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Apoptosis induced by modulation in selenium status involves p38 MAPK and ROS: implications in spermatogenesis.
1Department of Biophysics, Panjab University, Chandigarh, 160014, India.
Molecular and Cellular Biochemistry
|April 14, 2009
Summary
Selenium
Area of Science:
- Reproductive Biology
- Cellular Biology
- Toxicology
Background:
- Selenium is essential for male fertility and maintaining a balance between cell proliferation and apoptosis.
- Apoptosis, or programmed cell death, is crucial for spermatogenesis.
- Reactive oxygen species (ROS) are implicated in initiating apoptotic pathways.
Purpose of the Study:
- To investigate the role of selenium in regulating testicular apoptosis.
- To understand the mechanisms by which selenium affects spermatogenesis.
- To examine the involvement of p38 MAPK and ROS in selenite-induced apoptosis.
Main Methods:
- Modulating intracellular selenium levels through diet (deficient and excess) for 8 weeks.
- Monitoring reactive oxygen species (ROS) generation and lipid peroxidation.
- Analyzing mRNA and protein expression of p38 MAPK, caspases 3 and 8, and Bcl-2.
- Assessing DNA integrity to identify apoptotic cells.
Main Results:
- Altered selenium levels correlated with increased ROS generation and lipid peroxidation.
- Increased mRNA and protein expression of p38 MAPK, caspases 3, and 8.
- Decreased mRNA expression of the anti-apoptotic factor Bcl-2.
- Evidence of DNA damage, indicating apoptotic cell death.
Conclusions:
- Sodium selenite induces testicular apoptosis, with toxicity mediated by increased ROS.
- ROS generation is linked to the upregulation of p38 MAPK and caspases, and downregulation of Bcl-2.
- p38 MAPK plays a role in testicular apoptosis, highlighting selenium's importance in balancing cell death and proliferation for male fertility.
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