Alcohol, oxidative stress, and free radical damage
Title
Alcohol, oxidative stress, and free radical damage
Publication type
Journal Article
Year of Publication
2003
Authors
Journal
Alcohol Research and Health
Volume
27
Issue
4
Pagination
277 - 284
Date published
2003
ISBN
0090838X (ISSN)
Keywords
alcohol, Alcohol Drinking, alcohol liver disease, Alcoholic liver disorder, Animal, Animals, antioxidant, catalase, Chronic AODE (alcohol and other drug effects), cytochrome P450, DNA, DNA damage, drinking behavior, enzyme activation, enzyme activity, Ethanol, fat, free radical, Free Radicals, glutathione peroxidase, human, Humans, lipid oxidation, Lipids, liver cell, liver cell damage, metabolism, metal, Metals, NAD, NADH oxidoreductases, nonhuman, oxidative stress, Peroxidation, physiology, protein, Proteins, reactive oxygen metabolite, Reactive Oxygen Species, reduced nicotinamide adenine dinucleotide, review, superoxide dismutase
Abstract
Reactive oxygen species (ROS) are small, highly reactive, oxygen-containing molecules that are naturally generated in small amounts during the body's metabolic reactions and can react with and damage complex cellular molecules such as fats, proteins, or DNA. Alcohol promotes the generation of ROS and/or interferes with the body's normal defense mechanisms against these compounds through numerous processes, particularly in the liver. For example, alcohol breakdown in the liver results in the formation of molecules whose further metabolism in the cell leads to ROS production. Alcohol also stimulates the activity of enzymes called cytochrome P450s, which contribute to ROS production. Further, alcohol can alter the levels of certain metals in the body, thereby facilitating ROS production. Finally, alcohol reduces the levels of agents that can eliminate ROS (i.e., antioxidants). The resulting state of the cell, known as oxidative stress, can lead to cell injury. ROS production and oxidative stress in liver cells play a central role in the development of alcoholic liver disease.