Nguyen T T, Hayakawa T, Tsuge H
Department of Food Science, Faculty of Agriculture, Gifu University, Japan.
J Nutr Sci Vitaminol (Tokyo). 2001 Jun;47(3):188-94. doi: 10.3177/jnsv.47.188.
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.
研究了维生素B6缺乏对大鼠组织中B6维生素浓度、S-腺苷同型半胱氨酸（SAH）和S-腺苷甲硫氨酸（SAM）水平的影响。与对照组相比，B6缺乏组血浆中磷酸吡哆醛（PLP）和吡哆醛（PL）水平较低。在喂食实验饮食5周后，与对照组和配对喂食对照组相比，B6缺乏组组织中的PLP、磷酸吡哆胺（PMP）和PL浓度显著降低。B6缺乏组胸腺中的PLP和PL水平较低。B6缺乏组肝脏和胸腺中SAM的浓度分别降至约50%和25%。然而，与对照组和配对喂食对照组相比，SAH浓度分别高出3.5倍和2倍。因此，与对照组或配对喂食对照组相比，B6缺乏组中SAM/SAH的比值显著降低。此外，与配对喂食对照组和对照组相比，B6缺乏组肝脏和胸腺中S-腺苷同型半胱氨酸水解酶（EC 3.3.1.1）的活性分别增加了45%和15%。然而，L-甲硫氨酸S-腺苷转移酶（EC 2.5.1.6）的活性也未受影响。大鼠脑中SAH和SAM的浓度、SAM/SAH比值以及S-腺苷同型半胱氨酸水解酶和L-甲硫氨酸S-腺苷转移酶的活性不受B6缺乏的影响。我们推断，B6缺乏导致B6代谢改变，尤其是肝脏和胸腺中PLP含量降低，导致SAH积累以及SAM和SAM/SAH比值降低。SAM/SAH比值降低是由于甲硫氨酸通过转硫途径的分解代谢受阻。这些可能导致DNA、RNA和蛋白质的甲基化反应受到抑制，胸腺淋巴细胞的合成和功能受损，并导致组织损伤。
