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PubMed1981

Daily requirement for pyridoxine supplements in chronic renal failure.

Vitamin B6 deficiency was evaluated in 37 patients with chronic renal failure and in 71 patients undergoing maintenance hemodialysis (HD) or intermittent peritoneal dialysis (PD). Vitamin B6 deficiency was assessed by the in vitro activity of erythrocyte glutamic pyruvic transaminase (EGPT), without (basal) and with (stimulated) the addition of pyridoxal-5-phosphate to the assay, and the EGPT index (stimulated activity ./. basal activity). Basal and stimulated EGPT activities were below normal in the HD patients, and the EGPT index was increased in each group of patients, indicating vitamin B6 deficiency. Supplemental pyridoxine hydrochloride was given to 30 HD patients who received 1.25 to 50 mg/day (37 studies), 6 PD patients who were given 1.25 or 2.5 mg/day (7 studies), and 8 nondialyzed patients with mild to severe renal failure who received 2.5 mg/ day. In all HD patients, 10 or 50 mg/day of pyridoxine hydrochloride rapidly corrected the abnormal EGPT index and maintained normal values; with supplements of 5.0 mg/day or less, the index was often abnormal, particularly in those who were septic or taking pyridoxine antagonists. In PD patients and nondialyzed patients with renal failure, 2.5 mg/day of pyridoxine hydrochloride was inadequate to correct rapidly the abnormal index in all patients. These findings suggest that HD patients should receive 10 mg/day of supplemental pyridoxine hydrochloride (8.2 mg/day pyridoxine). PD patients and patients with chronic renal failure should receive about 5.0 mg/day of supplemental pyridoxine hydrochloride (4.1 mg/day pyridoxine). When sepsis intervenes or vitamin B6 antagonists are taken, 10 mg/day of pyridoxine hydrochloride may be a safer supplement for all patients.

Adult↗
PubMed2005

Pipecolic acid as a diagnostic marker of pyridoxine-dependent epilepsy.

Pyridoxine-dependent epilepsy, although described some decades ago, may still be an underdiagnosed disorder. We have recently described isolated pipecolic acid elevations in the plasma and/or CSF of three patients with pyridoxine-dependent epilepsy with an intriguing inverse correlation to the oral intake of pyridoxine. We have now confirmed these findings in a further 6 unrelated patients with pyridoxine-dependent epilepsy. Pipecolic acid in plasma was 4.3- to 15.3 fold elevated compared to the upper normal range before pyridoxine and remained in the mildly elevated range while on pyridoxine. Pipecolic acid was even more markedly elevated in CSF. The extent of pipecolic acid elevation in CSF exceeded that of plasma by a factor of 2.2 to 4.8. This clearly discriminates pyridoxine-dependent epilepsy from other possible defects with elevated pipecolic acid. Determination of pipecolic acid in plasma and/or CSF should be included in the diagnostic work-up of patients with therapy-resistant seizures. It will in addition prevent patients with pyridoxine-dependent epilepsy from experiencing potentially dangerous pyridoxine-withdrawal, which until now has been necessary to prove the diagnosis.

Anticonvulsants↗
PubMed1988

Sympathetic stimulation and hypertension in the pyridoxine-deficient adult rat.

Pyridoxal phosphate is the coenzyme of various decarboxylases involved in the formation of monoamine neurotransmitters such as gamma-aminobutyric acid, serotonin, dopamine, and norepinephrine. Adult male Sprague-Dawley rats placed on a pyridoxine-deficient diet for 8 weeks showed significant hypertension compared with pyridoxine-supplemented controls. Hypothalamic contents of pyridoxal phosphate, gamma-aminobutyric acid, and serotonin in the pyridoxine-deficient rats were significantly lower than those in pyridoxine-supplemented controls. Hypertension was associated with sympathetic stimulation. Treatment of pyridoxine-deficient rats with a single dose of pyridoxine (10 mg/kg body weight) reversed the blood pressure to normal levels within 24 hours, with concomitant restorations of hypothalamic serotonin and gamma-aminobutyric acid as well as the return of plasma norepinephrine and epinephrine to normal levels. Also, pyridoxine treatment reversed the hypothalamic hypothyroidism observed in pyridoxine-deficient rats. These results indicate an association between pyridoxine deficiency and sympathetic stimulation leading to hypertension.

Animals↗
PubMed1981

Pyridoxine transport in brush border membrane vesicles of guinea pig jejunum.

Transport of [3H]pyridoxine was studied with membrane vesicles prepared from brush border of guinea pig jejunum, in which pyridoxal kinase was not detected. The imposition of an Na+ gradient across the membrane did not affect pyridoxine transport. The equilibrium level of pyridoxine uptake decreased with increasing osmolarity of the medium, which indicates that pyridoxine is transported into the membrane vesicles. The initial rate of pyridoxine uptake increased linearly with increasing pyridoxine concentration throughout the range of 0.18 microM to 7.4 microM both in the presence and absence of an Na+ gradient. 4'-Deoxypyridoxine and unlabeled pyridoxine, added in excessive amounts, did not inhibit pyridoxine transport into the membrane vesicles. These results substantiate the notion that pyridoxine passes through the brush border membrane by simple diffusion.

Animals↗
PubMed1976

Mineral metabolism in chicks on high dietary pyridoxine and magnesium.

The effect of high dietary pyridoxine and magnesium on tissue electrolytes was studied in day-old broiler-type male chicks. There were 15 treatments of 875, 1375 and 1875 mg. magnesium/kg. diet and pyridoxine at 1, 4, 31, 301, 3001 mg./kg. diet in a 3 x 5 factorial block design. The sodium concentration of the liver decreased linearly with increasing dietary magnesium concentration expressed as log 10. In the kidney, no such effect was observed. The response of sodium concentration in these two tissues to increasing dietary pyridoxine, also expressed as log 10, was curvilinear, decreasing to minimum concentrations at pyridoxine intakes estimated to be equal to 40 mg./kg. of diet for the liver and 50 for the kidney and thereafter increasing. Potassium concentration of the liver exhibited opposite trends to those for sodium concentration but the responses to dietary magnesium were not consistent at each dietary pyridoxine concentration. Kidney potassium content followed essentially opposite trends to those of sodium. Kidney calcium decreased with increases in either dietary magnesium or pyridoxine, but the decreases were not consistent. The magnesium content of the kidney tended to increase with increases in dietary magnesium. Dietary pyridoxine resulted in a curvilinear response only in those chicks fed the 1875 mg. diet, decreasing to a minimum value at a pyridoxine intake of 26 mg., and increasing at higher pyridoxine dietary concentrations. No significant effects on sodium, potassium, calcium and magnesium concentrations in the heart were observed. It was speculated that the maximum potassium retention estimated to occur in the livers of birds consuming a diet containing 48 mg. pyridoxine/kg. diet might be due to increased glycogen turnover or increased phosphorylase activity.

Animals↗
PubMedDate not supplied

[Pyridoxine dependence: the importance of the clinical diagnosis and early treatment].

OBJECTIVE: We described the electroclinical features, evolution and family history of two patients with definitive diagnosis of pyridoxine dependency. CASE REPORTS: The first patient is a 15-month-old girl who at 1 month of age started with seizures and irritability. At two months of age, pyridoxine was prescribed with a good control of seizures. At five months of age withdrawal response provoked 7 days after seizures recurrence. Pyridoxine was reintroduced and seizures disappeared. Her sister, at two months of age, started with refractory seizures. This sister also had mental retardation and at four years, she died. Her brother, 16 years old, presents mental retardation, refractory epilepsy and progressive motor and cognitive impairment. At 3 months of age, he started with seizures and at 15 years of age, pyridoxine was prescribed with a significative improvement the number of seizures and a better visual connection. The second patient is a 4-month-old girl who started with clonic seizures at 3 days of age and she had a good response to pyridoxine. Withdrawal response provoked seizure recurrence at 48 hours. Pyridoxine was introduced immediately with total control of seizures. She had two cousins with seizures who died at 3 months and 3 years of age respectively. CONCLUSION: When dealing with an infant with refractory seizures which start in the first two years of life and without etiology, we should consider the diagnosis of pyridoxine dependency. Early diagnosis and treatment with pyridoxine is crucial to avoid high risk morbidity and mortality. All infants in the two first years of life with refractory seizures without etiology must be prescribed oral pyridoxine (50-200 mg per day).

Female↗
PubMed1993

Double-blind trial of pyridoxine (vitamin B6) in the treatment of steroid-dependent asthma.

Pyridoxine has been reported to largely correct an abnormality of tryptophan metabolism present in patients with bronchial asthma and to reduce the symptoms of asthma in long-term studies. We enrolled 31 patients requiring steroids (oral or inhaled) for the treatment of their asthma in a double-blind, placebo-controlled assessment of 9 weeks' treatment with pyridoxine 300 mg per day (13) or placebo (18). Outcome variables included PEFR, FEV1, asthma symptom scores, 24 hour urinary 5-HIAA, skin test reactivity to histamine and compound 48/80 and blood serotonin levels. Plasma pyridoxine levels indicated overall patient compliance with a mean change from baseline to the end of the study of 82.5 +/- 27.7 ng/mL in patients on pyridoxine and -2.9 +/- 10.3 for those on placebo (P = .0001). Furthermore, patients routinely treated with theophylline had lower (10 +/- 8 ng/mL) plasma pyridoxine levels at baseline than those not on it (19 +/- 6 ng/mL; P = .01), suggesting that theophylline may lower plasma pyridoxine levels. There was no significant difference between the pyridoxine and placebo groups in the change from baseline to the last 2 weeks of treatment phase in any of the outcome variables. We conclude that under the conditions of the study, treatment with oral pyridoxine failed to improve the outcome variables in patients requiring steroids for the treatment of their asthma. The results of this study suggest that prescription or usage of oral pyridoxine for the treatment of asthma cannot be justified in such patients.

Administration, Inhalation↗
PubMed1997

Cytosolic pyridoxine-beta-D-glucoside hydrolase from porcine jejunal mucosa. Purification, properties, and comparison with broad specificity beta-glucosidase.

During studies of the nutritional utilization of pyridoxine 5'-beta-D-glucoside, a major form of vitamin B6 in plants, we detected two cytosolic beta-glucosidases in jejunal mucosa. As expected, one was broad specificity beta-glucosidase that hydrolyzed aryl beta-D-glycosides but not pyridoxine beta-D-glucoside. We also found a previously unknown enzyme, designated pyridoxine-beta-D-glucoside hydrolase, that efficiently hydrolyzed pyridoxine beta-D-glucoside. These were separated and purified as follows: broad specificity beta-glucosidase 1460-fold and pyridoxine-beta-D-glucoside hydrolase 36,500-fold. Purified pyridoxine-beta-D-glucoside hydrolase did not hydrolyze any of the aryl glycosides tested but did hydrolyze cellobiose and lactose. Pyridoxine-beta-D-glucoside hydrolase exhibited a pH optimum of 5.5 and apparent molecular mass of 130 kDa by SDS-polyacrylamide gel electrophoresis and 160 kDa by nondenaturing gel filtration, in contrast to 60 kDa for native and denatured broad specificity beta-glucosidase. Glucono-delta-lactone was a strong inhibitor of both enzymes. Ionic and nonionic detergents were inhibitory for each enzyme. Conduritol B epoxide, a potent inhibitor of lysosomal acid beta-glucosidase, inhibited pyridoxine-beta-D-glucoside hydrolase but not broad specificity beta-glucosidase, but both were inhibited by the mechanism-based inhibitor 2-deoxy-2-fluoro-beta-D-glucosyl fluoride. Our findings indicate major differences between these two cytosolic beta-glucosidases. Studies addressing the role of vitamin B6 nutrition in regulating the activity and its consequences regarding pyridoxine glucoside bioavailability are in progress.

Animals↗
PubMed1987

Pyridoxine deficiency and ethanol-induced liver injury.

It has been suggested that pyridoxine deficiency may potentiate ethanol-induced liver injury. Our purpose was to clarify the effect of pyridoxine deficiency on ethanol-associated liver injury by comparing liver histology, serum liver enzymes, and the viability of cultured hepatocytes from pyridoxine-deficient and pyridoxine-sufficient rats that had been chronically fed ethanol-enriched diets. Our data fail to substantiate that pyridoxine-deficient animals are more susceptible to the hepatotoxic effects of ethanol than pair-fed pyridoxine-sufficient controls. Furthermore, the addition of pyridoxine to hepatocyte cultures fails to prevent in vitro cytotoxicity of added ethanol. Pyridoxine deficiency may augment ethanol-induced enhancement of hepatic urea synthesis. These data suggest that pyridoxine deficiency may contribute to the abnormal plasma amino acid profiles and nitrogen balance of chronic alcoholics, but that it does not potentiate ethanol-induced liver injury.

Animals↗
PubMed1982

Role of glucose on fatty liver formation in pyridoxine-deficient rats.

Studies were made on whether glucose starvation causes fatty liver in pyridoxine-deficient male Wistar rats. Pyridoxine deficiency resulted in significantly lower levels of liver glucose than in pair-fed controls but no significant change in the serum glucose concentration. In non-starving animals, serum immuno-reactive insulin (IRI) was significantly lower in pyridoxine-deficient rats than in pair- or ad libitum-fed controls. Liver glucokinase activity in pyridoxine-deficient rats was also significantly lower than in ad libitum-fed controls. The extent of insulin deficiency was evaluated by examining the effect of administration of insulin on pyridoxine-deficient rats. Administration of insulin had no effect on the activity of liver glucokinase in pyridoxine-deficient rats, but induced the enzyme in ad libitum-fed controls. In response to a decrease in the activity of liver glucokinase or hexokinase in the deficient group, glycolytic activity, estimated as lactate production from glucose in the liver supernatant spun at 100,000 X g, was reduced to half the control level in pyridoxine-deficient rats. The effects of glucose administration on the liver lipid content, serum insulin and serum glucose were investigated. The serum glucose concentration was not significantly different in pyridoxine-deficient and control rats at any time after the glucose load. The level of serum IRI after the load was similar in the two groups after 30 min but then gradually decreased in the deficient group. The liver lipid content of the deficient rats tended to decrease whereas that of the controls remained unchanged throughout the experiment. Thus glucose starvation in pyridoxine-deficient rats is one factor responsible for fatty liver formation. Possible mechanisms of this phenomenon are discussed.

Animals↗
PubMed2006

Tat-mediated protein transduction of human brain pyridoxine-5-P oxidase into PC12 cells.

Pyridoxine-5-P oxidase catalyses the terminal step in the biosynthesis of pyridoxal-5-P, the biologically active form of vitamin B6 which acts as an essential cofactor. Here, a human brain pyridoxine-5-P oxidase gene was fused with a gene fragment encoding the HIV-1 Tat protein transduction domain (RKKRRQRRR) in a bacterial expression vector to produce a genetic in-frame Tat-pyridoxine-5-P oxidase fusion protein. Expressed and purified Tat-pyridoxine-5-P oxidase fusion protein transduced efficiently into PC12 cells in a time- and dose-dependent manner when added exogenously to culture media. Once inside the cells, the transduced Tat-pyridoxine-5-P oxidase protein showed catalytic activity and was stable for 48 h. Moreover, the formation of pyridoxal-5-P was increased by adding exogenous Tat-pyridoxine-5-P oxidase to media pre-treated with the vitamin B6 precursor pyridoxine. In addition, the intracellular concentration of pyridoxal-5-P was markedly increased when Tat-pyridoxal kinase was transduced together with Tat-pyridoxine-5-P oxidase into cells.These results suggest that the transduction of Tat-pyridoxine-5-P oxidase fusion protein presents a means of regulating the level of pyridoxal-5-P and of replenishing this enzyme in various neurological disorders related to vitamin B6.

Animals↗
PubMedDate not supplied

Potentiometric membrane sensors for the selective determination of pyridoxine hydrochloride (vitamin B6) in some pharmaceutical formulations.

The construction and general performance characteristics of two novel potentiometric PVC membrane sensors responsive to the pyridoxine hydrochloride known as vitamin B6 (VB6) are described. These sensors are based on the use of the ion-association complexes of the pyridoxine cation with phosphomolybdate, and phosphotungstate counter anions as ion pair in a plasticized PVC matrix. The electrodes show a stable, near-Nernstian response for 6x10(-5)-1x10(-2) M VB6 at 25 degrees C over the pH range 2-4 with a cationic slope of 54.0+/-0.5 and 54.5+/-0.4 per concentration decade for pyridoxine-phosphomolybdate and pyridoxine-phosphotungstate respectively. The two electrodes have the same lower detection limit (4x10(-5) M) and the response times are 45-60 and 30-45 s in the same order for both. Selectivity coefficients for VB6 relative to a number of interfering substances were investigated. There is negligible interference from many cations, some vitamins and pharmaceutical excipients. Direct potentiometric determination of 15-2000 microg/ml pyridoxine shows an average recovery of 98.0% and 99.0% with relative standard deviation 1.5% and 1.2% at 100.0 microg/ml for pyridoxine-phosphomolybdate and pyridoxine-phosphotungstate electrodes, respectively. The determination of VB6 in some pharmaceutical preparations using the proposed electrodes gave an average recovery of 98.0 and 99.0% of the nominal value and a mean standard deviation of 1.1% and 0.9% (n=10) for pyridoxine-phosphomolybdate and pyridoxine-phosphotungstate electrodes, respectively. The results compare favorably with data obtained by the British Pharmacopoeia method.

Ion-Selective Electrodes↗
PubMed1984

Mechanism of pyridoxine uptake by isolated rat liver cells.

Uptake of [3H]pyridoxine by isolated rat hepatocytes was detected at substrate concentrations as low as 0.5 microM. At this concentration, an initial uptake rate was 1.87 +/- 0.17 pmol/10(6) cells X min at 37 degrees C. Both the initial and a subsequent much slower pyridoxine accumulation were strongly inhibited by low temperature as well as by 10 mM ethionine, which competes for available ATP, or 1 microM carbonylcyanide-p-trifluoromethoxyphenylhydrazone, which inhibits oxidative phosphorylation and the supply of ATP. The uptake process is apparently insensitive to 1 mM ouabain and is Na+ independent. The initial uptake rate was saturable at higher concentrations of [3H]pyridoxine with an apparent Km of 28 +/- 8 microM and Vmax of 106 +/- 27 pmol/10(6) cells X min. The Km value corresponds to that reported for pyridoxine as a substrate of pyridoxal kinase. Moreover, the transport process was inhibited by structural analogs of [3H]pyridoxine even at concentrations equimolar to the normal substrate. The established order of inhibitory effectiveness, 4'-deoxypyridoxine greater than unlabeled pyridoxine greater than 5'-deoxypyridoxine, is in agreement with known properties of the kinase. It is concluded that pyridoxine uptake probably occurs by diffusion, simple or facilitated, followed by metabolic trapping due to pyridoxal kinase-catalyzed phosphorylation. Pyridoxine deficiency had no significant effect on uptake of this B6 vitamer by hepatocytes.

Adenosine Triphosphate↗
PubMed1994

The utilization of intravenously infused pyridoxine in humans.

The utilization of a usual dose of intravenously infused pyridoxine (100 mg pyridoxine hydrochloride) was investigated in ten healthy males. Blood plasma and erythrocytes were investigated by means of high-performance liquid chromatography. Detectable metabolites in blood plasma were pyridoxine, pyridoxal 5'-phosphate, pyridoxal and 4-pyridoxic acid. In erythrocytes pyridoxine, pyridoxal 5'-phosphate, pyridoxal, and pyridoxamine 5'-phosphate were found. From their concentration-time curves rate constants of elimination and invasion, volume of distribution (pyridoxine) and the areas under the curves were calculated. Values for concmax and tmax are reported. A comparison with earlier results of oral pyridoxine administration revealed a better utilization after intravenous than after oral application, i.e. a greater build-up of coenzyme forms. A regulatory phenomenon in erythrocytes caused by high doses of pyridoxine is described. In view of the potential toxicity of pyridoxine the doses used in parenteral nutrition are called into question.

Adult↗
PubMed1980

Transport and metabolism of pyridoxine in rat liver.

Evidence, obtained with in situ perfused rat liver, indicated that pyridoxine is taken up from the perfusate by a non-concentrative process, followed by metabolic trapping. These conclusions were reached on the basis of the fact that at low concentrations (0.125 microM), the 3H of [3H]pyridoxine accumulated against a concentration gradient, but high concentrations (333 microM) of pyridoxine or 4-deoxypyridoxine prevented this apparent concentrative uptake. Under no conditions did the tissue water:perfusate concentration ratio of [3H]pyridoxine exceed unity. The perfused liver rapidly converted the labeled pyridoxine to pyridoxine phosphate, pyridoxal phosphate and pyridoxamine phosphate and released a substantial amount of pyridoxal and some pyridoxal phosphate into the perfusate. Since muscle and erythrocytes failed to oxidize pyridoxine phosphate to pyridoxal phosphate, it is suggested that the liver plays a major role in oxidizing dietary pyridoxine and pyridoxamine as their phosphate esters to supply pyridoxal phosphate which then reaches to other organs chiefly as circulating pyridoxal.

Absorption↗
PubMed1998

Photosensitive dermatitis caused by pyridoxine hydrochloride.

Few photosensitive reactions caused by pyridoxine hydrochloride have been reported. There have been no reports of detailed photosensitivity studies on patients who have developed photosensitivity from pharmacologic doses of pyridoxine. Two patients with pyridoxine photosensitivity are described. Photopatch tests were positive for pyridoxine hydrochloride. The minimal erythematous dose (MED) for UVA decreased after the intravenous injection of pyridoxine hydrochloride in both patients. Normal controls gave negative results in photopatch tests for pyridoxine hydrochloride and phototest for vitamin B complex containing pyridoxine hydrochloride. On the basis of these results, we believe both patients had a photoallergic reaction to pyridoxine hydrochloride.

Dermatitis, Photoallergic↗
PubMed2002

Biochemical deficiency of pyridoxine does not affect interleukin-2 production of lymphocytes from patients with Sjögren's syndrome.

BACKGROUND: There is evidence that pyridoxine deficiency may alter the immune response. It is not known whether a deficiency of this vitamin is evident in subjects with primary Sjögren's syndrome (SS). OBJECTIVE: We studied whether subjects with primary SS showed a biochemical deficiency of pyridoxine, and if it is associated with abnormal production of interleukin-2 from lymphocytes stimulated in vitro with phytohemagglutinin (PHA). DESIGN: Two studies were conducted, (i) biochemical and nutritional assessments were performed in a cross-over study in subjects with primary SS, who were supplemented with 25 mg/day of pyridoxine or placebo for 3 months. After 1 month washout, they were supplemented for 3 months with placebo, (ii) patients with SS and matched controls received pyridoxine or placebo for 45 days, and a blood sample was obtained to study IL-2 production and expression in T-lymphocytes stimulated with PHA. RESULTS: Subjects with primary SS showed limited dietary intake of pyridoxine and biochemical deficiency of this vitamin assessed through the activation coefficient of the erythrocyte aspartate aminotransferase. The biochemical deficiency did not affect production nor mRNA expression of IL-2 from T-lymphocytes stimulated in vitro with PHA compared with the control group. Supplementation of subjects with primary SS with 25 mg/day with pyridoxine for 45 days did not produce any significant change as compared to those patients supplemented with placebo. CONCLUSIONS: Subjects with primary SS showed biochemical deficiency of pyridoxine, possibly due to limited intake of this vitamin which was corrected by supplementation with pyridoxine. However, IL-2 production and mRNA expression from stimulated lymphocytes were unaffected by supplementation, probably because the deficiency was not severe enough to affect the immune system. SPONSORSHIP: This work was supported by the National Council of Science and Technology (CONACYT), Mexico, grant no. 212226-5-0902PM.

Adult↗
PubMed1976

Influence of pyridoxine supplementation on vitamin B-6 levels in milk of rats deficient in the vitamin.

Levels of vitamin B-6 in milk from pyridoxine deficient dams were used as an indicator of the ability of pyridoxine to protect offspring against the effects of the deficiency. Sprague Dawley rats were fed a basal diet containing 30.0 (control) or 1.2 (deficient) mg pyridoxine-HC1/kg diet from weaning throughout growth, gestation and until 5 days postpartum. At this time, deficient dams were supplemented by a single intraperitoneal injection of 600 mug pyridoxine-HC1, or by adding 30 or 60 mg pyridoxine-HC1/kg to the diet. The vitamin B-6 content in milk form the group supplemented by injection exceeded the control level of 38.8 mug/100 ml milk 30 minutes after the injection, and reached a peak level of 110.7 mug/100 ml at 4 hours with a subsequent decline to 27mug/100 ml at 20 hours. In rats supplemented orally with 30 or 60 mg pyridoxine-HC1/kg diet, the vitamin B-6 level in the milk reached the control value in 24 and 6 hours, respectively. At 120 hours, orally supplemented dams had significantly higher levels of vitamin B-6 in the milk than control animals. Vitamin supplementation of dams by a single injection of pyridoxine-HC1 was sufficient to overcome the pyridoxine deficiency syndrome in the pups, but was not adequate for optimum growth.

Animals↗