Cigarette smoke induces rat testicular injury via mitochondrial apoptotic pathway

• Published in: Molecular reproduction and development 2017-10, Vol.84 (10), p.1053-1065
• Main Authors: He, Lijuan, You, Shuping, Gong, Haiyan, Zhang, Jing, Wang, Li, Zhang, Chen, Huang, Yunfei, Zhong, Chunxue, Zou, Ying
• Format: Article
• Language: English
• Subjects: animal model; Animals; Apoptosis; Apoptosis - drug effects; Apoptosis - genetics; Bcl-2 protein; Caspase; Caspase-3; Caspase-9; Cigarette smoke; cigarette smoking; Cigarettes; Exposure; Female; Gene Expression - drug effects; Germ cells; Inhalation; Inhalation Exposure - adverse effects; Leukemia; Lymphocytes B; Lymphoma; Male; Mitochondria; Mitochondria - drug effects; Mitochondria - genetics; Mitochondria - pathology; mitochondrial apoptotic pathway; molecular mechanism; Proteins; Rats; Rats, Sprague-Dawley; Reproductive system; Smoke; Smoke inhalation; Smoking - adverse effects; Testes; Testis - drug effects; Testis - metabolism; Testis - pathology; Tobacco smoke; Tobacco Smoke Pollution - adverse effects
• ISSN: 1040-452X; 1098-2795
• DOI: 10.1002/mrd.22863

An understanding of the causative mechanisms of the harmful effects of cigarette smoke on the male reproductive system remains incomplete. Here, we investigated three different inhaled cigarette smoke doses over five different exposure durations to identify how the testis is affected. The effects of cigarette smoke exposure on testicular germ cells were characterized by morphological changes and a significant elevation in the number of apoptotic cells. Caspase 3 activation increased dramatically after cigarette smoke exposure, accompanied by significant time‐dependent expression of the pro‐apoptotic proteins Bak (B cell lymphoma/leukemia 2 [Bcl‐2] homologous antagonist killer), Bcl2l11 (a BH3 domain‐only protein related to Bcl‐2), Apaf1 (Apoptotic protease‐activating factor‐1), and Caspase 9. Conversely, the abundance of anti‐apoptotic Bcl2l2 decreased. Taken together, our findings suggest that extensive inhalation of cigarette smoke damages testicular germ cells through the induction of the mitochondrial apoptotic pathway through the Bcl‐2 protein family.