MitoQ Mitigates Radiation‐Induced Testicular Injury: Molecular Docking and Toxicity Implications

This study assessed the possible mitigating effect of a mitochondrion-targeted antioxidant (MitoQ) against gamma irradiation-induced testicular damage. The rats were distributed into five groups. The first group served as a control, the second group received MitoQ (2 mg/kg/day; i.p.) for 7 days, the third group was exposed to gamma radiation (5 gray as a single dose), the fourth group received MitoQ prophylactically before irradiation, and the last group was exposed to gamma radiation and then treated with MitoQ. The rats were killed 7 days after irradiation. MitoQ replenished mitochondrial ROS, indicating its antioxidant effect. MitoQ inhibited the intrinsic apoptosis cascade via a reduction in Bax and alleviated Bcl-2. MitoQ improved steroidogenesis, as verified by an increase in testosterone and upregulation of 3β-HSD and 17β-HSD expression, in addition to increasing complex I and succinate dehydrogenase activity. Likewise, sperm evaluation corroborated these findings. The acute toxicity profile of MitoQ was investigated in mice and was found to be 75 mg/kg body weight. Additionally, a molecular docking study of MitoQ showed a good fit to the active site of succinate dehydrogenase. In conclusion, this study introduces MitoQ as a new approach for the management of testicular damage triggered by gamma irradiation.