Maternal exposure to fine particle matters cause autophagy via UPR-mediated PI3K-mTOR pathway in testicular tissue of adult male mice in offspring.

Epidemiological studies have shown that particulate matters are closely related to human infertility. However, the long-term risk of particulate matters exposure in early life is rarely considered. For the first time this study is designed to explore and elucidate the mechanism of maternal exposure to fine particle matters (PM2.5) on autophagy in spermatogenic cells of adult offspring. Pregnant C57BL/6 mice were randomly divided into four groups. The 4.8 mg/kg.b.w group and the 43.2 mg/kg.b.w group were administered with different doses of PM2.5. The membrane control group was administered with PM2.5 sampling membrane and the control group received no treatment. The exposure was performed every three days from the day after vaginal plug was checked until delivery for a total of 6 times. The results showed that sperms motility and sperms concentration decreased, and sperm deformity increased in adult male offspring. The expression of SOD decreased and MDA increased. Moreover, the level of GRP78/ATF6 and P62 was upregulated, and the expression of PI3K/Akt/mTOR/p-mTOR was down-regulated. This suggests that early-life exposure to PM2.5 can induce autophagy through the PI3K/Akt/mTOR pathway mediated by unfolded protein response in adult testicular tissue. PM2.5 may pose a significant role and long-term threat to adult after early-life exposure.