A critical role of superoxide anion in selenite-induced mitophagic cell death

Eun Hee Kim and Kyeong Sook Choi

volume 4 | issue 1

1 January 2008
Pages: 76 - 78

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Mitochondria, which are a major source of intracellular reactive oxygen species (ROS), are extremely vulnerable to oxidative stress. We recently reported that selenite treatment of various glioma cells induced a non-apoptotic cell death accompanied by excessive mitophagy (selective autophagy of damaged mitochondria). Examination of various ROS revealed that the superoxide anion played a key role in selenite-induced mitochondrial damage, mitophagy and cell death. Treatment with superoxide generators (diquat and paraquat) was sufficient to trigger mitophagy in glioma cells. Small interfering RNA-mediated knockdown of ATG6 or ATG7 attenuated selenite-induced mitophagy and cell death, demonstrating that the mitophagic pathway contributes to selenite-induced cell death. The effect of selenite in glioma cells may thus provide an example of superoxide-mediated mitophagic cell death, i.e., cell death caused by excessive mitophagy.

Addendum to: Kim EH, Sohn S, Kwon HJ, Kim SU, Kim MJ, Lee SJ, Choi KS. Sodium selenite induces superoxide-mediated mitochondrial damage and subsequent autophagic cell death in malignant glioma cells. Cancer Res 2007; 67:6314-24

Authors

Eun Hee Kim

Institue for Medical Sciences, Ajou University School of Medicine

Kyeong Sook Choi

Institue for Medical Sciences, Ajou University School of Medicine

We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link: