The effect of vitamin B-6-deficiency on the B-6-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 B-6-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 B-6-deficient group compared to the control and the pair-red control groups. Thymus PLP and PL levels were lower in the B-6-deficient group. The concentration of SAM in the B-6-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 B-6-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 B-6-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 B-6-deficiency. We infer that the alteration of B-6 metabolism. especially the reduction of PLP contents in liver and thymus, caused by the B-6 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 or transmethylation reaction of DNA, RNA and protein, the synthesis and function of thymic lymphocyte and result in damage to tissues.