Early-life exposure tofine particle matterscause autophagy via UPR-mediated PI3K-mTOR pathwayin spermatogenic cells of adult male mice
【摘要】：Background: Epidemiological studies have shown that particulate matters are closely related to human infertility. However, a less considered long-term risk of particulate matters exposure in early life. For the first time this study was designed to determine the mechanism of early-life exposure to fine particle matters(PM_(2.5)) on autophagy in spermatogenic cells of adult. METHODS Pregnant C57 mice were randomly divided into four groups. 4.8 mg·kg~(-1) b.w group and 43.2 mg·kg~(-1) b.w groupwere administered with different doses PM_(2.5). Membrane control group was administered with PM_(2.5) sampling membrane and Control group without any treatment. The exposure began from the day after vaginal plug checked and was conducted every three days until delivery, in total 6 times. RESULTS The results shown that a decline in sperms motility and sperms concentration, increased sperm deformity in adult male mice of offspring. The expression of SOD was decreased and MDA was increased. The level of GRP78/ATF6 and P62 was upregulated, and the expression of PI3K/Akt/mTOR/p-mTOR was downregulated. CONCLUSION It is implied that early-life exposure to PM_(2.5) can induce autophagyvia the PI3K/Akt/mTOR pathway mediated by unfolded protein response in spermatogenic cells in adult.PM2.5 may pose a significant role and long lasting threat to adult after early-life exposure.