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Lipid peroxidation induced by H2O2 alters the sensitivity of complex III to oxidative stress by increasing iron labile pool
Author(s) -
CortésRojo Christian,
EstradaVillagómez M. Mirella,
CalderónCortés Elizabeth,
MontoyaPérez Rocío,
SaavedraMolina Alfredo
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.510.3
Subject(s) - mitochondrion , chemistry , degree of unsaturation , oxidative stress , lipid peroxidation , reactive oxygen species , biochemistry , mitochondrial ros , redox , biophysics , oxidative phosphorylation , inner mitochondrial membrane , electron transport chain , biology , chromatography , inorganic chemistry
The electron transport chain (ETC) is a target for H 2 O 2 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 H 2 O 2 due to enhanced membrane damage. To test this hypothesis, we studied the effects of H 2 O 2 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 H 2 O 2 and lipoperoxidation was increased in +C18:3 mitochondria, while complex III inhibition by H 2 O 2 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.