title: Effect of vitamin B6 deficiency on the synthesis and accumulation of S-adenosylhomocysteine and S-adenosylmethionine in rat tissues.
abstract: The effect of vitamin B6-deficiency on the B6-vitamer concentrations, level of S-adenosylhomocysteine (SAH) and S-adenosylmethionine (SAM) were studied in rat tissues. The plasma pyridoxal 5'-phosphate (PLP) and, pyridoxal (PL) levels were lower in the B6-deficient group compared to the control group. After 5 weeks of feeding the experimental diets, tissue PLP, pyridoxamine 5'-phosphate (PMP) and PL concentrations were significantly lower in the B6-deficient group compared to the control and the pair-fed control groups. Thymus PLP and PL levels were lower in the B6-deficient group. The concentration of SAM in the B6-deficient group decreased to approximately 50% and 25% in liver and thymus, respectively. However SAH concentration was 3.5 and 2 fold higher compared to the control and the pair-fed control groups. Thus, the ratio of SAM/SAH was significantly decreased in the B6-deficient group compared to the control or the pair fed-control group. In addition, the S-adenosylhomocysteine hydrolase (EC 3.3.1.1) activity increased by 45% and 15% in liver and thymus, respectively, in the B6-deficient group compared to the pair-fed control and the control groups. However, the activity of L-methionine S-adenosyltransferase (EC 2.5.1.6) was also unaffected. Concentrations of SAH and SAM, SAM/SAH ratio and activities of S-adenosylhomocysteine hydrolase and L-methionine S-adenosyltrasferase in rat brain were not affected by the B6-deficiency. We infer that the alteration of B6 metabolism, especially the reduction of PLP contents in liver and thymus, caused by the B6 deficiency, resulted in accumulation of SAH as well as reduction of SAM and the SAM/SAH ratio. The reduction of the SAM/SAH ratio was due to a block in the catabolism of methionine via the trans-sulfuration pathway. These may lead to inhibition of transmethylation reaction of DNA, RNA and protein, the synthesis and function of thymic lymphocyte and result in damage to tissues.
authors.affiliation: Department of Food Science, Faculty of Agriculture, Gifu University, Japan.
authors.forename: T T
authors.initials: TT
authors.lastname: Nguyen
authors.forename: T
authors.initials: T
authors.lastname: Hayakawa
authors.forename: H
authors.initials: H
authors.lastname: Tsuge
mesh_terms: D000818:Animals; D001921:Brain / Q000378:metabolism; D002851:Chromatography, High Pressure Liquid / Q000379:methods; D008099:Liver / Q000201:enzymology / Q000378:metabolism; D008297:Male; D011730:Pyridoxal / Q000097:blood; D011732:Pyridoxal Phosphate / Q000097:blood; D011733:Pyridoxamine / Q000031:analogs & derivatives* / Q000097:blood; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D012435:S-Adenosylhomocysteine / Q000378:metabolism*; D012436:S-Adenosylmethionine / Q000096:biosynthesis / Q000378:metabolism*; D013950:Thymus Gland / Q000201:enzymology / Q000378:metabolism; D013997:Time Factors; D026681:Vitamin B 6 Deficiency / Q000378:metabolism*
chemical_list: D011730:Pyridoxal; D011732:Pyridoxal Phosphate; D011733:Pyridoxamine; D012436:S-Adenosylmethionine; D012435:S-Adenosylhomocysteine; C010627:pyridoxamine phosphate