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The fungicide Carbendazim Methyl-2-benzimidazole carbamate (MBC) is known to produce male reproductive toxicity. The present study has been undertaken to investigate the impact of vitamin E, an antioxidant against the testicular toxicity induced by MBC. HPLC analysis showed that the amount of MBC in testis and serum was 57.40 +/- 3.38 nmol/g and 14.10 +/- 0.84 nmol/ml, respectively, in rats treated with carbendazim + vitamin-E, which were significantly lower than that of rats treated with carbendazim alone (240 +/- 15.60 nmol/g and 318.70 +/- 22.52 nmol/ml, respectively). MBC treatment significantly decreased the testicular weight while co-administration of vitamin-E registered normal testicular weight. Histomorphometric analysis revealed a significant decrease (P < 0.05) in the diameter of the seminiferous tubules and lumen in MBC-treated rats compared to control whereas they remained normal in vitamin E + MBC-treated rats. Leydig cells appeared dispersed and hypertrophic after MBC treatment. Various histopathological changes were observed in testis of rats treated with MBC whereas these changes were absent in vitamin-E + MBC-treated rat testis. In conclusion protection against MBC-induced toxicity was observed with co-administration of vitamin E with MBC.

The effect of treatment with prolactin or bromocryptine on testicular steroidogenesis and serum hormone levels were studied in immature and mature bonnet monkeys. Leydig cells alone showed the presence of 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD) and 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD) in normal immature and mature monkeys. Administration of prolactin increased the activity of 3 beta-HSD and 17 beta-HSD in Leydig cells from mature monkeys, and also increased the serum levels of testosterone. Bromocryptine treatment induced exactly the opposite effect. These changes occurred in the absence of any change in serum gonadotrophin levels. In immature monkeys, prolactin and bromocryptine had no significant effect. These results suggest a direct stimulatory effect of prolactin on testicular steroidogenesis in mature monkeys.