Extracellular iron (II) can protect cells from hydrogen peroxide.

摘要: Abstract We hypothesized that exposure of cells to H2O2plus Fe2+would increase formation cell-derived lipid peroxides would inactivate prostaglandin H synthase, resulting in decreased synthesis. Therefore, we treated human endothelial with 0–100 μ m H2O2followed immediately by addition 0–200 Fe2+. After oxidant exposure, were stimulated 20 arachidonic acid induce I2(PGI2) Adding 100 H2O2prior PGI2synthesis more than 80%. However, our surprise, the Fe2+, increasing amounts, progressively protected against harmful effects H2O2. A ratio one part H2O2to two parts Fe2+offered almost complete protection, whereas Fe3+did not protect from found H2O2was cytolytic; however, 250 Fe2+protected this cytotoxicity. In addition, extracellular Fe2+prevented rise intracellular calcium caused H2O2and Fe2+preserved glutathione H2O2-exposed cells. Electron paramagnetic resonance spin trapping demonstrated Fe2+generated hydroxyl free radical, HO•, outside cell. speculate Fe2+protects space H2O2by initiating Fenton reaction This reductive cleavage H2O2generates HO•in space, where much HO•will react noncellular components, thereby protecting cell interior.