Mito-TEMPO protects against bisphenol-A-induced testicular toxicity: an in vivo study

Bisphenol-A (BPA) is a common environmental toxin which alters testicular function in both animals and humans. BPA exerts its cytotoxic potential by altering mitochondrial oxidative stress and functioning. Therefore, protecting mitochondria from oxidative stress may prevent BPA-induced testicular damage. In the present study, modulation of BPA toxicity by mitochondria-targeted antioxidant, mito-TEMPO was studied in male Wistar rats. Rats were administered mito-TEMPO (0.1 mg/kg b.w, i.p.) twice a week, followed by BPA (10 mg/kg b.w., orally) once a week for 4 weeks. After 4 weeks, sperm parameters were evaluated in the testis along with histopathological analysis. The mitochondrial oxidative stress, mitochondrial membrane potential (MMP) and enzymatic activity of mitochondrial complex II and IV were estimated in the testicular tissue. Pretreatment of mito-TEMPO protected animals from toxic effects of BPA as indicated by the normalization of sperm parameters and preserved histoarchitecture of testis. BPA treatment to animals significantly increased mitochondrial reactive oxygen species (ROS) and lipid peroxidation (LPO). A significant decrease in the activity of mitochondrial complex II was also observed after BPA exposure whereas, mitochondrial complex II activity was increased. In addition, an increase in MMP was also observed in BPA group. Mito-TEMPO successfully normalized mitochondrial ROS and LPO formation. Similar normalization effect was also noted in the activity of mitochondrial complex II, complex IV, and MMP. Results suggested that mito-TEMPO pretreatment significantly protected BPA-induced oxidative stress and thereby mito-TEMPO effectively prevented testicular damage.

Automated summary

The study suggests that the mitochondria-targeted antioxidant mito-TEMPO can protect against testicular damage induced by BPA. Pretreatment with mito-TEMPO normalizes sperm parameters, preserves testicular histopathology, and repairs oxidative stress and dysfunction in mitochondria.