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Précis Abnormal methionine challenge test results cannot be explained by a deficiency in pyridoxal phosphate, folic acid, or cobalamin. The methionine challenge test is reliable for demonstrating hyperhomocysteinemia. Objective. To research the status of pyridoxal phosphate, folic acid, and cobalamin as part of an examination for hyperhomocysteinemia and to establish their relationship to the results of methionine challenge tests in women, who were tested at least 3 months after they had ended a pregnancy which was complicated by preeclampsia or other vascular-related pregnancy complications. Methods. In the Isala clinics in Zwolle, women with vascular-related complications of pregnancy were tested at least 3 months postpartum for hyperhomocysteinemia, by performing a methionine challenge test, as well as tests to measure their vitamin status. The diagnosis of hyperhomocysteinemia was made after two abnormal test results. The χ2 test was used to compare the vitamin status of the group with normal results to those with an abnormal result of methionine challenge tests. Results. No statistically significant differences in the vitamin status were found between the group of women with an abnormal and the group with normal results of the methionine challenge tests. Conclusion. Abnormal methionine challenge test results cannot be explained by a deficiency in pyridoxal phosphate, folic acid, or cobalamin. We demonstrate that, when women are tested 3 months postpartum, the methionine challenge test is reliable for demonstrating hyperhomocysteinemia as a risk factor for vascular-related complications of pregnancy. [ABSTRACT FROM AUTHOR]

Abstract: Purpose: Pyridoxine-Dependent Epilepsy (PDE) is a rare autosomal recessive disease with neonatal seizures resistant to conventional anti-epileptic drugs. This metabolic disease has to be diagnosed early and treated to improve outcome. We report on two new mutations that open new prenatal prospects and suggest a new diagnostic procedure. Case report: We describe PDE in a neonate carrying two novel mutations in the ALDH7A1 gene: c.[852_856delCTTAG] + [1230C > A]; p.[(Phe410Leu)] + p.[(Leu285CysfsX26)]. This case also illustrates that diagnosis could have been made without any pyridoxine withdrawal, thanks to the measurement of biomarkers. The patient was successfully treated with pyridoxine supplementation and currently shows normal neurological development. [ABSTRACT FROM AUTHOR]

There is good agreement concerning average requirements and reference intakes for vitamin B6 but less agreement over safe upper levels from supplements. High-dose supplements cause sensory nerve damage. Supplements of vitamin B6 have been advocated for treatment of the premenstrual syndrome, with little evidence of efficacy. There are plausible mechanisms for an antidepressant action and protection against steroid hormone—dependent cancers but no evidence from clinical trials. Pyridoxamine reduces the glycation of proteins and so could be beneficial in preventing the adverse effects of poor glycemic control in diabetes. There are plausible mechanisms for an antihypertensive action but only suggestive evidence from small intervention trials. There is no evidence that supplements of vitamin B6 have any beneficial effect in hyperhomocysteinemia. There is neither a plausible mechanism nor any evidence from controlled trials for any effect of supplements of vitamin B6 in preventing a decline in cognitive function with aging, amelioration of dementia or autism, or improvement of the carpal tunnel syndrome. [ABSTRACT FROM PUBLISHER]

Deficiencies of the vitamins folate, B, and B are associated with neurological and psychological dysfunction and with congenital defects. In the elderly, cognitive impairment and incident dementia may be related to the high prevalence of inadequate B vitamin status and to elevations of plasma homocysteine. Plausible mechanisms include homocysteine neurotoxicity, vasotoxicity, and impaired S-adenosylmethionine-dependent methylation reactions vital to central nervous system function. In light of this, it is imperative to find safe ways of improving vitamin B status in the elderly without exposing some individuals to undue risk. [ABSTRACT FROM AUTHOR]

Objective: To find out the prevalence of hyperhomocysteinemia, and deficiencies of folate, vitamin B6 and vitamin B12 in an urban population in Karachi, Pakistan. Methodology: In a pre and post experimental study, eight hundred and seventy-two apparently healthy adults (aged 18-60 years; 355 males and 517 females) were recruited from a low-income urban locality in East of Karachi from February 2006 to March 2007. Fasting venous blood was obtained. Serum was analyzed for folate and vitamin B12. Plasma was analyzed for pyridoxal phosphate (PLP, coenzymic form of B6) and total homocysteine. A group of vitamin-deficient individuals (n=194) was given 3-week supplementation with folic acid (5mg/ day), methycobalamin (0.5mg/day) and pyridoxine hydrochloride (vitamin B6, 50 mg/day). After supplementation, serum/plasma levels of folate, vitamin B12, PLP and homocysteine were again determined. Results: Prevalence of hyperhomocysteinemia (>15μmol/l) was 32%. Similarly percent values of folate deficiency (<3.5ng/ml), vitamin B6 deficiency (PLP<20 nmol/l) and vitamin B12 deficiency (<200pg/ml) in the study population were 27.5%, 33.7% and 9.74%, respectively. Hyperhomocysteinemia was associated with male sex, folate deficiency, vitamin B12 deficiency [OR (95%CI), 8.3(5.7-12.1); 2.5(1.76-3.58); 2.6(1.5-4.5), respectively]. A 3-week supplementation with folic acid, methycobalamin and pyridoxine hydrochloride in vitamindeficient subjects decreased plasma homocysteine levels by 37%. Conclusion: High prevalence estimates of folate, vitamin B12, and vitamin B6 deficiencies appear to be the major determinants of hyperhomocysteinemia in a low income general population in Karachi. [ABSTRACT FROM AUTHOR]

J. Neurochem. (2010) 114, 87–96. Pyridoxal 5′-phosphate, the active form of vitamin B6, is an essential cofactor for multiple enzymes, including aromaticl-amino acid decarboxylase that catalyses the final stage in the production of the neurotransmitters dopamine and serotonin. In two patients with inherited disorders of vitamin B6 metabolism, we observed reductions in plasma aromaticl-amino acid decarboxylase activity. In one patient, this change was related to an increase in Km for pyridoxal 5′-phosphate. Furthermore, pyridoxal 5′-phosphate-deficient human SH-SY5Y neuroblastoma cells were found to exhibit reduced levels of aromaticl-amino acid decarboxylase activity and protein but with no alteration in expression. Further reductions in activity and protein were observed with the addition of the vitamin B6 antagonist 4-deoxypyridoxine, which also reduced aromaticl-amino acid decarboxylase mRNA levels. Neither pyridoxal 5′-phosphate deficiency nor the addition of 4-deoxypyridoxine affected aromaticl-amino acid decarboxylase stability over 8 h with protein synthesis inhibited. Increasing extracellular availability of pyridoxal 5′-phosphate was not found to have any significant effect on intracellular pyridoxal 5′-phosphate concentrations or on aromaticl-amino acid decarboxylase. These findings suggest that maintaining adequate pyridoxal 5′-phosphate availability may be important for optimal treatment of aromaticl-amino acid decarboxylase deficiency andl-dopa-responsive conditions. [ABSTRACT FROM AUTHOR]

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Introduction: The aim of this study was to evaluate lipid peroxidation (LP) and free radical scavenging enzyme activities in kidney tissue of vitamin B6-deficient rats. Material and Methods: The rats were divided into control and vitamin B6-deficient groups. After 4 weeks of feeding, animals in all groups were anesthetized by thiopental sodium (50 mg/kg). Thoraces were opened, 2 mL blood samples were taken from aortas, then the rats were killed by cervical dislocation, and kidney tissues were removed. Biochemical measurements in kidney tissue were carried out using a spectrophotometer. Results: Total superoxide scavenger activity (TSSA), nonenzymatic superoxide scavenger activity (NSSA), superoxide dismutase (SOD) activities, and antioxidant potential (AOP) values in the vitamin B6-deficient group were significantly lower than those of the control group, whereas glutathione peroxidase (GSH-Px), glutathione reductase (GRD), glutathione- S-transferase (GST) activities, and malondialdehyde (MDA) level were significantly higher than those of the control group ( p < 0.05). Discussion: The results show that vitamin B6 deficiency causes an attenuation in antioxidant defense system and an increase in oxidative stress in kidney tissue of rats. [ABSTRACT FROM AUTHOR]

Aim: Little is known about pyridoxine nutriture of children treated with isoniazid (INH) regimens. This study documents plasma pyridoxal 5′-phosphate (PLP) concentrations in children, HIV-infected and HIV-uninfected, receiving INH regimens. Methods: Children from the Western Cape of South Africa hospitalized for tuberculosis (TB) management were studied. Plasma PLP concentrations were determined on enrolment, 1-month after commencing TB treatment, and again after 4-month’s treatment. The children received a supplement meeting pyridoxine requirements. Results: Nineteen HIV-infected and 33 HIV-uninfected children received INH (dosage range 4–20 mg/kg) daily. Mean PLP plasma concentrations on enrolment were 8.32 (SD 6.75) ng/mL and 11.28 (SD 3.02) ng/mL in HIV-infected and HIV-uninfected children, respectively (p = 0.11) and after 4-month’s treatment 6.75 (SD 2.71) ng/mL and 14.76 (SD 7.96) ng/mL (p < 0.001). On enrolment 9 (50%) HIV-infected and 5 (15%) HIV-uninfected children (p = 0.016) had suboptimal PLP concentrations (<6 ng/mL); after 4-month’s treatment 8 (42%) and 2 (6%) (p = 0.004). Conclusion: Plasma PLP concentrations in children treated for TB were low on enrolment in HIV-infected and HIV-uninfected children; after 4-month’s treatment low values were still common in HIV-infected children. Additional pyridoxine supplementation of malnourished children treated for tuberculosis is advisable, particularly those HIV-infected. [ABSTRACT FROM AUTHOR]

Esmond E. Snell (1914–2003) was a giant of B-vitamin and enzyme research. His early research in bacterial nutrition had lead to the discovery of vitamins such as lipoic acid and folic acid, and an anti-vitamin avidin. He developed microbiological assay methods for riboflavin and other vitamins and amino acids, which are still used today. He also investigated the metabolism of vitamins, discovered pyridoxal and pyridoxamine as the active forms of vitamin B6 and revealed the mechanism of transamination and other reactions catalysed by vitamin B6 enzymes. His research in later years on pyruvoyl-dependent histidine decarboxylase unveiled the biogenesis mechanism of this first built-in cofactor. Throughout his career, he was a great mentor of many people, all of whom are inspired by his philosophy of science. [ABSTRACT FROM PUBLISHER]

Abstract: Epidemiological and clinical studies indicate that elevated circulating level of homocysteine (Hcy) is a risk factor for developing Alzheimer’s disease (AD). Dietary deficiency of folate, vitamin B6 and B12 results in a significant increase of Hcy levels, a condition also known as hyperhomocysteinemia (HHcy). In the present study we tested the hypothesis that a diet deficient for these three important factors when administered to a mouse model of AD, i.e. Tg2576, will result in HHcy and in an acceleration of their amylodotic phenotype. Compared with Tg2576 mice on regular chow, the ones receiving the diet deficient for folate, B6 and B12 developed HHcy. This condition was associated with a significant increase in Aβ levels in the cortex and hippocampus, and an elevation of Aβ deposits in the same regions. No significant changes were observed for steady-state levels of total APP, BACE-1, ADAM-10, PS1 and nicastrin in the brains of mice with HHcy. No differences were observed for the main Aβ catabolic pathways, i.e. IDE and neprilysin proteins, or the Aβ chaperone apolipoprotein E. Our findings demonstrate that a dietary condition which leads to HHcy may also result in increased Aβ levels and deposition in a transgenic mouse model of AD-like amylodosis. They further support the concept that dietary factors can contribute to the development of AD neuropathology. [Copyright &y& Elsevier]

The frequency of the methylenetetrahydrofolate reductase enzyme (MTHFR) C677T mutation was determined using polymerase chain reaction (PCR) and with measurement of plasma total homocysteine (tHcy), folate, vitamins B6, B12 and disease severity in 102 SS children from Yemen. The homozygous TT genotype for MTHFR C677T was present in 2% (2/102), and heterozygous CT in 10.8% (11/102), giving an allele frequency of 7.35%. The T allele was not associated with raised plasma tHcy or increased disease severity. The mean [±SD (standard deviation)] tHcy was 2.8 ± 1.7 μmol/L, increased with age and was highest in children >10 years (3.6 ± 2.5 vs. 2.5 ± 1.2 μmol/L, p <0.05). Whole blood folate and plasma vitamin B12 levels were normal or elevated, and 4% had vitamin B6 deficiency. In Yemeni children with sickle cell disease the frequency of the MTHFR C677T mutation was not higher than expected in the general population and was not associated with disease severity. [ABSTRACT FROM AUTHOR]

Low circulating pyridoxal 5'-phosphate (PLP) concentrations have been linked to inflammatory markers and the occurrence of inflammatory diseases. However, the implications of these findings are unclear. The measurement of PLP and C-reactive protein (CRP) in blood samples collected from participants in the 2003-2004 NHANES afforded us the opportunity to investigate this relationship in the general U.S. population. Dietary and laboratory data were available for 3864 of 5041 interviewed adults, 2686 of whom were eligible lie, provided reliable dietary data and were not diabetic, pregnant, lactating, or taking hormones or steroidal antiinflammatory drugs). Vitamin B-6 intake was assessed using 2 24-h diet recalls and supplement use data. After multivariate adjustment for demographics, smoking, BMI, alcohol use, antioxidant vitamin status, intakes of protein and energy, and serum concentrations of creatinine and albumin, high vitamin B-6 intake was associated with protection against serum CRP concentrations >10 mg/L compared with ⩽3 mg/L. However, plasma PLP ⩾⩾ 20 nmol/L compared with <20 nmol/L was inversely related to serum CAP independently of vitamin 8-6 intake (P< 0.0011. Among participants with vitamin B-6 intakes from 2 to 3 mg/d, the multivariate-adjusted prevalence of vitamin B-6 inadequacy was <10% in participants with serum CRP ⩽3 mg/L but close to 50% in those with serum CAP > 10 mg/L (P < 0.001). In conclusion, higher vitamin B-6 intakes were linked to protection against inflammation and the vitamin El-6 intake associated with maximum protection against vitamin B-6 inadequacy was increased in the presence compared to absence of inflammation [ABSTRACT FROM AUTHOR]

Low circulating pyridoxal 5'-phosphate (PLP) concentrations have been linked to inflammatory markers and the occurrence of inflammatory diseases. However, the implications of these findings are unclear. The measurement of PLP and C-reactive protein (CRP) in blood samples collected from participants in the 2003-2004 NHANES afforded us the opportunity to investigate this relationship in the general U.S. population. Dietary and laboratory data were available for 3864 of 5041 interviewed adults, 2686 of whom were eligible lie, provided reliable dietary data and were not diabetic, pregnant, lactating, or taking hormones or steroidal antiinflammatory drugs). Vitamin B-6 intake was assessed using 2 24-h diet recalls and supplement use data. After multivariate adjustment for demographics, smoking, BMI, alcohol use, antioxidant vitamin status, intakes of protein and energy, and serum concentrations of creatinine and albumin, high vitamin B-6 intake was associated with protection against serum CRP concentrations >10 mg/L compared with ⩽3 mg/L. However, plasma PLP ⩾⩾ 20 nmol/L compared with <20 nmol/L was inversely related to serum CAP independently of vitamin 8-6 intake (P< 0.0011. Among participants with vitamin B-6 intakes from 2 to 3 mg/d, the multivariate-adjusted prevalence of vitamin B-6 inadequacy was <10% in participants with serum CRP ⩽3 mg/L but close to 50% in those with serum CAP > 10 mg/L (P < 0.001). In conclusion, higher vitamin B-6 intakes were linked to protection against inflammation and the vitamin El-6 intake associated with maximum protection against vitamin B-6 inadequacy was increased in the presence compared to absence of inflammation [ABSTRACT FROM AUTHOR]

The article presents a study which examines the effect of marginal vitamin B-6 deficiency on the rate of red blood cell glutathione synthesis. Subjects and methods of the study are offered, along with a discussion on the protective roles of glutathione in the human body. Result of the study reveals that dietary vitamin B-6 restriction reduces the red blood cell glutathione synthesis rate without affecting glutathione concentration in plasma.

The article presents abstracts on kidney diseases and management which include the efficacy nutraceutical products for kidney stone diseases, subcapsular hematoma as complication of extracorporeal shock wave lithotripsy, and the increased risk of urinary calcium oxalate and uric acid stone formation due to depletion of vitamin B1 and B6 in the diet.

We experimented with a mathematical model for 1-carbon metabolism and glutathione (GSH) synthesis to investigate the effects of vitamin B-6 deficiency on the reaction velocities and metabolite concentrations in this metabolic network. The mathematical model enabled us to independently alter the activities of each of the 5 vitamin B-6-dependent enzymes and thus determine which inhibitions were responsible for the experimentally observed consequences of a vitamin B-6 deficiency. The effect of vitamin B-6 deficiency on serine and glycine concentrations in tissues and plasma was almost entirely due to its effects on the activity of glycine decarboxylase. The effect of vitamin B-6 restriction on GSH concentrations appeared to be indirect, arising from the fact that vitamin B-6 restriction increases oxidative stress, which, in turn, affects several enzymes in 1-carbon metabolism as well as the GSH transporter. Vitamin B-6 restriction causes an abnormally high and prolonged homocysteine response to a methionine load test. This effect appeared to be mediated solely by its effects on cystathionine β-synthase. Reduction of the enzymatic activity of serine hydroxymethyltransferase (SHMT) had negligible effects on most metabolite concentrations and reaction velocities. Reduction or total elimination of cytoplasmic SHMT had a surprisingly moderate effect on metabolite concentrations and reaction velocities. This corresponds to the experimental findings that a reduction in the enzymatic activity of SHMT has little effect on 1-carbon metabolism. Our simulations showed that the primary function of SHMT was to increase the rate by which the glycine-serine balance was reequilibrated after a perturbation. [ABSTRACT FROM AUTHOR]

AbstractBackgroundLower levels of B vitamins (particularly folate, vitamin B12and vitamin B6) may be associated with psychological distress. Little is known about the impact of childhood nutrition on psychological distress in adult life.ObjectiveWe investigated whether prospectively measured childhood and adult dietary intakes of thiamin, riboflavin, niacin, folate, vitamin B6and vitamin B12were related to the psychological distress of women in mid-age, taking into account socio-economic, behavioural and lifestyle factors.DesignProspective data were collected from a cohort of 636 British women followed up since their birth in 1946. Participants completed a 28-item, scaled version of the General Health Questionnaire (GHQ-28) to measure psychological distress at age 53 years. Dietary intakes in childhood (at age four) were determined by 24h recall and in adulthood (at age 36, 43 and 53 years) by a 5d food record.ResultsLow dietary vitamin B12intake at age 53 was associated with higher psychological distress at that age. Women in the lowest third of vitamin B12intake in adulthood had a higher GHQ-28 score compared with those in the highest third (percentage change, adjusted regression coefficient, 21 (95% CI 3, 39)). There were no other significant associations between dietary B vitamin intake in childhood or adulthood and psychological distress in the cohort.ConclusionsOverall, there is evidence that intake of vitamin B12at age 53 is related to adult psychological distress but there is no evidence for the effects of other adult B vitamin intakes or childhood intakes on psychological distress. [ABSTRACT FROM AUTHOR]

Abstract: Purpose: We investigated the effect of a vitamin B6 deficiency and pair-feeding on tissue trace element status. Method: Tissue zinc, copper and iron concentrations were measured in 3 groups of young, male Wistar rats receiving a diet of 3.5mg/kg (control group), 0mg/kg (deficient group) and a pair-fed group over 8 weeks. The pair-fed group received the same diet consumed by the control. Tissue trace element analysis was performed using atomic absorption spectrophotometry and plasma vitamin B6 status was determined using HPLC. Results: Deficiency resulted in elevation in liver iron concentration and reduction in muscle iron concentration. Muscle copper concentrations were reduced in the pair-fed and deficient groups vs. the control group. Tissue zinc concentrations remained unaffected by the deficiency. Kidney iron and heart copper levels were elevated in the pair-fed group. Conclusions: The liver and muscle iron changes were due to the deficiency and not to reduced calorie intake and the latter may be due to impaired heme synthesis. The differences in copper between the groups were due to reduced food intake. Zinc seems to form a fixed pool in these animals. A dietary deficiency of vitamin B6 impacts on the trace element status of certain tissues in key metabolic tissues and hence needs to be factored into the amelioration of the condition. [Copyright &y& Elsevier]

The article presents a study on the incidence, risk factors and management of pyridoxal-5′ -phosphate (PLP) deficiency following the multivisceral and intestinal transplantation in adult. It highlights the clinical nutritional autonomy (CNA) measurement of serum PLP and homocysteine concentrations before and after transplant to prevent deficiency. It also emphasizes the establishment of an effective repletion algorithmic protocol for the achievement of full CNA.

Objective:To study the prevalence of vitamin B6 deficiency in common variable immunodeficiency and the impact of vitamin B6 supplementation on immune function in the disorder.Design:Open, non-blinded.Setting:Medical School Hannover, Hannover, Germany.Subjects:Plasma vitamin B6 concentrations were measured in all the 54 common variable immunodeficiency (CVID) patients visiting our outpatients' clinics in 2005.Interventions:The 17 patients with a decreased vitamin B6 concentration were recommended to take 50 mg of vitamin B6/day for 3 months. Then, vitamin B6 concentrations, absolute number of lymphocyte populations and immunoglobulin concentrations were controlled.Results:Vitamin B6 concentrations were reduced in 17/54 patients. All 11/17 patients following our advice to substitute vitamin B6 had normal vitamin B6 plasma concentrations 3 months later. In parallel, the number of CD4+ T cells significantly increased. In contrast, concentrations of serum immunoglobulins were not improved.Conclusions:Vitamin B6 deficiency is common in CVID. The vitamin deficiency is not the cause of CVID and vitamin supplementation does not relieve humoral immunodeficiency. Nevertheless, vitamin B6 should be measured in CVID to avoid possible long-term complications of its deficiency.European Journal of Clinical Nutrition (2008) 62, 332–335; doi:10.1038/sj.ejcn.1602694; published online 21 February 2007 [ABSTRACT FROM AUTHOR]

We studied the effects of an intravenous hydroxypyruvate load on endogenous oxalogenesis in rats receiving a standard diet or a vitamin-B6-deficient diet. Twelve male Wistar rats were randomized to two groups and were fed either a standard diet or a vitamin-B6-deficient diet for 3 weeks. Then the animals received an intravenous infusion of 100 mg/ml (960.6 μmol/ml) of hydroxypyruvate slowly over 10 min. Urine samples were collected just before hydroxypyruvate infusion and at hourly intervals until 5 h afterward. Urinary oxalate, glycolate, and citrate levels were measured by capillary electrophoresis. Hourly urinary oxalate excretion peaked within 2 h, while urinary glycolate excretion peaked at 1 h, after the hydroxypyruvate load in both control and vitamin-B6-deficient rats. Both urinary oxalate and glycolate excretion were higher in vitamin-B6-deficient rats than in control rats. Infusion of hydroxypyruvate increased the 5-h urinary oxalate and glycolate excretion to 0.68% (6.56 μmol) and 0.53% (5.10 μmol) of the administered dose (mol/mol), respectively, in the control rats, while oxalate and glycolate excretion, respectively, increased to 2.43% (23.36 μmol) and 0.79% (7.59 μmol) of the dose in the vitamin-B6-deficient rats. Urinary citrate excretion was significantly lower at baseline and all other times in the vitamin-B6-deficient rats than in the control rats. In conclusion, a hydroxypyruvate load increased endogenous oxalate synthesis in control rats, and its synthesis was even greater in vitamin-B6-deficient rats. Vitamin B6 deficiency also resulted in significant hypocitraturia. [ABSTRACT FROM AUTHOR]

Multiple aspects of homocysteine metabolism were studied to understand the mechanism responsible for hyperhomocysteinemia toxicity in Alzheimer disease. Besides oxidative stress and vascular damage, homocysteine has also a great importance in regulating DNA methylation through S-adenosylmethionine, the main methyl donor in eukaryotes. Alterations of S-adenosylmethionine and methylation were evidenced in Alzheimer disease and in elderly. In order to clarify whether DNA methylation can provide the basis for amyloid-beta overproduction, we used human SK-N-BE neuroblastoma and A172 glioblastoma cell lines. We tested the effects of folate, B12 and B6 deprivation and S-adenosylmethionine addition on methylation metabolism. Our results indicate that homocysteine accumulation induced through vitamin B deprivation could impair the "Methylation Potential" with consequent presenilin 1, BACE and amyloid-beta upregulation. Moreover, we found that homocysteine alterations had an effect on neuroblastoma but not on glioblastoma cells; this suggests a possible differential role of the two cell types in Alzheimer disease. [ABSTRACT FROM AUTHOR]

The effects of an intravenous hydroxyproline load on endogenous oxalogenesis were compared in rats fed a standard diet or a vitamin B6-deficient diet. Twelve male Wistar rats were randomized to two groups and were fed either a standard diet (control group) or a vitamin B6-deficient diet for 3 weeks. Then the animals were intravenously administered 100 mg (762.6 μmol)/ml hydroxyproline. In the control group, infusion of hydroxyproline increased the 5-h urinary oxalate and glycolate excretion above baseline to 0.27% (2.02 ± 1.11 μmol) and 0.32% (2.43 ± 1.60 μmol) of the administered dose (mol/mol), while it was respectively 2.01% (15.24 ± 2.13 μmol) and 0.00% (−0.02 ± 0.19 μmol) of the dose in the vitamin B6-deficient group. Therefore, vitamin B6 deficiency augmented endogenous synthesis of oxalate from hydroxyproline by 7.56-fold (15.24/2.02) compared with that in the control group. Urinary citrate excretion was significantly lower at baseline and all other times in the vitamin B6-deficient group compared with the control group. In conclusions, l-hydroxyproline loading augmented endogenous oxalogenesis in the vitamin B6-deficient group without causing hyperglycolic aciduria, and also led to significant hypocitraturia. These findings suggest that hydroxyproline is not metabolized to oxalate via glycolate, but rather via the 4-hydroxyglutamate to glyoxylate pathway (usually requiring vitamin B6-dependent enzymes) even in the presence of vitamin B6 deficiency. [ABSTRACT FROM AUTHOR]

Background: Vitamin B6 is thought to be a most versatile coenzyme that participates in more than 100 biochemical reactions. It is involved in amino acid and homocysteine metabolism, glucose and lipid metabolism, neurotransmitter production and DNA/RNA synthesis. Vitamin B6 can also be a modulator of gene expression. Nowadays, clinically evident vitamin B6 deficiency is not a common disorder, at least in the general population. Nevertheless, a subclinical, undiagnosed deficiency may be present in some subjects, particularly in the elderly. Objective: This review gives a complete overview over the metabolism and interactions of vitamin B6. Further, we show which complications and deficiency symptoms can occur due to a lack of vitamin B6 and possibilities for public health and supplemental interventions. Methods: The database Medline (www.ncvi.nlm.nih.gov) was searched for terms like "vitamin B6", "pyridoxal", "cancer", "homocysteine", etc. For a complete understanding, we included studies with early findings from the forties as well as recent results from 2006. These studies were summarised and compared in different chapters. Results and conclusion: In fact, it has been proposed that suboptimal vitamin B6 status is associated with certain diseases that particularly afflict the elderly population: impaired cognitive function, Alzheimer's disease, cardiovascular disease, and different types of cancer. Some of these problems may be related to the elevated homocysteine concentrations associated to vitamin B6 deficiency, but there is also evidence for other mechanisms independent of homocysteine by which a suboptimal vitamin B6 status could increase the risk for these chronic diseases. [ABSTRACT FROM AUTHOR]

Abstract: Objective: The purpose of this study was to investigate the association between plasma pyridoxal 5′-phosphate (PLP) status and lipid profiles and to estimate the relation to the risk of coronary artery disease (CAD). Methods: Patients who were identified by cardiac catheterization as having ≥70% stenosis of one major coronary artery were assigned to the case group (n = 184). The control group (n = 516) was comprised of healthy individuals with normal blood biochemical values. Plasma PLP, homocysteine, high-sensitivity C-reactive protein, lipid profiles (total cholesterol, low-density lipoprotein, high-density lipoprotein, very low-density lipoprotein, and triacylglycerol) were determined. Results: Subjects with a plasma PLP level <30 nmol/L exhibited a significantly increased risk of CAD compared with subjects with a plasma PLP level ≥30 nmol/L (odds ratio, 1.85; 95% confidence interval, 1.16–2.95) after adjusting for homocysteine and high-sensitivity C-reactive protein. The association between PLP and the risk of CAD remained significant after each lipid profile was additionally adjusted. In addition, the combined presence of low PLP level and an abnormal lipid level increased the risk of CAD to an even greater degree. Conclusions: A borderline vitamin B6 deficiency (plasma PLP concentration <30 nmol/L) is strongly associated with the risk of CAD. The combined presence of low PLP and abnormal lipid levels increased the risk of CAD even further. [Copyright &y& Elsevier]

The transsulfuration pathway, which aids in regulating homocysteine concentration and mediates cysteine synthesis, may be sensitive to vitamin B-6 status because cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CGL) require pyridoxal 5'-phosphate (PLP). To assess relations between vitamin B-6 and transsulfuration, we evaluated the effects of dietary pyridoxine (PN) on the hepatic concentration of relevant metabolites and in vitro activity of CBS and CGL. Growing rats were fed AIN-93G- or AIN-76A-based diets that ranged from adequate to deficient in vitamin B-6 (2, 1, 0.5, 0.1, or 0 mg of PN/kg diet, n = 5). This design allowed assessment of the effects of supplemental methionine (AIN-76A) vs. cysteine (AIN-93G) in common research diets over a range of vitamin B-6 levels. CBS activity, assayed in the presence or absence of added S-adenosylmethionine, was independent of diet type and PN level. CGL activity was independent of diet type but proportional to dietary PN. Rats fed deficient (0 and 0.1 mg PN/kg) diets exhibited only approximately 30% of the CGL activity of those fed the 2 mg PN/kg diets. Hepatic cystathionine increased from 20 to 30 nmol/g for the 1-2 mg PN/kg diets to approximately 85 nmol/g for the 0 mg PN/kg diet; however, cysteine was reduced only in B-6-deficient rats consuming the AIN-93G diet (means of 30-40 nmol/g for adequate to 11.6 nmol/g for 0 mg PN/kg AIN-76A diet). In spite of these effects, hepatic glutathione concentration increased in vitamin B-6 deficiency. These results suggest that vitamin B-6-dependent changes in transsulfuration do not limit hepatic glutathione production. [ABSTRACT FROM AUTHOR]

Summary: Background and aims: The aim of this study was to evaluate the lipid peroxidation and antioxidant function in liver tissue of vitamin B6 deficient rats and investigate relationship among these parameters in either group. Methods: Twenty-four male rats with a weight of 48–59g were used for the experiment. The rats were divided into control () and vitamin B6 deficient groups. After 4 weeks of feeding, the rats were killed by cervical dislocation and liver tissues were removed. Biochemical measurements in liver tissue were carried out using a spectrophotometer. Results: Liver tissue antioxidant potential, superoxide dismutase, glutathione peroxidase, glutathione-S-transferase, total (enzymatic plus non-enzymatic) superoxide scavenger activity, non-enzymatic superoxide scavenger activity, glutathione levels were significantly lower in vitamin B6 deficient rats than in control group. However, liver tissue glutathione reductase activity, and MDA values were significantly higher in vitamin B6 deficient rats than in control group. Conclusions: These results explicitly indicate that vitamin B6 deficiency causes a decrease in antioxidant defense system and an increase in oxidant stress in liver tissue in rats. [Copyright &y& Elsevier]

The mechanism of pellagrous changes in skin caused by a deficiency of vitamin B_{6} was studied in respect to neogenesis of proline in skin collagen and glucose metabolism. In vitamin B_{6} deficiency the insulin/glucagon coefficient in serum decreased significantly from 3.02 to 2.32, indicating a metabolic change towards gluconeogenesis. A deficiency of vitamin B_{6} caused a decrease in the levels of vitamin B_{6}-dependent enzymes, such as ornithine aminotransferase, alanine aminotransferase, and aspartate aminotransferase, which also contribute to gluconeogenesis. Because the conversion of ornithine to proline via pyrroline-5-carboxylate was suppressed due to the decrease in ornithine aminotransferase activity, the amount of proline in the skin collagen fraction also decreased significantly in vitamin B_{6}-deficient rats compared with the pair-fed control. These results suggest that the pellagrous lesions in vitamin_{6}-deficiency are caused by an impaired synthesis of proline from ornithine, which results in the suppression of collagen neogenesis in the skin. [ABSTRACT FROM AUTHOR]

Vitamin B-6-deficient animals exhibit motor abnormalities. To investigate the possible physiologic alterations in the dopaminergic nervous system in vitamin B-6 deficiency, dopamine release in the striatum of vitamin B-6-deficient rats was determined using in vivo electrochemistry. Male Sprague-Dawley rats, 3 wk old, weighing 50-60 g, were randomly assigned to a control (7 mg pyridoxine HCI/kg diet), vitamin B-6-deficient (0 mg pyridoxine HCI/kg diet), or pair-fed (7 mg pyridoxine HCI/kg diet) group. After 8 wk of dietary treatment, plasma concentrations of pyridoxal 5'-phosphate as well as the striatal pyridoxal 5'-phosphate and pyridoxamine 5'- phosphate were significantly lower in the vitamin B-6-deficient group than in the control and pair-fed groups. The dopamine concentrations of the striatum and the magnitude of the dopamine release after local application of KCI did not differ among the groups. However, the time required for KCI-evoked dopamine release to reach its peak level was significantly longer for the vitamin B-6-deficient rats than for controls. In addition, the decay time from the peak to one-half of the KCI-evoked dopamine release was also significantly prolonged in vitamin B-6-deficient rats compared with the control group. The results indicate that the cellular content of dopamine does not reflect the functional state of dopaminergic neurons in vitamin B-6 deficiency. The time course for release of dopamine and decay of the released dopamine is prolonged by vitamin B-6 deficiency, which might contribute to the motor abnormalities of the deficient rats. [ABSTRACT FROM AUTHOR]

Experimental and human studies describe the adverse effect of iron or vitamin B6 deficiencies on polyunsaturated fatty acid metabolism. Iron is present in end proteins of the δ6-desaturase enzyme complex, and vitamin B6 deficiency can affect the transmethylation reaction of proteins. Plasma polyunsaturated fatty acid content was estimated in apparently healthy subjects of the general population with no consumption of fish and low vitamin B6 serum levels (<3 μg/l; n = 21) or with low iron serum levels (men: <12 μmol/l; women: <10 μmol/l; n = 16) and compared to a control group (n = 22) with normal vitamin B6 and iron serum levels (in reference range). The activities of the δ6-desaturase enzyme complex were calculated as product/precursor (conversion indices). In groups of subjects with low vitamin B6 and low iron levels, δ6-desaturase activity together with δ5-desaturase activity (conversion of α-linolenic/18:3,n–3/ into eicosapentaenoic acid/20:5,n–3/) as well as the conversion index of docosahexaenoic acid formation (22:6,n–3) from 22:5,n–3 (second δ6-desaturase activity) were significantly reduced. The inhibition effect on fatty acid synthesis was more pronounced in subjects with low iron levels than in those with low vitamin B6 levels. The conversion indices correlated significantly positively with vitamin B6 or iron levels. Copyright © 2004 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

The issue of estimating usual intake distributions using daily intake data as collected by nationwide food consumption surveys is discussed. Of interest are not only the usual nutrient intake distributions based on food intake alone, but also the total nutrient intake distributions that must be based on information on food and supplement consumption. The problems of estimating usual food intake distributions and distinguishing between frequently consumed and infrequently consumed food items are considered. Data needs as well as statistical methodologies available to carry out each of the tasks outlined above are discussed, with particular reference to the integrated National Health and Nutrition Examination Survey that is now in the field. The replicated 24-h recalls should be augmented with a propensity questionnaire to improve on the estimation of intake distributions for infrequently consumed nutrients, supplements and food items. [ABSTRACT FROM AUTHOR]

Marginal deficiency of vitamin B6 has recently been related to cardiovascular diseases. Because of that there is an increasing interest in a suitable and reliable method for quantifying this vitamin in routine laboratory medicine. We have developed a HPLC-based method able to quantify the B6 vitamers pyridoxal 5′-phosphate (PLP), pyridoxal (PL), pyridoxamine 5′-phosphate (PMP), pyridoxine (PN), and pyridoxamine (PM) and the degradation product 4-pyridoxic acid (4-PA). The separation was accomplished using a C18 (ODS) analytical column and an ion-pair reversed-phase chromatography. B6 vitamers were eluted with a gradient of acetonitrile (0.5–15%) in a potassium phosphate buffer with 1-octanesulfonic acid and triethylamine, pH 2.16. The concentration of the vitamers was determined with fluorescence detector (328 nm excitation, 393 nm emission) after postcolumn derivatization with phosphate buffer containing 1 g/L sodium bisulfite. The performance of the assay was evaluated by analyzing six plasma samples with interrelated concentration and two control samples (unspiked and vitamer spiked) over a 3-months period. The HPLC method was able to identify PLP, 4-PA, PM, PL, PN, and PMP from all other compounds in plasma in an analytical run of 46 min. The imprecisions and mean values (presented in parenthesis in nmol/L) were (unspiked and spiked sample) 9–8% (41–65) for PLP, 12–7% (18–40) for 4-PA, 67–28% (4–19) for PL, 15% (21) for PN, 10% (27) for PM, and 27% (17) for PMP. All three B6 vitamers (PLP, 4-PA, and PL) present in unspiked plasma showed an excellent linearity within the range of (nM) 8–60 (4-PA), 1–19 (PL), and 11–99 (PLP). In conclusion, we report a HPLC-based method that separates and detects nanomolar quantities of six B6 vitamers and demonstrate that the method will be suitable for routine quantitation of PLP and 4-PA in human plasma. [Copyright &y& Elsevier]

Examines the mechanism and regulation of vitamin B[sub 6] uptake by renal tubular epithelia. Characteristics of pyridoxine uptake; Upregulation of pyridoxine uptake by maintaining opossum kidney cells in a vitamin B[sub 6]-deficient growth medium; Inhibition of upregulation by cyclohexamide and actinomycin D.

Examines the effects of folate and vitamin B6 deficiency on homocysteine, serine and methionine kinetics. Analysis on one-carbon metabolism; Depression of methionine synthesis by homocysteine remethylation; Risk factors for plasma homocysteine elevation.

Little is known about the micronutrient status of Chinese women of childbearing age. We assessed nonfasting plasma concentrations of folic acid, vitamin B-12, vitamin B-6 (as pyridoxal-5'-phosphate), hemoglobin (Hb), ferritin and transferrin receptor (TfR) in 563 nonpregnant textile workers aged 21-34 y from Anqing, China. All women had obtained permission to become pregnant and were participating in a prospective study of pregnancy outcomes. Mean (SD) plasma concentrations were 9.7 (4.1) nmol/L folic acid, 367 (128) pmol/L vitamin B-12, 40.2 (15.8) nmol/L vitamin B-6, 108 (12. 9) g/L Hb, 42.6 (34.2) microgram/L ferritin and 5.2 (2.7) mg/L TfR. Twenty-three percent of women had biochemical evidence of folic acid deficiency, 26% were deficient in vitamin B-6 and 10% had low vitamin B-12. Overall, 44% of women were deficient in at least one B vitamin. Although anemia (Hb < 120 g/L) was detected in 80% of women, only 17% had depleted iron stores (ferritin < 12 microgram/L); 11% had elevated TfR concentrations. Distinct seasonal trends were observed in the prevalence of moderate anemia (Hb < 100 g/L) and deficiencies of folic acid and vitamin B-6, with significantly lower concentrations of folate and Hb occurring in summer and lower concentrations of vitamin B-6 occurring in winter and spring than in other seasons. We conclude that deficiencies of folic acid, vitamin B-6 and iron were relatively common in this sample of Chinese women of childbearing age and were contributing to the high prevalence of anemia. Without appropriate supplementation, these deficiencies could jeopardize the women's health and increase their risk of adverse pregnancy outcomes. [ABSTRACT FROM AUTHOR]

Examines the link between perinatal Vitamin B6 deficiency and poverty. Effects of Vitamin B6 deficiency on the immune system; Effects of Vitamin B6 deficiency on behavior and brain cell development; Elements of metabolic imprinting based on the concept of the 'fetal origins hypothesis.'

Micronutrient deficiencies such as vitamin A, iron, zinc, and selenium have been known to occur as a consequence of pancreaticoduodenectomy (PD), but vitamin B6 deficiency has not been previously reported. We report two post-PD patients who developed anemias attributed to vitamin B6 deficiency. Oral supplementations of vitamin B6 significantly improved anemias in both cases. Micronutrients including vitamin B6 should be monitored in post-PD patients, and supplementations should be carried out when necessary. [ABSTRACT FROM AUTHOR]

Background: Limited evidence is available to describe the prevalence, causes, and consequences of zinc and vitamin B 6 deficiencies in those with acutely exacerbated inflammatory bowel disease (IBD). Zinc is important for immune function and wound healing, and B 6 is needed for metabolic and neurological function. Patients with IBD are at risk of micronutrient deficiencies, particularly during flares., Presentations: The cases of 2 patients with IBD exacerbations were reviewed in which deficiencies of both zinc and vitamin B 6 were identified., Conclusions: These cases highlight the need for increased screening for zinc and pyridoxine deficiencies in IBD population, especially during disease exacerbation. Therefore, we recommend a comprehensive nutrition workup with physical exam, diet history, and a complete micronutrient panel while ruling out contributing factors. If patients are susceptible to deficiencies during flares, prophylactic oral zinc and pyridoxine supplementation may be considered, with close monitoring for subsequent iron and copper deficiencies., (© 2021 American Society for Parenteral and Enteral Nutrition.)

Presents information on a study which investigated the prevalence of nausea and vomiting among pregnant women and characterize the distribution of severity and the role of Vitamin B6 deficiency. Methodology; Result; Discussion on the findings.

Presents information on a study which determined plasma pyridoxal-5-phosphate concentrations as an indicator of vitamin B6 deficiency through the application of a high performance liquid chromatography. Materials and methods; Results; Discussion; Conclusion.

Suggests that vitamin B6 deficiency is an essential factor in carpal tunnel syndrome. Examination of the hypothesis; Study conducted on active industrial workers; Recruitment of study participants; Description of medical survey procedures used; Procedures for measuring vitamin B6 status; Regression analyses of indices of vitamin B6 status; Results of the study.

First in a series. Discusses the relationship between maternal vitamin B6 deficiency in nutrition and infant cognitive development. Vitamin B6 nutritional requirement of pregnant and lactating women; Effect on learning behavior and central nervous system; N-methyl-D-aspartate (NMDA) glutamate receptor mechanism's role in memory formation.

Investigates the physiological effect of vitamin B6 deficiency in chicks. Abnormalities in the extracellular matrix of the connective tissues; Measurements done in the articular cartilages; Presence of proteolysis; Adhesive properties of collagen associated proteoglycans.

Investigates the physiological effect of vitamin B-6 deficiency in rats. Digestive enzyme activity of the pancreas; Antioxidant enzyme levels; Levels of glutathione reductase; Amylase and trypsinogen messenger RNA; Effect of pyridoxine intake on the exocrine pancreatic functions.