Mitochondrion-mediated apoptosis is involved in reproductive damage caused by BPA in male rats |
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| Affiliation: | 1. Key Laboratory of Agricultural Animal Genetics, Breeding and Reproduction of Ministry of Education, College of Animal Science and Technology, Huazhong Agricultural University, Wuhan, 430070, Hubei, China;2. Stowers Institute for Medical Research, 1000 East 50th Street, Kansas City, MO, 64110, USA;3. Biochip Laboratory, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, 264000, Shandong, China;1. School of Nursing, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China;2. MOE (Ministry of Education) Key Lab of Environment and Health, Department of Occupational and Environmental Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China;3. Department of Epidemiology and Health Statistics, School of Public Health, Medical College, Wuhan University of Science and Technology, Wuhan, 430030, China;4. Department of Clinical Laboratory, Taihe Hospital, Hubei University of Medicine, Shiyan, 442000, China;5. Family Planning Research Institute, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China;1. Department of Oriental Medicine Biotechnology, Kyung Hee University, Yongin 17104, Republic of Korea;2. Kwang-Dong Pharmaceutical Co., Ltd., Seoul 06650, Republic of Korea |
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| Abstract: | Bisphenol A (BPA) is a widely used environmental endocrine disruptor. Many studies have reported that BPA exposure shows reproductive toxicity and causes apoptosis in spermatogenic cells. However, few studies have investigated the relationship between the mitochondrial pathway and BPA-induced apoptosis. This study investigated the role of the mitochondrial pathway in apoptosis induced by BPA, which resulted in compromised male rat spermatogenesis and reproductive damage. Rats were exposed to various BPA concentrations (0, 50, 100, or 200 mg of BPA/kg body weight per day), and factors in the mitochondrial signal transduction pathway and the apoptosis indices of spermatogenic cells were measured and sperm characteristics were analyzed. Our data revealed that BPA exposure increased the protein and mRNA levels of cytochrome C, apoptosis-inducing factor, caspase-3/9, and Bax; caspase-3 and caspase-9 activities; and the apoptosis indices of spermatogenic cells. In addition, abnormal structure of mitochondria and decreased protein and gene levels of Bcl-2 were observed following BPA exposure. These results suggest that apoptosis in the mitochondrial pathway mediates compromised reproductive system function caused by BPA exposure. |
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| Keywords: | Mitochondria Apoptosis Spermatogenic cells Bisphenol A Reproductive toxicity |
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