Phosphorylation of pyridoxine by human blood platelets—Effects of structure analogs and metabolic inhibitors

Gaut, Zane N.; Solomon, Harvey M.

doi:10.1016/0006-2952(72)90391-7

Cited by 13 publications

(2 citation statements)

References 15 publications

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“…A possible inhibitory effect of 4-PA on vitamin B6 metabolism has also been discussed. Experimental data have shown the inhibitory effect of 4-PA on PL kinase 37 , 38 . Additionally, an observational study showed that the plasma 4-PA level was a stronger covariate with homocysteine (an independent CHD risk factor) than the plasma PLP level 39 .…”

Section: Discussionmentioning

confidence: 99%

Investigation of novel metabolites potentially involved in the pathogenesis of coronary heart disease using a UHPLC-QTOF/MS-based metabolomics approach

Zhang

et al. 2017

Sci Rep

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Coronary heart disease (CHD) is associated with complex metabolic disorders, but its molecular aetiology remains unclear. Using a novel nontargeted metabolomics approach, we explored the global metabolic perturbation profile for CHD. Blood samples from 150 patients with severe obstructive CHD and 150 angiographically normal controls were collected. Metabolic fingerprinting was performed by ultra-high performance liquid chromatography coupled to quadruple time-of-flight mass spectrometry (UHPLC-QTOF/MS) technique. After adjusting for CHD traditional risk factors and metabolic batch, a comprehensive list of 105 metabolites was found to be significantly altered in CHD patients. Among the metabolites identified, six metabolites were discovered to have the strongest correlation with CHD after adjusting for multiple testing: palmitic acid (β = 0.205; p < 0.0001), linoleic acid (β = 0.133; p < 0.0001), 4-pyridoxic acid (β = 0.142; p < 0.0001), phosphatidylglycerol (20:3/2:0) (β = 0.287; p < 0.0001), carnitine (14:1) (β = 0.332; p < 0.0001) and lithocholic acid (β = 0.224; p < 0.0001); of these, 4-pyridoxic acid, lithocholic acid and phosphatidylglycerol (20:3/2:0) were, to the best of our knowledge, first reported in this study. A logistic regression model further quantified their positive independent correlations with CHD. In conclusion, this study surveyed a broad panel of nontargeted metabolites in Chinese CHD populations and identified novel metabolites that are potentially involved in CHD pathogenesis.

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Section: Discussionmentioning

confidence: 99%

Investigation of novel metabolites potentially involved in the pathogenesis of coronary heart disease using a UHPLC-QTOF/MS-based metabolomics approach

Zhang

et al. 2017

Sci Rep

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“…A possible inhibitory effect of PA on vitamin B 6 metabolism is discussed [7]. Experimental data evidenced PL kinase inhibition by PA [19]. Although a low PLP concentration was associated with an increased risk for having coronary artery disease [20] or hypertension [21], data supporting a possible role for PA as a cardiovascular risk factor have not been published to date.…”

Section: Discussionmentioning

confidence: 99%

Vitamin B<sub>6</sub> Metabolism in Chronic Kidney Disease – Relation to Transsulfuration, Advanced Glycation and Cardiovascular Disease

Busch¹,

Gobert²,

Franke³

et al. 2009

Nephron Clin Pract

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Background: Vitamin deficiency is common in chronic kidney disease (CKD). Data on B₆ supply and possible relationships to cardiovascular events (CVE) in CKD are rare. Pyridoxamine exerts inhibitory effects on the formation of advanced glycation endproducts (AGE) implicated in the pathogenesis of CKD and atherosclerosis. Methods: In 48 CKD patients at stage 2–4, 72 hemodialysis patients (HD), 38 renal transplant recipients (RTR) and 141 healthy controls (mean age 58 ± 13, 61 ± 12, 50 ± 12 and 54 ± 16 years, respectively), plasma and red blood cell (RBC) concentrations of pyridoxal-5′-phosphate (PLP), pyridoxal (PL), 4-pyridoxic acid (PA), pyridoxamine-5′-phosphate (PMP) and of the AGE pentosidine were measured by high-performance liquid chromatography, N^Ε-(carboxymethyl)lysine and imidazolone by an ELISA, and total homocysteine and cystathionine by gas chromatography-mass spectrometry. Results: Despite routine low-dose vitamin supplementation in HD, plasma PLP was decreased in HD (79 ± 69 nmol/l) compared with CKD stage 2–4 patients (497 ± 944 nmol/l), RTR (416 ± 604 nmol/l) and controls (159 ± 230 nmol/l; p < 0.001). Plasma PA was significantly increased in HD (11,667 ± 17,871 nmol/l) in comparison with CKD stage 2–4 (435 ± 441 nmol/l), RTR (583 ± 668 nmol/l) and controls (46 ± 49 nmol/l; p < 0.001). B₆ forms were significantly affected by renal function (R = 0.792, p < 0.001 for CKD stage 2–4). There was no relation of vitamers with a history of CVE. Relationships between B₆ forms and AGE (RBC-PMP with pentosidine in CKD stage 2–4: R = –0.351, p < 0.05) were found. Conclusion: HD patients showed a deficiency in PLP in plasma but not in RBC. Prospective trials are needed to elucidate the potential role of elevated PA on cardiovascular and renal outcome in CKD. Vitamin B₆ supplementation might be successful in preventing AGE-related pathologies.

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Homocysteine and atherosclerosis in dialysis patients

Sunder‐Plassmann¹,

Födinger²

2004

Replacement of Renal Function by Dialysis

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Phosphorylation of pyridoxine by human blood platelets—Effects of structure analogs and metabolic inhibitors

Cited by 13 publications

References 15 publications

Investigation of novel metabolites potentially involved in the pathogenesis of coronary heart disease using a UHPLC-QTOF/MS-based metabolomics approach

Investigation of novel metabolites potentially involved in the pathogenesis of coronary heart disease using a UHPLC-QTOF/MS-based metabolomics approach

Vitamin B<sub>6</sub> Metabolism in Chronic Kidney Disease – Relation to Transsulfuration, Advanced Glycation and Cardiovascular Disease

Homocysteine and atherosclerosis in dialysis patients

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