Brain age-dependent effects of acute endotoxemia on oxidative damage and mitochondrial function

CIMOLAI, MARIA CECILIA; VANASCO, VIRGINIA; EVELSON, PABLO; BUGGER, HEIKO; ALVAREZ, SILVIA

Friburgo

Conferencia; 17th European Bioenergetics Conference (EBEC); 2012

Endotoxemia is a systemic inflammatory state secondary to the activation of the innate immune system. Its pathogenic mechanism is still incompletely understood. Impaired mitochondrial function and increased oxidative damage have been proposed as responsible for the septic final state: multi-organ failure. The incidence of endotoxemia and sepsis is increased in elderly adults, and age is an independent predictor of mortality. The mitochondrial theory of aging hypothesizes that mitochondria are the pacemakers of tissue aging due to the continuous production of oxygen and nitrogen free radicals and related reactive species. Endotoxemia and aging are situations characterized by an increased damage to cellular structures due to increased or cumulative production of reactive oxygen species. Thus, the aim of the present work was to study the occurrence of oxidative stress and mitochondrial contribution to the response in an acute model of endotoxemia, analyzing the effect in animals grouped by age (young adults: 3 mo.; old adults: 12 mo.). O2 utilization was assessed by measuring O2 consumption in whole tissue and mitochondria. Whole tissue O2 consumption was found invariable in young animals (control: 3.88 ± 0.42. 103 nmol O2 / min. g tissue), being non-mitochondrial O2 consumption increased in a 45% (p