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

VANASCO, VIRGINIA; SAEZ, TRINIDAD; MAGNANI, NATALIA; PEREYRA, LEONARDO; MARCHINI, TIMOTEO; CORACH, ALEJANDRA; VACCARO, MARIA INES; CORACH, DANIEL; EVELSON, PABLO; ALVAREZ, SILVIA

FREE RADICAL BIOLOGY AND MEDICINE

ELSEVIER SCIENCE INC

Lugar: Amsterdam; Año: 2014 vol. 77 p. 1 - 9

0891-5849

Mitochondrial biogenesis emerges as a compensatory mechanism involved in the recovery process in endotoxemia and sepsis. The aim of this work was to analyze the time course of the cardiac mitochondrial biogenesis process occurring during endotoxemia, with emphasis on the quantitative analysis of mitochondrial function. Female Sprague-Dawley rats (45 days old) were ip injected with LPS (10 mg/kg). Measurements were performed at 0?24 h after LPS administration. PGC-1α and mtTFA expression for biogenesis and p62 and LC3 expression for autophagy were analyzed by Western blot; mitochondrial DNA levels by qPCR, and mitochondrial morphology by transmission electron microscopy. Mitochondrial function was evaluated as oxygen consumption and respiratory chain complex activity. PGC-1α and mtTFA expression significantly increased in every time point analyzed, and mitochondrial mass was increased by 20% (P