Dear Colleagues,

Oxygen is a double edged sword for life. It is a key element for optimal energy production (e.g., aerobic glycolysis, tricarboxylic acid cycle, oxidative phosphorylation), but also a toxic compound, involved in the generation of reactive oxygen species (ROS) able to damage DNA, proteins, and lipids, and also in the formation of reactive nitrogen species (RNS).  Oxidative damage activates proinflammatory cytokines production, and, together with RNS, ROS damage mitochondrial enzymatic chain. Mitochondrial damage and proinflammatory cytokines amplify the deleterious effects of ROS, creating a harmful positive feed-back loop, ultimately leading to cell death. Also, lipid peroxidation promotes ferroptosis, another important pathway involved in cell injury, and oxidative damage to histone proteins and/or DNA may lead to altered gene expression.  As a defense against the toxic effects of oxygen, several enzymatic pathways (e.g, superoxide dismutases) developed, since probably very early in the evolution of life. Together with other non-enzymatic compounds, such as urate, bilirubin, several vitamins, and reduced glutathione, and with enzymes involved in the maintenance of cell function and DNA repair during oxidative injury, antioxidants are usually in homeostatic balance with oxidative damage. However, chronic exposure to ethanol, by many mechanisms, may alter this delicate equilibrium, leading to accumulation of ROS and to ongoing disease, not only in the liver but also affecting other organs, especially those with highest oxygen consumption, such as muscle, heart and brain.

Despite intensive research in this field many aspects are still poorly understood, including for instance the role of ferroptosis, or that of the acetaldehyde/advanced glycation end-products on oxidative damage, the relation of epigenetic changes induced by alcoholism, among many others, so studies devoted to shed light on any of the still obscure aspects of the mechanisms and consequences of altered redox equilibrium in alcoholic liver disease are strongly welcome.

Contributions need not be limited to the fields mentioned in the keywords. We look forward to your contribution.

Dr. Iván Ferraz-Amaro
Dr. María Candelaria Martín-González
Guest Editors

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• alcoholism
• alcoholic liver disease
• reactive oxygen species
• reactive nitrogen species
• oxidative damage
• lipid peroxidation
• proinflammatory cytokines
• ferroptosis
• advanced glycation end-products
• epigenetic changes
• altered redox equilibrium