Zearalenone induces apoptosis of rat Sertoli cells through Fas‐Fas ligand and mitochondrial pathway
- College of Veterinary Medicine Yangzhou University Yangzhou Jiangsu China, Jiangsu Co‐innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses Yangzhou Jiangsu China, Joint International Research Laboratory of Agriculture and Agri‐Product Safety of the Ministry of Education of China Yangzhou University Yangzhou Jiangsu China
- College of Veterinary Medicine Yangzhou University Yangzhou Jiangsu China, Jiangsu Co‐innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses Yangzhou Jiangsu China
Abstract Zearalenone (ZEA) is an estrogen‐like toxin produced by Fusarium that is widely found in cereals worldwide. In recent years, ZEA has been found to cause reproductive dysfunction in male animals, but the underlying mechanism remains unclear. This study examined the apoptosis of rat Sertoli cells induced by different concentrations (0, 5, 10, and 20 μmol/L) of ZEA via Fas‐Fas ligand and mitochondrial signaling pathway in vitro. Apoptosis rate was detected by flow cytometry. The mitochondrial membrane potential was detected by immunofluorescence assay and flow cytometry. Western Blot and qRT‐PCR were used to identify the signaling pathway. The results revealed that ZEA induced apoptosis of rat Sertoli cells, significantly reduced the transcription and expression of the anti‐apoptotic protein Bcl‐2, increased the transcription and expression of pro‐apoptotic proteins Bax and tBID, and Fas, FasL, FADD, and caspase‐8. ZEA also increased the activation of caspase‐8 and caspase‐9, and promoted the release of cytochrome C from mitochondria to cytoplasm. Moreover, addition of caspase‐8 inhibitor Z‐IETD‐FMK led to significant decrease in the mitochondrial membrane potential and apoptosis rate of the ZEA + Z‐IETD‐FMK group as compared to the ZEA treatment group. The release of cytochrome C from mitochondria to cytoplasm and the activation of caspase‐9 and caspase‐3 were significantly decreased in the ZEA + Z‐IETD‐FMK group. These results suggested that ZEA can induce apoptosis of rat Sertoli cells, activate the Fas‐Fas ligand signaling pathway and participate in the regulation of mitochondrial apoptosis pathway.
- Sponsoring Organization:
- USDOE
- OSTI ID:
- 1489294
- Journal Information:
- Environmental Toxicology, Journal Name: Environmental Toxicology Vol. 34 Journal Issue: 4; ISSN 1520-4081
- Publisher:
- Wiley Blackwell (John Wiley & Sons)Copyright Statement
- Country of Publication:
- United States
- Language:
- English
Web of Science
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