Premium
Effect of Lipid Restriction on Mitochondrial Free Radical Production and Oxidative DNA Damage
Author(s) -
SANZ ALBERTO,
CARO PILAR,
SANCHEZ JOSE GOMEZ,
BARJA GUSTAVO
Publication year - 2006
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1354.024
Subject(s) - mitochondrial dna , caloric theory , oxidative stress , mitochondrion , oxidative phosphorylation , reactive oxygen species , mitochondrial ros , biochemistry , biology , ingestion , dna oxidation , nuclear dna , dna damage , dna , chemistry , oxidative damage , endocrinology , gene
Many studies have shown that caloric restriction (40%) decreases mitochondrial reactive oxygen species (ROS) generation in rodents. Moreover, we have recently found that 7 weeks of 40% protein restriction without strong caloric restriction also decreases ROS production in rat liver. This is interesting since it has been reported that protein restriction can also extend longevity in rodents. In the present study we have investigated the possible role of dietary lipids in the effects of caloric restriction on mitochondrial oxidative stress. Using semipurified diets, the ingestion of lipids in male Wistar rats was decreased by 40% below controls, while the other dietary components were ingested at exactly the same level as in animals fed ad libitum . After 7 weeks of treatment the liver mitochondria of lipid‐restricted animals showed significant increases in oxygen consumption with complex I‐linked substrates (pyruvate/malate and glutamate/malate). Neither mitochondrial H 2 O 2 production nor oxidative damage to mitochondrial or nuclear DNA was modified in lipid‐restricted animals. Oxidative damage to mitochondrial DNA was one order of magnitude higher than that of nuclear DNA in both dietary groups. These results deny a role for lipids and reinforce the possible role of dietary proteins as being responsible for the decrease in mitochondrial ROS production and DNA damage in caloric restriction.