Testicular injury to rats fed on soybean protein-based vitamin B12-deficient diet can be reduced by methionine supplementation.

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Yamada K, Kawata T, Wada M, Mori K, Tamai H, Tanaka N, Tadokoro T, Tobimatsu T, Toraya T, Maekawa A

Testicular injury to rats fed on soybean protein-based vitamin B12-deficient diet can be reduced by methionine supplementation.

J Nutr Sci Vitaminol (Tokyo). 2007 Apr;53(2):95-101.

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17615995 [ View in PubMed

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Abstract

We have previously reported that rats fed on a vitamin B12 (B12)-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 B12-deficiency on B12-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 B12-deficient diet for 120 d. We confirmed that those rats were in serious B12-deficiency by measuring urinary methylmalonic acid excretion and B12 content in tissues. Methionine synthase activity in the testis of the B12-deficient rats was less than 2% of that in B12-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 B12-deficient diet did not affect urinary methylmalonic acid excretion of B12-deficient rats. The testicular histology of rats fed the methionine-supplemented B12-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 B12-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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Drug Targets

Drug	Target	Kind	Organism	Pharmacological Action	Actions
Methionine	Methionine synthase	Protein	Humans	Unknown	Product of	Details