Zinc deficiency and corticosteroids in the pathogenesis of alcoholic brain dysfunction--a review.
Chronic alcoholism is associated with hypercortisolemia and low serum zinc (Zn). Hypercortisolemia could be responsible for alcoholic cerebral atrophy and is also associated with enhanced NMDA neurotoxicity. It is hypothesized that low brain Zn, noted in chronic alcoholics, enhances NMDA excitotoxicity and ethanol withdrawal seizure susceptibility. Also, Zn deficiency can produce neuronal damage through increased free radical formation. Clinically, Zn replacement therapy may be a rational approach to the treatment of alcohol withdrawal seizures and alcohol-related brain dysfunction.
Neuropharmacology Program, Playfair Neuroscience Unit, University of Toronto, Ontario, Canada.
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D000305:Adrenal Cortex Hormones / Q000502:physiology*; D000430:Alcohol Withdrawal Delirium / Q000503:physiopathology* / Q000534:rehabilitation; D000437:Alcoholism / Q000503:physiopathology* / Q000534:rehabilitation; D001284:Atrophy; D001921:Brain / Q000473:pathology*; D005609:Free Radicals; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D011604:Psychoses, Alcoholic / Q000503:physiopathology* / Q000534:rehabilitation; D016194:Receptors, N-Methyl-D-Aspartate / Q000187:drug effects / Q000502:physiology; D012307:Risk Factors; D015032:Zinc / Q000172:deficiency*
D000305:Adrenal Cortex Hormones; D005609:Free Radicals; D016194:Receptors, N-Methyl-D-Aspartate; D015032:Zinc; D006854:Hydrocortisone