Chronic Exposure to Diesel Exhaust Particulate Matter Impairs Meiotic Progression during Spermatogenesis in a Mouse Model

Abstract

Background: Exposure to air pollutants represented by diesel exhaust PM2.5 (DEP) correlates with the decline of semen quality, but the underlying biological mechanism has not been fully understood. In the present study, mice were intratracheally instilled with DEP for around 7 months, and the effects of PM2.5 exposure on the spermatogenic process as well as the alterations of testicular gene expression profile were assessed. Results: Our results show that chronic exposure to DEP significantly impairs the fertility of male mice without influencing their libido. Compared with Vehicle-exposed group, the sperm count and motility from DEP-exposed mice were significantly decreased. In addition, immunohistological staining of γH2AX and DMC1, biomarkers for meiotic double strand breaks (DSBs), demonstrated that chronic exposure to DEP comprised the repair of meiotic DSBs, thus disrupts the spermatogenesis. Deep RNA sequencing test shows massive altered expressions of testicular genes including the GnRH signaling pathway. Conclusion: In summary, our research demonstrates that chronic exposure to PM2.5 disrupts spermatogenesis through targeting the meiotic recombination, providing a new perspective for the research on the male reproductive system damage caused by air pollution.