Zinc deficiency and corticosteroids in the pathogenesis of alcoholic brain dysfunction--a review.

Abstract

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.

• Authors: E Menzano, P L Carlen
• Journal: Alcoholism, clinical and experimental research (Alcohol Clin Exp Res) Vol. 18 Issue 4 Pg. 895-901 (Aug 1994) ISSN: 0145-6008 [Print] England
• PMID: 7978102 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)

Chemical References

• Adrenal Cortex Hormones
• Free Radicals
• Receptors, N-Methyl-D-Aspartate
• Zinc
• Hydrocortisone

Topics

• Adrenal Cortex Hormones (physiology)
• Alcohol Withdrawal Delirium (physiopathology, rehabilitation)
• Alcoholism (physiopathology, rehabilitation)
• Atrophy
• Brain (pathology)
• Free Radicals
• Humans
• Hydrocortisone (blood)
• Psychoses, Alcoholic (physiopathology, rehabilitation)
• Receptors, N-Methyl-D-Aspartate (drug effects, physiology)
• Risk Factors
• Zinc (deficiency)