Molecules and Cells

Korean Society for Molecular and Cellular Biology (한국분자세포생물학회)
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Suppression of Arsenic Trioxide-induced Apoptosis in HeLa Cells by N-Acetylcysteine

  • Han, Yong Hwan (Department of Physiology, Medical School, Institute for Medical Sciences, Center for Healthcare Technology Development, Chonbuk National University) ;
  • Kim, Sung Zoo (Department of Physiology, Medical School, Institute for Medical Sciences, Center for Healthcare Technology Development, Chonbuk National University) ;
  • Kim, Suhn Hee (Department of Physiology, Medical School, Institute for Medical Sciences, Center for Healthcare Technology Development, Chonbuk National University) ;
  • Park, Woo Hyun (Department of Physiology, Medical School, Institute for Medical Sciences, Center for Healthcare Technology Development, Chonbuk National University)
  • Received : 2007.10.24
  • Accepted : 2008.01.14
  • Published : 2008.07.31
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Abstract

Arsenic trioxide (ATO) can affect many biological functions such as apoptosis and differentiation in various cells. We investigated the involvement of ROS and GSH in ATO-induced HeLa cell death using ROS scavengers, especially N-acetylcysteine (NAC). ATO increased intracellular ${O_2}^{{\cdot}-}$ levels and reduced intracellular GSH content. The ROS scavengers, Tempol, Tiron and Trimetazidine, did not significantly reduce levels of ROS or GSH depletion in ATO-treated HeLa cells. Nor did they reduce the apoptosis induced by ATO. In contrast, treatment with NAC reduced ROS levels and GSH depletion in the ATO-treated HeLa cells and prevented ATO-induced apoptosis. Treatment with exogenous SOD and catalase reduced the depletion of GSH content in ATO-treated cells. Catalase strongly protected the cells from ATO-induced apoptosis. In addition, treatment with SOD, catalase and NAC slightly inhibited the G1 phase accumulation induced by ATO. In conclusion, NAC protects HeLa cells from apoptosis induced by ATO by up-regulating intracellular GSH content and partially reducing the production of ${O_2}^{{\cdot}-}$.

Keywords

Acknowledgement

Supported by : Korean Science and Engineering Foundation, Korea Research Foundation

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