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Published on: December 28, 2021
In vitro mechanistic study of endosulfan-induced spermatogenic cell apoptosis in the mouse
Ying Xu1, Na Wang1, Zhi-Xiong Shi1
1Department of Health Toxicology and Health Chemistry, School of Public Health, Capital Medical University, Beijing, People's Republic of China Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing, People's Republic of China.
Abstract:
To investigate the mechanisms of endosulfan-induced reproductive toxicity, the spermatogenic cell lines (GC-1 spg) of mice were treated with 0, 6, 12, and 24 μg/ml endosulfan for 24 h in vitro The results showed that endosulfan induced apoptosis as well as oxidative stress and mitochondrial dysfunction. Reactive oxygen species and damage of mitochondrial structure were considered as major factors to GC-1 spg cells apoptosis. We further examined the expression of apoptosis-related proteins in mitochondria pathway by Western blot and immunohistochemistry analysis as well as activities. The results showed that endosulfan significantly improved the expressions of cytochrome c and B-cell lymphoma 2 (Bcl-2)-associated X protein and increased the activities of caspases 9 and 3 as well as the downregulation of the expression of Bcl-2 in GC-1 spg cells. The results suggested that exposure to endosulfan might induce the apoptosis of spermatogenic cells via mitochondria-dependent pathway mediated by oxidative stress resulting in the damage of mitochondrial structure and mitochondrial dysfunction.
Insights
Endosulfan exposure induces reproductive toxicity by causing oxidative stress and mitochondrial damage in mouse spermatogenic cells. This leads to apoptosis via the mitochondria-dependent pathway, impacting male fertility.
Area of Science:
- Toxicology
- Reproductive Biology
- Cell Biology
Background:
- Endosulfan is an organochlorine pesticide with known reproductive toxicity.
- Spermatogenic cell dysfunction is a key factor in male infertility.
Purpose of the Study:
- To elucidate the mechanisms underlying endosulfan-induced reproductive toxicity in mouse spermatogenic cells.
- To investigate the role of oxidative stress and mitochondrial dysfunction in endosulfan toxicity.
Main Methods:
- In vitro exposure of mouse spermatogenic GC-1 spg cells to varying concentrations of endosulfan.
- Assessment of apoptosis, oxidative stress, and mitochondrial function.
- Western blot and immunohistochemistry analysis of apoptosis-related proteins.
- Measurement of caspase activities.
Main Results:
- Endosulfan induced apoptosis, oxidative stress, and mitochondrial dysfunction in GC-1 spg cells.
- Reactive oxygen species and mitochondrial structural damage were identified as key factors in apoptosis.
- Endosulfan altered the expression of apoptosis-related proteins (cytochrome c, Bax, Bcl-2) and increased caspase 9 and 3 activities.
Conclusions:
- Endosulfan induces spermatogenic cell apoptosis through a mitochondria-dependent pathway.
- Oxidative stress and subsequent mitochondrial damage mediate endosulfan's toxic effects on male reproductive cells.
