부산대학교 도서관

Background : Mercury exerts a variety of toxic effects on both neurons and glia and also may play a role in pathophysiological mechanisms of Alzheimer's disease in neuroblastoma cells. Studies in vivo and in vitro have shown that mercury generates reactive oxygen species (ROS) and increases lipid peroxidation in various tissues including brain, suggesting that oxidative stress may contribute to the development of neurodegenerative disorders caused by mercury intoxication. However, whether lipid peroxidation plays an important role in mercury cytotoxicity is not clear. Methods : The present study was undertaken to determine (1) the involvement of individual ROS in mediating mercury cytotoxicity and (2) whether mercury0induced cell death is resulted from lipid peroxidation in human glioma cells. HgCl2 caused the loss of cell viability in a dose- and time-dependent manner. Results : The loss of viability was prevented by the hydroxyl radical scavenger dimethylthiourea, but the superoxide scavenger superoxide dismutase and the hydrogen peroxide scavengers catalase and pyruvate showed no beneficial effect. The potent antioxidant DPPD exerted partial protective effect, but BHA, Trlox, and melatonin were not effective. HgCL2-induced loss of viability was prevented by the ferrous iron chelator phenanthroline, but no the ferric iron ATP depletion, which was prevented by the agents protecting HgCl2-induced cell death. Conclusion : These results suggest that (1) HgCl2-induced cell death is associated with generation of hydroxyl radicals resulting from an iron-dependent mechanism and (2) lipid peroxidation does not play a critical role in HgCl2 cytotoxicity in human glioma cells.