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ROLE OF LIPOPEROXIDATION ON OXIDATIVE DAMAGE TO MITOCHONDRIAL RESPIRATORY CHAIN
Author(s) -
CortésRojo Christian,
EstradaVillagómez Mirella,
CoronaGómez Rosalía,
CalderónCortés Elizabeth,
ClementeGuerrero Mónica,
EsquivelGutiérrez Edgar,
CaudilloNoriega Evangelina,
NoriegaCisneros Ruth,
ManzoÁvalos Salvador,
SaavedraMolina Alfredo
Publication year - 2007
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.21.5.a662-c
Subject(s) - spheroplast , lipid peroxidation , mitochondrion , oxidative phosphorylation , biochemistry , chemistry , yeast , polyunsaturated fatty acid , fatty acid , degree of unsaturation , oxidative stress , biology , chromatography , escherichia coli , gene
During pathological conditions, uncontrolled amounts of free radicals are produced in mitochondria. Polyunsaturated fatty acids from mitochondrial membranes lipids are the main targets of ROS attack. Susceptibility of fatty acids (FA) to peroxidation depends on the number of unsaturations in its hydrophobic tail. Consequently, we hypothesize that increase on unsaturation degree of FA will augment the sensitivity of mitochondrial function to oxidative inactivation due to lipid peroxidation stimulation, which may lead to accelerated cell death. We used S. cerevisiae yeast as model because its membrane fatty acid composition can be easily manipulated. Yeast membranes possess mainly monounsaturated FA (C18:1). Under this condition, lipoperoxidation was poorly induced with Fe2+, in both isolated mitochondria and spheroplasts. However, when linolenic acid (C18:3) was incorporated to membranes a 10‐times increase on lipoperoxidation was observed. It was observed that functionality of C18:3 mitochondria and spheroplasts was strongly inhibited by treatment with Fe2+. In contrast, in C18:1 mitochondria and spheroplasts, higher concentrations were needed to achieve the same effect. Also, it was observed that 400 μM Fe2+ caused complete lost of viability on C18:3 cells, while in C18:1 cells, only 10% loss viability. These results show that lipid peroxidation sensitize mitochondrial function to oxidative damage leading to cellular collapse. Acknowledgments: The authors appreciate the partial economic support from the grants of CONACYT (43705) and CIC‐UMSNH (2.16‐2006).