[The possible role of acetaldehyde in the brain damage caused by the chronic consumption of alcohol].
OBJECTIVE
The purpose of this study is to collect and evaluate the experimental evidence suggesting that acetaldehyde, the first oxidative metabolite of ethyl alcohol (ethanol), plays a mediating role in the brain damage associated with the chronic consumption of this substance.


METHODS
Although the brain damage associated with the chronic consumption of ethanol is multifactorial and, possibly, dependent on the numerous actions of this substance on the central nervous system (CNS), there is data to suggest that the oxidative metabolism of ethanol and resulting substances are involved in the aetiology of such processes. Similarly, the generation of free radicals and the formation of adducts between the products of this metabolism and substrates contained in the CNS could be the main mediators in such pathological processes. This idea is supported by the fact that the adducts derived from the metabolism of ethanol are formed in the same areas of the brain as those which present structural and functional disorders in chronic consumers of alcohol.


CONCLUSIONS
There are currently different experimental findings that appear to support the proposal that the substances resulting from the metabolism of ethanol can be important mediators in the brain damage associated with the chronic consumption of alcohol. Although more research is required, this theoretical proposal is very interesting, not just because of its relative novelty, but also because it is based on the same principles put forward to explain the toxic effects of alcohol consumption on organs and tissues.
Forn-Frías
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Departamento de Psicología Básica, Clínica y Psicobiología, Universidad Jaume I, Castelló, España.
Sanchis-Segura
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C
D000079:Acetaldehyde / Q000378:metabolism* / Q000494:pharmacology; D000428:Alcohol Drinking / Q000009:adverse effects*; D000437:Alcoholism / Q000150:complications* / Q000378:metabolism; D001921:Brain / Q000378:metabolism / Q000473:pathology*; D000431:Ethanol / Q000378:metabolism*; D005609:Free Radicals / Q000378:metabolism; D006801:Humans; D009422:Nervous System Diseases / Q000209:etiology / Q000473:pathology; D010084:Oxidation-Reduction
D005609:Free Radicals; D000431:Ethanol; D000079:Acetaldehyde