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Influence of lipoperoxidation on the generation of mitochondrial membrane potential
Author(s) -
EstradaVillagómez M. Mirella,
CortésRojo Christian,
CalderónCortés Elizabeth,
MontoyaPérez Rocío,
ClementeGuerrero Mónica,
ManzoAvalos Salvador,
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.511.1
Subject(s) - mitochondrion , reactive oxygen species , electron transport chain , membrane , oxidative stress , membrane potential , inner mitochondrial membrane , chemistry , yeast , biophysics , oxidative phosphorylation , biochemistry , cytoplasm , microbiology and biotechnology , biology
Mitochondria are the main site of ATP synthesis, which requires the buildup of a membrane potential (ΔΨ). Reactive oxygen species (ROS) generated during electron transport can damage electron transport chain (ETC) components. Unsaturated lipids from mitochondrial membranes are the main targets of ROS attack, leading to ETC dysfunction due to membrane disruption. The hypothesis of this work is that lipoperoxidation resistance may also confer resistance to other mitochondrial parameters (i.e. ΔΨ generation) under oxidative stress conditions. We used the yeast S. cerevisiae as model due to the intrinsic resistance of yeast to lipoperoxidation. Also, the sensitivity of yeast to lipoperoxidation can be enhanced through incorporation of linolenic acid (C18:3) to membranes. Our results shown that in −C18:3 cells, the cytoplasmic and mitochondrial ΔΨ was observed even at concentrations of Fe 2+ up to 50 μM, while in +C18:3 cells, lower Fe 2+ concentrations inhibited ΔΨ buildup. As comparison, ΔΨ from rat liver mitochondria, which are prone to lipoperoxidation, was also inhibited by Fe 2+ treatment. These results suggest that membranes resistant to lipoperoxidation preserve its structural integrity even under strong oxidative conditions and allow a better function of mitochondrial ETC than the observed in lipoperoxidation‐prone mitochondria.