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- W2290965293 abstract "The electron transport chain (ETC) is a target for H2O2 due to the presence of thiol groups (−SH) that undergoes reversible oxidation. −SH serves as a redox sensor that modulates complex activity and avoids further ROS production. Our hypothesis is that the increment on unsaturation degree of mitochondrial membranes disrupts −SH-mediated ETC reversible inhibition by H2O2 due to enhanced membrane damage. To test this hypothesis, we studied the effects of H2O2 on lipoperoxidation levels, ETC activity, ROS production and free Fe concentration on native yeast mitochondria (−C18:3, lipoperoxidation resistant) and yeast mitochondria enriched with linolenic acid (+C18:3, lipoperoxidation sensitive). Sensitivity of complex III to H2O2 and lipoperoxidation was increased in +C18:3 mitochondria, while complex III inhibition by H2O2 was poorly reverted by a −SH reductanct. Furthermore, increases in ROS production and free Fe concentration were detected only in +C18;3 mitochondria. These results suggest that lipoperoxidation promote Fe release from mitochondrial pools enhancing ROS production and sensitivity of complex III to oxidative damage due to ROS attack in other enzyme components different than −SH groups." @default.
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- W2290965293 date "2010-04-01" @default.
- W2290965293 modified "2023-09-27" @default.
- W2290965293 title "Lipid peroxidation induced by H2O2 alters the sensitivity of complex III to oxidative stress by increasing iron labile pool" @default.
- W2290965293 doi "https://doi.org/10.1096/fasebj.24.1_supplement.510.3" @default.
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