Abstract
Severity of ischemia/reperfusion injury accompanied with generation of reactive oxygen species is reduced by hypoxic preconditioning, the precise mechanisms of which are not completely understood. We found that cobalt-induced hypoxia-inducible factor-1α activity ameliorated suppression of cell growth caused by H2O2 through protecting mitochondrial DNA from oxidative damage.
Keywords: HIF-1α, cobalt, H2O2, cell growth, mitochondria, DNA damage
Letters in Drug Design & Discovery
Title: HIF-1α as a Target for Drug Design in Ischemic Injury: Effect of Cobalt Treatment on Mitochondrial DNA Damage in Cells Exposed to H2O2
Volume: 3 Issue: 3
Author(s): Yasutomo Nomura, Hiroyuki Fujiwara, Kohei Ito, Hirobumi Fuchigami, Michihiko Sato, Eiji Takahashi, Yasukazu Hozumi, Kaoru Goto, Zhonggang Feng and Takao Nakamura
Affiliation:
Keywords: HIF-1α, cobalt, H2O2, cell growth, mitochondria, DNA damage
Abstract: Severity of ischemia/reperfusion injury accompanied with generation of reactive oxygen species is reduced by hypoxic preconditioning, the precise mechanisms of which are not completely understood. We found that cobalt-induced hypoxia-inducible factor-1α activity ameliorated suppression of cell growth caused by H2O2 through protecting mitochondrial DNA from oxidative damage.
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Nomura Yasutomo, Fujiwara Hiroyuki, Ito Kohei, Fuchigami Hirobumi, Sato Michihiko, Takahashi Eiji, Hozumi Yasukazu, Goto Kaoru, Feng Zhonggang and Nakamura Takao, HIF-1α as a Target for Drug Design in Ischemic Injury: Effect of Cobalt Treatment on Mitochondrial DNA Damage in Cells Exposed to H2O2, Letters in Drug Design & Discovery 2006; 3 (3) . https://dx.doi.org/10.2174/157018006776286952
DOI https://dx.doi.org/10.2174/157018006776286952 |
Print ISSN 1570-1808 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-628X |
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