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A new method for the assay of tissue. S-adenosylhomocysteine and S-adenosylmethione. Effect of pyridoxine deficiency on the metabolism of S-adenosylhomocysteine, S-adenosylmethionine and polyamines in rat liver.

ABSTRACT: The hepatic synthesis and accumulation of S-adenosylhomocysteine, S-adenosylmethionine and polyamines were studied in normal and vitamin B-6-deficient male albino rats. A method involving a single chromatography on a phosphocellulose column was developed for the determination of S-adenosylhomocysteine and S-adenosylmethionine from tissue samples. Feeding the rat with pyridoxine-deficient diet for 3 or 6 weeks resulted in a four- to five-fold increase in the concentration of S-adenosylhomocysteine, whereas that of S-adenosylmethionine was only slighly elevated. The concentration of putrescine was decreased to half, that of spermidine was somewhat decreased and that of spermine remained fairly constant. The activities of L-ornithine decarboxylase, S-adenosyl-L-methionine decarboxylase, L-methionine adenosyltransferase and S-adenosyl-L-homocysteine hydrolase were moderately increased. S-Adenosylmethionine decarboxylase showed no requirement for pyridoxal 5'-phosphate. The major effect of pyridoxine deficiency of S-adenosylmethionine metabolism seems to be a block in the utilization of S-adenosylhomocysteine, resulting in the accumulation of this metabolite to a concentration that may inhibit biological methylation reactions.

SUBMITTER: Eloranta TO

PROVIDER: S-EPMC1164235 | biostudies-other | 1976 Nov

REPOSITORIES: biostudies-other

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Project description:Background: Patients suffering from chronic kidney disease (CKD) have a high risk of premature cardiovascular morbidity and mortality. It has been suggested that elevated homocysteine (Hcy) or disturbances in the transmethylation pathway may contribute to this high cardiovascular risk burden due to epigenetic mechanisms. The objective of this study was to explore the prognostic value of Hcy, S-adenosylhomocysteine (SAH) and S-adenosylmethionine (SAM) (one-carbon (C1)-metabolites) among patients with CKD. Methods: Plasma concentrations of Hcy, SAM and SAH were measured among 297 participants with CKD (KDIGO GFR category G2-G5). The predefined endpoint was the occurrence of major cardiovascular events (MACE), defined as carotid, coronary and peripheral arterial revascularization, stroke, acute myocardial infarction, major amputation, cardiovascular death and all-cause mortality during a median (IQR) follow-up period of 4.0 [3.2; 4.3] years. Results: Among all participants, the median (IQR) of plasma Hcy, SAH, and SAM levels were 16.6 [13.5; 21.2] µmol/L, 41.5 [26.6; 63.9] nmol/L, 183.4 [151.1; 223.5] nmol/L, respectively. Estimated glomerular filtration rate (eGFR) correlated more strongly with plasma SAH (r = -0.588) than with SAM (r = -0.497) and Hcy (r = -0.424). During the follow-up period, 55 participants experienced MACE. In a univariate Kaplan Meier analysis, all three C1-metabolites were significantly associated with the occurrence of the primary outcome. In a Cox-regression analysis, the association between Hcy and MACE was not significant after adjustment for age and sex (hazard ratio (HR) and 95% confidence intervals (95% CI) for the 3rd vs. 1st tertile = 1.804 (0.868-3.974)). Both SAH and SAM were not associated with MACE after adjustment for age, sex and additionally for renal function markers (SAH: HR 3rd vs. 1st tertile 1.645 95% (0.654-4.411); SAM: HR 3rd vs. 1st tertile 1.920 95% CI (0.764-5.138)). Conclusions: In people with CKD, plasma Hcy, SAH and SAM were not independent predictors of MACE after adjustment for age, sex and renal function. Disturbed renal function may explain elevated C1-metabolites and disturbed transmethylation, while this pathway is not likely to be an appropriate access point to modify the risk of cardiovascular events in CKD patients.

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A new method for the assay of tissue. S-adenosylhomocysteine and S-adenosylmethione. Effect of pyridoxine deficiency on the metabolism of S-adenosylhomocysteine, S-adenosylmethionine and polyamines in rat liver.

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