BPA-induced apoptosis of rat Sertoli cells through Fas/FasL and JNKs/p38 MAPK pathways |
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| Affiliation: | 1. Department of Anatomy, Physiology and Biochemistry, Swedish University of Agricultural Sciences, Box 7011, 75007, Sweden;2. Division of Diet, Disease Prevention and Toxicology, Technical University of Denmark, Building 202, 2800 Kgs Lyngby, Denmark;3. Iranian Research Institute for Information Science and Technology (IranDoc) Tehran Province, No. 1090, Enghelab, Tehran, Iran;4. Department of Medical Sciences, Occupational and Environmental Medicine, Akademiska sjukhuset, 751 85 Uppsala, Uppsala University, Sweden;5. ARUP Institute for Clinical and Experimental Pathology, Salt Lake City, UT 84108, USA;6. Department of Pathology, University of Utah, Salt Lake City, UT, USA;1. Department of Physiology, School of Basic Medical Sciences, Nanchang University, Nanchang, 330006, PR China;2. Nursing School of Nanchang University, Nanchang, 330006, PR China;3. Jiangxi Provincial Key Laboratory of Reproductive Physiology and Pathology, Nanchang University, Nanchang, 330006, PR China |
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| Abstract: | Bisphenol-A was examined for its effects on cultured Sertoli cells established from 18 to 22-day-old rat testes. Results indicated that exposure to BPA (0, 30, 50 and 70 μM) decreased the cell viability in a concentration-dependent manner and induced cell apoptosis. Apoptosis-caused cell death was observed in cells exposed to 50 and 70 μM BPA. The mRNA expressions of Fas, FasL and caspase-3 were all elevated, and the protein expressions of FasL and cleaved caspase-3 were also increased. In addition, levels of phosphorylation of JNKs/p38 MAPK were also increased and then activated JNKs/p38 MAPK up regulated target gene expressions, such as c-jun and CHOP. Translocation of NF-κB into nuclei indicated the activation of NF-κB after treatment with BPA. Taken together, observed results suggest that BPA induces apoptosis of Sertoli cells by the activation of JNKs/p38 MPAK and translocation of NF-κB, and Fas/FasL system plays a critical role in the initiation of apoptosis. |
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| Keywords: | Bisphenol-A MAPK NF-κB Fas/FasL Cells apoptosis |
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