Coenzyme Q addition to an n-6 PUFA-rich diet resembles benefits on age-related mitochondrial DNA deletion and oxidative stress of a MUFA-rich diet in rat heart.
Age-related changes in cardiomyocytes reduce the capacity to recover from acute injury or to adapt during chronic disease in advanced age. N-6 polyunsaturated fatty acids (n-6PUFA) lead to higher lipid peroxidation during aging than the less oxidizable monounsaturated fatty acids (MUFA); and coenzyme Q (CoQ)-supplemented n-6PUFA lengthens the lifespan and reduces peroxidation in comparison to non-supplemented n-6PUFA. Here, lifelong feeding on MUFA, n-6PUFA, and n-6 PUFA+CoQ was compared regarding age-related alterations in rat heart. Less mitochondrial area and perimeter were reported for aged n-6 PUFA-fed animals while MUFA led to a higher density of mitochondrial cristae. Mitochondrial complexes and cytochrome c oxidase activity decreased with aging (except complex I and cytochrome c oxidase in n-6 PUFA+CoQ), while increased apoptosis-inducing factor was found with aging. MUFA led to lower mitochondrial DNA-deletion frequency. The lowest hydroperoxide levels for aged animals were found for n-6 PUFA+CoQ, which also showed lower concentrations than did n-6 PUFA. For protein oxidation, specific carbonyl compounds were lower in aged animals; meanwhile lipoxidation-derived protein-oxidation markers were higher. The results suggest that MUFA can protect mitochondria from age-related changes, and that CoQ supplementation to n-6 PUFA partially resembles MUFA benefits. Moreover, under our experimental conditions, lipid-derived oxidative damage appears to be more important than the pure protein-derived oxidative damage during aging.
Quiles
José L
JL
Institute of Nutrition and Food Technology José Mataix Verdú, Department of Physiology, University of Granada, Granada, Spain. jlquiles@ugr.es
Pamplona
Reinald
R
Ramirez-Tortosa
M Carmen
MC
Naudí
Alba
A
Portero-Otin
Manuel
M
Araujo-Nepomuceno
Eduardo
E
López-Frías
Magdalena
M
Battino
Maurizio
M
Ochoa
Julio J
JJ
D000367:Age Factors; D000375:Aging / Q000235:genetics / Q000378:metabolism; D000818:Animals; D051033:Apoptosis Inducing Factor / Q000378:metabolism; D004272:DNA, Mitochondrial / Q000378:metabolism*; D004032:Diet; D019587:Dietary Supplements; D045222:Electron Transport Chain Complex Proteins / Q000378:metabolism; D005229:Fatty Acids, Monounsaturated / Q000008:administration & dosage / Q000378:metabolism*; D043371:Fatty Acids, Omega-6 / Q000008:administration & dosage / Q000378:metabolism*; D017353:Gene Deletion; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D008929:Mitochondria, Heart / Q000187:drug effects* / Q000378:metabolism / Q000648:ultrastructure; D032383:Myocytes, Cardiac / Q000187:drug effects* / Q000378:metabolism / Q000648:ultrastructure; D000069463:Olive Oil; D018384:Oxidative Stress / Q000187:drug effects*; D010938:Plant Oils / Q000378:metabolism; D050050:Protein Carbonylation / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D000074242:Sunflower Oil; D014451:Ubiquinone / Q000008:administration & dosage*
C494831:Aifm1 protein, rat; D051033:Apoptosis Inducing Factor; D004272:DNA, Mitochondrial; D045222:Electron Transport Chain Complex Proteins; D005229:Fatty Acids, Monounsaturated; D043371:Fatty Acids, Omega-6; D000069463:Olive Oil; D010938:Plant Oils; D000074242:Sunflower Oil; D014451:Ubiquinone