0000000000364861
AUTHOR
Juan B. Miñana
Mitochondrial oxidative stress and CD95 ligand: A dual mechanism for hepatocyte apoptosis in chronic alcoholism
Apoptosis plays an important role in the progression of alcohol-induced liver disease to cirrhosis. Oxidative stress is an early event in the development of apoptosis. The major aim of this study was to study the conditions in which oxidative stress occurs in chronic alcoholism and its relationship with apoptosis of hepatocytes. We have found that oxidative stress is associated with chronic ethanol consumption in humans and in rats, in the former independently of the existence of alcohol-induced liver disease. Ethanol or acetaldehyde induces apoptosis in hepatocytes isolated from alcoholic rats, but not in those from control rats. Inhibition of aldehyde dehydrogenase, but not of cytochrome …
Chronic ethanol feeding causes oxidative stress in rat liver mitochondria. Prevention by S-adenosyl methionine
Mitochondrial function in liver disease.
Oxidative stress is involved in the pathogenesis and progression of different liver diseases, such as alcoholic liver disease and biliary cirrhosis. The increased mitochondrial production of O2(-) at complexes I and III, and consequently of H2O2 and other reactive oxygen species (ROS), triggered by NADH overproduction seems the major cause of mitochondrial and cellular oxidative stress and damage in chronic alcoholism. The mitochondrial oxidative stress renders hepatocytes susceptible to ethanol- or acetaldehyde-induced mitochondrial membrane permeability transition (MMPT) and apoptosis. Nitrosative stress contributes to cell death by peroxynitrite formation. The expression of the death rec…
Hyperoxemia caused by resuscitation with pure oxygen may alter intracellular redox status by increasing oxidized glutathione in asphyxiated newly born infants
In a prospective, randomized, blinded trial we have studied the effects of resuscitation upon oxygenation in a group of asphyxiated newly born infants receiving room air or 100% oxygen as the gas source. During the acute phase of asphyxia and until the resuscitation procedure concluded, we determined serial blood gases as well as reduced and oxidized glutathione, enzymes involved in the glutathione redox cycle, and antioxidant enzyme activities. The use of 100% oxygen caused a remarkable increase of partial pressures of oxygen in arterial blood, with values that were frequently above physiological levels (>100 mm Hg). In addition, we have found a significant correlation between hyperoxemia …
The Relationship between Alcohol–induced Apoptosis and Oxidative Stress in the Liver
This chapter discusses the relationship of apoptosis and oxidative stress induced by alcohol in the liver. Oxidative stress is involved in the pathogenesis and progression of alcohol-induced liver disease. Chronic alcoholism always causes oxidative stress independently of the presence of liver disease. Two key mechanisms are responsible for it: (1) the mitochondrial respiratory chain and (2) cytochrome P450 2El activity. Increased production of reactive oxygen species at complexes I and III together with NADH overproduction would be the major cause for mitochondrial oxidative stress in chronic alcoholism. Reactive Oxygen Species (ROS) cause oxidative damage, which may lead to cell death by …