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Melatonin protects bovine cerebral endothelial cells from hyperoxia-induced DNA damage and death
A Y Shaikh1, J Xu, Y Wu
1Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Abstract:
Hyperoxia leads to excessive formation of reactive oxygen species (ROS). ROS cause damage to many cellular components, including DNA. Exposure of bovine cerebral endothelial cells to 95 or 100% oxygen resulted in an increase in DNA fragmentation, the appearance of DNA ladders, and cell death with morphological features suggestive of apoptosis. Melatonin, an antioxidant, reduced hyperoxia-induced DNA fragmentation and cell death in a dose-dependent manner. Results from the present study support the contention that ROS play a major role in DNA damage and apoptotic death. Melatonin is an effective agent in reducing ROS-mediated DNA fragmentation and death in bovine cerebral endothelial cells.