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Published on: January 10, 2015
Cigarette smoke induces rat testicular injury via mitochondrial apoptotic pathway
Lijuan He1, Shuping You2, Haiyan Gong3
1Department of Social Medicine, School of Public Health, Xinjiang Medical University, Urumqi, Xinjiang, P.R. China.
Abstract:
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.
Insights
Cigarette smoke exposure damages testicular germ cells by triggering apoptosis via the mitochondrial pathway. This involves increased pro-apoptotic proteins like Bak and decreased anti-apoptotic Bcl2l2, impacting male reproductive health.
Area of Science:
- Reproductive Biology
- Toxicology
- Cellular Biology
Background:
- The mechanisms by which cigarette smoke harms the male reproductive system are not fully understood.
- Testicular germ cell damage is a known consequence of smoking.
Purpose of the Study:
- To investigate the effects of varying cigarette smoke doses and exposure durations on the testis.
- To elucidate the molecular pathways involved in cigarette smoke-induced testicular damage.
Main Methods:
- Exposure of testes to three different inhaled cigarette smoke doses.
- Assessment of five different exposure durations.
- Characterization of morphological changes and apoptosis in testicular germ cells.
- Measurement of apoptotic and anti-apoptotic protein expression (Caspase 3, Bak, Bcl2l11, Apaf1, Caspase 9, Bcl2l2).
Main Results:
- Cigarette smoke exposure caused morphological changes and increased apoptotic germ cells.
- Significant time-dependent increases in pro-apoptotic proteins (Bak, Bcl2l11, Apaf1, Caspase 9) and Caspase 3 activation were observed.
- A decrease in the anti-apoptotic protein Bcl2l2 was noted.
Conclusions:
- Cigarette smoke induces testicular germ cell damage through the mitochondrial apoptotic pathway.
- The Bcl-2 protein family plays a critical role in mediating cigarette smoke-induced germ cell apoptosis.
- Findings highlight the detrimental impact of inhaled cigarette smoke on male reproductive function.
