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

Authors
Kim, EH; Choi, KS
Citation
Autophagy, 4(1):76-78, 2008
Journal Title
Autophagy
ISSN
1554-86271554-8635
Abstract
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.
MeSH terms
Antineoplastic Agents/metabolismCell Death/physiology*Glioma/metabolismHerbicides/metabolismHumansMitochondria/metabolism*Oxidative StressParaquat/metabolismReactive Oxygen Species/metabolismSodium Selenite/metabolism*Superoxides/metabolism*
PMID
17952022
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Biochemistry & Molecular Biology
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