The oxidative stress and the mitochondrial dysfunction caused by endotoxemia are prevented by alpha-lipoic acid.
The aims of this work were to study the mitochondrial function and to evaluate (a) the oxidative stress in real time in an acute model of endotoxemia and (b) the effect of alpha-lipoic acid (LA, 100 mg/kg) as a therapeutic strategy to be considered. In rats treated with lipopolisaccharide (LPS, 10 mg/kg), a 1.4-fold increase was observed in in situ skeletal muscle chemiluminescence. Experimental sepsis increased oxygen consumption in tissue cubes (1 mm(3)) by 30% for heart and diaphragm and impaired state 3 mitochondrial respiration rate in the three organs (liver, diaphragm and heart) studied. Only complex I activity in heart and diaphragm and complex IV activity in diaphragm were found impaired in this septic model. The production of NO by submitochondrial membranes was found increased by 80% in the diaphragm and by 35% in the heart of septic rats. The treatment with LA prevented the oxidative stress and mitochondrial dysfunction observed in this model.
Vanasco
Virginia
V
Laboratory of Free Radical Biology, School of Pharmacy and Biochemistry, University of Buenos Aires, Buenos Aires, Argentina.
Cimolai
Maria Cecilia
MC
Evelson
Pablo
P
Alvarez
Silvia
S
D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D019446:Endotoxemia / Q000473:pathology*; D005260:Female; D008070:Lipopolysaccharides / Q000378:metabolism; D008928:Mitochondria / Q000378:metabolism / Q000473:pathology*; D018482:Muscle, Skeletal / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000378:metabolism; D018384:Oxidative Stress; D010100:Oxygen / Q000378:metabolism; D010101:Oxygen Consumption; D051381:Rats; D017207:Rats, Sprague-Dawley; D018805:Sepsis; D008063:Thioctic Acid / Q000378:metabolism*
D000975:Antioxidants; D008070:Lipopolysaccharides; D009569:Nitric Oxide; D008063:Thioctic Acid; D019001:Nitric Oxide Synthase; D010100:Oxygen