LAUSR

Aging is an irreversible process associated with a variety of diseases where mitochondria play an essential role. Redox balance and the level of unsaturation in membrane phospholipids can modulate the aging process. Attenuating oxidative damage and decreasing the content of long-chain polyunsaturated fatty acids (PUFAs) in mitochondrial membranes can contribute to extend lifespan of many organisms. Calorie restriction without malnutrition (CR) promotes a healthy aging phenotype increasing monounsaturated fatty acids and decreasing PUFAs without any observed changes in saturated fatty acids. On the other hand, the identification of enzymes which the capacity of modulating aging is starting to emerge. NADH-cytochrome b5 reductase-3 (CYB5R3) is a flavoprotein that uses NADH and several quinones including coenzyme Q (CoQ) as substrates. Our previous studies have shown that overexpressing in mice extends longevity. However, how CYB5R3 transgenic mice respond to nutritional interventions is largely unknown. Based on this, the aim of our work was to determine the impact of CR, fat source variations and genotype using the in vivo model of mice overexpressing CYB5R3, paying especial attention to those pathways that modulate metabolism, the prevention of oxidative stress, and CoQ system.