiation of a health claim related to a combination of thiamin, riboflavin, niacin, pantothenic acid, pyridoxine, D-biotin and pumpkin seed oil (Cucurbita pepo L. and maintenance of normal hair. The Panel considers that the specified combination is sufficiently characterised. The claimed effects are “contributes to reduce hair loss” and “increases the number of hair”. The target population proposed by the applicant is healthy adults in the general population. The Panel considers that maintenance of normal hair is a beneficial physiological effect. The applicant identified one publication as being pertinent to the health claim. This study did not use the food which is the subject of the claim. No conclusions can be drawn from this study for the scientific substantiation of the claim. The Panel concludes that a cause and effect relationship has not been established between the consumption of a combination of thiamin, riboflavin, niacin, pantothenic acid, pyridoxine, D-biotin and pumpkin seed oil (Cucurbita pepo L. and maintenance of normal hair.

  17. Electrochemical Behavior and Determination of Pyridoxine Hydrochloride at the Poly Nicotinic Acid Modified Electrode%盐酸吡哆辛在聚烟酸修饰电极上的电化学行为及测定

    Institute of Scientific and Technical Information of China (English)

    顾小燕; 唐鹏鹏; 李宁波; 刘欢; 俞静; 何凤云

    2014-01-01

    采用电聚合方法制备了聚烟酸修饰玻碳电极(PNA/GCE),并利用循环伏安法(CV)和差分脉冲伏安法(DPV)考察了盐酸吡哆辛(VB6)在该修饰电极上的电化学行为。结果表明,VB6在 PNA/GCE 上的氧化峰电流显著提高,电极反应为扩散控制的一电子两质子反应。利用差分脉冲伏安法对 VB6进行测定,线性范围为0.08~400μmol/L,VB6的检出限为0.02μmol/L,测定结果的相对标准偏差为3.1%(n=8),加标回收率为95.8%~103.7%。该方法可用于 VB6片中 VB6含量的测定。%Poly(nicotinic acid) modified electrode (PNA/GCE) was prepared and the electrochemical behavior of pyridoxine hydrochloride(VB6) was investigated at the modified electrode by cyclic voltammetry(CV) and differential pulse voltammetry(DPV). Results showed that the oxidation current of VB6 at the PNA/GCE was obviously larger than that at GCE. The oxidation process of VB6 was an irreversible diffusion–controlled process involving one electron and two protons. The liner range between the peak current of DPV and the concentration of VB6 was 0.08–400 μmol/L, and the detection limit was 0.02 μmol/L. The modified electrode showed a good reproducibility with a relative standard deviation of 3.1%(n=8). The recoveries were between 95.8% and 103.7%. The method can be applied to the analysis of vitamin B6 content in vitamin B6 tablets.

  18. Clinical analysis of pyridoxine-dependent epilepsy in a child and ALDH7A1 mutation%吡哆醇依赖性癫(癎)的临床及乙醛脱氢酶7家庭成员A1基因突变分析

    Institute of Scientific and Technical Information of China (English)

    杨志仙; 杨小玲; 王静敏; 张月华; 姜玉武; 秦炯

    2013-01-01

    目的 分析1例吡哆醇依赖性癫(癎)(PDE)的临床诊治过程及乙醛脱氢酶7家庭成员A1(ALDH7A1)基因突变特征.方法 对1例以早期癫(癎)起病的PDE患儿行临床诊治观察、神经电生理及神经影像学检查、以及ALDH7A1基因突变分析.结果 患儿出生2个月出现反复癫(癎)发作,多种抗癫(癎)药均不能控制发作,多次住院过程中在抗癫(癎)药治疗基础上给予吡哆醇静脉滴注使发作控制,出院后仅用抗癫(癎)药而未用吡哆醇维持治疗,癫(癎)发作分别在吡哆醇撤药后13 d、14 d及38 d出现复发,减停抗癫(癎)药物后仅单纯口服吡哆醇使发作完全控制.治疗前后多次EEG正常,头颅MRI检查正常.ALDH7A1基因检测发现1对新的复合杂合突变,第5外显子c.410G> A(p.G137E)和第11内含子IVS11 +1G>A剪切位点突变,其父携带G137E突变,其母携带IVS11 +1G>A突变.结论 本例癫(癎)发作早期起病、经吡哆醇治疗有效、撤药后复发临床提示了PDE的可能,ALDH7A1基因分析最终确诊了国内第1例PDE,本例携带的2个基因突变位点均为国际未报道的新位点.%Objective To analyze clinical diagnosis and treatment,aldehyde dehydrogenase 7 family member A1 (ALDH7A1) gene mutations in 1 Chinese child with pyridoxine dependent epilepsy(PDE).Methods The clinical manifestations and course of treatment were observed in a PDE patient with early epilepsy onset.Video-electroencephalogram(VEEG) and magnetic resonance imaging (MRI) were performed.The mutations of ALDH7A1 gene were examined.Results At the age of 2 months,recurrent epileptic seizures occurred and the child was resistant to antiepileptic drugs.Patient hospitalized several times due to frequent seizures and pyridoxine was used intravenously for several days.For each hospital stay,the frequent seizures were controlled completely under the treatment of pyridoxine and antiepileptic drugs.Seizures recurred at intervals of 13,14 and 38 days due to

  19. Pyridoxine-responsive seizures as the first symptom of infantile hypophosphatasia caused by two novel missense mutations (c.677T>C, p.M226T; c.1112C>T, p.T371I) of the tissue-nonspecific alkaline phosphatase gene.

    Science.gov (United States)

    Baumgartner-Sigl, Sara; Haberlandt, Edda; Mumm, Steven; Scholl-Bürgi, Sabine; Sergi, Consolato; Ryan, Lawrence; Ericson, Karen L; Whyte, Michael P; Högler, Wolfgang

    2007-06-01

    Pyridoxine-responsive seizures (PRS) and the role of pyridoxine (PN, vitamin B(6)) in hypophosphatasia (HPP) are incompletely understood. Typically, PRS and HPP are rare, independent, metabolic disorders. In PRS, seizures resist standard anticonvulsants apart from PN, yet have a good prognosis. In HPP, inactivation of the tissue nonspecific isoenzyme of alkaline phosphatase (TNSALP) impairs skeletal mineralization and causes rickets in infants that can be fatal. Here, we report a 7-month-old girl, newly diagnosed with infantile HPP, who presented as a neonate with PRS but without bony abnormalities. Analysis of biogenic amines in cerebrospinal fluid (CSF) suggested brain pyridoxal 5'-phosphate (PLP) deficiency, although PLP in CSF was not decreased. She had normal cognitive milestones but failure to thrive and rickets. Nearly undetectable serum ALP activity, elevated plasma PLP and urinary phosphoethanolamine (PEA) and inorganic pyrophosphate (PPi) levels, hypercalcemia, hypercalciuria and nephrocalcinosis were consistent with infantile HPP. Only prednisolone reduced serum calcium levels. Despite improved growth and weight gain, she developed rib fractures and died from respiratory failure at age 9 months. Sequence analysis of the TNSALP gene revealed novel missense mutations in exon 7 (c.677T>C, p.M226T) and exon 10 (c.1112C>T, p.T371I). Our patient demonstrated that PRS in neonates may not necessarily be "idiopathic"; instead, such seizures can be caused by severe HPP that becomes clinically apparent later in infancy. The pathophysiology of PRS in HPP differs from the three other genetic defects known to cause PRS, but all may lead to brain PLP deficiency reducing seizure thresholds. All reported HPP patients with neonatal seizures died within 18 months of birth, suggesting that PRS is an indicator of HPP severity and lethal prognosis. We recommend that assessment of any neonate with PRS should include measurement of serum ALP activity.

  20. 21 CFR 184.1676 - Pyridoxine hydrochloride.

    Science.gov (United States)

    2010-04-01

    ... hydrochloride that is prepared by chemical synthesis. (b) The ingredient meets the specifications of the Food... chapter; meat products as defined in § 170.3(n)(29) of this chapter; milk products as defined in § 170.3(n)(31) of this chapter; plant protein products as defined in § 170.3(n)(33) of this chapter; and...

  1. Site-directed mutation of pyridoxine 5'-phosphate oxidase from Bombyx mori and activity assay of the mutants in vitro%家蚕磷酸吡哆醇氧化酶的体外定点突变及其活性鉴定

    Institute of Scientific and Technical Information of China (English)

    童宁; 张剑韵; 黄龙全

    2011-01-01

    [目的]研究家蚕Bombyx mori磷酸吡哆醇氧化酶(pyridoxine 5’-phosphate oxidase,PNPO)个别保守氨基酸残基对PNPO酶活性的影响.[方法]用重叠延伸法把氨基酸残基Lys111 (AAA)突变为Glu (GAA),Ser160(AGC)定点突变为Ala(GCC);构建重组表达载体,在大肠杆菌Escherichia coli Rosetta中诱导表达,经亲和纯化后进行酶活鉴定.[结果]重组蛋白的分子量约为45.0 kDa.体外酶活分析发现,家蚕氨基酸残基Lys111突变体K11lE活性降低了约78.0%,Ser160突变体S160A的活性降低了67.4%.[结论]结果提示氨基酸残基Lys111和Ser160对维持家蚕PNPO的酶活性有重要作用.本研究明确了家蚕磷酸吡哆醇氧化酶个别保守氨基酸残基的酶学功能.%[Aim] To study the effects of single conserved amino acid residue of pyridoxine 5'-phosphate oxidase (PNPO) from Bombyx mori on its activity. [Methods] Lys111 (AAA) and Ser160 (AGC) , two of the most conserved residues, were mutated to Glu ( GAA) and Ala ( GCC ) by using over-lap extension, respectively. The obtained expression plasmids were over-expressed in Escherichia coli Rosetta by IPTG induction, and then the expressed products were purified with affinity chromatography and the activity of the purified PNPO were determined. [ Results ] The molecular mass of the target recombinant protein was ~45.0 kDa. Compared with the wild type PNPO, the activities of the mutants K111E and S160A were reduced by 78.0% and 67.4% , respectively. [ Conclusion] The results suggest that the residues Lys and Ser are important to maintain the activity of PNPO. This study confirms the significance of single conserved amino acid residues on the catalytic function of PNPO of B. Mori.

  2. Aplicação de métodos de calibração multivariada para a determinação simultânea de riboflavina (VB2, tiamina (VB1, piridoxina (VB6 e nicotinamida (VPP UV spectrophotrometry and chemometrics methods for simultaneous determinations of riboflavin (VB2, thiamine (VB1, pyridoxine (VB6 and nicotinamide (VPP

    Directory of Open Access Journals (Sweden)

    Rosângela C. Barthus

    2007-01-01

    Full Text Available In this work, the artificial neural networks (ANN and partial least squares (PLS regression were applied to UV spectral data for quantitative determination of thiamin hydrochloride (VB1, riboflavin phosphate (VB2, pyridoxine hydrochloride (VB6 and nicotinamide (VPP in pharmaceutical samples. For calibration purposes, commercial samples in 0.2 mol L-1 acetate buffer (pH 4.0 were employed as standards. The concentration ranges used in the calibration step were: 0.1 - 7.5 mg L-1 for VB1, 0.1 - 3.0 mg L-1 for VB2, 0.1 - 3.0 mg L-1 for VB6 and 0.4 - 30.0 mg L-1 for VPP. From the results it is possible to verify that both methods can be successfully applied for these determinations. The similar error values were obtained by using neural network or PLS methods. The proposed methodology is simple, rapid and can be easily used in quality control laboratories.

  3. 左旋精氨酸与维生素B6对低密度脂蛋白抑制兔胸主动脉内皮舒张功能的影响%Effect of LDL on the Endothelium of Rabbit Aortic Rings by L-arginine and Pyridoxine

    Institute of Scientific and Technical Information of China (English)

    刁建欣; 韩艺; 黄艳; 许逸; 季勇

    2004-01-01

    目的:观察正常人的低密度脂蛋白(native low density lipoprotein,nLDL),人工氧化的低密度脂蛋白(oxidized lowdensity lipoprotein,ox-LDL)及非胰岛素依赖型糖尿病(Non-insulin dependent diabetes mellitus,MDDM)患者的低密度脂蛋白(diabetic low density lipoprotein,dLDL)对兔胸主动脉环内皮的损伤作用及左旋精氨酸(L-arginine,L-Arg),维生素B6(pyridoxine,VB6)的拮抗效应.方法:采用离体动脉环灌流的方法,观察兔胸主动脉环对乙酰胆碱(acetycholine,Ach),钙离子载体A23187的舒张反应.结果:3种LDL均抑制动脉环对Ach及A23187的舒张,损伤强度为ox-LDL>dLDL>nLDL,并具有浓度依赖性;L-Arg、VB6能明显拮抗LDL的抑制作用,但并不能完全逆转.以SOD作为保护药对照,250 U/ml的浓度能够显著抑制dLDL对内皮的损伤.结论:3种低密度脂蛋白主要可能通过降低NO生物活性损伤内皮,L-Arg、VB6具有内皮保护作用.

  4. 吡哆醇依赖性癫痫的临床和遗传学特点及尿液哌啶酸的检测%Clinical and genetic characteristics and detection of urinary pipecolic acid in pyridoxine dependent epilepsy

    Institute of Scientific and Technical Information of China (English)

    薛姣; 杨志仙; 李慧; 钱萍; 吴晔; 姜玉武; 刘晓燕

    2016-01-01

    Objective To analyze the clinical and genetic characteristics of patients with pyridoxine dependent epilepsy (PDE),and build a method to detect and analyze the concentration of urinary pipecolic acid in PDE patients receiving pyridoxine treatment.Method Twelve patients (8 were male,4 were female) were diagnosed as PDE in Peking University First Hospital between April 2012 and September 2015.The clinical manifestations,diagnosis and treatment process,video-electroencephalogram,magnetic resonance imaging were retrospectively analyzed.ALDH7A1 gene was detected using Sanger sequencing or targeted next-generation sequencing.The concentration of urinary pipecolic acid in PDE patients was detected with gas chromatography-mass spectrometry (GC-MS),as well as in some non-PDE children served as normal control.All controls,58 cases totally,were neonates born in our hospital or children came to our hospital for reasons such as syncope (without disturbing pipecolic acid metabolism) from November 2015 to January 2016.Of them,25 were ≤6 months old(14 were male,11 were female),33 were >6 months old (14 were male,19 were female).The Student's t-test or Mann-Whitney U test was used for comparing the pipecolic acid between the two groups.Correlation analysis was conducted using Pearson or Spearman test.Result Of the 12 patients,seven of them were abnormal at birth.The age of epilepsy onset was from 5 h to 5 months,within 10 d in 8 patients.After a diagnostic delay time of 15 d to 20 months,seizures in all patients were controlled by pyridoxine monotherapy,at a dose of higher than 10.0 mg/(kg · d) in 10 patients,and 8.5 and 2.5 mg/(kg · d) in the other 2 patients respectively.The range of maintenance dose was 2.5-20.0 mg/(kg · d) during the follow up.Interictal electroencephalogram showed nonspecific abnormality in 10,normal in 2.Brain magnetic resonance imaging showed nonspecific abnormality in 7,normal in 5.ALDH7A1 mutations were found in all patients,including 15 different

  5. 盐酸吡哆辛在石墨烯-碳纳米管/聚烟酸复合修饰电极上的电化学行为研究及其测定%Electrochemical Behavior and Determination of Pyridoxine Hydrochloride at Graphene-Carbon Nanotubes/Poly(nicotinic acid) Modified Electrode

    Institute of Scientific and Technical Information of China (English)

    何凤云; 俞静; 刘欢; 顾小燕; 唐鹏鹏; 周宏; 陈昌云; 陆国飞

    2014-01-01

    Graphene ( GN) and multiwalled carbon nanotubes ( MWCNT) composites were coated on glassy carbon electrode ( GCE ) and then poly ( nicotinic acid ) ( PNA ) was electrodeposited on the modified electrode. The electrochemical behavior of pyridoxine hydrochloride ( VB6 ) was investigated at the modified electrode by cyclic voltammetry ( CV ) and differential pulse voltammetry ( DPV ) . Results showed the oxidation current of VB6 at the GN-MWCNT/PNA/GCE was obviously larger than that at GCE, PNA/GCE and GN/MWCNT/GCE. The oxidation process of VB6 was an irreversible diffusion-controlled process involving one electron and two protons. The liner range between the peak current intensity of DPV and the concentration of VB6 was 0 . 05-200 μmol/L with a detection limit of 0 . 02 μmol/L ( S/N=3 ) . The modified electrode showed a good reproducibility with a relative standard deviation of 3 . 1% ( n=8 ) . The proposed method was applied to the analysis of vitamin B6 in vitamin B6 tablets and compound vitamin B tablets with recoveries between 96 . 1%-104 . 5%.%通过滴涂和电聚合的方法制备了石墨烯( GN)-多壁碳纳米管( MWCNTs)/聚烟酸( PNA)修饰玻碳电极。利用循环伏安法和差分脉冲伏安法考察了盐酸吡哆辛( VB6)在此修饰电极上的电化学行为和测定方法。结果表明,VB6在此修饰电极上有一明显的不可逆氧化峰(Epa=1.049 V),该电极与 GCE、PNA/GCE以及GN/MWCNT/GCE相比,VB6的氧化峰电流显著提高,电极反应为扩散控制的一电子两质子反应。利用差分脉冲伏安法对VB6进行测定,线性范围为0.05~200μmol/L,检出限为0.02μmol/L,相对平均偏差为3.1%(n=8)。本方法可用于测定VB6片和B族维生素片中的VB6含量测定,加标回收率为在96.1%~104.5%之间。

  6. 大剂量吡哆醇对大鼠睾丸一氧化氮合酶和细胞凋亡的影响%Effcet of high-dose pyridoxine on nitric oxide synthase and apoptosis of rat testis

    Institute of Scientific and Technical Information of China (English)

    闫蓓; 李积胜; 刘亚华; 杨烽

    2006-01-01

    [Objective] To study the changes of testis nitric oxide synthase (NOS) and apoptosis in high dose pyridoxine (PN) for the understanding of the molecular mechanism of high dose PN injurious action on the development and function oftestis. [Methods] DNA and RNA of testicular cells were stained in situ with nick translation (ISNT) technique.[Results] Comparing with the control guoup, the testes demonstrated only very slight histopathological changes in NOS positive leydig cells after a 3 days PN treatment. The 7 days PN treatment caused obvious decrease in the staining of the testis cellular DNA and RNA, distinctive increase of NOS reactive density under the fluorescent light microscope, and significantly higher number of apoptotic testis spermatogenic cells (38.41 ± 8.20) in comparison with the control group ( 11.39 ± 4.86), ( P < 0.01 ). [ Conclusion] It is concluded that high dose of PN treatment could accelerate the apoptosis of testicular cells and the activity of NOS positive cells, which might be one of the molecular mechanisms of the injurious action of high dose PN on the development and function of the testis.%[目的]为探讨大剂量吡哆醇(PN)对睾丸结构和功能损害的分子机制,研究其对睾丸一氧化氮合酶(NOS)和细胞凋亡的影响.[方法]实验采用吖啶橙荧光染色法显示睾丸细胞DNA和RNA,黄递酶(NADPHd)组织化学法显示睾丸细胞NOS,采用原位缺口平移技术检测睾丸生精细胞凋亡的数目.[结果]与对照组相比,注射PN 3 d,大鼠睾丸间质细胞NOS反应活性明显增强,睾丸生精细胞凋亡数目(38.41±8.20)较相应对照组(11.39±4.86)明显增多,差异有显著性(P<0.01).[结论]提示大剂量PN腹腔注射后,大鼠睾丸细胞NOS活性和凋亡细胞数目明显增加,这些变化可能是PN损害睾丸结构和功能的分子机制之一.

  7. Changes in the transcriptional levels of pyridoxal kinase and pyridoxine-5'-phosphate oxidase post exogenous hormone treatment in the silkworm,Bombyx mori%外源激素处理后家蚕吡哆醛激酶和磷酸吡哆醇氧化酶转录水平的变化

    Institute of Scientific and Technical Information of China (English)

    杨欢欢; 姚丽丽; 张剑韵; 黄龙全

    2015-01-01

    [目的] 研究家蚕Bombyx mori经蜕皮激素(20-hydroxyecdysone,20-E)和保幼激素类似物(juvenile hormone analogue,JHA)处理后引起吡哆醛激酶(pyridoxal kinase,PLK)和磷酸吡哆醇氧化酶(pyridoxine-5'-phosphateoxidase,PNPO)的转录水平变化,为进一步研究激素对蚕体营养代谢等工作奠定基础.[方法]以20-E和JHA分别喂食不同发育时期(5龄第1,3和5天)的家蚕幼虫,以喂食蒸馏水的家蚕为对照,采用实时荧光定量PCR(real-time quantitative PCR)方法在处理后24和48 h对各组幼虫后部丝腺中PLP合成酶PLK和PNPO的转录水平进行分析.[结果]5龄第1天幼虫经20-E处理24和48 h后,PLK和PNPO的转录水平出现上调且与对照的差异达到极显著(P<0.01);5龄第3天幼虫经20-E处理,PLK的转录水平在48 h出现下调且与对照的差异达到显著(P<0.05),PNPO的转录水平在24和48 h均出现上调且与对照的差异达到极显著(P<0.01);5龄第5天幼虫经20-E处理后PLK和PNPO的转录水平无变化.5龄第1天幼虫经JHA处理后PLK和PNPO的转录水平未受到影响;5龄第3天幼虫经JHA处理后,PLK的转录水平在48 h出现显著下调且与对照的差异达到显著(P<0.05),PNPO的转录水平在24和48 h后均出现显著下调且与对照的差异达到极显著(P<0.05);5龄第5天幼虫经JHA处理24和48 h后,PLK和PNPO的转录水平出现下调且与对照的差异达到极显著(P<0.01).[结论]20-E和JHA显著影响家蚕5龄幼虫PLK和PNPO的转录水平,20-E提高5龄前期家蚕PLK和PNPO的转录水平,JHA降低5龄后期它们的转录水平,为深入研究激素对VB6的调控奠定基础.

  8. Study on fluorescence spectra of thiamine, riboflavin and pyridoxine

    Science.gov (United States)

    Yang, Hui; Xiao, Xue; Zhao, Xuesong; Hu, Lan; Lv, Caofang; Yin, Zhangkun

    2016-01-01

    This paper presents the intrinsic fluorescence characteristics of vitamin B1, B2 and B6 measured with 3D fluorescence Spectrophotometer. Three strong fluorescence areas of vitamin B2 locate at λex/λem=270/525nm, 370/525nm and 450/525nm, one fluorescence areas of vitamin B1 locates at λex/λem=370/460nm, two fluorescence areas of vitamin B6 locate at λex/λem=250/370nm and 325/370nm were found. The influence of pH of solution to the fluorescence profile was also discussed. Using the PARAFAC algorithm, 10 vitamin B1, B2 and B6 mixed solutions were successfully decomposed, and the emission profiles, excitation profiles, central wavelengths and the concentration of the three components were retrieved precisely through about 5 iteration times.

  9. Pyridoxine deficiency affects biomechanical properties of chick tibial bone

    Science.gov (United States)

    Masse, P. G.; Rimnac, C. M.; Yamauchi, M.; Coburn, S. P.; Rucker, R. B.; Howell, D. S.; Boskey, A. L.

    1996-01-01

    The mechanical integrity of bone is dependent on the bone matrix, which is believed to account for the plastic deformation of the tissue, and the mineral, which is believed to account for the elastic deformation. The validity of this model is shown in this study based on analysis of the bones of vitamin B6-deficient and vitamin B6-replete chick bones. In this model, when B6-deficient and control animals are compared, vitamin B6 deficiency has no effect on the mineral content or composition of cortical bone as measured by ash weight (63 +/- 6 vs. 58 +/- 3); mineral to matrix ratio of the FTIR spectra (4.2 +/- 0.6 vs. 4.5 +/- 0.2), line-broadening analyses of the X-ray diffraction 002 peak (beta 002 = 0.50 +/- 0.1 vs. 0.49 +/- 0.01), or other features of the infrared spectra. In contrast, collagen was significantly more extractable from vitamin B6-deficient chick bones (20 +/- 2% of total hydroxyproline extracted vs. 10 +/- 3% p < or = 0.001). The B6-deficient bones also contained an increased amount of the reducible cross-links DHLNL, dehydro-dihydroxylysinonorleucine, (1.03 +/- 0.07 vs. 0.84 +/- 0.13 p < or = 0.001); and a nonsignificant increase in HLNL, dehydro-hydroxylysinonorleucine, (0.51 +/- 0.03 vs. 0.43 +/- 0.03, p < or = 0.10). There were no significant changes in bone length, bone diameter, or area moment of inertia. In four-point bending, no significant changes in elastic modulus, stiffness, offset yield deflection, or fracture deflection were detected. However, fracture load in the B6-deficient animals was decreased from 203 +/- 35 MPa to 151 +/- 23 MPa, p < or = 0.01, and offset yield load was decreased from 165 +/- 9 MPa to 125 +/- 14 MPa, p < or = 0.05. Since earlier histomorphometric studies had demonstrated that the B6-deficient bones were osteopenic, these data suggest that although proper cortical bone mineralization occurred, the alterations of the collagen resulted in changes to bone mechanical performance.

  10. Antihypertensive and neuroprotective actions of pyridoxine and its derivatives.

    Science.gov (United States)

    Dakshinamurti, Shyamala; Dakshinamurti, Krishnamurti

    2015-12-01

    Vitamin B6 plays a crucial role in the nervous system as the amino acid decarboxylases involved in the synthesis of all putative neurotransmitters requires the coenzyme pyridoxal phosphate. Vitamin B6 in its various forms has antioxidant properties. Pyridoxal phosphate has a role in regulating cellular calcium transport through both the voltage-mediated and ATP-mediated purinergic mechanisms of cellular calcium influx and, hence, has a role in the control of hypertension. Pharmacological doses of vitamin B6 appear to decrease the high blood pressure associated with both genetic and nongenetic models of hypertension. Vitamin B6 has a crucial role in the normal function of the central and peripheral nervous systems. It also protects against ischemia and glutamate-induced neurotoxicity.

  11. Pyridoxine hydrochloride treatment of carpal tunnel syndrome: a review.

    Science.gov (United States)

    Aufiero, Elaine; Stitik, Todd P; Foye, Patrick M; Chen, Boqing

    2004-03-01

    It has been hypothesized that idiopathic carpal tunnel syndrome (CTS) is a manifestation of vitamin B6 deficiency. Some claim that B6 supplementation can alleviate symptoms. Others argue that pain relief occurs because of vitamin B6's anti-nociceptive properties or because B6 supplementation addresses an unrecognized peripheral neuropathy. Few studies on CTS and B6 employed electrodiagnostic techniques in diagnosis, and few showed a correlation between symptoms and improved electrodiagnostic parameters with supplementation. Other studies failed to measure or estimate B6 levels. Nevertheless, it appears reasonable to recommend vitamin B6 supplementation to people with CTS. Some patients will improve symptomatically with low risks of toxicity in recommended doses.

  12. [Pyridoxine (vitamin B6) influence on endogenic melatonin production during the experiment].

    Science.gov (United States)

    2007-12-01

    The purpose of the study was to investigate the role of vitamin B6 in the process of melatonin biosynthesis. 30 laboratory white rats were divided into two groups - experimental and control groups. The animals in the first group were treated with vitamin B6 injection. Every other day at 22 00, melatonin concentration was defined by means of ELISA. The experiment has lasted for two months. At the end of the experiment, the plasma level of melatonin increased by 35,95% in the first group of animals in comparison with the second control group. It is found that, B6 vitamin injections strengthens melatonin biosynthesis; consequently strengthening of melatonin biosynthesis influences positive therapeutic effects,; one of the reasons for pathological processes, developed in organism on the background of B6 vitamin deficiency, is reduction of endogen melatonin production.

  13. Neuroprotection of Grape Seed Extract and Pyridoxine against Triton-Induced Neurotoxicity

    Directory of Open Access Journals (Sweden)

    Heba M. Abdou

    2016-01-01

    Full Text Available Triton WR-1339 administration causes neurotoxicity. Natural products and herbal extracts can attenuate cerebral injury. In the present study, we investigated the neuroprotective role of grape seed extract and/or vitamin B6 against triton-induced neurotoxicity. Thirty-five adult male albino rats of the Sprague-Dawley strain, weighing 140–145 g, were divided into five groups: control, triton, grape seed extract + triton, grape seed extract + triton + vitamin B6, and vitamin B6 + triton. The hematological and biochemical analyses were carried out. Alteration in iNOS mRNA gene expression was determined using reverse-transcriptase PCR analysis. In addition, qualitative DNA fragmentation was examined using agarose gel electrophoresis. Triton-treatment caused significant disturbances in the hematological parameters, the neurological functions, and the antioxidant profile. Also, triton significantly increased the iNOS mRNA expression and DNA damage. Our results showed that grape seed extract and/or vitamin B6 could attenuate all the examined parameters. These natural substances could exhibit protective effects against triton-induced neurological damage because of their antioxidative and antiapoptotic capacities.

  14. Infantile Hypophosphatasia Secondary to a Novel Compound Heterozygous Mutation Presenting with Pyridoxine-Responsive Seizures

    OpenAIRE

    2013-01-01

    Hypophosphatasia (HPP) is a rare metabolic disease with the hallmark finding of deficient serum tissue nonspecific alkaline phosphatase (TNSALP) activity. TNSALP is primarily known for its role in mineralization; hence, HPP is characterized by defective mineralization of bone and/or teeth. TNSALP is also necessary for proper vitamin B6 metabolism and its participation as a cofactor for neurotransmitters in the central nervous system. Defective TNSALP activity in the brain can result in intrac...

  15. Synthesis of Pyridoxine Hydrochloride%盐酸吡哆醇的合成

    Institute of Scientific and Technical Information of China (English)

    英智威; 段梅莉; 冀亚飞

    2009-01-01

    L-丙氨酸、过量草酸和乙醇在苯中同步进行乙酯化和草酰化制得N-乙氧草酰基-L-丙氨酸乙酯,再经环合、水解、脱羧制得4-甲基-5-乙氧基噁唑,进而与马来酸二乙酯经Diels-Alder加成、芳构化、还原后成盐得到维生素B6吡哆醇盐酸盐,总收率为56%.

  16. Synthesis of pyridoxine dipalmitate%吡哆醇二棕榈酸酯的合成

    Institute of Scientific and Technical Information of China (English)

    郭雪飞; 廖发盆; 黄小华

    2006-01-01

    采用吡哆醇与棕榈酸为原料,水溶剂法合成吡哆醇二棕榈酸酯.通过正交实验得到适宜的反应条件为:棕榈酰氯与吡哆醇的质量比为2:1,反应温度16℃,反应时间20 h,以吡哆醇计产率58.4%,纯度88.9%.

  17. Pyridoxine-dependent seizures%吡哆醇依赖性癫痫

    Institute of Scientific and Technical Information of China (English)

    杨斌; 叶小飞

    2008-01-01

    吡哆醇依赖性癫痫(PDS)是一种少见的常染色体遗传性疾病,也是婴幼儿期发病的难治性癫痫之一。该病在50多年前已被人们所了解,但其致病机制目前仍不十分清楚。PDS发病率一般认为1:500000左右,但实际发病率很可能高于此比例,可能有与很多临床病例未被明确诊断有关。本文就该病的病因学、临床表现、实验室检查、分子生物学研究进展作一简要综述。

  18. Pyridoxin-responsive anaemia in a patient with a history of polycythaemia vera

    NARCIS (Netherlands)

    vanGameren, [No Value; Wijnja, L; Louwes, H; deWolf, JTM

    1997-01-01

    Pancytopenia in the course of polycythaemia vera (PV) following the proliferative and stable phase, ultimately leads to a spent phase characterized by extensive marrow fibrosis. We describe a patient with a history of PV and pancytopenia caused by myelodysplasia, before a genuine end stage myelofibr

  19. [Hemochromatotic cirrhosis complicating pyridoxine-sensitive hereditary sideroblastic anemia. Case report].

    Science.gov (United States)

    Abadia, R; Rochant, H; Levy, V G

    1983-01-01

    A further case of sporadic congenital sideroblastic anaemia is reported. Despite no contributing factors such as blood transfusion, oral ingestion of iron or alcoholic beverages, were present excessive iron stores occurred with consecutive tissue damage resulting in cirrhosis of the liver, portal hypertension and diabetes mellitus. HLA phenotype was A3 B7 as in primary hemochromatosis. Correction of anemia was obtained by vitamin B6 administration. Improvement of iron overload was achieved through the use of daily subcutaneous infusions of the iron chelating drug desferrioxamine with a portable infusion pump.

  20. Pyridoxin-responsive anaemia in a patient with a history of polycythaemia vera

    NARCIS (Netherlands)

    vanGameren, [No Value; Wijnja, L; Louwes, H; deWolf, JTM

    1997-01-01

    Pancytopenia in the course of polycythaemia vera (PV) following the proliferative and stable phase, ultimately leads to a spent phase characterized by extensive marrow fibrosis. We describe a patient with a history of PV and pancytopenia caused by myelodysplasia, before a genuine end stage myelofibr

  1. Fenugreek seed extract treats peripheral neuropathy in pyridoxine induced neuropathic mice

    OpenAIRE

    2013-01-01

    Trigonella foenum graecum commonly known as Fenugreek exerts normoglycemic and insulinotropic effects in humans by compounds from its seed and leaf extracts. Some studies reported that treating pregnant mice with fenugreek seed could cause toxic effects on the nervous system of its pubs during developmental growth, while in some other studies neuroprotective properties were considered for it. Safety of anti-diabetic drugs for nervous system is very important because peripheral neuropathy is a...

  2. Drug: D04913 [KEGG MEDICUS

    Lifescience Database Archive (English)

    Full Text Available D04913 Mixture, Drug Thiamine chloride hydrochloride - pyridoxine hydrochloride - cyanocobalamin...3179 Others D04913 Thiamine chloride hydrochloride - pyridoxine hydrochloride - cyanocobalamin mixt PubChem: 17398216 ...

  3. Drug: D04917 [KEGG MEDICUS

    Lifescience Database Archive (English)

    Full Text Available D04917 Mixture, Drug Octotiamine - riboflavin - pyridoxine hydrochloride - cyanocobalamin...9 Others D04917 Octotiamine - riboflavin - pyridoxine hydrochloride - cyanocobalamin mixt PubChem: 17398219 ...

  4. A missense mutation in the cystathionine {beta}-synthase (CBS) gene associated with pyridoxine (B{sub 6}) responsive homocystinuria

    Energy Technology Data Exchange (ETDEWEB)

    Shih, V.E.; Fringer, J.M.; Mandell, R. [Massachusetts General Hospital, Boston, MA (United States)] [and others

    1994-09-01

    CBS deficiency is an autosomal recessive disorder characterized by homocystinuria and multisystem clinical disease. B{sub 6} responsive patients usually have a milder clinical phenotype than B{sub 6} nonresponsive patients. In our ongoing studies of the molecular defects in CBS deficiency, we reported a T-833 to C transition causing a substitution of threonine for isoleucine at position 278 (I278T). By PCR amplification and sequencing of exon 8 from genomic DNA we have now identified 2 index patients who are homozygous and 5 who are heterozygous for this mutation in a group of 32 patients with CBS deficiency. The mutation was detected in 7 of 10 unrelated families with in vivo B{sub 6} responsiveness, including one with a partial response, and in 0 of 22 B{sub 6} nonresponsive patients. The mutations on the other allele in the compound heterozygotes are still under investigation. We have now observed the I278T mutation in 9 of 20 independent alleles of varied ethnic backgrounds in the subgroup of B{sub 6} responsive patients. These findings, together with the previous report of this mutation in one allele of a B{sub 6} responsive patient, suggest that the I278T mutation is associated with B{sub 6} responsiveness in CBS deficiency. In compound heterozygotes, the degree of B{sub 6} responsiveness may also depend upon the nature of the other mutant allele and/or the interaction between the polypeptide subunits produced by the two mutant allelic genes.

  5. Phosphorimetric Assay of Pyridoxine%吡哆辛的光分析法及应用

    Institute of Scientific and Technical Information of China (English)

    黄如衡

    2001-01-01

    吡哆辛(VB6)在碱液中有强的光(λex316 nm,λem444 nm,寿命1.8 s),经紫外光照射后光消失.光照前后光强度差(Δ P)与吡哆辛含量呈线性关系.建立了吡哆辛的低温光分析法,并应用于制剂及一些生物组织中吡哆辛含量分析.

  6. Chemical stability study of vitamins thiamine, riboflavin, pyridoxine and ascorbic acid in parenteral nutrition for neonatal use

    Directory of Open Access Journals (Sweden)

    Cabral Lúcio M

    2011-05-01

    Full Text Available Abstract Background The objective of this work was to study the vitamins B1, B2, B6 and C stability in a pediatric formulation containing high amounts of calcium in the presence of organic phosphate, amino acids, glucose, sodium chloride, magnesium sulfate, pediatric vitamins and trace elements under different conditions using developed and validated analytical methods. Methods The study was carried out during 72 h with formulations packaged in recommended storage temperature (4°C and 25°C, with and without photoprotection. Results The results showed that the methodologies used for assessing the chemical stability of vitamins B1, B2, B6 and C in the formulation were selective, linear, precise and accurate. The vitamins could be considered stable in the formulation during the three days of study if stored at 4°C. When stored at 25°C vitamin C presented instability after 48 h. Conclusion The pediatric formulation containing high amount of calcium in the presence of organic phosphate, amino acids, glucose, sodium chloride, magnesium sulphate, pediatric vitamins and trace elements packaged in bag-type trilaminate presented a shelf life of the 72 h, when maintained under refrigeration, between 2°C and 8°C. This shelf life was measured considering the vitamins studied. Further studies are needed including all the vitamins present in this formulation.

  7. Pyridoxine (Vitamin B6) and the Glutathione Peroxidase System; a Link between One-Carbon Metabolism and Antioxidation

    Science.gov (United States)

    Dalto, Danyel Bueno; Matte, Jean-Jacques

    2017-01-01

    Vitamin B6 (B6) has a central role in the metabolism of amino acids, which includes important interactions with endogenous redox reactions through its effects on the glutathione peroxidase (GPX) system. In fact, B6-dependent enzymes catalyse most reactions of the transsulfuration pathway, driving homocysteine to cysteine and further into GPX proteins. Considering that mammals metabolize sulfur- and seleno-amino acids similarly, B6 plays an important role in the fate of sulfur-homocysteine and its seleno counterpart between transsulfuration and one-carbon metabolism, especially under oxidative stress conditions. This is particularly important in reproduction because ovarian metabolism may generate an excess of reactive oxygen species (ROS) during the peri-estrus period, which may impair ovulatory functions and early embryo development. Later in gestation, placentation raises embryo oxygen tension and may induce a higher expression of ROS markers and eventually embryo losses. Interestingly, the metabolic accumulation of ROS up-regulates the flow of one-carbon units to transsulfuration and down-regulates remethylation. However, in embryos, the transsulfuration pathway is not functional, making the understanding of the interplay between these two pathways particularly crucial. In this review, the importance of the maternal metabolic status of B6 for the flow of one-carbon units towards both maternal and embryonic GPX systems is discussed. Additionally, B6 effects on GPX activity and gene expression in dams, as well as embryo development, are presented in a pig model under different oxidative stress conditions. PMID:28245568

  8. Aromatic Amino Acid Decarboxylase Deficiency Not Responding to Pyridoxine and Bromocriptine Therapy: Case Report and Review of Response to Treatment

    OpenAIRE

    2014-01-01

    Aromatic L-amino acid decarboxylase (AADC) deficiency (MIM #608643) is an autosomal recessive inborn error of monoamines. It is caused by a mutation in the DDC gene that leads to a deficiency in the AADC enzyme. The clinical features of this condition include a combination of dopamine, noradrenaline, and serotonin deficiencies, and a patient may present with hypotonia, oculogyric crises, sweating, hypersalivation, autonomic dysfunction, and progressive encephalopathy with severe developmental...

  9. Does use of oral contraceptives enhance the toxicity of carbon disulfide through interactions with pyridoxine and tryptophan metabolism?

    Science.gov (United States)

    Calabrese, E J

    1980-01-01

    It is proposed that oral contraceptive (OC) users are at increased risk to experiencing adverse psychological disorders (e.g. irritability, depression) from exposures to elevated levels of carbon disulfide (CS2). This theory is based on studies indicating that both OCs and CS2 induce either a vitamin B6 deficiency and/or enhance its requirement. Since disruptions of B6 metabolism are thought to explain, at least in part, the adverse psychological effects of OCs and CS2, it is speculated that joint exposure to these substances may result in an exaggerated disruption of B6 metabolism with the development of CS2 induced adverse psychological effects occurring at exposure levels below those normally associated with adverse effects.

  10. Pyridoxine neuropathy: correlation of functional tests and neuropathology in beagle dogs treated with large doses of vitamin B6.

    Science.gov (United States)

    Schaeppi, U; Krinke, G

    1982-10-01

    Neurologic examination, electrophysiologic testing and microscopic post-mortem examination was used to study the neuropathy induced in the beagle dog by administration of excessive amounts of vitamin B6. Two female dogs received repeated daily oral doses of 3 g. The treatment was ceased when the dogs developed severe general morbidity, including uncoordinated gait and abnormal neurologic symptoms. The symptoms were most severe during and early after cessation of treatment, and in general they regressed during the subsequent 2 months of treatment-free observation. Sensory central and peripheral maximum nerve conduction velocity started to decrease after a considerable delay; the decrease progressed until late after termination of treatment and failed to fully regress. Morphologic lesions were confined to large, first order sensory neurons. The neurologic examination thus revealed the early changes, while electrodiagnostics and microscopic neuropathology were indicators of more advanced stages of toxic neuropathy and disclosed selective lesions in individuals whose gait appeared to be unremarkable.

  11. Drug: D10357 [KEGG MEDICUS

    Lifescience Database Archive (English)

    Full Text Available D10357 Mixture, Drug Doxylamine succinate - pyridoxine hydrochloride mixt; Diclegis... (TN) Doxylamine succinate [DR:D02327], Pyridoxine hydrochloride [DR:D02179] Treatment of nausea and vomitin...noalkyl ethers R06AA59 Doxylamine, combinations D10357 Doxylamine succinate - pyridoxine hydrochloride mixt USP dr...ug classification [BR:br08302] Antiemetics Antiemetics, Other Doxylamine Succinate/Pyridoxine Hydrochl...oride D10357 Doxylamine succinate - pyridoxine hydrochloride mixt PubChem: 172232450 ...

  12. Dietary pyridoxine requirement for juvenile cobia( Rachycentron canadum)%军曹鱼幼鱼对吡哆醇的需要量

    Institute of Scientific and Technical Information of China (English)

    刘凯; 麦康森; 艾庆辉; 张文兵; 王小洁; 肖林栋; 任鸣春

    2010-01-01

    以初始体重(3.23±0.06)g的军曹鱼为研究对象,以酪蛋白(不合维生素)、明胶、鱼肉浓缩蛋白为蛋白源,在基础饲料中分别添加0、2、4、8、16和32 mg PN/kg,配制出6种实验饲料,使饲料中吡哆醇的水平分别达到0.22、1.89、3.87、7.54、14.75和29.88 mg PN/kg,研究军曹鱼对吡哆醇的需要量.养殖实验在室内流水系统中(250 L)进行,每个处理设3个重复,每个重复放养军曹鱼25尾.养殖实验过程中,海水盐度为30~34,水温28~32℃,溶氧>7mg/L,养殖实验持续9周.实验结果显示,在0.22~3.87 mg PN/kg水平范围内,随着饲料中吡哆醇含量的升高,实验鱼特定生长率显著升高,当饲料吡哆醇水平达到或高于3.87mg/kg时,各饲料组实验鱼的特定生长率(2.68~2.71%/d)无显著差异,而都显著高于0.22和1.89 mg/kg饲料组的特定生长率(1.17~2.06%/d)P<0.05).军曹鱼肝脏吡哆醇含量、吡哆醛含量、谷丙转氨酶活力、谷草转氨酶活力均与特定生长率有相似的变化趋势,即在3.87mg/kg饲料组接近或者达到最大值,在达到或超过3.87 mg/kg时达到或近似达到一平台.根据实验结果,以军曹鱼幼鱼特定生长率和谷丙转氨酶活力、谷草转氨酶活力分别拟合折线模型,得到军曹鱼幼鱼对饲料中吡哆醇的需要量为3.09~3.26 mg/kg饲料.

  13. 维生素B6与苯巴比妥的相互作用%The interactions between pyridoxine and phenobarbital

    Institute of Scientific and Technical Information of China (English)

    胡朝欣; 陈湛芳; 单若冰; 张玉华; 王志燕

    2002-01-01

    目的:探讨大剂量维生素B6与苯巴比妥的相互作用.方法:分析两例新生儿合并使用大剂量维生素B6后其苯巴比妥血药浓度代谢速度与群体药动学参数的差异.结果:患者苯巴比妥血药浓度代谢速度较群体代谢速度快近一倍.结论:大剂量维生素B6可加快苯巴比妥的代谢速度.

  14. The Delayed-Release Combination of Doxylamine and Pyridoxine (Diclegis®/Diclectin®) for the Treatment of Nausea and Vomiting of Pregnancy

    OpenAIRE

    2014-01-01

    Nausea and vomiting of pregnancy (NVP) affects up to 85 % of all pregnancies. Effective treatment can greatly improve a woman’s quality of life, reduce the risk for maternal and fetal complications, and reduce healthcare costs. Unfortunately, many women receive either no pharmacological treatment or are recommended therapies for which fetal safety and efficacy have not been established. First-line treatment of NVP, as recommended by several leading healthcare and professional organizations, i...

  15. Lysine-restricted diet and mild cerebral serotonin deficiency in a patient with pyridoxine-dependent epilepsy caused by ALDH7A1 genetic defect

    Directory of Open Access Journals (Sweden)

    Saadet Mercimek-Mahmutoglu

    2014-01-01

    Stricter lysine restriction would be necessary to normalize CSF α-AASA levels, but might increase the risks associated with the diet. Patients are at risk of cerebral serotonin deficiency and should be monitored by CSF neurotransmitter measurements.

  16. Drug: D04935 [KEGG MEDICUS

    Lifescience Database Archive (English)

    Full Text Available D04935 Mixture, Drug Thiamine disulfide phosphate - pyridoxine hydrochloride - cyanocobalamin...arations 3179 Others D04935 Thiamine disulfide phosphate - pyridoxine hydrochloride - cyanocobalamin mixt PubChem: 17398223 ...

  17. Drug: D04911 [KEGG MEDICUS

    Lifescience Database Archive (English)

    Full Text Available D04911 Mixture, Drug Benfotiamine - pyridoxine hydrochloride - cyanocobalamin mixt;... 31 Vitamins 317 Multivitamin preparations 3179 Others D04911 Benfotiamine - pyridoxine hydrochloride - cyanocobalamin mixt PubChem: 17398215 ...

  18. Pyridoxal phosphate-dependent neonatal epileptic encephalopathy.

    Science.gov (United States)

    Bagci, S; Zschocke, J; Hoffmann, G F; Bast, T; Klepper, J; Müller, A; Heep, A; Bartmann, P; Franz, A R

    2008-03-01

    Pyridox(am)ine-5'-phosphate oxidase converts pyridoxine phosphate and pyridoxamine phosphate to pyridoxal phosphate, a cofactor in many metabolic reactions, including neurotransmitter synthesis. A family with a mutation in the pyridox(am)ine-5'-phosphate oxidase gene presenting with neonatal seizures unresponsive to pyridoxine and anticonvulsant treatment but responsive to pyridoxal phosphate is described. Pyridoxal phosphate should be considered in neonatal epileptic encephalopathy unresponsive to pyridoxine.

  19. Drug: D04904 [KEGG MEDICUS

    Lifescience Database Archive (English)

    Full Text Available D04904 Mixture, Drug Thiamine disulfide - pyridoxine hydrochloride - hydroxocobalam...in acetate mixt; Dai medine (TN) Thiamine disulfide [DR:D03299], Pyridoxine hydrochloride [DR:D02179], Hydro...xocobalamin acetate [DR:D02707] Therapeutic category: 3179 Therapeutic category of drugs in Japan [BR:br0830...thers D04904 Thiamine disulfide - pyridoxine hydrochloride - hydroxocobalamin acetate mixt PubChem: 17398213 ...

  20. High-yield production of aryl alcohol oxidase under limited growth conditions in small-scale systems using a mutant Aspergillus nidulans strain.

    Science.gov (United States)

    Pardo-Planas, Oscar; Prade, Rolf A; Wilkins, Mark R

    2017-02-01

    Aryl alcohol oxidase (MtGloA) is an enzyme that belongs to the ligninolytic consortium and can play an important role in the bioenergy industry. This study investigated production of an MtGloA client enzyme by a mutant strain of Aspergillus nidulans unable to synthesize its own pyridoxine. Pyridoxine limitation can be used to control cell growth, diverting substrate to protein production. In agitated culture, enzyme production was similar when using media with 1 mg/L and without pyridoxine (26.64 ± 6.14 U/mg mycelia and 26.14 ± 8.39 U/mg mycelia using media with and without pyridoxine, respectively). However, the treatment lacking pyridoxine had to be supplemented with pyridoxine after 156 h of fermentation to sustain continued enzyme production. Use of extremely diluted pyridoxine levels allowed reduced fungal growth while maintaining steady enzyme production. Concentrations of 9 and 13.5 µg/L pyridoxine allowed MtGloA production with a growth rate of only 5% of that observed when using the standard 1 mg/L pyridoxine media.

  1. Effects of pyridoxine on rat testis cells in Sertoli-germ cell co-culture system%用睾丸细胞共培养探讨吡哆醇对大鼠睾丸细胞的毒性

    Institute of Scientific and Technical Information of China (English)

    黄厚今; 王瑞淑; 徐维光; 杨青

    1999-01-01

    目的 探讨吡哆醇(PN)对大鼠睾丸的体外毒性.方法 采用在Williams方法的基础上改进的Sertoli-germ细胞共培养系统,观察PN在不同剂量和接触时间对培养细胞的作用.结果 脱落生精细胞数随PN浓度的增高和接触时间的延长而增加,并有明显的剂量-效应和时间-效应关系.同时,还观察到Sertoli细胞骨架出现松弛、回缩等效应.结论 PN对大鼠生精细胞的体外效应反映了其对Sertoli细胞的损害.睾丸细胞共培养方法对探讨PN对大鼠睾丸的毒性作用具有实用价值.

  2. Fluorescence Characteristic of Hemoglobin-Pyridoxine-Peroxynitrite and Its Application in the Determination of Peroxynitrite%血红蛋白-维生素B6-ONOO-体系的荧光特性及ONOO-分析

    Institute of Scientific and Technical Information of China (English)

    曹启花; 蔡汝秀

    2008-01-01

    在中性pH值的缓冲溶液中,血红蛋白作催化剂,维生素B6与过氧亚硝酸活性氧(ONOO-)发生反应,维生素B6原来位于391 nm处的强烈的荧光发射峰消失,而在384 nm和424 nm处出现了两个新的荧光峰.据此建立了血红蛋白一维生素B6体系高灵敏检测ONOO-活性氧的新方法.方法的线性范围为5.24×10-8~2.62×10-6mol/L,检出限为2.62×10-9mol/L,对1.31×10-7mol/L的ONOO-溶液测定的相对标准偏差为3.75%(n=7).

  3. 吡哆醇对水稻、烟草生理活性及生长的影响试验初报%Effect of pyridoxine on physiological viabilities and growth of rice and tobacco

    Institute of Scientific and Technical Information of China (English)

    何虹桦

    2004-01-01

    用不同浓度的吡哆醇(PDL)浸泡处理水稻种子,及加入到营养液中对烟苗进行通气水培,结果表明,经吡哆醇处理能增加作物苗期的抗寒性,促进氮磷钾等营养元素的吸收利用,对植株根系的生长也具有明显的促进效果,说明吡哆醇对作物生长具有一定的积极意义.

  4. Effect of high-dose pyridoxine on nitric oxide synthase activity in rat testis%大剂量吡哆醇对大鼠睾丸一氧化氮合酶活性的影响

    Institute of Scientific and Technical Information of China (English)

    李积胜; 汪超; 王鹏; 贺智; 张玉和; 徐鹏霄; 姚班

    2001-01-01

    目的探讨大剂量吡哆醇(PN)对睾丸结构和功能损害的分子机制,研究其对睾丸一氧化氮合酶(NOS)的影响.方法选用2月龄Wistar雄性大鼠36只,均分为实验组和对照组,每日分别自腹腔注射PN(800mg/kg)和等量生理盐水,于第3 d和7 d后,采用NADPH-黄递酶(NADPH-d)组织化学法显示睾丸细胞NOS.结果与对照组相比,注射PN 3 d,实验组大鼠睾丸间质细胞NOS反应活性轻度增加;注射PN7 d后,睾丸间质细胞NOS活性明显增强.结论大剂量PN腹腔注射后;大鼠睾丸细胞NOS活性明显增加,这些变化可能是PN损害睾丸结构和功能的分子机制之一.

  5. In Silico Cloning of Pyridoxine Biosynthesis Protein Gene from Soybean and Evolution Analysis%大豆吡哆醇生物合成蛋白基因(PDX)的电子克隆和进化分析

    Institute of Scientific and Technical Information of China (English)

    李蕊; 孟宪萍; 胡英考; 蔡民华; 李雅轩

    2007-01-01

    电子克隆(In silico cloning)是随着基因组计划和EST计划实施而发展起来的利用生物信息学手段进行基因克隆的新方法.根据物种间同源基因相对保守的特点,以拟南芥(Arabidopsis thaliana)吡哆醇生物合成蛋白cDNA序列为信息探针,对大豆(Glycine max)EST数据库进行同源搜索和序列拼接,获得了1 280 bp长的大豆吡哆醇生物合成蛋白的基因序列(GenBank登陆号为DQ139265).经过RT-PCR扩增、基因组PCR扩增、分子克隆和序列分析验证,结果表明与电子克隆序列完全一致.该基因具有完整的开放阅读框架(ORF,20~955 bp),编码311个氨基酸.通过与水稻、日本百脉根、烟草、截形苜蓿等物种的吡哆醇生物合成蛋白序列比对,发现该基因具有高度的保守性.表明根据物种间同源基因序列,对跨物种间EST数据库进行同源检索、筛选、拼接,是克隆基因的有效途径.

  6. The Conformation, Spectroscopy and Thermodynamic Properties of the 3-bromo-6-methyl Pyridoxine%3-溴-6-甲基哒嗪的结构、光谱和热力学性质

    Institute of Scientific and Technical Information of China (English)

    徐友辉

    2009-01-01

    3-澳-6-甲基哒嗪是一种新近合成的哒嗪重要衍生物,从理论上对其结构、光谱和热力学性质的研究还未见报道.采用Gaussian03计算程序在B3LYP/6-311++G**水平对3-澳-6-甲基哒嗪进行结构优化和频率、热力学性质计算,得到它们的红外光谱以及热容、熵、焓等热力学性质与温度之间的函数关系式,有助干哒嗪类化合物的合成及其它性质研究.

  7. Determination of pyridoxine by reversed-phase high performance liquid chromatography with chemiluminescence detection%反相高效液相色谱 -增敏化学发光测定VB6

    Institute of Scientific and Technical Information of China (English)

    王莉; 周光明; 游水英; 沈祥

    2006-01-01

    基于维生B6对于鲁米诺(Luminol)和高碘酸钾(KIO4)化学发光反应的增敏作用原理,建立了反相高效液相色谱(RP-HPLC)分离柱后化学发光检测VB6的新方法,并成功运用于饮料中VB6的测定.其中在鲁米诺中加入KBr可以大大增敏该反应.该方法测定VB6的线性范围为5.0×10-7~5.0×10-4g/mL,检测限为2 0×10-8g/mL.对1.0×10-5g/mL的VB6进行连续5次测定的相对标准偏差分别为2.8%,回归方程为Y=954.472X+1.488.

  8. Study of the inhibitory effect of pyridoxine on liver cancer cell line H22 in vitro%吡哆醇对小鼠肝癌细胞H22体外抑制作用的研究

    Institute of Scientific and Technical Information of China (English)

    江平; 陈兴; 张乃哲

    2002-01-01

    目的研究吡哆醇对体外培养小鼠肝细胞H22的细胞毒作用.方法应用MTT法,测定吡哆醇在不同浓度及不同作用时间对小鼠肝癌细胞的抑制作用.结果同阴性对照组相比,吡哆醇浓度为3 mmol/L时对肝癌细胞有轻度抑制作用(R=36.8%),6mmol/L时为高度抑制(IR=55.6%,P<0.01).回归分析显示,IR%与给药浓度和作用时间呈正相关,尤以48小时为显著,呈线性趋势(r=0.9764,P<0.01),其相应的IC50=5mmol/L.结论吡哆醇对体外培养的H22小鼠肝癌细胞系的生长具有抑制作用,且二者之间有剂量-效应关系和时间-效应趋势.

  9. 大剂量吡哆醇对大鼠睾丸细胞DNA和RNA影响的研究%Effect of high-dose pyridoxine on DNA & RNA content in testicular cells of rats

    Institute of Scientific and Technical Information of China (English)

    白银; 闫蓓; 杨敏; 王大宁

    2003-01-01

    目的:探讨大剂量吡哆醇(PN)对睾丸结构和功能影响的分子机制,研究其对睾丸细胞DNA和RNA的影响.方法:选用2m龄Wistar雄性大鼠32只,均分为实验组和对照组,每日分别自腹腔注射PN(800mg/kg)和等量生理盐水,于第3d和7d后,采用吖啶橙荧光染色法显示睾丸细胞DNA和RNA.结果:与对照组相比,注射3d实验组大鼠睾丸细胞DNA和RNA反应活性未见明显减弱或消失,注射7d实验组大鼠睾丸DNA和RNA反应活性明显减弱.结论:大剂量PN腹腔注射后,大鼠睾丸细胞DNA和RNA活性明显减少,这些变化可能是PN损害睾丸结构和功能的重要原因之一.

  10. In silico cloning of biosynthesis gene of pyridoxine from Medicago truncatula and its evolution analysis%截形苜蓿吡哆醇生物合成基因的电子克隆和进化分析

    Institute of Scientific and Technical Information of China (English)

    李蕊; 孟宪萍; 胡英考; 蔡民华; 李雅轩

    2007-01-01

    电子克隆是随着基因组计划和EST计划实施而发展起来的、利用生物信息学手段进行基因克隆的新方法.根据物种间同源基因相对保守的特点,利用生物信息学的方法,以拟南芥吡哆醇生物合成蛋白基因(PDX)cDNA序列为探针,在GenBank的HTGs数据库中找到与之高度同源的截形苜蓿的基因组序列--mth2-17p16克隆,通过GenScan软件预测和序列拼接得到了截形苜蓿吡哆醇生物合成基因序列(GenBank登录号为DQ139263).用该序列对GenBank中的est-others进行相似性搜索,获得了25条截形苜蓿的EST序列,经拼接后发现与基因组预测的基因序列一致,表明该基因是真实存在和表达的.该cDNA序列长度为1 257 bp,具有完整的开放式阅读框(ORF 29-973bp),推测编码314个氨基酸.通过对日本百脉根(Lotus corniculatus var.japonicus)、烟草(Nicotiana tabacum)、拟南芥(Arabidopsis thaliana)、大豆(Glycine max)、小麦(Triticum aestivum)和水稻(Oryza sativa)等进行吡哆醇生物合成蛋白序列同源比较,发现该基因具有高度的保守性.

  11. Nerve Regeneration Microenvironment in Pyridoxine-induced Ganglionopathy Rats Model Following Nerve Crush Injury%吡哆醇诱导性大鼠感觉神经元病的神经再生微环境

    Institute of Scientific and Technical Information of China (English)

    张在强; 曹世俭; 王拥军

    2009-01-01

    目的 观察吡哆醇诱导的感觉神经元病大鼠在坐骨神经挤压伤后神经再生相关蛋白的表达水平,探讨神经元分子微环境变化对神经再生修复的重要意义.方法 制作吡哆醇诱导的感觉神经元病模型,在此基础上制作双侧坐骨神经挤压伤模型.观察神经挤压损伤后7、14、21和28 d大鼠的背根神经节TUNEL标记阳性细胞百分比变化;利用蛋白印迹技术,观察神经再生相关蛋白(GAP-43)和神经生长因子受体(trk A)表达水平变化.结果 背根神经节细胞早期有较多的TUNEL标记细胞,但21~28 d由于大部分细胞变性坏死,TUNEL标记细胞反而减少.背根神经节细胞GAP-43和trk A蛋白有一定水平的表达,但总体水平低于单纯坐骨神经损伤时.结论 中毒造成的感觉神经节病变危及神经元的生存,导致基因表达体系不完整,使损伤神经的再生修复能力下降.

  12. 维生素B6在微电极上的电化学行为及测定%The electrochemical behavior and determination of pyridoxine at microelectrode

    Institute of Scientific and Technical Information of China (English)

    任艳艳; 金根娣; 胡效亚

    2010-01-01

    用伏安法研究了维生素B6(VB6)在碳纤维微电极(CFME)上的电化学行为及其测定.以0.1 mol/L的邻苯二甲酸氢钾(pH 5)的缓冲液为底液,在最佳实验条件下,VB6在0.94 V(vs, SCE)的氧化峰峰电流与VB6在5.0×10-6 ~8.0×10-4 mol/L范围内呈良好的线性关系,检出限为1.0×10-6 mol/L (S/N=3).方法用于药剂中的VB6的分析.

  13. Efeitos de diferentes níveis das vitaminas tiamina, riboflavina e piridoxina sobre o desempenho de frangos de corte Effects of different levels of thiamine, riboflavin and pyridoxine on broiler performance

    Directory of Open Access Journals (Sweden)

    Ana Lúcia Pozzobon de Souza

    1996-12-01

    Full Text Available O experimento foi conduzido para analisar os efeitos de níveis altos e baixos das vitaminas tiamina (B1, riboflavina (B2 e piridoxina (B6 sobre o desempenho de frangos de corte. Um total de 576 pintos de corte de um dia, foram distribuídos em desenho experimental trifatorial (2³, inteiramente casualizado onde dois níveis (alto e baixo de cada vitamina foram testados: vitamina B1 (A=3 mg/kg; B=2 mg/kg, vitamina B2 (A=6 mg/kg; B=4 mg/kg e vitamina B6 (A=4,5 mg/kg; B=3 mg/kg. Deste modo, dezoito aves por tratamento (8, em quatro repetições, foram distribuídas em boxes sobre piso e receberam dietas isonutritivas, variando somente em relação às vitaminas estudadas. Os dados foram submetidos a análise de variância e teste de Tukey. Não foram observadas diferenças significativas (P>0,05 entre os tratamentos para todos os parâmetros estudados. Portanto, os resultados deste trabalho sugerem que os níveis das vitaminas B1, B2 e B6, para frangos de corte, podem ser reduzidos em até 66% dos níveis atualmente utilizados, sem prejuízo na performance dos mesmos.An experiment was carried out to evaluate the effècts of high and low levels of vitamins thiamine (B1 ribofiavin (B2 andpyridoxin (B3 on the performance of boilers. A total of 576 day old broiler chicks of both sexes was distributed in a trifactorial (23 completely randomized experimental desing, where two levels (high and low} of each vitamin were tested: vitamin B1 (A=3 mg/kg; B=2 mg/kg; vitamin B2 (A=6 mg/kg; B=4 mg/kg and vitamin B6 (A=4,5 mg/kg; B=3 mg/kg. Therefore, eighteenth birds in each treatment (8, in four replications, were distributed in floor pens andreceived isonutritious diets, varying only in respect to the vitamins studied. Data were submitted to the analysis of variance and Tukey test. No significant differences (P>0.05 among treatments were observed for all parameters studied. Then, the results from this work suggest that the levels of vitamins B1, B2 and B6, for broilers, can be lowered to 66% of the usual levels actually used, without reduction in the performance of broilers.

  14. Dicty_cDB: Contig-U10476-1 [Dicty_cDB

    Lifescience Database Archive (English)

    Full Text Available ospora nicotianae pyridoxine s... 89 1e-16 CP000497_204( CP000497 |pid:none) Pichia... 4 pd... 87 7e-17 AF363613_1( AF363613 |pid:none) Aspergillus nidulans pyridoxine (p... 89 8e-17 AF294268_1( AF294268 |pid:none) Cerc

  15. Drug: D02179 [KEGG MEDICUS

    Lifescience Database Archive (English)

    Full Text Available ic category of drugs in Japan [BR:br08301] 3 Agents affecting metabolism 31 Vitamins 313 Vitamin B preparations 3134 Vitamin B6 prepa...A11H OTHER PLAIN VITAMIN PREPARATIONS A11HA Other plain vitamin preparations A11HA02 Pyridoxine (vit B6) D02...rations D02179 Pyridoxine hydrochloride (JP16/USP) Anato

  16. Disease: H01124 [KEGG MEDICUS

    Lifescience Database Archive (English)

    Full Text Available hy with severe seizures which do not respond to anticonvulsant drugs or pyridoxine but shows a dramatic resp... are not responsive to anticonvulsant drugs and pyridoxine. Patients with this deficiency have very low conc...phate oxidase (PNPO) deficiency is a rare autosomal recessive disorder that causes intractable seizures that

  17. Isoniazid-induced convulsions.

    Science.gov (United States)

    Coyer, J R; Nicholson, D P

    1976-03-01

    Acute isoniazid overdose and toxicity may be complicated by convulsions and death. Six patients are reported, one of whom ingested simultaneously 15 gm of isoniazid and 5 gm of pyridoxine hydrochloride (vitamin B6); no convulsions resulted. In the light of this and other experience, suggestions are made for the use of pyridoxine in the treatment and prevention of acute isoniazid poisoning.

  18. Drug: D04930 [KEGG MEDICUS

    Lifescience Database Archive (English)

    Full Text Available D04930 Mixture, Drug Benfotiamine - pyridoxine hydrochloride - Hydroxocobalamin hydr...ochloride mixt; Vitamedin-S (TN) Benfotiamine [DR:D01255], Pyridoxine hydrochloride [DR:D02179], Hydroxocobalamin hydrochloride [DR:D04929] See [DR:D04911] PubChem: 17398222 ...

  19. Vitamin B6: deficiency diseases and methods of analysis.

    Science.gov (United States)

    Ahmad, Iqbal; Mirza, Tania; Qadeer, Kiran; Nazim, Urooj; Vaid, Faiyaz Hm

    2013-09-01

    Vitamin B6 (pyridoxine) is closely associated with the functions of the nervous, immune and endocrine systems. It also participates in the metabolic processes of proteins, lipids and carbohydrates. Pyridoxine deficiency may result in neurological disorders including convulsions and epileptic encephalopathy and may lead to infant abnormalities. The Intravenous administration of pyridoxine to patients results in a dramatic cessation of seizures. A number of analytical methods were developed for the determination of pyridoxine in different dosage forms, food materials and biological fluids. These include UV spectrometric, spectrofluorimetric, mass spectrometric, thin-layer and high-performance liquid chromatographic, electrophoretic, electrochemical and enzymatic methods. Most of these methods are capable of determining pyridoxine in the presence of other vitamins and complex systems in µg quantities. The development and applications of these methods in pharmaceutical and clinical analysis mostly during the last decade have been reviewed.

  20. Vitamin B deficiencies in a critically ill autistic child with a restricted diet.

    Science.gov (United States)

    Baird, J Scott; Ravindranath, Thyyar M

    2015-02-01

    An 11-year-old male with autism became less responsive and was hospitalized with hepatomegaly and liver dysfunction, as well as severe lactic acidosis. His diet for several years was self-limited exclusively to a single "fast food"-a particular type of fried chicken-and was deficient in multiple micronutrients, including the B vitamins thiamine and pyridoxine. Lactic acidosis improved rapidly with thiamine; 2 weeks later, status epilepticus-with low serum pyridoxine-resolved rapidly with pyridoxine. Dietary B vitamin deficiencies complicated the care of this critically ill autistic child and should be considered in this setting.

  1. Vitamins of group B in the food and in certain organs of the carp, the white amur and the tench, under natural feeding conditions. 5. Vitamin content in the natural diet and in the artificial food of the fishes

    National Research Council Canada - National Science Library

    Tryapsene, O.P; Jankyavicius, K.K

    1978-01-01

    The results of the experiments in 1971-1972 showed that B vitamin complex: meso-inositole, biotine, pantothenic acid, thiamine, pyridoxine and nicotinic acid were found in the natural nutriment and artificial forage of the fish...

  2. Plasma Levels of Folates, Riboflavin, Vitamin B6, and Ascorbate in Severely Disturbed Children.

    Science.gov (United States)

    Sankar, D. V. Siva

    1979-01-01

    The plasma levels of folic acid, ascorbic acid, pyridoxine, and riboflavin were studied in 125 severely emotionally disturbed children (ages 5-16 years) to determine whether they had overt vitamin deficiencies. (Author/DLS)

  3. Fortify Your Knowledge about Vitamins

    Medline Plus

    Full Text Available ... 3 (niacin): flushing, redness of the skin, upset stomach. B-6 (pyridoxine, pyridoxal, and pyridoxamine): Nerve damage ... trouble walking, and pain. C (ascorbic acid): Upset stomach, kidney stones, increased iron absorption. Folic Acid (folate): ...

  4. Pharmaceutical Approval Update

    OpenAIRE

    Choy, Mary

    2017-01-01

    Olaratumab (Lartruvo) for the treatment of soft tissue sarcoma; bezlotoxumab (Zinplava) for use with an antibiotic to reduce recurrence of C. difficile infection; and doxylamine succinate/pyridoxine hydrochloride (Bonjesta) for the treatment of nausea and vomiting during pregnancy

  5. EFFECT OF CALITROPIS PROCERA AQUEOUS ROOT EXTRACT ...

    African Journals Online (AJOL)

    ABUBAKAR

    The hepatocurative effect of aqueous root extract of Calitropis Procera on CCl4 induced hepatotoxicity in rabbits was studied in groups of rabbit and the levels of liver enzymes; aspartate .... and inhibitors and presence of pyridoxine (vitamin.

  6. Fortify Your Knowledge about Vitamins

    Medline Plus

    Full Text Available ... If you are an older adult, have dark skin, or are exposed to insufficient ultraviolet band radiation ( ... Vitamins B-3 (niacin): flushing, redness of the skin, upset stomach. B-6 (pyridoxine, pyridoxal, and pyridoxamine): ...

  7. Cisplatin Injection

    Science.gov (United States)

    ... Dilantin), bumetanide (Bumex), ethacrynic acid (Edecrin), furosemide (Lasix), pyridoxine (Vitamin B-6). Your doctor may need to ... looks like coffee grounds Cisplatin may increase the risk that you will develop other cancers. Talk to ...

  8. Fortify Your Knowledge about Vitamins

    Medline Plus

    Full Text Available ... If you are an older adult, have dark skin, or are exposed to insufficient ultraviolet band radiation ( ... Vitamins B-3 (niacin): flushing, redness of the skin, upset stomach. B-6 (pyridoxine, pyridoxal, and pyridoxamine): ...

  9. Disease: H01247 [KEGG MEDICUS

    Lifescience Database Archive (English)

    Full Text Available , Baxter P, Baumgartner M, Willemsen MA, Omran H, Tacke U, Uhlenberg B, Weschke B, Clayton PT Mutations in a...Scharer G, Struijs E, Tein I, Jakobs C, Clayton P, Van Hove JL Pyridoxine depende

  10. Multiple B-vitamin depletion in large areas of the coastal ocean

    National Research Council Canada - National Science Library

    Sergio A. Sañudo-Wilhelmy; Lynda S. Cutter; Reginaldo Durazo; Emily A. Smail; Laura Gómez-Consarnau; Eric A. Webb; Maria G. Prokopenko; William M. Berelson; David M. Karl

    2012-01-01

    .... Therefore, cellular metabolism of marine vitamin-requiring (auxotrophic) phytoplankton and bacteria would likely be significantly compromised if B vitamins (thiamin B₁, riboflavin B₂, pyridoxine B₆, biotin B₇, and cobalamin B₁₂) were unavailable...

  11. Silane Reduction of 5-Hydroxy-6-methyl-pyridine-3,4-dicarboxylic Acid Diethyl Ester: Synthesis of Vitamin B6

    Directory of Open Access Journals (Sweden)

    Andrew G. Gum

    2003-12-01

    Full Text Available Alternative methods for the synthesis of pyridoxine have been investigated. The key intermediate, 5-hydroxy-6-methyl-pyridine-3,4-dicarboxylic acid diethyl ester (5, was reduced with either a silane monomer (MeSiH(OEt2 or a polysiloxane (polymethylhydrosiloxane, PMHS to afford crude pyridoxine. An isolation technique utilizing a commercially available resin was devised, affording the desired product, vitamin B6, in an overall yield of 38-54 % and a purity of 76%.

  12. Encephalopathy secondary to isoniazid in patients on hemodialysis

    OpenAIRE

    2013-01-01

    We report isoniazid (INH)-induced encephalopathy in two male patients on hemodialysis. One of them had tuberculous adenitis, and the other had pulmonary tuberculosis. Both were given rifampicin, INH, pyrazinamide, and ethambutol with pyridoxine 40 mg/day. Two patients developed disturbances in consciousness. After excluding other causes, INH-induced encephalopathy was suspected so the drug was stopped and dose of pyridoxine increased. Both patients retained their consciousness within 1 week a...

  13. Pyridoxal phosphate-dependent neonatal epileptic encephalopathy

    OpenAIRE

    2009-01-01

    Pyridox(am)ine-5′-phosphate oxidase converts pyridoxine phosphate and pyridoxamine phosphate to pyridoxal phosphate, a cofactor in many metabolic reactions, including neurotransmitter synthesis. A family with a mutation in the pyridox(am)ine-5′-phosphate oxidase gene presenting with neonatal seizures unresponsive to pyridoxine and anticonvulsant treatment but responsive to pyridoxal phosphate is described. Pyridoxal phosphate should be considered in neonatal epileptic encephalopathy unrespons...

  14. Synthesis and in vitro microbial evaluation of La(III), Ce(III), Sm(III) and Y(III) metal complexes of vitamin B6 drug

    Science.gov (United States)

    Refat, Moamen S.; Al-Azab, Fathi M.; Al-Maydama, Hussein M. A.; Amin, Ragab R.; Jamil, Yasmin M. S.

    2014-06-01

    Metal complexes of pyridoxine mono hydrochloride (vitamin B6) are prepared using La(III), Ce(III), Sm(III) and Y(III). The resulting complexes are investigated. Some physical properties, conductivity, analytical data and the composition of the four pyridoxine complexes are discussed. The elemental analysis shows that the formed complexes of La(III), Ce(III), Sm(III) and Y(III) with pyridoxine are of 1:2 (metal:PN) molar ratio. All the synthesized complexes are brown in color and possess high melting points. These complexes are partially soluble in hot methanol, dimethylsulfoxide and dimethylformamide and insoluble in water and some other organic solvents. Elemental analysis data, spectroscopic (IR, UV-vis. and florescence), effective magnetic moment in Bohr magnetons and the proton NMR suggest the structures. However, definite particle size is determined by invoking the X-ray powder diffraction and scanning electron microscopy data. The results obtained suggested that pyridoxine reacted with metal ions as a bidentate ligand through its phenolate oxygen and the oxygen of the adjacent group at the 4‧-position. The molar conductance measurements proved that the pyridoxine complexes are electrolytic in nature. The kinetic and thermodynamic parameters such as: Ea, ΔH*, ΔS* and ΔG* were estimated from the DTG curves. The antibacterial evaluation of the pyridoxine and their complexes were also performed against some gram positive, negative bacteria as well as fungi.

  15. Vitamin B6 related epilepsy during childhood.

    Science.gov (United States)

    Wang, Huei-Shyong; Kuo, Meng-Fai

    2007-01-01

    In some patients without vitamin B6 deficiency, epilepsy can not be controlled without an extra supplement of vitamin B6. The therapeutic role of pyridoxal phosphate (PLP), the active form of vitamin B6, may not be replaced with other forms of vitamin B6 sometimes. Until now, four inborn errors of metabolism are known to affect vitamin B6 concentrations in the brain. Three of them are hyperprolinemia type 2, antiquitin deficiency, and pyridoxine phosphate oxidase deficiency. The fourth disorder occurs in neonates with hypophosphatasia and congenital rickets. All patients with these conditions present with early-onset epilepsy that is resistant to conventional antiepileptic medications. Patients with three of the conditions respond to any form of vitamin B6. Only those with pyridoxine phosphate oxidase deficiency respond to PLP instead of pyridoxine. Interestingly, the authors have successfully treated many patients without the above four disorders using vitamin B6, and have found that the treatment was more effective with PLP than with pyridoxine, though the mechanism is not known. Since PLP is as inexpensive as pyridoxine, we suggest replacing PLP for pyridoxine when treating children with epilepsy.

  16. Typical and atypical phenotypes of PNPO deficiency with elevated CSF and plasma pyridoxamine on treatment.

    Science.gov (United States)

    Ware, Tyson L; Earl, John; Salomons, Gajja S; Struys, Eduard A; Peters, Heidi L; Howell, Katherine B; Pitt, James J; Freeman, Jeremy L

    2014-05-01

    Pyridox(am)ine phosphate oxidase (PNPO) deficiency causes severe early infantile epileptic encephalopathy and has been characterized as responding to pyridoxal-5'-phosphate but not to pyridoxine. Two males with PNPO deficiency and novel PNPO mutations are reported and their clinical, metabolic, and video-electroencephalographic (EEG) findings described. The first child showed electro-clinical responses to pyridoxine and deterioration when pyridoxine was withheld. At last review, he has well-controlled epilepsy with pyridoxal-5'-phosphate monotherapy and an autism spectrum disorder. The second child had a perinatal middle cerebral artery infarct and a myoclonic encephalopathy. He failed to respond to pyridoxine but responded well to pyridoxal-5'-phosphate. At the age of 21 months he has global developmental delay and hemiparesis but is seizure-free with pyridoxal-5'-phosphate monotherapy. Plasma and cerebrospinal fluid pyridoxamine levels were increased in both children during treatment with pyridoxine or pyridoxal-5'-phosphate. These observations indicate that differential responses to pyridoxine and pyridoxal-5'-phosphate treatment cannot be relied upon to diagnose PNPO deficiency.

  17. STUDY ON QUANTITATIVE ANALYSIS OF PYRIDOXINE HYDROCHLORIDE AND ITS PREPARATION BY SECONDARY DERIVATIVE DIFFERENTIAL PULSE POLAROGRAPHY%盐酸吡哆辛及其制剂的二阶导数差示脉冲极谱法定量研究

    Institute of Scientific and Technical Information of China (English)

    王连朋; 申永壮; 梁云爱

    2003-01-01

    建立盐酸吡哆辛及其制剂的二阶导数差示脉冲极谱定量分析方法.盐酸吡哆辛在0.1 mol/L氢氧化钠溶液-0.1 mol/L磷酸二氢钾溶液-水(体积比为1.2:8.8:990)的混合溶液中,于-0.140 V(vs@Ag/AgCl)处出现一良好的二阶导数差示脉冲极谱峰,盐酸吡哆辛浓度在3.6×10-4~9.6×10-4mol/L范围内与其峰幅值呈显著的线性关系(P<0.01),线性相关系数r=0.9997,检出限为9.0 nmol/L.

  18. Effect of High-Dose Pyridoxine on Nitric Oxide Synthase(NOS)and Apoptosis of Rat Testis%大剂量吡哆醇对大鼠睾丸一氧化氮合酶和细胞凋亡的影响

    Institute of Scientific and Technical Information of China (English)

    李积胜; 焦富勇

    2000-01-01

    为探讨大剂量吡哆醇(PN)对睾丸结构和功能损害的分子机制,研究其对睾丸一氧化氮合酶(NOS)和细胞凋亡的影响.实验采用吖啶橙荧光染色法显示睾丸细胞DNA和RNA,黄递酶(NADPH-d)组织化学法显示睾丸细胞NOS,采用原位缺口平移技术检测睾丸生精细胞凋亡的数目.结果表明 ,与对照组相比,注射PN 3 d,大鼠睾丸间质细胞NOS反应活性轻度增加;注射PN 7 d后,大鼠睾丸细胞DNA和RNA荧光显色明显减弱,间质细胞NOS活性明显增强,睾丸生精细胞凋亡数目(38.41±8.20)较相应对照组(11.39±4.86)明显增多,差异有显著性(P<0.01).提示大剂量PN腹腔注射后,大鼠睾丸细胞NOS活性和凋亡细胞数目明显增加,这些变化可能是PN损害睾丸结构和功能的分子机制之一.

  19. 家蚕酸吡哆醇氧化酶cDNA克隆、鉴定及基因结构分析%Cloning,Identification and Genomic Organization of the cDNA Encoding Pyridoxine 5'-phosphate Oxidase in Bombyx mori

    Institute of Scientific and Technical Information of China (English)

    张剑韵; 石瑞君; 黄硕豪; 黄龙全

    2008-01-01

    [目的]了解家蚕维生素B6关键代谢酶磷酸吡哆醇氧化酶(PNP0)的基因结构.[方法]利用生物信息学原理和PeR方法,克隆出编码家蚕(Bombyx mori)PNPO的cDNA(GenBank登录号:DQ452398);采用T7启动子/T7 RNA聚合酶原核表达系统对cDNA进行体外表达,并通过酶活检测进行表达产物的功能鉴定;依据家蚕基因组数据库信息和得到的cDNA,对家蚕PNPO基因结构进行分析.[结果]克隆到的cDNA含有771 bp的完整可读框,编码一条分子量为29.86 kD、含257个氨基酸残基的蛋白质.序列比对显示此蛋白质与人类PNPO具有51.44%的同源性,包含PNPO家族共有的保守序列,但在人和大肠杆菌PNPO中具有重要作用的几个氨基酸残基在此蛋白质中被替换.在以磷酸吡哆醇(PNP)为底物时,表达产物Pro-PNPO的酶活力约为17 nmol·min-1·mg-1.家蚕PNPO基因包含5个外显子和4个内含子,跨越3.5 kb DNA序列,所有外显子/内含子交接点都遵从gt/ag剪接规则,基因的5'端启动子调控区发现有TATA-box和CAAT-box保守基序.[结论]获得家蚕PNPO基因,可利用该基因在分子水平上研究家蚕的VB6代谢特征,弄清PNPO家族的特征及其在生物进化过程中的演变规律.

  20. 吡哆醇对脑淋巴引流阻滞所致SAH后神经细胞凋亡加重的影响%Cerebral lymphatic blockage aggravates apoptosis of cortical neurons after SAH in rat and pyridoxine has a certain role in the mitigation

    Institute of Scientific and Technical Information of China (English)

    王轩; 陈锋; 高兵; 高向东; 贾丽丽; 杨明峰; 孙保亮

    2010-01-01

    目的 探讨脑淋巴引流阻滞(CLB)对蛛网膜下腔出血(SAH)后神经细胞凋亡的影响和吡哆醇的缓解作用及相关机制.方法 健康成年Wistar大鼠,随机分为正常对照组、SAH组、SAH+CLB组、SAH+CLB+吡哆醇组、SAH+CLB+生理盐水组.采用枕大池2次注血法建立SAH模型.于第2次注血3 d后检测相关指标.SAH+CLB+吡哆醇组于CLB术前30 min按50 mg·kg-1腹腔注射吡哆醇生理盐水溶液,每天以上述半量重复注射2次.采用TUNEL荧光标记法检测原位凋亡情况;免疫组织化学激光共聚焦检测大鼠皮层神经细胞Caspase-3和Bcl-2的蛋白表达.结果 ①与正常对照组比较,其余各组大鼠TUNEL阳性细胞表达均明显升高,而SAH+CLB组和SAH+CLB+生理盐水组又明显高于SAH组(P<0.01),SAH+CLB+吡哆醇组与SAH+CLB组比较表达有所减弱(P<0.01).②与正常对照组比较,其余各组大鼠皮层神经细胞Caspase-3蛋白表达均明显升高,而SAH+CLB组和SAH+CLB+生理盐水组最高,与SAH组比较差异具有显著性(P<0.01),SAH+CLB+吡哆醇组与SAH+CLB组比较表达有所减弱(P<0.01).③与正常对照组比较,其余各组大鼠皮层神经细胞Bcl-2蛋白表达均明显升高,而SAH+CLB组和SAH+CLB+生理盐水组明显低于SAH组(P<0.01),SAH+CLB+吡哆醇组较SAH+CLB组表达增强.结论 脑淋巴引流阻滞可以通过Caspase-3高表达和Bcl-2低表达加重SAH后大鼠皮层神经细胞的凋亡,而吡哆醇具有一定的缓解作用.

  1. Determination of Thiamine, Riboflavin, Pyridoxine Hydrochloride and Nicotinamide in Weikang Capsules by HPLC%高效液相色谱法测定维康胶囊中硫胺素、核黄素、盐酸吡多辛及烟酰胺

    Institute of Scientific and Technical Information of China (English)

    邓富良; 陈本美; 陈新; 周平; 陈国华; 邓世林; 梁绍先

    2005-01-01

    水溶性维生素是人体维持正常生理代谢所必需的一类重要的有机化合物。近来的研究发现许多水溶性维生素对肿瘤有防治作用;缺乏硫胺素、核黄素均会对脑发育产生不利影响。维康胶囊是一种含多种维生素和矿物质的新药。笔者在文献的基础上研究建立了以DL-樟脑-10-磺酸为离子对试剂的高效液相色谱法同时测定维康胶囊中水溶性维生素硫胺素、核黄素、盐酸吡多辛及烟酰胺含量的方法。该方法简单、快速、灵敏度高、重复性好,为产品质量的控制及多维类药物中水溶性维生素浓度的检测提供了可靠依据。

  2. 盐酸吡哆辛在聚对氨基苯磺酸修饰电极上的电化学行为与测定%Electrochemical Behavior and Determination of Pyridoxine Hydrochloride at Poly p-Aminobenzene Sulfonic Acid Modified Electrode

    Institute of Scientific and Technical Information of China (English)

    何凤云; 潘兆瑞; 周宏; 刘欢; 俞静; 顾小燕; 唐鹏鹏

    2015-01-01

    通过电聚合法制备了聚对氨基苯磺酸(PABSA)修饰玻碳电极(GCE),采用循环伏安法(CV)和差分脉冲伏安法(DPV)研究了盐酸吡哆辛(VB6)在该修饰电极上的电化学行为.结果表明,VB6在该修饰电极上的氧化电流显著增加,为裸电极上的7.5倍.在pH值3.0~6.5的醋酸缓冲溶液中,VB6在PABSA/GCE上的电极反应为吸附控制的一电子两质子的不可逆氧化反应.在优化条件下,使用DPV对VB6进行了定量检测,线性范围为0.04 ~ 100μmol/L,检出限为0.01 μnol/L,是目前所报道的电化学方法测定VB6的最低检出限,相对平均偏差为3.1%(n=8).采用本方法对维生素B6片中的VB6进行检测,回收率为106% ~ 108%.

  3. Determination of allantoin and pyridoxine hydrochloride in eye charm V eye drops by HPLC%高效液相色谱法测定中新滴眼液中尿囊素与维生素B6 的含量

    Institute of Scientific and Technical Information of China (English)

    梁蔚阳

    2002-01-01

    目的建立同时测定中新滴眼液中尿囊素与维生素B6含量的高效液相色谱法.方法采用Nova-Pak C18柱,流动相为甲醇-0.03 mol/L磷酸二氢钠溶液(10∶90),流速1.0 ml/min,检测波长230 nm,外标法计算.结果线性范围分别是:尿囊素0.205 4~4.108 mg/ml;维生素B6 0.010 1~0.202 0 mg/ml.回收率:尿囊素99.4%(RSD0.37%,n=5);维生素B6 99.5%(RSD 0.64%,n=5).结论此法分离效果好,辅料无干扰,快速、简便,适用于该制剂两组分的同时测定.

  4. 脑淋巴阻滞对大鼠蛛网膜下腔出血后脑血管痉挛的影响及吡哆醇的干预作用%Influence of cerebral lymphatic blockade on cerebral vasospasm after subarachnoid hemorrhage and the interventional effect of Pyridoxine in rats

    Institute of Scientific and Technical Information of China (English)

    王轩; 贾丽丽; 高向东; 高兵; 杨明峰; 孙保亮

    2010-01-01

    目的 探讨脑淋巴阻滞(CLB)对大鼠蛛网膜下腔出血(SAH)后脑血管痉挛(CVS)的影响及吡哆醇的干预作用.方法 60只Wistar大鼠随机分为正常对照组、SAH组、SAH+CLB组(CLB组)、SAH+CLB+吡哆醇组(吡哆醇组)、SAH+CLB+生理盐水组(生理盐水组).采用自体动脉血枕大池二次注血法建立SAH模型;用结扎颈部淋巴管、摘除淋巴结制作CLB模型;吡哆醇组于制模前30 min及随后每12 h腹腔注射吡哆醇.第二次注血后48 h,在体观察各组大鼠基底动脉(BA)管径,检测BA对乙酰胆碱(Ach)的反应性,HE染色观察BA病理学变化.结果 (1)BA管径:SAH组明显小于正常对照组(P<0.01);CLB组和生理盐水组明显小于SAH组(均P<0.01);吡哆醇组较CLB组明显增大(P<0.01).(2)BA对Ach反应性:SAH组较正常对照组降低(P<0.01);CLB组和生理盐水组较SAH组更低(均P<0.01);吡哆醇组较CLB组明显改善(P<0.01).(3)BA病理学变化:正常对照组BA内膜光滑;SAH组血管内皮细胞肿胀,管腔狭窄,与正常对照组比较差异有统计学意义(P<0.01);CLB组、生理盐水组管腔最窄,管壁最厚,大部分内皮细胞脱落(均P<0.01);吡哆醇组血管损害较CLB组明显减轻(均P<0.01).结论 CLB可加重大鼠SAH后CVS及脑血管损害;吡哆醇可以减轻这些损害.

  5. Content determination of pyridoxine hydrochloride and the related substance in Vitamin B6 Tablets by HPLC%高效液相色谱法测定维生素B6片中盐酸吡哆辛的含量和有关物质

    Institute of Scientific and Technical Information of China (English)

    郭栩丰

    2008-01-01

    目的:建立维生素B6片中盐酸吡哆辛含量测定及其有关物质检查方法.方法:高效液相色谱(HPLC)法,Hypersil ODS C18柱,以甲醇-0.2%磷酸(45∶55)为流动相,流速为1ml/min,检测波长为291 nm.结果:盐酸吡哆辛在0.2032~2.0320 μg范围内与峰面积线性关系良好,r=-0.999 8,平均回收率为99.71%,RSD为0.36%(n=6).结论:本方法简便,准确,迅速,重现性好.

  6. MORPHOFUNCTIONAL CHARACTERISTICS OF FIBROBLASTS (MCCOY CELL LINE CULTURED WITH MAGNESIUM PREPARATIONS

    Directory of Open Access Journals (Sweden)

    L. V. Didenko

    2015-01-01

    Full Text Available Aim. To study the effect of magnesium orotate, magnesium/pyridoxine combination and magnesium sulfate on fibroblast morphofunctional characteristics in cell culture of fibroblasts (McCoy line.Material and methods. The study of fibroblasts (McCoy line with the addition of magnesium-containing preparations (magnesium orotate, magnesium/pyridoxine combination, magnesium sulphate to the culture medium was performed using scanning and transmission electron microscopy.Results. When adding into the media magnesium orotate or magnesium/pyridoxine combination, significant changes in morphofunctional state of fibroblasts were noted, which were absent when adding magnesium sulfate. At that fibroblasts significantly promoted synthetic and secretory activity. This was expressed in the formation of amorphous and fibrous components in well-formed cell layers.Conclusion. Stimulation by magnesium ions of the proliferative activity of fibroblasts is shown in the morphological analysis of the effect of magnesium orotate or magnesium in combination with pyridoxine and magnesium sulfate on morphological and functional organization of fibroblasts. Revealed the predominant influence of magnesium orotate, and a less pronounced effect of magnesium in combination with pyridoxine on biosynthetic processes in the cells, including the synthesis of amorphous and fibrous components (protocollagen and elastin of the extracellular matrix founded.

  7. Thiamine and cyanocobalamin relieve neuropathic pain in rats: synergy with dexamethasone.

    Science.gov (United States)

    Caram-Salas, Nadia L; Reyes-García, Gerardo; Medina-Santillán, Roberto; Granados-Soto, Vinicio

    2006-01-01

    Treatment of neuropathic pain is an area of largely unmet medical need. Therefore, this pain may require the development of novel drug entities. In the search for alternatives, B vitamins have been found to be a clinically useful pharmacological tool for patients with neuropathic pain. However, preclinical studies supporting this use are lacking. In this study, we assessed the possible antiallodynic effects of thiamine, pyridoxine, and cyanocobalamin as well as dexamethasone and their combination on spinal nerve ligation induced allodynia. Sub cutaneous administration of thiamine (75-600 mg/kg), pyridoxine (75-600 mg/kg), cyanocobalamin(0.75-6 mg/kg), and dexamethasone (4-32 mg/kg) significantly reduced tactile allodynia in rats. Maximal antiallodynic effects were reached with 600 mg/kg of thiamine (approximately 58%), 600 mg/kg of pyridoxine (approximately 22%), 6 mg/kg of cyanocobalamin (approximately 73%), and 32 mg/kg of dexamethasone (approximately 68%). Since a small antiallodynic effect was observed with pyridoxine, this drug was not further analyzed in the combinations. Coadministration of thiamine or cyanocobalamin and dexamethasone remarkably reduced spinal nerve ligation induced allodynia (approximately 90%), showing a synergistic interaction between either thiamine or cyanocobalamin and dexamethasone. Our data indicate that thiamine and pyridoxine as well as the combination of B vitamins and dexamethasone are able to reduce tactile allodynia in rats and suggest the possible clinical use of these drugs in the treatment of neuropathic pain in human beings. Copyright 2006 S. Karger AG, Basel.

  8. Acute isoniazid neurotoxicity in childhood.

    Science.gov (United States)

    Citak, Agop; Kaya, Ozlen; Uçsel, Raif; Karaböcüoğlu, Metin; Uzel, Nedret

    2002-01-01

    Acute isoniazid (INH) poisoning is uncommon in children. Although most physicians are aware of INH hepatotoxicity, acute INH poisoning and its treatment are not well recognized. INH is increasingly being used to control the spread of tuberculosis, and physicians should know its potentially fatal effects. INH overdose is known to result in rapid onset of seizures, metabolic acidosis and prolonged obtundation. We report two cases of obtundation secondary to INH overdose that was immediately reversed by pyridoxine. Parenteral pyridoxine administration is an effective method in INH intoxication. The intravenous form of pyridoxine must be available in the emergency care units, and INH toxicity should be suspected in any patient with refractory seizures and metabolic acidosis.

  9. Vincristine induced cranial polyneuropathy.

    Science.gov (United States)

    Bay, Ali; Yilmaz, Cahide; Yilmaz, Nebi; Oner, Ahmet Faik

    2006-06-01

    We describe a 5-year-old girl showed recovery of vincristine induced cranial polyneuropathy with pyridoxine and pyridostigmine treatment. A 5-year-old girl was diagnosed preB cell Acute Lymphoblastic Leukemia (ALL). She received chemotherapy according to the previously described modified St. Jude total therapy studies XIII. Five days after the fourth dose of vincristine, she presented with bilateral ptosis. Neurological examination revealed bilateral ptosis, and complete external opthalmoplegia with normal pupillary and corneal reflexes. She received 3.8 mg cumulative dose of vincristin before development of ptosis. A neuroprotective and neuroregenerative treatment attempt with pyridoxine and pyridostigmine was initiated. The bilateral ptosis markedly improved after 7 days of pyridoxine and pyridostigmine treatment and completely resolved after two weeks. The both agents were given for 3 weeks and were well tolerated without any side effects. During the follow up period we did not observe residue or recurrence of the ptosis.

  10. Abnormal vitamin levels in patients receiving home total parenteral nutrition.

    Science.gov (United States)

    Mikalunas, V; Fitzgerald, K; Rubin, H; McCarthy, R; Craig, R M

    2001-01-01

    The administration of multivitamins to patients receiving home parenteral nutrition (HPN) was decreased from once daily to three times weekly during the parenteral multivitamin shortage in 1997. Blood vitamin levels were measured to examine whether the decrement in the infused vitamins affected the levels. Six patients with normal renal and liver function, receiving HPN for 6 months to 10 years, were studied 6 months after the institution of 10 mL of multivitamins thrice weekly. Two patients with renal insufficiency who required hemodialysis and HPN were also studied. Multivitamin administration was eliminated in one patient and was reduced to once weekly when elevated pyridoxine levels were found in association with possible neurotoxicity. Five of the six patients with normal renal function had low serum ascorbic acid levels. Serum riboflavin levels were found to be low in one patient, serum pyridoxine was low in one, serum retinoids were low in three, and serum niacin was low in one. There were no clinically obvious untoward effects caused by the vitamin deficiencies. Each of the dialysis patients had elevated serum pyridoxine levels and had some neurologic disturbance (peripheral neuropathy, involuntary movements). The serum pyridoxine levels fell to normal in each after the cessation or decrease of the multivitamin preparation. Ascorbic acid levels were low in one patient and fell into abnormally low levels in the other when the parenteral multivitamins were reduced, but they corrected with the separate administration of intravenous vitamin C. In conclusion, the reduced administration of multivitamins in 1997 resulted in diminished ascorbic acid levels in seven of eight patients receiving total parenteral nutrition. Less often, low levels of retinoids, niacin, pyridoxine, and riboflavin were seen. Patients with chronic renal failure receiving HPN with multivitamins may develop elevated pyridoxine levels, which might result in neurologic sequelae.

  11. Atypical Vitamin B-6 Deficiency A Rare Cause of Unexplained Neonatal and Infantile Epilepsies

    DEFF Research Database (Denmark)

    Baumgart, A.; von Spiczak, S.; Verhoeven-Duif, N. M.

    2014-01-01

    . We identified 1 patient with an epilepsy phenotype resembling Dravet syndrome and likely pathogenic mutations in ALDH7A1. Presenting features were highly atypical of pyridoxine-dependent epilepsy, including febrile seizures, response to anticonvulsive drugs, and periods of seizure freedom without......ALDH7A1 and PNPO deficiencies are rare inborn errors of vitamin B-6 metabolism causing perinatal seizure disorders. The phenotypic variability, however, is broad. To assess the frequency of these deficiencies in unexplained infantile epilepsy, we screened 113 patients for mutations in both genes...... pyridoxine treatment. "Hidden" vitamin B-6 deficiencies might be rare but treatable causes of unexplained epilepsy extending beyond the classical phenotypes....

  12. A new pharmacologic treatment for nausea and vomiting of pregnancy.

    Science.gov (United States)

    Fantasia, Heidi Collins

    2014-01-01

    Nausea and vomiting of pregnancy (NVP) affects up to 80 percent of pregnant women. This condition is usually self-limiting, but the symptoms can be distressing and interfere with work, social activities and sleep. Symptoms can often be managed by diet and lifestyle changes, but these interventions may not be successful for everyone. In April 2013, the U.S. Food and Drug Administration approved doxylamine succinate 10 mg/pyridoxine hydrochloride 10 mg (Diclegis) as the first medication to specifically treat NVP in more than 30 years. This article reviews the indications, dosage and nursing interventions associated with using doxylamine succinate/pyridoxine to treat NVP.

  13. Roles of Breast Cancer Susceptibility Genes BRCA’s in Mammary Epithelial Cell Differentiation

    Science.gov (United States)

    2006-03-01

    associated factor 3 - 3.0 IFNAR1 AA133989 interferon (alpha, beta and omega) receptor 1 -3.1 PDXK AW449022 pyridoxal ( pyridoxine , vitamin B6...IFNAR1 AA133989 Interferon (, , and ) receptor 1 3.1 PDXK AW449022 Pyridoxal ( pyridoxine , vitamin B6) kinase 4.0 HTATIP2 BC002439 HIV-1 Tat...evaluate the risk of breast cancer. N Engl J Med 336, 1409-1415. 26 Cullmann, G., Fien, K., Kobayashi, R., and Stillman, B. (1995). Characterization

  14. HPLC法同时测定多维元素胶囊中烟酰胺、维生素B6、维生素B1和维生素B2的含量%Determination of the contents of nicotinamide, pyridoxine hydrochloride, thiamine hydrochloride and riboflavin in oil-and water-soluble vitamins with minerals capsule by HPLC

    Institute of Scientific and Technical Information of China (English)

    王琛; 陈彬彬; 邹梅娟; 程刚

    2010-01-01

    目的 建立多维元素胶囊中烟酰胺、维生素B6、维生素B1和维生素B2的HPLC含量测定方法.方法 采用DiamonsiL C18柱(5μm,4.6mm×250mm),流动相为庚烷磺酸钠溶液(取庚烷磺酸钠0.6g,1000mL水溶解,加三乙胺2.8mL,用冰醋酸调节pH值至3.0)-甲醇(体积比6:1);流速:1.0 mL·min-1;检测波长:选择280nm;柱温:40℃;进样量:20μL.结果 烟酰胺在30.0~152.0μg·mL-1(r=0.9997)、维生素B6在1.0~5.0μg·mL-1(r=0.9998)、维生素B1在10.5~52.5μg·mL-1(r=0.9998)、维生素B2在10.5~52.0μg·mL-1(r=0.9997)范围内均呈良好的线性关系,平均回收率分别为99.95%(RSD=0.43%)、100.50%(RSD=1.33%)、100.30%(RSD=0.88%)和100.50%(RSD=0.90%).结论 建立的方法灵敏度高、准确度和重现性好,可作为多维元素胶囊的质量控制方法之一.

  15. AcEST: DK946064 [AcEST

    Lifescience Database Archive (English)

    Full Text Available DDVNHINKH 526 ESEVLT ADD +HINK+ Sbjct: 121 ESEVLTLADDAHHINKN 137 >sp|O59905|PDX1_CERNC Pyridoxine biosynthesis protein PDX1 OS=Cercos...pora nicotianae GN=PDX1 PE=1 SV=1 Length = 343 Score = 195 bits (496), Expect = 1e-

  16. Preparação e caracterização espectroscópica de complexos de boro: uma proposta para uma prática integrada de química inorgânica Preparation and spectroscopic characterization of boron complexes: a proposal for an integrated inorganic laboratory

    Directory of Open Access Journals (Sweden)

    Karl Eberhard Bessler

    2010-01-01

    Full Text Available As a proposal for an undergraduate second or third year inorganic laboratory course, the present paper describes the preparation of three representative boron complexes: potassium tetrafluoroborate, pyridoxin boron complex and potassium bis(oxalatoborate. The complexes are characterised by infrared and multinuclear magnetic resonance spectroscopy (¹H, 11B and 19F where isotopic effects are demonstrated.

  17. The measurement of urinary Delta(1)-piperideine-6-carboxylate, the alter ego of alpha-aminoadipic semialdehyde, in Antiquitin deficiency.

    NARCIS (Netherlands)

    Struys, E.A.; Bok, L.A.; Emal, D.; Houterman, S.; Willemsen, M.A.A.P.; Jakobs, C.

    2012-01-01

    The assessment of urinary alpha-aminoadipic semialdehyde (alpha-AASA) has become the diagnostic laboratory test for pyridoxine dependent seizures (PDS). alpha-AASA is in spontaneous equilibrium with its cyclic form Delta(1)-piperideine-6-carboxylate (P6C); a molecule with a heterocyclic ring structu

  18. EFSA Panel on Dietetic Products, Nutrition and Allergies (NDA); Scientific Opinion on the substantiation of a health claim related to KF2BL20 and maintenance of normal hair pursuant to Article 13(5) of Regulation (EC) No 1924/2006

    DEFF Research Database (Denmark)

    Tetens, Inge

    related to KF2BL20, which is a combination of keratin, copper, zinc, niacin, pantothenic acid, pyridoxine and D-biotin, and maintenance of normal hair. The Panel considers that KF2BL20 is sufficiently characterised. The claimed effect is “helps to reinforce hair strength and normal hair function...

  19. Effect of consumption of red wine, spirits and beer on serum homocysteine

    NARCIS (Netherlands)

    Gaag, M.S. van der; Ubbink, J.B.; Sillanaukee, P.; Nikkari, S.; Hendriks, H.F.J.

    2000-01-01

    Serum homocysteine increases after moderate consumption of red wine and spirits, but not after moderate consumption of beer. Vitamin B6 in beer seems to prevent the alcohol-induced rise in serum homocysteine. Chemicals/CAS: Homocysteine, 454-28-4; Pyridoxine, 65-23-6

  20. Drug: D08830 [KEGG MEDICUS

    Lifescience Database Archive (English)

    Full Text Available D08830 Mixture, Drug Retinol palmitate - thiamine nitrate - riboflavin - pyridoxine...tic category of drugs in Japan [BR:br08301] 3 Agents affecting metabolism 31 Vita...mins 317 Multivitamin preparations 3179 Others D08830 Retinol palmitate - thiamine nitrate - riboflavin - py

  1. Effect of exogenous hormones on transcription levels of pyridoxal 5'-phosphate biosynthetic enzymes in the silkworm (Bombyx mori).

    Science.gov (United States)

    Huang, ShuoHao; Yang, HuanHuan; Yao, LiLi; Zhang, JianYun; Huang, LongQuan

    2016-01-01

    Vitamin B6 includes 6 pyridine derivatives, among which pyridoxal 5'-phosphate is a coenzyme for over 140 enzymes. Animals acquire their vitamin B6 from food. Through a salvage pathway, pyridoxal 5'-phosphate is synthesized from pyridoxal, pyridoxine or pyridoxamine, in a series of reactions catalyzed by pyridoxal kinase and pyridoxine 5'-phosphate oxidase. The regulation of pyridoxal 5'-phospahte biosynthesis and pyridoxal 5'-phospahte homeostasis are at the center of study for vitamin B6 nutrition. How pyridoxal 5'-phosphate biosynthesis is regulated by hormones has not been reported so far. Our previous studies have shown that pyridoxal 5'-phosphate level in silkworm larva displays cyclic developmental changes. In the current study, effects of exogenous juvenile hormone and molting hormone on the transcription level of genes coding for the enzymes involved in the biosynthesis of pyridoxal 5'-phospahte were examined. Results show that pyridoxal kinase and pyridoxine 5'-phosphate oxidase are regulated at the transcription level by development and are responsive to hormones. Molting hormone stimulates the expression of genes coding for pyridoxal kinase and pyridoxine 5'-phosphate oxidase, and juvenile hormone appears to work against molting hormone. Whether pyridoxal 5'-phosphate biosynthesis is regulated by hormones in general is an important issue for further studies.

  2. Antitubercular drug poisoning in a pregnant woman

    Directory of Open Access Journals (Sweden)

    Rahul Dutta

    2010-01-01

    Full Text Available A 20-year-old female in her third month of pregnancy, presented with generalised tonic clonic seizures, metabolic acidosis and coma following suicidal ingestion of antitubercular medication. We successfully managed the case with pyridoxine, sodium bicarbonate and mechanical ventilation.

  3. Suture supported P C IOL in a homocystinuric child.

    Directory of Open Access Journals (Sweden)

    Bhatti S

    1996-01-01

    Full Text Available A homocystinuric child presented with a secondary pupillary block glaucoma due to anteriorly subluxated lens. After removal of the subluxated lens, a suture supported posterior chamber IOL was implanted. Postoperative complication of cerebral venous thrombosis following general anaesthesia was managed with high doses of pyridoxine special diet and drugs.

  4. Diversity of cystathionine ß-synthase haplotypes bearing the most common homocystinuria mutation c.833T>C: a possible role for gene conversion

    DEFF Research Database (Denmark)

    Vyletal, P; Sokolová, J; Cooper, DN;

    2007-01-01

    Homozygosity or compound heterozygosity for the c.833T>C transition (p.I278 T) in the cystathionine beta-synthase (CBS) gene represents the most common cause of pyridoxine-responsive homocystinuria in Western Eurasians. However, the frequency of the pathogenic c.833C allele, as observed in healthy...

  5. Chinese restaurant syndrome

    Directory of Open Access Journals (Sweden)

    Balachandran C

    1991-01-01

    Full Text Available A 24-year-old Chinese student with history of recurrent attacks of flushing with burning and dryness of face of 4 years duration showed exacerbation of the symptoms after oral provocation with 1 mg of Chinese salt. Patient was treated with 50 mg pyridoxine daily and restriction of the Chinese salt in diet with moderate improvement.

  6. An intriguing "silent" mutation and a founder effect in antiquitin (ALDH7A1).

    NARCIS (Netherlands)

    Salomons, G.S.; Bok, L.A.; Struys, E.A.; Pope, L.L.; Darmin, P.S.; Mills, P.B.; Clayton, P.T.; Willemsen, M.A.A.P.; Jakobs, C.

    2007-01-01

    Recently, alpha-aminoadipic semialdehyde (alpha-AASA) dehydrogenase deficiency was shown to cause pyridoxine-dependent epilepsy in a considerable number of patients. alpha-AASA dehydrogenase deficiency is an autosomal recessive disorder characterized by a neonatal-onset epileptic encephalopathy in w

  7. The biochemistry of vitamin B6 is basic to the cause of the Chinese restaurant syndrome.

    Science.gov (United States)

    Folkers, K; Shizukuishi, S; Willis, R; Scudder, S L; Takemura, K; Longenecker, J B

    1984-03-01

    The concept of this basic research was that monosodium L-glutamate could reveal a deficiency of vitamin B6 by the neurological reactions known as the Chinese Restaurant Syndrome. An other amino acid, tryptophan, administered to subjects, is known to reveal a deficiency of vitamin B6 by the excretory xanthurenic acid, etc. The presence and degree of a deficiency of vitamin B6 in 155 students on no supplemental B6 was determined by the differential assay of aspartate transaminase of erythrocytes which also allows each subject to be a control. Twenty-seven of 155 students had extraordinarily low basal specific activities of the transaminase, less than 0.26 mumol pyruvate/(h X 10(8) erythrocytes). These 27 were challenged with glutamate and a placebo. Twelve of 27 revealed the Chinese Restaurant Syndrome, and 15 did not. By double blind trials, the 12 "responders" were treated with pyridoxine and a placebo for twelve weeks, and then were rechallenged with glutamate and a placebo. Decoding showed 3 of 12 received placebo to pyridoxine and then revealed the symptoms of the syndrome again to glutamate; 9 of 12 received pyridoxine and then 8 of 9 failed to respond to glutamate. These results show, p less than 0.01, that the symptoms of the Chinese Restaurant Syndrome to oral glutamate fail to reoccur after treatment which pyridoxine, and that the biochemistry of vitamin B6 is basic to the cause of the Chinese Restaurant Syndrome.

  8. Neonatal vitamin-responsive epileptic encephalopathies.

    Science.gov (United States)

    Gospe, Sidney M

    2010-01-01

    The treatment of neonatal seizures generally relies on the use of one or more anticonvulsant medications along with evaluation and management of any underlying etiology. In some circumstances, neonatal seizures are refractory to therapy and result in poor outcomes, including death. Certain rare vitamin- responsive inborn errors of metabolism may present as neonatal encephalopathy with anticonvulsant-resistant seizures. Therefore, it is vital for the clinicians of caring for seizing encephalopathic newborns to consider these particular disorders early in the hospital course. Pyridoxine-dependent seizures are due to deficiency of alpha-aminoadipic semialdehyde dehydrogenase (antiquitin) which is encoded by ALDH7A1. Seizures in infants who are pyridoxine-dependent must be treated using pharmacologic doses of pyridoxine (vitamin B(6)), and life-long therapy is required. Despite medical therapy, developmental handicaps, particularly in expressive language, are common. Folinic acidresponsive seizures are treated with supplements of folinic acid (5-formyltetrahydrofolate). Recently, patients with this condition were also demonstrated to be antiquitin deficient. Pyridoxal phosphate-dependent seizures result from a deficiency of pyridox(am)ine 5'-phosphate oxidase which is encoded by PNPO. Patients with this cause of seizures respond to pyridoxal phosphate but not to pyridoxine. This review discusses our current understanding of these three neonatal vitamin-responsive epileptic encephalopathies and a diagnostic and treatment protocol is proposed.

  9. The Effects of Various Levels of Ascorbic Acid Intake Upon Oral Wound Healing in Guinea Pigs.

    Science.gov (United States)

    1983-01-01

    Carotene, ppm 3 Thiamin, ppm 5 Ribof’lavin, ppm 6 Niacin, ppm 50 Pantothenic Acid, ppm 19 Choline, ppm X 100 18 Folic Acid, ppm 4 Pyridoxines ppm 4...Overnutrition in Prenatal and Neonatal Life: A Problem? Can. Ned. Assoc. J. .Us 893, 1965. 814. Lowry, O.H., Bessey, O.A., and Burch, R.B.s Effects of Prolonged

  10. Preparative Production of Acetylcholinesterase and Paraoxonase in Procaryotic and Eucaryotic Expression in Systems

    Science.gov (United States)

    2006-01-01

    agar and screened with the target substrate. Positive colonies (as determined by the appearance of a colored or fluorescent product) were transferred...natural amino acids, with the exception of L-methionine, 40µg/ml of seleno-L-methionine, 1µg/ml of vitamins ( Riboflavin , Niacinamide, Pyridoxine

  11. Pantothenic acid (Vitamin B5)

    Science.gov (United States)

    ... vitamin B5 (pantothenic acid), vitamin B6 (pyridoxine), vitamin B12 (cyanocobalamin), and folic acid. However, some products do ... Pantothenas, Calcium D-Pantothenate, Calcium Pantothenate, Complexe de Vitamines B, D-Calcium Pantothenate, D-Panthenol, D-Panthénol, ...

  12. Maternal dietary B vitamin intake, other than folate, and the association with orofacial cleft in the offspring.

    NARCIS (Netherlands)

    Krapels, I.P.C.; Rooij, I.A.L.M. van; Ocke, M.C.; Cleef, B. van; Kuijpers-Jagtman, A.M.; Steegers-Theunissen, R.P.M.

    2004-01-01

    BACKGROUND: Periconceptional folic acid supplementation is suggested to prevent orofacial clefts (OFCs). Other B vitamins however may be beneficial as well. AIM OF THE STUDY: To investigate the maternal periconceptional dietary intake of thiamine, riboflavin, niacin, pyridoxine and cobalamin in asso

  13. Interaction of Inorganic Nanoparticles With Cell Membranes

    Science.gov (United States)

    2008-10-20

    Apart from differences in glucose content the main differences lie in the presence/absence of e.g. sodium pyruvate pyridoxine , L-arginine, L-proline and...Science Foundation Projects., especially in the Framework of the new Swiss National Research Program “Changes and Risk of Nanotechnology” which is

  14. Dietary intake of the water-soluble vitamins B1, B2, B6, B12 and C in 10 countries in the European Prospective Investigation into Cancer and Nutrition

    NARCIS (Netherlands)

    Olsen, A.; Halkjaer, J.; van Gils, C. H.; Buijsse, B.; Verhagen, H.; Jenab, M.; Boutron-Ruault, M. C.; Ericson, U.; Ocke, M. C.; Peeters, P. H. M.; Touvier, M.; Niravong, M.; Waaseth, M.; Skeie, G.; Khaw, K. T.; Travis, R.; Ferrari, P.; Sanchez, M. J.; Agudo, A.; Overvad, K.; Linseisen, J.; Weikert, C.; Sacerdote, C.; Evangelista, A.; Zylis, D.; Tsiotas, K.; Manjer, J.; van Guelpen, B.; Riboli, E.; Slimani, N.; Bingham, S.

    2009-01-01

    Objectives: To describe the intake of vitamins thiamine (B1), riboflavin (B2), B6 (pyridoxine), B12 (cobalamine) and C (ascorbic acid) and their food sources among 27 centres in 10 countries participating in the European Prospective Investigation into Cancer and Nutrition (EPIC) study. Methods: Betw

  15. An intriguing "silent" mutation and a founder effect in antiquitin (ALDH7A1).

    NARCIS (Netherlands)

    Salomons, G.S.; Bok, L.A.; Struys, E.A.; Pope, L.L.; Darmin, P.S.; Mills, P.B.; Clayton, P.T.; Willemsen, M.A.A.P.; Jakobs, C.

    2007-01-01

    Recently, alpha-aminoadipic semialdehyde (alpha-AASA) dehydrogenase deficiency was shown to cause pyridoxine-dependent epilepsy in a considerable number of patients. alpha-AASA dehydrogenase deficiency is an autosomal recessive disorder characterized by a neonatal-onset epileptic encephalopathy in w

  16. Physical Characteristics of Magnetic Bacteria and Their Electromagnetic Properties in the Frequency Range of 1 - 400 GHz

    Science.gov (United States)

    1987-05-14

    Vitamin medium containing per liter: Biotin 20 mg Folic acid 20 mg B-6 ( pyridoxine HCI) 100 mg B-1 (thiamine CId) 50 mg B-2 (riboflavin) 50 mg Niacin 50 mg...protrusions (MM). Cup-shaped depressions with raised rims (MM) were interpreted to be regions through which the fracture plane had passed with removal of

  17. Massive venlafaxine overdose resulted in a false positive Abbott AxSYM (R) urine immunoassay for phencyclidine

    NARCIS (Netherlands)

    Bond, GR; Steele, PE; Uges, DRA

    2003-01-01

    Case report: A 13-yr-old girl overdosed on 48 x 150 mg venlafaxine (Effexor XR(R)). She was taking venlafaxine regularly for depression. Her only other medications included topical Benzamycin and pyridoxine 50 mg daily for acne. The Abbott AxSYM(R) assay was positive only for phencyclidine, but GC/M

  18. Effect of Monomethylhydrazine on Insulin Levels in Rats

    Science.gov (United States)

    1976-08-01

    pyridoxine was effective against MMH-induced hyper- glycemia (Dost et al., 1973). The following experiments were done to deter- mine if the...or 6 carbon positions to 1 4C02 is depressed in rats exposed to MEIH. Since the turnover of pyruvate-2- 1 4G, acetate-2-1 4 C and butyric acid-l- 1 4

  19. Fatal overdose from Bendectin.

    Science.gov (United States)

    Bayley, M; Walsh, F M; Valaske, M J

    1975-05-01

    A three-year old male ingested approximately 100 tablets of Bendectin. He developed tonic-clonic seizures followed by cardiac arrest. Toxicologic analysis yielded high levels of doxylamine, dicyclomine, and pyridoxine in blood, peritoneal fluid, and tissue homogenates. The antihistamine, doxylamine succinate appears to be the toxic constituent. Analytical methods used to document the case are herein described.

  20. Isoniazid overdose in the Cambodian population of Olmsted County, Minnesota.

    Science.gov (United States)

    Blanchard, P D; Yao, J D; McAlpine, D E; Hurt, R D

    1986-12-12

    Eight cases of suicidal isoniazid overdose by Cambodian refugees are reviewed. In all patients generalized seizures and metabolic acidosis developed. Treatment included supportive measures and intravenous pyridoxine hydrochloride. There were no deaths. Psychiatric evaluation of each patient revealed usual and extraordinary life and social adjustment stresses. Indochinese immigrants are a subpopulation at risk for isoniazid overdose.

  1. Proprioceptive neuropathy affects normalization of the H-reflex by exercise after spinal cord injury.

    Science.gov (United States)

    Ollivier-Lanvin, Karen; Keeler, Benjamin E; Siegfried, Rachel; Houlé, John D; Lemay, Michel A

    2010-01-01

    The H-reflex habituates at relatively low frequency (10 Hz) stimulation in the intact spinal cord, but loss of descending inhibition resulting from spinal cord transection reduces this habituation. There is a return towards a normal pattern of low-frequency habituation in the reflex activity with cycling exercise of the affected hind limbs. This implies that repetitive passive stretching of the muscles in spinalized animals and the accompanying stimulation of large (Group I and II) proprioceptive fibers has modulatory effects on spinal cord reflexes after injury. To test this hypothesis, we induced pyridoxine neurotoxicity that preferentially affects large dorsal root ganglia neurons in intact and spinalized rats. Pyridoxine or saline injections were given twice daily (IP) for 6 weeks and half of the spinalized animals were subjected to cycling exercise during that period. After 6 weeks, the tibial nerve was stimulated electrically and recordings of M and H waves were made from interosseous muscles of the hind paw. Results show that pyridoxine treatment completely eliminated the H-reflex in spinal intact animals. In contrast, transection paired with pyridoxine treatment resulted in a reduction of the frequency-dependent habituation of the H-reflex that was not affected by exercise. These results indicate that normal Group I and II afferent input is critical to achieve exercise-based reversal of hyper-reflexia of the H-reflex after spinal cord injury.

  2. Acute isoniazid intoxication: an uncommon cause of convulsion, coma and acidosis.

    Science.gov (United States)

    Uzman, Sinan; Uludağ Yanaral, Tümay; Toptaş, Mehmet; Koç, Alparslan; Taş, Aytül; Bican, Gülşen

    2013-01-01

    Despite the widespread use, suicidal ingestion of isoniazid is a rare condition in Turkey. We reported a case of acute isoniazid intoxication associated with alcohol intake presenting with convulsion, coma and metabolic acidosis. The patient was treated successfully with intravenous pyridoxine administration. Early recognation and appropriate treatment in the intensive care unit is very important to prevent mortality in patients with acute isoniazid toxicity.

  3. Epilepsy due to PNPO mutations: genotype, environment and treatment affect presentation and outcome

    Science.gov (United States)

    Mills, Philippa B.; Camuzeaux, Stephane S.M.; Footitt, Emma J.; Mills, Kevin A.; Gissen, Paul; Fisher, Laura; Das, Krishna B.; Varadkar, Sophia M.; Zuberi, Sameer; McWilliam, Robert; Stödberg, Tommy; Plecko, Barbara; Baumgartner, Matthias R.; Maier, Oliver; Calvert, Sophie; Riney, Kate; Wolf, Nicole I.; Livingston, John H.; Bala, Pronab; Morel, Chantal F.; Feillet, François; Raimondi, Francesco; Del Giudice, Ennio; Chong, W. Kling; Pitt, Matthew

    2014-01-01

    The first described patients with pyridox(am)ine 5’-phosphate oxidase deficiency all had neonatal onset seizures that did not respond to treatment with pyridoxine but responded to treatment with pyridoxal 5’-phosphate. Our data suggest, however, that the clinical spectrum of pyridox(am)ine 5’-phosphate oxidase deficiency is much broader than has been reported in the literature. Sequencing of the PNPO gene was undertaken for a cohort of 82 individuals who had shown a reduction in frequency and severity of seizures in response to pyridoxine or pyridoxal 5’-phosphate. Novel sequence changes were studied using a new cell-free expression system and a mass spectrometry-based assay for pyridoxamine phosphate oxidase. Three groups of patients with PNPO mutations that had reduced enzyme activity were identified: (i) patients with neonatal onset seizures responding to pyridoxal 5’-phosphate (n = 6); (ii) a patient with infantile spasms (onset 5 months) responsive to pyridoxal 5’-phosphate (n = 1); and (iii) patients with seizures starting under 3 months of age responding to pyridoxine (n = 8). Data suggest that certain genotypes (R225H/C and D33V) are more likely to result in seizures that to respond to treatment with pyridoxine. Other mutations seem to be associated with infertility, miscarriage and prematurity. However, the situation is clearly complex with the same combination of mutations being seen in patients who responded and did not respond to pyridoxine. It is possible that pyridoxine responsiveness in PNPO deficiency is affected by prematurity and age at the time of the therapeutic trial. Other additional factors that are likely to influence treatment response and outcome include riboflavin status and how well the foetus has been supplied with vitamin B6 by the mother. For some patients there was a worsening of symptoms on changing from pyridoxine to pyridoxal 5’-phosphate. Many of the mutations in PNPO affected residues involved in binding flavin

  4. Effect of dietary B vitamins on BMD and risk of fracture in elderly men and women: the Rotterdam study.

    Science.gov (United States)

    Yazdanpanah, Nahid; Zillikens, M Carola; Rivadeneira, Fernando; de Jong, Robert; Lindemans, Jan; Uitterlinden, André G; Pols, Huibert A P; van Meurs, Joyce B J

    2007-12-01

    A mildly elevated homocysteine (Hcy) level is a novel and potentially modifiable risk factor for age-related osteoporotic fractures. Elevated Hcy levels can have a nutritional cause, such as inadequate intake of folate, riboflavin, pyridoxine or cobalamin, which serve as cofactors or substrates for the enzymes involved in the Hcy metabolism. We examined the association between intake of Hcy-related B vitamin (riboflavin, pyridoxine, folate and cobalamin) and femoral neck bone mineral density BMD (FN-BMD) and the risk of fracture in a large population-based cohort of elderly Caucasians. We studied 5304 individuals aged 55 years and over from the Rotterdam Study. Dietary intake of nutrients was obtained from food frequency questionnaires. Incident non-vertebral fractures were recorded during a mean follow-up period of 7.4 years, and vertebral fractures were assessed by X-rays during a mean follow-up period of 6.4 years. We observed a small but significant positive association between dietary pyridoxine (beta = 0.09, p = 1 x 10(-8)) and riboflavin intake (beta = 0.06, p = 0.002) and baseline FN-BMD. In addition, after controlling for gender, age and BMI, pyridoxine intake was inversely correlated to fracture risk. As compared to the three lowest quartiles, individuals in the highest quartile of age- and energy-adjusted dietary pyridoxine intake had a decreased risk of non-vertebral fractures (HR = 0.77, 95% CI = 0.65-0.92, p = 0.005) and of fragility fractures (HR = 0.55, 95% CI = 0.40-0.77, p = 0.0004). Further adjustments for other dietary B vitamins (riboflavin, folate and cobalamin), dietary intake of calcium, vitamin D, vitamin A and vitamin K, protein and energy intake, smoking and BMD did not essentially modify these results. We conclude that increased dietary riboflavin and pyridoxine intake was associated with higher FN-BMD. Furthermore, we found a reduction in risk of fracture in relation to dietary pyridoxine intake independent of BMD. These findings

  5. Vitamin B6 in clinical neurology.

    Science.gov (United States)

    Bernstein, A L

    1990-01-01

    Many conditions in clinical neurology may be responsive to pyridoxine as a therapeutic agent. The current difficulty is in trying to isolate the conditions that are most likely to respond. Treating seizures is a major part of a neurologic practice. Our current therapeutic agents are only partially successful and limited by multiple side effects. One problem is that patients often have to take these agents for an entire lifetime, further raising the risk of toxicity. If pyridoxine supplementation can improve the efficacy of currently used medications, it will be gladly accepted into our therapeutic arsenal. Headache, chronic pain, and depression all appear to run together in many of our patients. The observations that serotonin deficiency is a common thread between them and that pyridoxine can raise serotonin levels open a wide range of therapeutic options. Small studies have been carried out with mixed success. Comparison with amitriptyline in the treatment of headache appears to show about equal efficacy, although side effects would be expected to be more of a problem with the amitriptyline. Behavioral disorders are relatively common and continue to be a major problem, disrupting the lives of the patients and their families. Current treatments are not acceptable to most people because of the risk of side effects with long-term usage. If, as Dr. Feingold suggests, many of these problems are caused by "toxic" exposures to chemicals that are pyridoxine antagonists, supplementation at early ages may reduce the incidence of hyperactivity and aggressive behavior. This raises the question of safety. Is pyridoxine safe for long-term use in large segments of the population, including children? The studies on children with Down's syndrome and autism, utilizing much higher doses than are used for other therapeutic purposes, seem to indicate relative safety if carefully monitored. Studies involving large population groups with carpal tunnel syndrome, all adults, using 100

  6. B6-responsive disorders: a model of vitamin dependency.

    Science.gov (United States)

    Clayton, Peter T

    2006-01-01

    Pyridoxal phosphate is the cofactor for over 100 enzyme-catalysed reactions in the body, including many involved in the synthesis or catabolism of neurotransmitters. Inadequate levels of pyridoxal phosphate in the brain cause neurological dysfunction, particularly epilepsy. There are several different mechanisms that lead to an increased requirement for pyridoxine and/or pyridoxal phosphate. These include: (i) inborn errors affecting the pathways of B(6) vitamer metabolism; (ii) inborn errors that lead to accumulation of small molecules that react with pyridoxal phosphate and inactivate it; (iii) drugs that react with pyridoxal phosphate; (iv) coeliac disease, which is thought to lead to malabsorption of B(6) vitamers; (v) renal dialysis, which leads to increased losses of B(6) vitamers from the circulation; (vi) drugs that affect the metabolism of B(6) vitamers; and (vii) inborn errors affecting specific pyridoxal phosphate-dependent enzymes. The last show a very variable degree of pyridoxine responsiveness, from 90% in X-linked sideroblastic anaemia (delta-aminolevulinate synthase deficiency) through 50% in homocystinuria (cystathionine beta-synthase deficiency) to 5% in ornithinaemia with gyrate atrophy (ornithine delta-aminotransferase deficiency). The possible role of pyridoxal phosphate as a chaperone during folding of nascent enzymes is discussed. High-dose pyridoxine or pyridoxal phosphate may have deleterious side-effects (particularly peripheral neuropathy with pyridoxine) and this must be considered in treatment regimes. None the less, in some patients, particularly infants with intractable epilepsy, treatment with pyridoxine or pyridoxal phosphate can be life-saving, and in other infants with inborn errors of metabolism B(6) treatment can be extremely beneficial.

  7. Drug-pyridoxal phosphate interactions.

    Science.gov (United States)

    Ebadi, M; Gessert, C F; Al-Sayegh, A

    1982-01-01

    In this review it has been pointed out that vitamin B6 and its vitamers can be involved in many interactions with a number of drugs, as well as with the actions of various endocrines and neurotransmitters. Nutritional deficiencies, especially of vitamins and proteins, can affect the manner in which drugs undergo biotransformation, and thereby may also modify the therapeutic efficacy of certain drugs. The differences between nutritional vitamin B6 deficiency and the hereditary disorder producing pyridoxine dependency are discussed. In addition to a pyridoxine deficiency being able to adversely affect drug actions, the improper supplementation with vitamin B6 can in some instances also adversely affect drug efficacy. A decrease by pyridoxine in the efficacy of levodopa used in the treatment of Parkinsonism is an example. The interrelationships and enzymatic interconversions among pyridoxine vitamers, both phosphorylated and non-phosphorylated, are briefly discussed, particularly regarding their pharmacokinetic properties. The ways in which the normal biochemical functions of vitamin B6 may be interfered with by various drugs are reviewed. (1) The chronic administration of isoniazid for the prevention or treatment of tuberculosis can produce peripheral neuropathy which can be prevented by the concurrent administration of pyridoxine. An acute toxic overdose of isoniazid causes generalized convulsions, and the intravenous administration of pyridoxine hydrochloride will prevent or stop these seizures. (2) The acute ingestion of excessive monosodium glutamate will, in some individuals, cause a group of symptoms including among others headache, weakness, stiffness, and heartburn, collectively known as the 'Chinese Restaurant Syndrome.' These symptoms can be prevented by prior supplementation with vitamin B6. The beneficial effect is ascribed to the correction of a deficiency in the activity of glutamic oxaloacetic transaminase, an enzyme that is dependent on pyridoxal

  8. An open-label pilot study to assess the effectiveness of krill oil with added vitamins and phytonutrients in the relief of symptoms of PMS

    Directory of Open Access Journals (Sweden)

    Wakeman MP

    2013-09-01

    Full Text Available Michael P Wakeman School of Cancer Sciences, University of Birmingham, Edgbaston, Birmingham, West Midlands, UK Abstract: An open-label pilot study over 4 months to evaluate the effectiveness of a compound formulation of ingredients, which individually have been demonstrated to be implicated in the pathogenesis of premenstrual syndrome to ameliorate the most troublesome symptoms of the condition. The supplement provided thiamine, riboflavin, pyridoxine, vitamin D, soy isoflavones, rosemary extract, and krill oil and was taken each day for the 3 months of the trial. Statistically significant effect was reported by the 29 women who completed the study in relief of anxiety, bloating, mood swings, breast tenderness, skin outbreaks, food cravings, fatigue, forgetfulness, insomnia, and headache after 3 months of treatment compared with baseline. This pilot study indicates the formulation to be effective, and a larger placebo-controlled trial is now planned. Keywords: thiamine, riboflavin, pyridoxine, vitamin D, soy isoflavones, rosemary extract, premenstrual syndrome

  9. Synthesis of B6 vitamin

    Directory of Open Access Journals (Sweden)

    Vučijak Nevena Ž.

    2009-01-01

    Full Text Available The importance of vitamin B6 has been known since its discovery in the 1940's. Chemical tests, elestrometric titration determinations, and absorption spectrum studies showed that this vitamin exists in three major chemical forms: pyridoxine (an alcohol, pyridoxal (an aldehyde, and pyridoxamine (a primary amine. Vitamin B6 is needed for more than 100 enzymes involved in protein metabolism, and it is assumed that this vitamin is cofactor of metabolic processes more important than any other substance. A deficiency of vitamin B6 in the human diet leads to severe disorders. Vitamin B6 is necessary for the proper function of the immune and nervous system, and helps the body convert protein to energy. This paper describes the history, properties and applications of vitamin B6, elucidation of chemical structure, and different procedures for synthesis of pyridoxine and pyridoxamine.

  10. An intriguing "silent" mutation and a founder effect in antiquitin (ALDH7A1).

    Science.gov (United States)

    Salomons, Gajja S; Bok, Levinus A; Struys, Eduard A; Pope, Lorna Landegge; Darmin, Patricia S; Mills, Philippa B; Clayton, Peter T; Willemsen, Michèl A; Jakobs, Cornelis

    2007-10-01

    Recently, alpha-aminoadipic semialdehyde (alpha-AASA) dehydrogenase deficiency was shown to cause pyridoxine-dependent epilepsy in a considerable number of patients. alpha-AASA dehydrogenase deficiency is an autosomal recessive disorder characterized by a neonatal-onset epileptic encephalopathy in which seizures are resistant to antiepileptic drugs but respond immediately to the administration of pyridoxine (OMIM 266100). Increased plasma and urinary levels of alpha-AASA are associated with pathogenic mutations in the alpha-AASA dehydrogenase (ALDH7A1/antiquitin) gene. Here, we report an intriguing "silent" mutation in ALDH7A1, a novel missense mutation and a founder mutation in a Dutch cohort (10 patients) with alpha-AASA dehydrogenase deficiency.

  11. Organic growth factor requirements of some yeasts.

    Science.gov (United States)

    Madan, M; Gulati, N

    1980-01-01

    Some sporogenous yeasts (Brettanomyces bruxellensis, Debaryomyces hansenii, Hansenula ciferrii, Hansenula polymorpha, Pichia polymorpha, Saccharomycopsis guttulata, and Saccharomyces chevalieri), isolated from various fruits have been examined for their organic growth factor requisites. H. ciferrii was completely deficient in thiamine, biotin, inositol, riboflavin, niacin, and partially deficient in pantothenic acid. It required an external supply of 0.1-1.0 ppm thiamine, 0.01-0.1 ppm biotin, 10.0 ppm inositol, 0.10 ppm niacin and riboflavin for its optimum growth. H. polymorpha showed partial deficiency only in xanthine. P. polymorpha gave indications of partial deficiencies in thiamine and biotin. S. guttulata was completely deficient in biotin, and partially deficient in adenine sulphate. It required 0.01 ppm biotin for optimum growth. S chevalieri was completely deficient in pyridoxine and partially deficient in thiamine. It required 0.1 ppm pyridoxine for maximum growth. D. hansenii and B bruxellensis were auxoautotrophic for the various growth factors studied.

  12. Review of NVP and HG and Early Pharmacotherapeutic Intervention

    Directory of Open Access Journals (Sweden)

    Shannon M. Clark

    2012-01-01

    Full Text Available NVP occurs in 50–90% of pregnancies, making it a common medical condition in pregnancy. Women present differently with any combination of signs and symptoms. It is appropriate to take the pregnancy-related versus nonpregnancy-related approach when determining the cause of nausea and vomiting but other causes should be considered. The most common etiologies for NVP include the hormonal changes associated with pregnancy, the physiologic changes in the gastrointestinal tract, and a genetic predisposition. Up to 10% of women will require pharmacotherapy to treat the symptoms of NVP despite conservative measures. ACOG currently recommends that a combination of oral pyridoxine hydrochloride and doxylamine succinate be used as first-line treatment for NVP if pyridoxine monotherapy does not relieve symptoms. A review of NVP and early pharmacotherapeutic management is presented due to the fact that NVP is largely undertreated, and investigations into the safe and effective pharmacotherapies available to treat NVP are lacking.

  13. Acute isoniazid intoxication: seizures, acidosis and coma.

    Science.gov (United States)

    Temmerman, W; Dhondt, A; Vandewoude, K

    1999-08-01

    Isoniazid (INH) is the most widely used of the antituberculosis drugs. An acute overdose is potentially fatal and is characterized by the clinical triad of repetitive seizures unresponsive to the usual anticonvulsants, metabolic acidosis with a high anion gap and coma. The diagnosis of INH overdose should be considered in any patient who presents with an unexplained metabolic acidosis and convulsions. The cornerstone of therapy consists in pyridoxine (vitamin B6) and the dose should be equal to the amount of INH ingested. When conservative therapy fails or in case of renal insufficiency, dialysis must be considered. Severe central nervous toxicity can also be caused by chronic ingestion of higher than therapeutic doses of INH. In those cases pyridoxine-therapy can be useful as well. In the present paper a case of acute overdose of INH is reported, followed by a review of the literature.

  14. Isoniazid overdose : a case series, literature review and survey of antidote availability.

    Science.gov (United States)

    Maw, Graeme; Aitken, Peter

    2003-01-01

    Tuberculosis has re-emerged as a significant public health threat over the last decade both globally and within Australia. This is thought to be largely due to the HIV epidemic, a growing itinerant population, and immigration. The antibiotic isoniazid remains an integral part of drug therapy. With the numbers of patients receiving isoniazid remaining high, the number of cases of acute poisoning is expected to be significant. This paper presents a series of two cases of isoniazid poisoning presenting to a tertiary referral centre in North Queensland. Isoniazid toxicity produces a triad of coma, metabolic acidosis and seizures. The seizures are often refractory to traditional antiepileptics. A specific antidote is available (pyridoxine [vitamin B6]) and both patients were administered this as part of their treatment. We also surveyed all hospitals in Australia with an accredited adult Emergency Department to assess the availability of pyridoxine.

  15. [Sensory disturbances caused by multivitamin preparations].

    Science.gov (United States)

    de Kruijk, J R; Notermans, N C

    2005-11-12

    2 patients, men aged 60 and 65 years, presented with symptoms of chronic sensory polyneuropathy. Symptoms in the first patient were bilateral numbness in the hands and leg pain and, in the second patient, painful tingling in the legs. Pyridoxine (vitamin B6) toxicity due to daily use of multivitamin supplements was diagnosed. The patients were taking 24 and 40 mg per day, respectively. Neurotoxic syndromes due to pyridoxine overdose have been described before in patients taking high-dose vitamin B. These patients mostly developed progressive sersory neuronopathy with sensory ataxia. Chronic sensory polyneuropathy has not been associated with the use of vitamin supplements, which have previously been considered harmless. Both patients recovered after discontinuation of supplement intake.

  16. Isoniazid overdose: pharmacokinetics and effects of oral charcoal in treatment.

    Science.gov (United States)

    Siefkin, A D; Albertson, T E; Corbett, M G

    1987-11-01

    The pharmacokinetics of isoniazid following overdose in two patients is described. One patient was treated with haemodialysis for seizures and persistent coma without obvious immediate clinical improvement. In addition, three volunteer subjects were given isoniazid orally on two separate occasions. Isoniazid elimination pharmacokinetics were determined with and without concominant charcoal. Oral activated charcoal totally prevented the absorption of isoniazid. Current recommendations for treatment of isoniazid overdoses include intravenous pyridoxine (one gram IV pyridoxine for each gram of ingested isoniazid), intravenous diazepam or phenobarbital for continued seizures, and gastric decontamination with lavage and activated charcoal (1 g/kg). Extraordinary measures such as early haemodialysis and haemoperfusion should be reserved for those patients with persistent coma or refractory seizures.

  17. Elevated B6 levels and peripheral neuropathies.

    Science.gov (United States)

    Scott, K; Zeris, S; Kothari, M J

    2008-01-01

    Polyneuropathy related to decreased levels of Vitamin B6 are well known. In contrast, the association between elevated levels of pyridoxine and neuropathy is not well described. This study is a retrospective review of patients in our neuromuscular clinic that were found to have elevated B6 levels. Twenty-six patients were found to have elevated serum B6 levels. The mean B6 level was 68.8 ng/ml. Twenty patients (76.9%) reported daily vitamin use. Twenty-one patients (80.8%) reported only sensory complaints. The most common symptoms reported were numbness (96%), burning pain (49.9%), tingling (57.7%), balance difficulties (30.7%), and weakness (7.8%). Nine (out of 26) had an abnormal EMG/NCS. Eight patients had an abnormal quantitative sensory study. We conclude that elevated pyridoxine levels should be considered in the differential diagnosis of any sensory or sensorimotor polyneuropathy.

  18. Repletion of Zinc and Iron Deficiencies Improves Cognition of Premenopausal Women.

    Science.gov (United States)

    1997-10-01

    Folic acid, vitamin B12 , pyridoxine, and homocystine are being measured in blood before and after treatment to determine effects of repletion of...34extracted" and "nonextracted" specimens. From such rigid analyses the evidence of lack of contamination can be easily verified. 56 Appendix III...iron and zinc status we are now targeting ads at vegetarians . e. We shared our concerns about recruitment with the contracting officer and proposed

  19. Homocysteine Is an Oncometabolite in Breast Cancer, Which Promotes Tumor Progression and Metastasis

    Science.gov (United States)

    2014-09-01

    diseases and also a pregnancy disorder known as preeclampsia. Polymorphisms in MTHFR that decrease the catalytic activity of the enzyme are common in the...low. Therefore, the nutritional status of individuals in terms of these three vitamins will also have an impact on the growth, progression, and...patients to take vitamin supplements to improve their nutritional status of folic acid, vitamin B12, and pyridoxine so as to reduce the homocysteine

  20. Pharmacokinetics of metadoxine for injection after repeated doses in healthy volunteers

    Institute of Scientific and Technical Information of China (English)

    L(U) Yuan; KANG Zi-sheng; LIU Yan; LI Tian-yun; XIAO Yong-hong

    2007-01-01

    @@ Alcohol-induced liver disease is one of the main epidemic problems nowadays. Metadoxine is a pyridoxine-pyrrolidone carboxylate with significant scavenging property. Metadoxine is able to accelerate the elimination of alcohol from the blood and tissues, help restore the functional structure of the liver and relieve neuro-psychological disorders associated with alcohol intoxication.1-3 The purpose of the study was to assay the pharmacokinetics of domestic metadoxine after repeated doses.

  1. Docetaxel-induced palmoplantar erythrodysesthesia syndrome and long-lasting multiple nail changes

    Directory of Open Access Journals (Sweden)

    Gulsen Akoglu

    2014-01-01

    Full Text Available Palmoplantar erythrodysesthesia syndrome (PPES and nail changes are common presentations of cutaneous toxicity of docetaxel chemotherapy, which deteriorate the quality of life of patients. Herein, we describe a female patient who developed PPES and multiple nail changes due to docetaxel treatment for infiltrative ductal carcinoma. Cold application and elevation of extremities during docetaxel infusion, potent topical steroids and oral pyridoxine increased the tolerance to chemotherapy and provided regression of painful cutaneous lesions without cessation of the treatment.

  2. Impact of

    OpenAIRE

    K. Velmurugan; A.P. Sathiyagnanam

    2016-01-01

    The uses of biodiesel in diesel engines result in reduction of exhaust emissions, though many researchers described that the biodiesel produces higher NOx emissions than diesel, which is detract from the inflation of the market for these fuels. The aim of the present study was to analyze the experimental exploration of the three antioxidants DEA (Di-Ethyl Amine), PHC (Pyridoxine Hydro Chloride) and TBHQ (Tert Butyl Hydro Quinone) on engine emission and performance of a single cylinder diesel ...

  3. RP-HPLC Determination of vitamins B1, B3, B6, folic acid and B12 in multivitamin tablets

    OpenAIRE

    2005-01-01

    Abstract:Asimple and sensitive reversed-phase, ion-pair HPLC method was developed and validated for the simultaneous determination of B-group vitamins, thiamine chloride hydrochloride (B1), nicotinamide (B3), pyridoxine hydrochloride (B6) and folic acid in Pentovit® coated tablets. The cyanocobalamine (B12) was determined separately, because of its low concentration in the investigated multivitamin preparation. RP-HPLC analysis was performed with a LKB 2150 HPLC system, equipped with a UV/VI...

  4. Overproduction of Hydrogen From an Anaerobic Bacterium

    Science.gov (United States)

    2008-12-01

    ADM002187. Proceedings of the Army Science Conference (26th) Held in Orlando, Florida on 1-4 December 2008, The original document contains color images...0.02 mg/L folic acid, 0.1 mg/L pyridoxine-HCl, 0.05 mg/L thiamine-HCl, 0.05 mg/L riboflavin , 0.05 mg/L nicotinic acid, 0.05 mg/L calcium

  5. Recurrent dystonia in homocystinuria: a metabolic pathogenesis.

    Science.gov (United States)

    Sinclair, Alex J; Barling, Lucy; Nightingale, Simon

    2006-10-01

    Dystonia complicating homocystinuria is extremely rare in the absence of thromboembolic disease. We report a unique case of recurrent dystonia in a patient with homocystinuria secondary to pyridoxine-unresponsive cystathionine beta-synthase deficiency. Brain MRI was normal. Two biochemical markers for homocystinuria, homocystine and methionine, were markedly elevated during periods when our patient manifested dystonia. These findings suggest that accumulation of sulfur-containing amino acids may contribute to the pathophysiology of dystonia in patients with homocystinuria.

  6. Multiple enzymatic defects in mitochondria in hematological cells of patients with primary sideroblastic anemia.

    Science.gov (United States)

    Aoki, Y

    1980-07-01

    Activities of mitochondrial enzymes in blood cells from 69 patients with primary sideroblastic anemia were determined to elucidate the pathogenesis of the disease. In erythroblasts of patients with primary acquired type the activities of both delta-aminolevulinic acid synthetase and mitochondrial serine protease were inevitably decreased. The susceptibility to the protease of apo-delta-aminolevulinic acid synthetase prepared from erythroblasts of patients with this type was within the normal range, in contrast to that of pyridoxine-responsive anemia. The activities of mitochondrial enzymes such as cytochrome oxidase, serine protease, and oligomycin-sensitive ATPase, except citrate synthetase, were usually decreased in mature granulocytes of the patients. Patients with hereditary sideroblastic anemia also had decreased delta-aminolevulinic acid synthetase activity in erythroblasts, and decreased serine protease activity in both erythroblasts and mature granulocytes. Mature granulocytes obtained from patients with pyridoxine-responsive anemia before therapy had decreased cytochrome oxidase activity, however, the activity increased to a normal level when the patients were in remission. The activities of other mitochondrial enzymes in mature granulocytes were within normal range in these patients before pyridoxine therapy. The activities of these mitochondrial enzymes in lymphocytes were within normal range in all groups of patients with primary sideroblastic anemia. We suggest that patients with primary acquired, and possibly also those with hereditary sideroblastic anemia have impaired mitochondrial function in both erythroblasts and granulocytes. That only anemia is observed in these patients is because a functional abnormality of mitochondria in erythroblasts is most important because of the role of mitochondria in the formation of heme in erythrocyte development. In contrast to these two types of sideroblastic anemia, only delta-aminolevulinic acid synthetase in

  7. Metabolic Mapping of Breast Cancer with Multiphoton Spectral and Lifetime Imaging

    Science.gov (United States)

    2007-03-01

    37°C with 10% CO2. COS-7 cells were maintained in DMEM (containing high glucose, L-glutamine, sodium pyruvate and pyridoxine hydrochloride) plus 10...characterize, study, and combat breast cancer are of great significance. One of the largest risk factors for developing breast carcinoma is high...breast tissue density (Boyd et al. 2002). Dense breast tissue is linked to a four-to-six fold increased risk of breast carcinoma (Boyd et al. 1998

  8. Protective Effects of B Vitamins and Antioxidants on the Risk of Arsenic-Related Skin Lesions in Bangladesh

    OpenAIRE

    2008-01-01

    Background An estimated 25–40 million of the 127 million people of Bangladesh have been exposed to high levels of naturally occurring arsenic from drinking groundwater. The mitigating effects of diet on arsenic-related premalignant skin lesions are largely unknown. Objectives The purpose of this study was to clarify the effects of the vitamin B group (thiamin, riboflavin, niacin, pyridoxine, and cobalamin) and antioxidants (vitamins A, C, and E) on arsenic-related skin lesions. Methods We per...

  9. In Situ Dechlorination of Solvents in Saturated Soils

    Science.gov (United States)

    1996-05-01

    ccmail.aleq.tyndall.af.mil Guy Sewell, Ph.D. US Environmental Protection Agency, National Risk Management Research Laboratory Ada, OK 74821 USA Jim...the U. S. Air Force Armstrong Laboratory Environics Directorate (AL/EQ), the U. S. Navy, the U. S. Environmental Protection Agency National Risk ...EXTRACT CONCENTRATIONS Vitamin/Yeast Extract Concentration (mg/L) d-biotin 0.01 folic acid 0.01 pyridoxine hydrochloride 0.05 thiamin hydrochloride 0.025

  10. Quality Improvement of Cheese Spread

    Science.gov (United States)

    2008-02-25

    Annatto (2% bixin) 3.5 mL Use as needed to conform color Vitamin A 0.14 0.003 Not less than 800 retinol units Added to comply with product...for samples with citrates (CIT) and altered levels of phosphates (LP) (Table 7). Although the citrates and phosphates have similar ionic components...Effect of vitamins The guidelines for cheese spread fortification include the addition of retinol (vitamin A), thiamine (vitamin B1), pyridoxine

  11. Experimente ueber den Einflusse von Metaboliten und Antimetaboliten am Modell von Trichomonas Vaginalis. VI. (Experiments on the Influence of Metabolites and Antimetabolites on the Model of Trichomonas Vaginalis. VI. Communication: Effect of Vitamins and Vitamin-Like Substances),

    Science.gov (United States)

    A number of substances (folic acid, axerophtol, tokopherol and others) stimulate the growth of Trichomonas vaginalis and, therefore, are very well...group of vitamins (thiamine, lactoflavin, pyridoxine and others) are without recognizeable effect upon the growth of Trichomonas vaginalis . The third...inhibiting effect upon the growth of Trichomonas vaginalis . Further investigations with these substances within a combined inhibition system seem to be important. (Modified author abstract)

  12. Evaluation of emotional reactions to oral contraceptive use.

    Science.gov (United States)

    Kane, F J

    1976-12-15

    A review of available clinical studies indicates that 10 to 40 per cent of oral contraceptive users may suffer mild to moderate depression syndromes. Clinical and animal data indicate that a variety of mechanisms may be involved, including alterations in folate, pyridoxine, and vitamine B12 metabolism, as well as related effects on biogenic amine metabolism. Interactive effects may result, such as impairment of usual coping mechnisms and psychological defenses by altered central nervous system function.

  13. New developments in pediatric psychopharmacology.

    Science.gov (United States)

    Gualtieri, C T; Golden, R N; Fahs, J J

    1983-09-01

    This is a report on recent developments in pediatric psychopharmacology: new drugs and new applications for established drugs. The drugs reviewed include imipramine, amitryptiline, lithium, piracetam, propranolol, tryptophan, clonidine, pyridoxine and fenfluramine. Putative indications include prepubertal depression, school phobia, anorexia nervosa, explosive-aggressive behavior, learning disabilities, attention deficit disorder (hyperactivity), Tourette's syndrome, autism, and the Lesch-Nyhan syndrome. Some of the information presented in this report must be regarded as "preliminary," and caution is advised in its interpretation and application.

  14. Role of Lipotropes in Mammary Carcinogenesis.

    Science.gov (United States)

    1997-09-01

    Pyridoxine HC1 0.022 Calcium phosphate, 4.5 Riboflavin 0.022 dibasic L-Alanine 3.5 Thiamine HC1 0.022 L-Arginine HC1 12.1 Glycine 23.3 L-Asparagine 6.0 L...lipotrope-deficient diet depressed normal methylation of DNA by lowering the pool of AdoMet. When the cell prepares for normal division, methylation of the

  15. Advances in clinical toxicology.

    Science.gov (United States)

    Boehnert, M T; Lewander, W J; Gaudreault, P; Lovejoy, F H

    1985-02-01

    New data are reviewed in two areas in the management of the acute overdose: gastrointestinal decontamination and systemic antidotes. The mechanism and effectiveness of Ipecac syrup, gastric aspiration and lavage, activated charcoal, gastrointestinal dialysis, and saline cathartics are discussed. Special problems posed by disc batteries and packet ingestion of cocaine (in transporting contraband) are highlighted. The pharmacology and uses of pyridoxine and naloxone as antidotes are detailed.

  16. Vitamin B nutrition in the Nigerian tropical ataxic neuropathy.

    OpenAIRE

    1985-01-01

    Assessment of nutritional status of vitamin B components by plasma or blood levels indicated riboflavin deficiency and possibly thiamine deficiency in Nigerian patients who suffered from tropical ataxic neuropathy and neurologically normal Nigerians who subsisted on predominant cassava diet. Serum levels of folate, niacin, pyridoxine and panthothenic acid were normal. Vitamin deficiencies probably are minor factors, if any, in the pathogenesis of tropical ataxic neuropathy in Nigerians.

  17. An Industrial Ergonomics Bibliography: Prevention of Cumulative Trauma through Workplace Analysis

    Science.gov (United States)

    1991-12-05

    Rehabilitation, ?.(4), 18-37. 12 CARPAL TUNNEL Amadio, P. C. (1987). Carpal tunnel syndrome, pyridoxine , and the workplace. Journal of Hand Surger...Thermography in the detection of carpal tunnel syndrome and other compressive neuropathies . The Journal of Hand S , 12(5), 943-949. Hirsh, L. F. a. T., A... neuropathy at the wrist. Clinical Orthopaedics and Related Research, .a, 48-54. Jensen, R. C., Klein, B. P., and Sanderson, L. M. (1983, September). Motion

  18. ANALISIS FAKTOR PREDISPOSISI DOMINAN TERJADINYA ANGULAR CHEILITIS PADA ANAK-ANAK

    OpenAIRE

    ASNI, NURUL

    2013-01-01

    2013 Latar Belakang : Kesehatan gigi dan mulut merupakan salah satu faktor untuk mencapai kualitas hidup yang optimal. Salah satu masalah kesehatan gigi dan mulut yang sering ditemukan pada anak-anak adalah angular cheilitis. Menurut beberapa pendapat angular cheilitis disebabkan oleh defisiensi nutrisi terutama kekurangan vitamin B-2 (riboflavin), vitamin B-3 (niacin), vitamin B-6 (pyridoxine), atau vitamin B-12 (cyanocobalamin) dan kekurangan zat besi, selain itu kebiasaan membasahi bi...

  19. Callus and cell suspension cultures of carnation

    DEFF Research Database (Denmark)

    Engvild, Kjeld Christensen

    1972-01-01

    Callus cultures of carnation, Dianthus caryophyllus L. ev. G. J. Sim, were grown on a synthetic medium of half strength Murashige and Skoog salts, 3 % sucrose, 100 mg/l of myo-inositol, 0.5 mg/l each of thiamin, HCl, pyridoxin, HCl and nicotinic acid and 10 g/l agar. Optimal concentrations of gro......, but all attempts to induce formation of shoots or em-bryoids gave negative results....

  20. Biochemical Effects of Cadmium Exposure and the Potential Pharmacologic Significance of Cadmium Mediated Hydrolase Inhibition

    Science.gov (United States)

    1997-04-18

    increase Cd absorption from the intestines (Larson and Piscator 1971; Itokawa, Abe et al. 197 4; Pond and Walker 1975). Pyridoxine, vitamin B 6 , is...considerations on uptake and retention of cadmium in human kidney cortex. Cadmium in the Environment. L. Friberg, M. Piscator and G. F. Nordberg. Cleveland...Columbia, Missouri, University of Missouri. Larson, S.-E. and M. Piscator (1971). "Effect of cadmium on skeletal tissue in normal and calcium