Exposure to ambient PM_2.5 may correlate with the decline of semen quality, and the underlying biological mechanism has not been fully understood. In the present study, mice were intratracheally instilled with diesel exhaust PM_2.5 (DEP), and its effects on the spermatogenic process as well as the alterations of testicular gene expression profile were assessed. Our results showed that chronic exposure to DEP impaired 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 disrupting the spermatogenesis. Deep RNA sequencing test showed altered expressions of testicular genes including the GnRH signaling pathway. In summary, our research demonstrated that chronic exposure to DEP may disrupt spermatogenesis through targeting the meiotic recombination, providing a new perspective for the research on the male reproductive system damage caused by air pollution.

暴露于环境PM _2.5可能与精液质量下降有关，并且尚未完全理解其潜在的生物学机制。在本研究中，小鼠气管内滴注了柴油机尾气PM _2.5（DEP），及其对生精过程的影响以及睾丸基因表达谱的变化进行了评估。我们的结果表明，长期暴露于DEP会损害雄性小鼠的生育能力，而不会影响其性欲。与暴露于媒介物的组相比，暴露于DEP的小鼠的精子数量和运动能力显着降低。此外，γH2AX和DMC1（减数分裂双链断裂（DSBs）的生物标志物）的免疫组织学染色显示，长期暴露于DEP可修复减数分裂DSB，从而破坏精子发生。深度RNA测序测试显示，包括GnRH信号通路在内的睾丸基因表达发生了改变。总而言之，我们的研究表明，长期暴露于DEP可能通过靶向减数分裂重组而破坏精子发生，