期刊
JOURNAL OF CELLULAR BIOCHEMISTRY
卷 104, 期 3, 页码 862-878出版社
WILEY
DOI: 10.1002/jcb.21673
关键词
arsenic trioxide; ROS; GSH; apoptosis; mitochondria; Calu-6
Arsenic trioxide (ATO) can regulate many biological functions such as apoptosis and differentiation in various cells. We investigated an involvement of ROS such as H2O2 and O-2(.-), and GSH in ATO-treated Calu-6 cell death. The levels of intracellular H2O2 were decreased in ATO-treated Calu-6 cells at 72 h. However, the levels Of O-2(.-) were significantly increased. ATO reduced the intracellular GSH content. Many of the cells having depleted GSH contents were dead, as evidenced by the propidium iodine staining. The activity of CuZn-SOD was strongly down-regulated by ATO at 72 h while the activity of Mn-SOD was weakly up-regulated. The activity of catalase was decreased by ATO. ROS scavengers, Tiron and Trimetazidine did not reduce levels of apoptosis and intracellular O-2(.-) in ATO-treated Calu-6 cells. Tempol showing a decrease in intracellular O-2(.-) levels reduced the loss of mitochondrial transmembrane potential (Delta Psi(m)). Treatment with NAC showing the recovery of GSH depletion and the decreased effect on O-2(.-) levels in ATO-treated cells significantly inhibited apoptosis. In addition, BSO significantly increased the depletion of GSH content and apoptosis in ATO-treated cells. Treatment with SOD and catalase significantly reduced the levels Of O-2(.-) levels in ATO-treated cells, but did not inhibit apoptosis along with non-effect on the recovery of GSH depletion. Taken together, our results suggest that ATO induces apoptosis in Calu-6 cells via the depletion of the intracellular GSH contents rather than the changes of ROS levels.
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