Lesión oxidativa de proteínas de hígado y corazón de rata durante el proceso de envejecimiento

Abstract

Objectives ageing affects all organisms and its basic mechanisms can be expected to be conserved across species. Protein oxidation has been proposed as one of the basic mechanisms linking oxygen radicals with the basic ageing process. If oxidative damage to proteins is involved in ageing, aged animals should show higher steady- state levels of specific markers of this kind of damage than younger adult animals. However, the evidence available on this prediction is limited when the use of specific chemical markers is considered. Material and method we measured steady-state levels of markers of different kinds of protein damage-oxidation (glutamic and aminoadipic semialdehydes), glycoxidation (carboxyethyl-lysine), mixed glyco- and lipoxidation (carboxymethyl-lysine), and lipoxidation (malondialdehydelysine)-, as well as fatty acid profile in the livers and hearts of young adult (8 months old) and aged (30 months old) male rats. Results oxidative and glycoxidative markers were significantly increased in both the liver and heart of aged rats. Lipoxidation damage was also significantly increased in aged rats. This result was probably associated with the significantly increased double bond and peroxidizability indexes found in liver and heart cell membranes. Steady-state levels of oxidation and lipoxidation damage were significantly higher in the heart than in the liver. In contrast, glycoxidation damage was greater in the liver than in the heart. Accumulation rates of protein damage were higher in the heart than in the liver during aging. Conclusions in the context of the oxidative stress theory of ageing, these results reveal differences between organs and reinforce the role of membrane unsaturation as well as the homeostatic mecha-nisms that maintain the steady-state level of protein damage in this biological process.