Cardiac mitochondrial biogenesis in endotoxemia is not accompanied by mitochondrial function recovery

VANASCO VIRGINIA; SAEZ TRINIDAD; MAGNANI NATALIA; PEREYRA LEONARDO; MARCHINI TIMOTEO; EVELSON PABLO; BOVERIS ALBERTO; ALVAREZ SILVIA

Buenos Aires

Congreso; VIII International Congress of SFRBM South American Group; 2013

Society for Free Radical Biology and Medicine

Endotoxemia is described as a paradigm of acute whole body inflammation, with massive increases of nitric oxide (NO) and inflammatory cytokines in biological fluids, systemic damage in the vascular endothelium, and impaired tissue and whole body respiration despite adequate O2 supply. Without timely and effective therapeutic intervention, this scenario evolves to multiple organ failure and ultimately to death mainly by heart failure. Cardiac mitochondrial dysfunction occurring during endotoxemia, plays a key role in the development of organ damage mainly by decreasing ATP availability and producing increased amounts of reactive oxygen and nitrogen species. However, it has also been proposed that endotoxemia might trigger the activation of mitochondrial biogenesis process as a compensatory mechanism in order to restore a functional mitochondrial population. Although mitochondrial biogenesis indicates increased mass of newly mitochondria, this observation does not necessarily imply functional mitochondria. To our knowledge, no studies have been carried out analyzing mitochondrial funtion during heart mitochondrial biogenesis in an in vivo acute inflamatory model as endotoxemia. The aim was to analyze the time course of mitochondrial biogenesis occurring in heart during endotoxemia, with emphasis in the quantitative analysis of mitochondrial function.