Leptin ameliorates testicular injury by altering expression of nitric oxide synthases in diabetic rats

We aimed to evaluate the effects of leptin and nitro-L-arginine methyl ester hydrochloride (L-NAME) on testicular damage and expression of nitric oxide synthase (NOS) types (neuronal, endothelial and inducible NOS) in streptozotocin (STZ) -induced diabetic and non-diabetic rats.

Testicular damage was evaluated histologically and expression of NOSs was evaluated immunohistochemically in testis. Plasma leptin level and blood glucose level were assessed.

Blood glucose levels increased in all diabetic groups. L-NAME reduced it, but leptin had no effect. Three types NOS expression were shown in germ cells immunohistochemically. Increased eNOS and iNOS expression and decreased nNOS expression was detected in diabetic group. Testicular damage was observed in diabetic groups. Leptin ameliorated the damage by reducing iNOS expression and L-NAME partially prevented injury by supressing excessive NO production in diabetic rats.

It can be suggested that leptin and L-NAME partially prevents testicular damage by ameliorating histopathological changes by stimulating and /or supressing three types of NOS expression in diabetic rats. Leptin exhibited its effects by reducing iNOS expression in diabetic rats. This is the first report demonstrating the relationship between leptin and nitric oxide in testicular tissue in STZ-induced diabetic rats (Fig. 3, Ref. 33).