Cigarette smoke induces rat testicular injury via mitochondrial apoptotic pathway

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...

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Bibliographic Details
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
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Summary: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.
ISSN:1040-452X
1098-2795
DOI:10.1002/mrd.22863