Abstract
Zearalenone (ZEA) is a nonsteroidal estrogenic mycotoxin found in several food commodities worldwide. ZEA causes reproductive disorders, genotoxicity, and testicular toxicity in animals. However, little is known about the functions of apoptosis and autophagy after exposure to ZEA in granulosa cells. This study investigated the effects of ZEA on chicken granulosa cells. The results show that ZEA at different doses significantly inhibited the growth of chicken granulosa cells by inducing apoptosis. ZEA treatment up-regulated Bax and downregulated Bcl-2 expression, promoted cytochrome c release into the cytosol, and triggered mitochondria-mediated apoptosis. Consequently, caspase-9 and downstream effector caspase-3 were activated, resulting in chicken granulosa cells apoptosis. ZEA treatment also upregulated LC3-II and Beclin-1 expression, suggesting that ZEA induced a high level of autophagy. Pretreatment with chloroquine (an autophagy inhibitor) and rapamycin (an autophagy inducer) increased and decreased the rate of apoptosis, respectively, in contrast with other ZEA-treated groups. Autophagy delayed apoptosis in the ZEA-treated cells. Therefore, autophagy may prevent cells from undergoing apoptosis by reducing ZEA-induced cytotoxicity. In addition, our results further show that the autophagy was stimulated by ZEA through PI3K-AKT-mTOR and MAPK signaling pathways in chicken granulosa cells.
Highlights
Zearalenone (ZEA) is an estrogen-like non-steroidal mycotoxin produced by a variety of fusarium fungi
Key Contribution: In this study, we found that ZEA could protect cell apoptosis by activating autophagy, and it was found that ZEA could regulate autophagy and apoptosis through PI3K-AktmTOR and MAPK signaling pathways
To investigate whether ZEA had an adverse effect on the viability of chicken granulosa cells, we cultured chicken granulosa cells
Summary
Zearalenone (ZEA) is an estrogen-like non-steroidal mycotoxin produced by a variety of fusarium fungi. It is often found in grain crops and animal feed as a pollutant, causing serious harm to animal husbandry [1,2]. Numerous studies have confirmed the harmful effects of exposure to ZEA and its metabolites on animals and humans, resulting in a variety of diseases and significant economic losses [3,4]. Many reports have shown that exposure to ZEA causes early puberty in children, endometrial adenocarcinoma, female breast cancer, and reduced testicular germ cells [5,6]. In livestock production, low and high concentrations of ZEA have all been shown to have adverse effects, leading to hyperestrogenemia, abortion, and reproductive failure [7,8,9]
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