Regulation of Reactive Oxygen Species by Nerve Growth Factor but not Bcl-2 as a Novel Mechanism of Protection of PC12 Cells from Superoxide Anion-Induced Death
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概要
- 論文の詳細を見る
Although neurotrophins protect PC12 cells and neurons from oxidative stress-induced death, the molecular mechanism of this effect is largely unknown. Xanthine (XA)+ xanthine oxidase (XO) increased the production of the superoxide anion (O-2) and hydrogen peroxide (H2O2), and the death of PC12 cells. Catalase but not superoxide dismutase (SOD) nor a NO scavenger protected PC12 cells from death, indicating that H2O2 is the main effector responsible for this cell death. Both nerve growth factor (NGF) and Bcl-2 protected PC12 cells from O2-induced toxicity. NGF enhanced the production of O-2 and suppressed that of H2O2, suggesting that it inhibits the conversion of O-2 to H2O2, while Bcl-2 had no such effect. These results suggested that NGF protected the cells from oxidative stress by altering the composition of the reactive oxygen species (ROS) without affecting their total level.
- 社団法人 日本生化学会の論文
著者
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Satoh Takumi
Division Of Cardiology Internal Medicine Tonan Hospital
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ISHIKAWA Yasuyuki
Division of Protein Biosynthesis, Institute for Protein Research, Osak University
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YAMADA Masashi
Division of Protein Biosynthesis, Institute for Protein Research, Osak University
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Uchiyama Yasuo
Department Of Anatomy Jichi Medical School
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YAMAGATA Tomoko
Division of Protein Biosynthesis, Institute for Protein Research, Osaka University
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Hatanaka Hiroshi
Department Of Microbiology Showa College Of Pharmacy
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