Mitochondria-Mediated Apoptosis Induced Testicular Dysfunction in Diabetic Rats: Ameliorative Effect of Resveratrol

The molecular mechanism underlying diabetes-induced testicular damage has not been thoroughly elucidated. The present study was conducted to elucidate the role of mitochondria-mediated apoptosis in diabetes-induced testicular dysfunction in rats and to explore the ameliorative effect of resveratrol. Diabetes suppressed sperm count, motility, and viability and increased sperm abnormalities. It decreased serum testosterone level and testicular mitochondria! membrane potential. The level of Bax and caspase-3 and -9 activities were increased in the testicular cytosol, while the level of Bcl-2 was decreased. Diabetes increased the Bax/Bcl-2 ratio. The cytochrome C level was decreased in the mitochondrial fraction, while its level was increased in the cytosol, a result that was supported by the immunohistochemistry of cytochrome C. Diabetes resulted in deleterious alterations in the architecture of testicular tissue, suppressed antioxidant enzymes, and increased H2O2 production, protein carbonyl content, and lipid peroxidation. However, administration of resveratrol at a dose of 50 mg kg/day for 4 successive weeks post diabetic induction, successfully ameliorated the testicular dysfunction. In conclusion, these findings strongly reveal that diabetes induces testicular damage, at least in part, by inducing mitochondrial-mediated apoptosis and oxidative stress. Administration of resveratrol to diabetic rats improves the diabetes-induced testicular damage. These impacts could be mediated through resveratrol antioxidant and anti-apoptotic effects.

Automated summary

Diabetes induces testicular damage, partially through inducing mitochondria-mediated apoptosis and oxidative stress. Resveratrol administration improves diabetes-induced testicular dysfunction through its antioxidant and anti-apoptotic effects.