Melatonin protects bovine cerebral endothelial cells from hyperoxia-induced DNA damage and death.
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.
Shaikh
A Y
AY
Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Xu
J
J
Wu
Y
Y
He
L
L
Hsu
C Y
CY
D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D002417:Cattle; D016923:Cell Death / Q000187:drug effects; D002478:Cells, Cultured; D002540:Cerebral Cortex / Q000166:cytology*; D004249:DNA Damage / Q000187:drug effects*; D004727:Endothelium / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D005609:Free Radicals / Q000378:metabolism; D018496:Hyperoxia / Q000188:drug therapy*; D008550:Melatonin / Q000494:pharmacology*; D018696:Neuroprotective Agents / Q000494:pharmacology*; D010100:Oxygen / Q000494:pharmacology
D000975:Antioxidants; D005609:Free Radicals; D018696:Neuroprotective Agents; D008550:Melatonin; D010100:Oxygen