Coenzyme Q amends testicular function and spermatogenesis in male mice exposed to cigarette smoke by modulating oxidative stress and inflammation.

This study explored the effects of coenzyme Q (CoQ) on the testicular functions of male mice exposed to cigarette smoke. Eight-week-old BALB/c male mice were divided into the following groups: the AV group (air with a vehicle), the AQ group (air with CoQ), the SV group (smoke with a vehicle), and the SQ group (smoke with CoQ). The results showed that the CoQ concentrations in the sera and testes were decreased in the groups subjected to smoke but they were improved after the administration of CoQ. Neither smoke nor CoQ supplementation affected the serum or testis testosterone concentrations. Regarding the antioxidant system in the testis, the exposure to smoke induced malondialdehyde and hydrogen peroxide production and decreased the catalase and glutathione peroxidase activities. Oral CoQ administration reversed the oxidative damage. In apoptosis, the cytochrome c, c-caspase 9, and c-caspase 3 proteins were increased in the groups exposed to smoke but they were decreased after the CoQ administration. In mitochondrial biogenesis, smoke exposure led to decreases in the PGC1-α, NRF1, and NRF2 levels, but CoQ increased the expressions of these proteins. Additionally, oral CoQ administration improved the mitochondrial copy numbers that were reduced following the exposure to smoke. In summary, CoQ administration reduces smoke-induced testicular damage by regulating the antioxidant capacity, the cell apoptosis, the mitochondrial biogenesis, and the copy numbers in the testes.