Journal
TOXICOLOGY LETTERS
Volume 226, Issue 2, Pages 182-191Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.toxlet.2014.02.003
Keywords
Zearalenone; Apoptosis; Autophagy; Leydig cells
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Funding
- National Science Foundation of the Higher Education institutions of Jiangsu Province, China [08KJD230002]
- Graduate Training Innovative Projects Foundation of Jiangsu Province, China [CXLX13_921]
- Priority Academic Program Development of Jiangsu Higher Education Institutions
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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 Leydig cells. This study investigated the effects of ZEA on rat Leydig cells. Results showed that ZEA at different doses significantly inhibited the growth of Leydig cells by inducing apoptosis. ZEA treatment upregulated Bax expression, promoted cytochrome c release into the cytosol, and triggered mitochondria-mediated apoptosis. Consequently, caspase-9 and downstream effector caspase-3 were activated, followed by the cleavage of poly(ADP-ribose) polymerase (PARP), resulting in Leydig cell 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 to other ZEA-treated groups. Autophagy delayed apoptosis in the ZEA-treated Leydig cells. Therefore, autophagy may prevent cells from undergoing apoptosis by reducing ZEA-induced cytotoxicity. (C) 2014 Elsevier Ireland Ltd. All rights reserved.
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