Changes in the levels of coenzyme Q homologues, alpha-tocopherol and malondialdehyde in human tissue during the course of circulatory shock.
Following our previous findings on mitochondrial oxidative damage during the course of circulatory shock in human muscular tissue, in the present work we examined the pathogenic connections between the electron-transport-chain enzymic activity and the ubiquinone metabolism. The effects of the oxidative damage on the alpha-tocopherol content and malondialdehyde (MDA) levels were also studied. The results reveal an involvement of cytochrome oxidase and coenzyme Q10 in the oxidative damage due to shock; alpha-tocopherol seems to show a particularly increased antioxidant activity contemporary with the marked increase in MDA levels. These findings suggest that the significant fall in the mitochondrial oxidative capacity could generate an oxygen free-radical production with subsequent peroxidative damage of the mitochondrial inner-membrane bilayer.
D001794:Blood Pressure; D002302:Cardiac Output; D003576:Electron Transport Complex IV / Q000378:metabolism; D006339:Heart Rate; D006801:Humans; D008314:Malonates / Q000378:metabolism*; D008315:Malondialdehyde / Q000378:metabolism*; D009132:Muscles / Q000378:metabolism*; D012769:Shock / Q000378:metabolism / Q000503:physiopathology*; D012770:Shock, Cardiogenic / Q000378:metabolism / Q000503:physiopathology; D014451:Ubiquinone / Q000378:metabolism*; D014655:Vascular Resistance; D014810:Vitamin E / Q000378:metabolism*
D008314:Malonates; D014451:Ubiquinone; D014810:Vitamin E; D008315:Malondialdehyde; D003576:Electron Transport Complex IV