Running exercise training-induced impact on oxidative stress and mitochondria-related apoptosis in rat's testicles.

The current study has been designed to explore the effects of running exercise training protocols (ETPs), with different intensities, on testicular redox and antioxidant capacities. Moreover, the crosstalk between oxidative stress (OS) and mitochondria-related apoptosis was analysed. To this end, 24 Wistar rats were subdivided into sedentary control, low- (LICT), moderate- (MICT), and high (HICT)-intensity continuous running ETP groups. Following 8 weeks, the Johnsen score, sperm count, testicular malondialdehyde (MDA) content, total oxidant status (TOS), and redox biomarkers, including glutathione peroxidase (GPX), superoxide dismutase (SOD), and catalase (CAT) levels were evaluated. Additionally, the expression levels of Bcl-2, Bax, caspase-3, proteins involving in the mitochondria-related apoptosis, and the apoptotic index were analysed. The LICT and MICT running ETPs did not affect the spermatogenesis development, sperm count, and antioxidant and redox capacities. Accordingly, no significant changes were revealed in Bcl-2, Bax, and caspase-3 expression levels and apoptosis index compared to sedentary rats. In contrast, the HICT-induced rats showed a significant (p < 0.05) reduction in spermatogenesis development, sperm count, antioxidant and redox capacities versus control, LICT, and MICT groups. Moreover, the expression of Bcl-2 was decreased, while the Bax and caspase-3 expression levels were increased in the HICT-induced group. Finally, the apoptosis index was increased in the HICT group. In conclusion, the suppressed redox system after HICT can trigger the mitochondria-mediated ROS overload, result in OS condition in the testicular tissue, and reversely target the mitochondrial membrane permeability. All of these molecular alterations are suspected to initiate progressive mitochondria-related apoptosis after HICT.