Oxidative stress from alcohol in the brain.
An acute ethanol load administered to rats results in an enhancement in lipid peroxidation in the cerebellum, a brain area which is particularly sensitive to free radical attack. The ethanol load induces also a decrease in the cerebellar concentration of the three main endogenous anti-oxidant small molecules, i.e. alpha-tocopherol, ascorbate and glutathione. These findings are highly suggestive of a cerebellar oxidative stress due to acute ethanol administration. However this administration does not enhance brain mitochondrial superoxide production as well as cerebellar mitochondrial hydrogen peroxide production. An oxidative stress could also play a role in some effects of chronic alcohol intoxication on the brain. This is particularly suggested by the beneficial effects of the administration of desferrioxamine, an iron-chelator and free radical scavenger, on physical dependence on alcohol in rodents. A speculative synthesis of the mechanisms that might be involved in such an oxidative stress on the central nervous system is presented.
Nordmann
R
R
Department of Biomedical Research on Alcoholism, Université René Descartes, Paris, France.
D000437:Alcoholism / Q000378:metabolism; D000818:Animals; D001921:Brain / Q000187:drug effects* / Q000378:metabolism; D001923:Brain Chemistry / Q000187:drug effects; D002531:Cerebellum / Q000187:drug effects / Q000378:metabolism; D000431:Ethanol / Q000009:adverse effects* / Q000494:pharmacology; D005609:Free Radicals; D005978:Glutathione / Q000032:analysis; D008054:Lipid Peroxides / Q000378:metabolism; D010084:Oxidation-Reduction; D051381:Rats; D014810:Vitamin E / Q000032:analysis
D005609:Free Radicals; D008054:Lipid Peroxides; D014810:Vitamin E; D000431:Ethanol; D005978:Glutathione