A review of the role of reactive oxygen and nitrogen species in alcohol-induced mitochondrial dysfunction.

摘要: Our understanding of the mechanisms involved in development alcohol-induced liver disease has increased substantially recent years. Specifically, reactive oxygen and nitrogen species have been identified as key components initiating possibly sustaining pathogenic pathways responsible for progression from fatty to alcoholic hepatitis cirrhosis. Ethanol demonstrated increase production decrease several antioxidant liver. However, relative contribution proposed sites ethanol-induced within is still not clear. It that chronic ethanol-elicited alterations mitochondria structure function might result at level mitochondrion ethanol consumers. This turn oxidative modification inactivation mitochondrial macromolecules, thereby contributing further dysfunction a loss hepatic energy conservation. Moreover, ethanol-related increases may shift balance between pro- anti-apoptotic factors such there activation permeability transition, which would lead cell death after alcohol consumption. article will examine critical role these injury with specific emphasis on how ethanol-associated influence their disrupt conservation abuser.