Ethanol-induced oxidative stress: basic knowledge

Abstract

After a general introduction, the main pathways of ethanol metabolism (alcohol dehydrogenase, catalase, coupling of catalase with NADPH oxidase and microsomal ethanol-oxidizing system) are shortly reviewed. The cytochrome P 450 isoform (CYP2E1) specifically involved in ethanol oxidation is discussed. The acetaldehyde metabolism and the shift of the NAD/NADH ratio in the cellular environment (reductive stress) are stressed. The toxic effects of acetaldehyde are mentioned. The ethanolinduced oxidative stress: the increased MDA formation by incubated liver preparations, the absorption of conjugated dienes in mitochondrial and microsomal lipids and the decrease in the most unsaturated fatty acids in liver cell membranes are discussed. The formation of carbon-centered (1-hydroxyethyl) and oxygen-centered (hydroxyl) radicals during the metabolism of ethanol is considered: the generation of hydroxyethyl radicals, which occurs likely during the process of univalent reduction of dioxygen, is highlighted and is carried out by ferric cytochrome P 450 oxy-complex (P 450 -Fe 3? O 2 Á-) formed during the reduction of heme-oxygen. The ethanol-induced lipid peroxidation has been evaluated, and it has been shown that plasma F 2 -isoprostanes are increased in ethanol toxicity.

Feeding on ripening and over-ripening fruit: interactions between sugar, ethanol and polyphenol contents in a tropical butterfly

“…It is therefore possible that butterflies do not possess a type of ADH that can be induced by ethanol, as observed in adult D. melanogaster fruit flies (Geer et al, 1988;Hernández-Tobías et al, 2011). Butterflies lacking this physiological protective response would be expected to experience the detrimental effects of ethanol intake such as its pro-oxidant effects (Albano, 2006;Comporti et al, 2010). However, we did not detect any pro-oxidant effects following ethanol consumption, suggesting that butterflies were efficiently protected against ethanol exposure.…”

“…Indeed, ethanol consumption has been described as altering the oxidative balance of organisms by increasing the production of reactive oxygen species (ROS) and decreasing endogenous antioxidant defences, thereby increasing oxidative damage on biomolecules (Albano, 2006;Comporti et al, 2010). This variation in oxidative status can, in turn, negatively affect the fitness of animals by decreasing reproductive performance and survival probability (Monaghan et al, 2009).…”

Telomeres and Telomerase in The Aging Heart

“…Telomere shortening process is associated with these risk factors through increased tissue inflammation and oxidative stress. (92)(93)(94) Mechanistically, telomere dysfunction-driven tissue compromise is thought to be secondary to the activation of DNA damage signaling pathways that converge on p53, a central executor of the DNA damage response pathway. (95) The activation of p53 induces senescent and apoptosis pathways, particularly in stem cell and progenitor compartments of highly regenerative organs.…”

Alcohol hangover induces mitochondrial dysfunction and free radical production in mouse cerebellum

“…It was widely established that ethanol metabolism generates reactive oxygen species (ROS) which cause oxidative stress and lipid peroxidation in the brain (Calabrese et al, 1998;Comporti et al, 2010). Particularly, chronic alcohol exposure induces liver mitochondrial DNA damage mainly affecting respiratory complexes' activities (Cahill and Cunningham, 2000).…”