Document Type : Original Article
Authors
1
Biochemistry Division, Chemistry Department, Faculty of Science, Mansoura University
2
Center of Excellence for Genome and Cancer Research, Urology and Nephrology Center
3
Medical Physiology Department, Faculty of Medicine, Mansoura University, Mansoura
4
Biochemistry Division, Chemistry Department, Faculty of Science, Mansoura University, Mansoura 35516, Egypt
Abstract
This study investigates the mitigative effects of Selenium (Se) against Doxorubicin (DOX)-induced hepatotoxicity, particularly focusing on gene expressions of BCL2 and BAX as markers of cellular survival and apoptosis. Chemotherapy, notably with DOX, while effective against various malignancies, poses risks of hepatotoxicity, characterized by hepatocyte necrosis and fibrosis. The study explores Se's role, a vital trace mineral integral to Selenium nanoparticles, in combating oxidative stress induced by DOX. Employing a controlled experimental design, gene expressions in four groups (Control, Se, DOX, and DOX + Se) were studied using quantitative real-time PCR. Results showed that Se supplementation alone had minimal impact on BCL2 and BAX expressions. However, DOX treatment significantly decreased BCL2 levels and increased BAX levels, underscoring its hepatotoxic potential. The combined DOX+Se treatment moderated these effects, partially restoring BCL2 levels and reducing BAX expression, suggesting Se's protective capability against DOX-induced gene expression dysregulation. These results highlight the potential of Se in ameliorating the adverse effects of DOX, providing insights into protective strategies against chemotherapy-induced hepatotoxicity.
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