Aflatoxin B1 impairs leydig cells through inhibiting AMPK/mTOR-mediated autophagy flux pathway.

作者: Xianwu Chen , Chao Li , Yong Chen , Chaobo Ni , Xiuxiu Chen

DOI: 10.1016/J.CHEMOSPHERE.2019.05.273

关键词:

摘要: Aflatoxin B1 (AFB1), a potential endocrine disrupter, has been shown to induce hepatotoxicity in animal models, but the effects of AFB1 on Leydig cell function are unclear. In this study, in vivo exposure at 15 and 150 μg/kg/day lowered serum testosterone (T), luteinizing hormone (LH), follicle-stimulating (FSH) levels, reduced number, down-regulated expression biosynthesis-related genes. In vitro study showed that (10 μM) significantly increased ROS decreased T production cells by suppressing certain T-biosynthesis gene expressions. Moreover, induced apoptosis through lowering pAMPK/AMPK ratio increasing pmTOR/mTOR ratio, then further up-regulating autophagy proteins, LC3, BECLIN 1, BAX, as well down-regulating flux protein P62 anti-apoptosis BCL-2. AFB1-induced toxicity was characterized inhibiting expression, reducing promoting production, inducing via AMPK/mTOR-mediated pathway.

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