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PubMed1999

Nicotinic acid and pyridoxine modulate arachidonic acid metabolism in vitro and ex vivo in man.

The in vitro effects of nicotinic acid (10-1000 microM), pyridoxine (0.1-500 microM) and pyridoxal-5'-phosphate (0.1-500 microM) and the ex vivo effects of nicotinic acid (2500 mg orally during 12 h) and pyridoxine (600 mg orally daily for seven days) on arachidonic acid metabolism were investigated in calcium ionophore A23187 (calcimycin)-stimulated human whole blood. In vitro nicotinic acid stimulated prostaglandin E2, thromboxane B2 and leukotriene E4 synthesis. Pyridoxine at all concentrations and pyridoxal-5'-phosphate at the highest concentration stimulated prostaglandin E2 and thromboxane B2 production, but had no effect on leukotriene E4 synthesis. Nicotinic acid treatment increased ex vivo prostaglandin E2, thromboxane B2 and leukotriene E4 synthesis to 185%, 165% and 175% of the initial values, respectively. In the pyridoxine-treated subjects, ex vivo prostaglandin E2, thromboxane B2 and leukotriene E4 synthesis was decreased after seven days to 75%, 65% and 45% of the initial values, respectively. In the present study the effects of nicotinic acid on the 5-lipoxygenase pathway in arachidonic acid metabolism were studied for the first time and the drug was found to stimulate this pathway in vitro and ex vivo. In vitro pyridoxine and pyridoxal-5'-phosphate had no effect on the 5-lipoxygenase pathway. The inhibition of leukotriene synthesis by pyridoxine ex vivo might be of therapeutic importance.

Adult↗
PubMed2005

Amiloride uptake and toxicity in fission yeast are caused by the pyridoxine transporter encoded by bsu1+ (car1+).

Amiloride, a diuretic drug that acts by inhibition of various sodium transporters, is toxic to the fission yeast Schizosaccharomyces pombe. Previous work has established that amiloride sensitivity is caused by expression of car1+, which encodes a protein with similarity to plasma membrane drug/proton antiporters from the multidrug resistance family. Here we isolated car1+ by complementation of Saccharomyces cerevisiae mutants that are deficient in pyridoxine biosynthesis and uptake. Our data show that Car1p represents a new high-affinity, plasma membrane-localized import carrier for pyridoxine, pyridoxal, and pyridoxamine. We therefore propose the gene name bsu1+ (for vitamin B6 uptake) to replace car1+. Bsu1p displays an acidic pH optimum and is inhibited by various protonophores, demonstrating that the protein works as a proton symporter. The expression of bsu1+ is associated with amiloride sensitivity and pyridoxine uptake in both S. cerevisiae and S. pombe cells. Moreover, amiloride acts as a competitor of pyridoxine uptake, demonstrating that both compounds are substrates of Bsu1p. Taken together, our data show that S. pombe and S. cerevisiae possess unrelated plasma membrane pyridoxine transporters. The S. pombe protein may be structurally related to the unknown human pyridoxine transporter, which is also inhibited by amiloride.

Amiloride↗
PubMed2005

Epidemiology of pyridoxine dependent seizures in the Netherlands.

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 the Netherlands, and to determine whether the diagnosis is based on the appropriate criteria. METHODS: Nationwide all departments of paediatrics (n = 113) and of paediatric or neonatal neurology (n = 17) were asked to report cases of pyridoxine dependent seizures. Birth incidences were calculated using national data on live births from 1991 to 2003. RESULTS: Response was received from 67% of paediatric departments, including all university hospitals and 94% of child neurology departments. Thirteen patients were reported. Four definite (31%), three probable (23%), and four possible cases (31%) were identified. Two cases (15%) did not meet criteria for either of these groups. The birth incidence was 1:396,000 for definite and probable cases and 1:252,000 when possible cases are included. CONCLUSIONS: Thus far, epidemiological data on pyridoxine dependent seizures were only available from the UK and Ireland. A higher incidence was found in the Netherlands, in accordance with earlier suggestions of a regional difference. The study shows that the diagnosis is often made without performance of a formal trial of withdrawal. The importance of confirming the diagnosis, concerning the consequences as for individual prognosis, the potential side effects of prolonged pyridoxine substitution, and the possibility of treating the mother in case of future pregnancies are emphasised.

Epilepsy↗
PubMed1983

Pyridoxine dependent seizures--a wider clinical spectrum.

We report 4 infants with pyridoxine dependent seizures who had clinical features that led to diagnostic uncertainty. Their clinical course was unusual in 1 or more of the following: later onset of initial seizures; a seizure free period after taking of anticonvulsants, but before taking of pyridoxine; a long remission after withdrawal of pyridoxine; and atypical seizure type. This report illustrates a broader range of clinical features and highlights the need to consider the diagnosis of pyridoxine dependent seizures in any infant with intractable epilepsy, regardless of the pattern of seizures and the response to anticonvulsant medications. In such a case, 100 mg intravenous pyridoxine should be given and, if a definite clinical response is established, oral pyridoxine should be continued indefinitely.

Epilepsy↗
PubMed1984

Immunologic abnormalities in hemodialysis patients: improvement after pyridoxine therapy.

8 male patients undergoing maintenance hemodialysis were studied to determine the effect of administering supplements of pyridoxine hydrochloride, 50 mg/day for 3-5 weeks, on tests of immune function. In the 3 patients who initially had abnormal nitroblue tetrazolium reduction tests, the values returned to normal with therapy (p less than 0.05). The generation of chemotactic factors from plasma was defective in all evaluated patients and improved after pyridoxine therapy in 4 of 5 patients (p less than 0.01). The lymphocyte subpopulations changed with a rise in the populations of null cells after supplementation with pyridoxine. In addition, lymphocyte transformation in response to mitogens improved in the 3 patients who initially showed low values in these assays. The improvements occurred with pyridoxine therapy even though some patients who responded had no evidence for vitamin B6 deficiency before therapy, as indicated by a normal erythrocyte glumatic-pyruvic transaminase index. We conclude that several parameters of immune function are improved with pyridoxine supplementation. Studies are necessary to establish the minimum daily intake of pyridoxine which will maintain improved values of these tests of immune function in hemodialysis patients.

Adult↗
PubMed1995

Late-onset X-linked sideroblastic anemia. Missense mutations in the erythroid delta-aminolevulinate synthase (ALAS2) gene in two pyridoxine-responsive patients initially diagnosed with acquired refractory anemia and ringed sideroblasts.

X-linked sideroblastic anemia (XLSA) is caused by mutations of the erythroid-specific delta-aminolevulinate synthase gene (ALAS2) resulting in deficient heme synthesis. The characteristic hypochromic, microcytic anemia typically becomes manifest in the first three decades of life. Hematologic response to pyridoxine is variable and rarely complete. We report two unrelated cases of highly pyridoxine-responsive XLSA in geriatric patients previously diagnosed with refractory anemia and ringed sideroblasts. A previously unaffected 77-yr-old male and an 81-yr-old female were each found to have developed severe hypochromic, microcytic anemia with ringed sideroblasts in the bone marrow, which responded dramatically to pyridoxine with normalization of hemoglobin values. Sequence analysis identified an A to C transversion in exon 7 (K299Q) of the ALAS2 gene in the male proband and his daughter. In the female proband a G to A transition was identified in exon 5 (A172T). This mutation resulted in decreased in vitro stability of bone marrow delta-aminolevulinate synthase activity. Each patient's recombinant mutant ALAS2 enzyme had marked thermolability. Addition of pyridoxal 5'-phosphate in vitro stabilized the mutant enzymes, consistent with the observed dramatic response to pyridoxine in vivo. This late-onset form of XLSA can be distinguished from refractory anemia and ringed sideroblasts by microcytosis, pyridoxine-responsiveness, and ALAS2 mutations. These findings emphasize the need to consider all elderly patients with microcytic sideroblastic anemia as candidates for XLSA, especially if pyridoxine responsiveness is demonstrated.

5-Aminolevulinate Synthetase↗
PubMed1987

Pyridoxine dependency seizures: report of a case with unusual features.

Pyridoxine dependency is a rare cause of neonatal seizures. Newborns with this disorder are often hyperirritable and fail to respond to the usual anticonvulsants. The diagnosis is established by cessation of seizures after the administration of parenteral pyridoxine. Reported is a case of pyridoxine dependency that illustrates several problems in management. The amount of pyridoxine required to control seizures is variable and may exceed 100 mg per day. The electroencephalogram (EEG) may not change significantly during the initiation of therapy. During intercurrent illnesses, parenteral pyridoxine may need to be given. Additional pyridoxine may be needed even when the EEG is normal. Treatment should continue indefinitely.

Dose-Response Relationship, Drug↗
PubMed1975

Effect of chronic levodopa treatment on pyridoxine metabolism.

Pyridoxine metabolism was investigated in eight chronic levodopa-treated parkinsonian patients and in eight matched dopa-naive controls by measurement of plasma and erythrocyte pyridoxal-5-phosphate concentrations over a 24-hour period, following intravenous administration of pyridoxine. After both a 10 mg and 100 mg pyridoxine dosage, plasma and erythrocyte pyridoxal-5-phosphate concentrations were significantly higher in the chronic levodopa-treated group than in the controls. The percentage change in pyridoxal-5-phosphate concentrations as a function of the administered doses of pyridoxine was greater in the dopa-treated group. Chronic administration of levodopa may result in an adaptive alteration in the decarboxylase system with an increased cellular ability to synthesize pyridoxal-5-phosphate from pyridoxine, possibly through enzyme induction. This metabolic alteration would protect against pyridoxine deficiency states and may explain in part the progressive loss of levodopa effectiveness sometimes observed.

Aged↗
PubMed1993

Formation of beta-fructosyl compounds of pyridoxine in growing culture of Aspergillus niger.

Two pyridoxine compounds were found to be formed in a culture filtrate of Aspergillus niger and A. sydowi, when grown in a medium containing sucrose and pyridoxine. Each of the two compounds I and II was obtained as a white powdered preparation by preparative paper chromatography, gel filtration on Toyopearl HW-40S and Sephadex G-10 columns, DEAE-cellulose column chromatography, and lyophilization. Compounds I and II were identified as 5'-O-(beta-D-fructofuranosyl)-pyridoxine and 5'-O-[beta-D-fructofuranosyl-(2-->1)-beta-D-fructofuranosyl]-pyridoxine, on the basis of the various experimental results, viz., elementary analyses, UV, 1H-, and 13C-NMR spectra, products by hydrolysis with acid and yeast beta-D-fructofuranosidase, migration on paper electrophoresis, and Gibbs reaction in the presence and absence of boric acid. Levansucrase from Microbacterium laevaniformans and yeast beta-D-fructofuranosidase did not catalyze the beta-D-fructofuranosyl transfer from sucrose to pyridoxine to give rise to beta-D-fructofuranosyl-pyridoxine.

Aspergillus niger↗
PubMed1985

Pyridoxine deficiency in children treated with isoniazid.

Isoniazid-induced deficiency of pyridoxine (vitamin B6) is reportedly not uncommon in adults but rare in children. In the present study, 38 children had serum levels of pyridoxine tested while receiving therapy with isoniazid. A biologic assay using the protozoan Tetrahymena thermophila determined pyridoxine status after 2 to 18 months of therapy with isoniazid. Five children (13 percent) were deficient. None had definitive clinical symptoms or signs consistent with pyridoxine deficiency. Three had normal nerve conduction velocity. Children receiving isoniazid in dosages greater than 10 mg/kg/day had a higher incidence of deficiency. Present recommendations for withholding pyridoxine prophylaxis from children receiving isoniazid therapy must be reconsidered in light of these findings, particularly in those children who are debilitated or have a poor nutritional history with a known pyridoxine deficit prior to therapy with isoniazid.

Child↗
PubMed2005

Red cell aspartate aminotransferase saturation with oral pyridoxine intake.

CONTEXT AND OBJECTIVE: The coenzyme of aspartate aminotransferase is pyridoxal phosphate, generated from fresh vegetables containing pyridoxine. Vitamin B6-responsive sideroblastic anemia, myelofibrosis and Peyronies syndrome respond to high pyridoxine doses. The objective was to investigate the oral pyridoxine oral dose that would lead to maximized pyridoxal phosphate saturation of red cell aspartate aminotransferase. DESIGN AND SETTING: Controlled trial, in Hematology Division of Instituto Adolfo Lutz. METHODS: Red cell aspartate aminotransferase activity was assayed (before and after) in normal volunteers who were given oral pyridoxine for 15-18 days (30 mg, 100 mg and 200 mg daily). In vitro study of blood from seven normal volunteers was also performed, with before and after assaying of aspartate aminotransferase activity. RESULTS: The in vivo study showed increasing aspartate aminotransferase saturation with increasing pyridoxine doses. 83% saturation was reached with 30 mg daily, 88% with 100 mg, and 93% with 200 mg after 20 days of oral supplementation. The in vitro study did not reach 100% saturation. CONCLUSIONS: Neither in vivo nor in vitro study demonstrated thorough aspartate aminotransferase saturation with its coenzyme pyridoxal phosphate in red cells, from increasing pyridoxine supplementation. However, the 200-mg dose could be employed safely in vitamin B6-responsive sideroblastic anemia, myelofibrosis and Peyronies syndrome treatment. Although maximum saturation in circulating red cells is not achieved, erythroblasts and other nucleated and cytoplasmic organelles containing cells certainly will reach thorough saturation, which possibly explains the results obtained in these diseases.

Adult↗
PubMed1977

Effect of pyridoxine deficiency on cholesterogenesis in rats fed different levels of protein.

Hepatic cholesterol contents in rats fed a 70% or 20% casein diet with or without pyridoxine was determined. In the case of the 70% casein group, pyridoxine-deficient rats showed a higher content than the control. The increment was mainly due to the accumulation of an ester form of the cholesterol. On the other hand, pyridoxine-deficient rats in the 20% casein group showed a slightly lower content. The cholesterol content in liver microsomal fractions was lower in the 20% casein pyridoxine-deficient group and serum cholesterol level was lower in the 70%-casein pyridoxine-deficient group than those in respective control groups. Incorporation of [14C]acetate into cholesterol was studied using liver slices, and significant stimulation was observed in pyridoxine-deficient rat fed a 20% or 70% casein diet. There was no difference in intestinal cholesterogenesis between the control and the deficient groups.

Animals↗
PubMed1978

Pyridoxine and its relation to lipids. Studies with pyridoxineless mutants of Aspergillus nidulans.

The effect of pyridoxine deficiency on fat metabolism was studied using mutant strains of Aspergillus nidulans requiring pyridoxine for growth. Under pyridoxine deficiency the mutants exhibited increased levels of total lipid, sterols, phospholipids, and triacylglycerols. Total fatty acids were found to decrease with pyridoxine deficiency. An increase in saturated fatty acids and decrease in unsaturated fatty acids were seen with deficiency. Pyridoxine deficiency also increased lower carbon chain fatty acids. A possible involvement of pyridoxine in the elongation of fatty acid chain and in the desaturation of fatty acids in Aspergillus nidulans is suggested.

Aspergillus nidulans↗
PubMed1986

Regulation of ornithine aminotransferase in rat kidney by estradiol and pyridoxine.

Increased synthesis of ornithine aminotransferase [EC 2.6.1.13] (OAT) in the kidney of pyridoxine-deficient rats has been reported previously (Ikeda, M. and Okada, M. (1985): J. Nutr. Sci. Vitaminol., 31, 553-561). In this report the effects of 3,3',5'-triiodothyronine (T3) and estradiol on OAT activity in the kidney of rats given pyridoxine-deficient and control diets were studied. T3 induced renal OAT activity in rats given the control diet but not in those given the pyridoxine-deficient diet. On the other hand, estradiol induced renal OAT activity in both deficient and control rats, the levels induced in the two groups being the same. Maximal induction of OAT occurred at a lower dose of estradiol in pyridoxine-deficient rats than in the controls. When rats fed on pyridoxine-deficient diet were pretreated with pyridoxine for several days, OAT induction by estradiol was suppressed. Thus pyridoxal phosphate (PLP) may modulate OAT activity in rat kidney through the action of estradiol.

Animals↗
PubMed1988

Isolation and structural elucidation of three new pyridoxine-glycosides in rice bran.

Three new pyridoxine-glycosides were isolated from rice bran (10 kg) as colorless powder by various chromatographic techniques: compound A, 53 mg; compound B, 7.8 mg; compound C, 5.8 mg. Compound A was shown to consist of pyridoxine and glucose in a 1:2 molar ratio by beta-glucosidase hydrolysis, and by 1H-NMR and secondary ion mass spectrometry (SI-MS) data. On partial acid hydrolysis of the compound, cellobiose was liberated. Compound A showed the positive Gibbs color reaction, but the reaction was negative in the presence of boric acid. Thus, compound A was identified as 5'-O-(beta-cellobiosyl)pyridoxine. The 13C-NMR spectral data were compatible with this structure. Compounds B and C were proven to be triglucosides of pyridoxine by enzymic hydrolysis and SI-MS data. From the results of the Gibbs color reaction and partial hydrolyses which yielded compound A, compound B was concluded to be 4'-O-(beta-D-glucosyl)-5'-O-(beta-cellobiosyl)pyridoxine, and compound C to be 5'-O-(beta-glucotriosyl)pyridoxine in which a glucose molecule was bound to the cellobiosyl moiety of compound A through beta-glycosidic linkage.

Chromatography↗
PubMed2000

Pipecolic acid elevation in plasma and cerebrospinal fluid of two patients with pyridoxine-dependent epilepsy.

Diagnosis of pyridoxine-dependent epilepsy is based on the clinical response to high-dosage application of pyridoxine. Here, we report on 2 patients with pyridoxine-dependent epilepsy with significant elevation of pipecolic acid concentrations in plasma and cerebrospinal fluid (CSF) and further increase of pipecolic acid in CSF during a 72-hour pyridoxine withdrawal in 1 of them. Patients with non-pyridoxine-dependent epilepsy had normal pipecolic acid concentrations in plasma and significantly lower concentrations in CSF. High plasma and CSF pipecolic acid concentrations might provide a diagnostic marker in pyridoxine-dependent epilepsy.

2-Aminoadipic Acid↗
PubMed2001

[Antidepressive effect of pyridoxine (vitamin B6) in neuroleptic-treated schizophrenic patients with co-morbid minor depression--preliminary open-label trial].

BACKGROUND: Minor depression is reported in 20-60% of schizophrenic patients during various stages of their disorders; impairing patients' compliance, response to treatment and worsening their overall prognosis. Various anti-depressive treatments have been proposed for such cases but response rates are usually poor. Pyridoxine (Vitamin B6) in essential for the proper metabolism of various neurotransmitters that are considered relevant to the pathophysiology of depression and/or schizophrenia and it has been reported beneficial in ameliorating depressive symptoms as part of major depression, premenstrual syndrome or 'Chinese restaurant syndrome'. We hypothesized that addition of pyridoxine to on-going neuroleptic treatment could improve minor depression in schizophrenic patients. METHOD: Nine schizophrenic patients with co-morbid minor depression participated in this study. All participants had a stable unchanged clinical state (changes in Brief Psychiatric Rating Scale (BPRS). Scale for the Assessment of Positive Symptoms (SAPS), and Scale for the Assessment of Negative symptoms (SANS) scores < 5%) and all were maintained on unchanged doses of anti-psychotic drugs for at least 4 consecutive weeks prior to initiation of the study. Participants received, open-label, pyridoxine 150 mg/day in addition to their anti-psychotic treatment for 4 consecutive weeks. Mental status was evaluated before, during, and at the end of 4 weeks of pyridoxine administration using the BPRS, SAPS, SANS and HAM-D. RESULTS: Two of the nine patients (22%), characterized by higher initial HAM-D and SANS scores, and by older age and longer duration of illness, experienced marked improvements in depressive symptoms (23% and 28% decrease in HAM-D scores) following 4 weeks of pyridoxine administration. In one of these two, the improvement in depressive symptoms was accompanied by a parallel decrease in SANS Scores. CONCLUSION: A subgroup of schizophrenic patients with comorbid minor depression may benefit from pyridoxine addition to their on-going anti-psychotic treatment.

Adult↗
PubMed2002

The effect of pyridoxine administration on melatonin secretion in normal men.

OBJECTIVES: To determine pineal response to pyridoxine in normal men. MATERIAL AND METHODS: Twelve healthy men were given orally pyridoxine (100 mg) or placebo at 1700h. Serum melatonin levels were determined every 30 minutes with simultaneous measurement of core body temperature between 1700h to 0300h. Polysomnographic sleep recordings were performed between 1800h to 2000h. RESULTS: Serum melatonin levels after both placebo and pyridoxine showed a nocturnal rise occurring at 22:10+/-1:22h and 22:24+/-1:09h, respectively. The melatonin onset, peak, mean and area under the curve (AUC) values after pyridoxine (3.2+/-1.6 pg/ml, 47.2+/-22.6 pg/ml, 31.5+/-11.0 pg/ml and 173.5+/-138.4 pg/ml x min, respectively) were similar to the values after placebo administration (4.7+/-1.6 pg/ml, 53.9+/-26.0 pg/ml, 37.2+/-2.8 pg/ml and 205.3+/-137.8 pg/ml x min, respectively). CBT revealed a significant nocturnal decline but without significant difference between pyridoxine and placebo. Sleep amount and architecture were similar after the two treatments. CONCLUSIONS: In adult man, the oral administration of 100 mg-pyridoxine during the evening hours has no effect on melatonin secretion nor does it alter CBT or sleep quality.

Adult↗