P66shc and its role in mitochondrial homeostasis throughout the aging process

PÉREZ H, ELGUERO ME, VILLALBA NM, ALIPPE Y, PODEROSO JJ, CARRERAS MC.

Mar del Plata

Congreso; LX Reunión Científica de la Sociedad Argentina de Investigación Clínica; 2016

Sociedad Argentina de Investigación Clínica

In accordance to the free radicals dependent aging theory, It has been widely accepted that this process is triggered and sustained by the deleterious accumulative effect of oxidative damage caused by mitochondrial respiration generated ROS. P66shc has been proposed as a longevity genetic determinant that regulates both apoptosis and metabolism through ROS generation. In the present work we assessed p66shc function on mitochondrial metabolism and physiology throughout the aging process. With this in mind, and by means of a murine model consistent in p66shc (p66shc-/-) KO mice, we assessed oxidative metabolism in brain mitochondria of 3-24-month-old mice. The p66shc-/- mouse, presents a longer life expectancy (30% mas), show diminished weight, evidenced by a 25% body weight reduction and exhibit changes in mitochondrial function and physiology while aging, such as increased mitochondrial DNA content, decreased activity no significantly in the respiratory chain complexes, elevated ATP levels (P