HIF-1α as a Target for Drug Design in Ischemic Injury: Effect of Cobalt Treatment on Mitochondrial DNA Damage in Cells Exposed to H2O2
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
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