title: Mitochondrion-mediated apoptosis is involved in reproductive damage caused by BPA in male rats.
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 200mg 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.
authors.affiliation: Department of Clinical Laboratory, The First College of Clinical Medical Science of China Three Gorges University and Yichang Central People's Hospital, Yichang 433003, Hubei, China.
authors.forename: Peng
authors.initials: P
authors.lastname: Wang
authors.affiliation: Department of Clinical Laboratory, The First College of Clinical Medical Science of China Three Gorges University and Yichang Central People's Hospital, Yichang 433003, Hubei, China.
authors.forename: Chunhua
authors.initials: C
authors.lastname: Luo
authors.affiliation: Department of Clinical Laboratory, The First College of Clinical Medical Science of China Three Gorges University and Yichang Central People's Hospital, Yichang 433003, Hubei, China.
authors.forename: Qianyuan
authors.initials: Q
authors.lastname: Li
authors.affiliation: Department of Clinical Laboratory, The First College of Clinical Medical Science of China Three Gorges University and Yichang Central People's Hospital, Yichang 433003, Hubei, China.
authors.forename: Sai
authors.initials: S
authors.lastname: Chen
authors.affiliation: Department of Clinical Laboratory, The First College of Clinical Medical Science of China Three Gorges University and Yichang Central People's Hospital, Yichang 433003, Hubei, China. Electronic address: Yonghu1021@163.com.
authors.forename: Yong
authors.initials: Y
authors.lastname: Hu
mesh_terms: D000818:Animals; D017209:Apoptosis; D001559:Benzhydryl Compounds / Q000633:toxicity*; D020169:Caspases / Q000235:genetics / Q000378:metabolism; D005786:Gene Expression Regulation / Q000187:drug effects; D008297:Male; D008928:Mitochondria / Q000378:metabolism*; D010636:Phenols / Q000633:toxicity*; D051381:Rats; D012098:Reproduction / Q000187:drug effects*; D015398:Signal Transduction / Q000187:drug effects; D013091:Spermatogenesis / Q000187:drug effects*; D013737:Testis / Q000473:pathology* / Q000503:physiopathology; D000098826:Bisphenol A Compounds
chemical_list: D001559:Benzhydryl Compounds; D020169:Caspases; D010636:Phenols; C006780:bisphenol A; D000098826:Bisphenol A Compounds
keywords: Apoptosis; Bisphenol A; Mitochondria; Reproductive toxicity; Spermatogenic cells