Diesel exhaust particles induce reproductive toxicity in mice via oxidative stress and ATP5α1 S-sulfhydration inhibition.

Diesel exhaust particle (DEP) is a primary urban air pollutant that poses serious risks to human reproductive health. In this study, DEP-induced reproductive toxicity in mice was examined, focusing on oxidative stress and ATP5α1 S-sulfhydration. After 15 weeks of DEP exposure, male C57BL/6 J mice were sacrificed under isoflurane anesthesia, and tissue samples were collected. In addition, semen quality was assessed, and testicular histopathology analysis was conducted to evaluate the effects of DEP exposure on spermatogenesis. Subsequently, the S-sulfhydration of ATP5α1 and its association with testicular energy metabolism in DEP-exposed mice were further identified. Results showed that DEP exposure induces spermatogenesis impairment and testicular dysfunction in male mice, which are associated with oxidative stress. Furthermore, DEP exposure attenuates ATP synthase activity via suppression of ATP5α1 S-sulfhydration, thereby causing ATP depletion. Collectively, these results indicate that DEP exposure induces reproductive toxicity in mice through ATP5α1 S-sulfhydration-mediated mechanisms.