The effect of vitamin B₆-deficiency on the B₆-vitam.er concentrations, level of S-adenosylhomocysteine (SAH) and S-adenosylmethionine (SAM) were studied in rat tis-sues. 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 signifi-cantly 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 thy-mus, 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 de-creased 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 ac-tivities 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, re-sulted in accumulation of SAH as well as reduction of SAM and the SAM/SAH ratio. The re-duction of the SAM/SAH ratio was due to a block in the catabolism of methionine via the traps-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 dam-age to tissues.