Testicular injury to rats fed on soybean [Glycine max] protein-based vitamin B12-deficient diet can be reduced by methionine supplementation
2007
Yamada, K.(Okayama Univ. (Japan). Faculty of Engineering) | Kawata, T. | Wada, M. | Mori, K. | Tamai, H. | Tanaka, N. | Tadokoro, T. | Tobimatsu, T. | Toraya, T. | Maekawa, A.
We have previously reported that rats fed on a vitamin Bsub(12) (Bsub(12))-deficient diet containing 180 g soybean protein per kg diet showed marked histologic damage in their testes. In this paper, we report the effect of Bsub(12)-deficiency on Bsub(12)-dependent methionine synthase in the rats' testes and the effect of methionine supplementation of the diet on testicular damage. Rats were fed the soybean protein-based Bsub(12)-deficient diet for 120 d. We confirmed that those rats were in serious Bsub(12)-deficiency by measuring urinary methylmalonic acid excretion and Bsub(12) content in tissues. Methionine synthase activity in the testis of the Bsub(12)-deficient rats was less than 2% of that in Bsub(12)-supplemented (control) rats. To complement disrupted methionine biosynthesis, methionine was supplied in the diet. A supplement of 5 g D,L-methionine per kg diet to the Bsub(12)-deficient diet did not affect urinary methylmalonic acid excretion of Bsub(12)-deficient rats. The testicular histology of rats fed the methionine-supplemented Bsub(12)-deficient diet was almost indistinguishable from that of control rats. Thus, we conclude that the lowered testicular methionine synthase activity is the primary cause of the histologic damage due to Bsub(12)-deficiency and that methionine supplementation to the diet can reduce the damage. These findings would indicate the importance of the methionine synthase activity, especially for testicular function.
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