Document Detail


The genesis of alcoholic brain tissue injury.
MedLine Citation:
PMID:  2198037     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
1. Acetaldehyde has been implicated in the pathogenesis of alcohol-related liver damage by two mechanisms. Adduct formation with many tissue constituents, especially proteins, makes them immunologically foreign or reduces enzyme activity and formation of cytotoxic free radicals from acetaldehyde metabolism. Adduct formation damage to microtubule associated proteins and to hepatocyte membranes impedes protein movement into, out of and around the cell. 2. Evidence that these mechanisms also have a role in alcoholic brain damage includes raised blood acetaldehyde in alcoholics, especially in those chemically dependent, or in other abnormal states; effects of extra-hepatic free radical toxicity, including induction of superoxide dismutase activity and damaged, abnormal variants of the thiamin-dependent enzyme transketolase and extrahepatic acetaldehyde-adduct formation with haemoglobin. That acetaldehyde-mediated impairment of microtubule systems also damages the brain is suggested by its importance for the maintenance by protein transport of often greatly extended brain cell processes. 3. Oxygen-derived free radicals can damage brain tissue, the effects including cerebral oedema, neuronal loss and damage to the blood-brain barrier, all changes also reported in the brains from alcoholic patients. Alcohol-related pathology in the brain differing from that in the liver, shows sharper regional variations in vulnerability and adverse effects due to nutritional deficiencies, especially of B-group vitamins. Even though some such deficits are capable of causing encephalopathy in the non-alcoholic, the strong association between them and chronic alcoholism points to possible aggravation by metabolic interactions at various levels between acetaldehyde and thiamin or other B-vitamins. Selective regional vulnerability may reflect differences in ease of acetaldehyde access or to important metabolic differences. Alteration of animal behaviour by acetaldehyde points to a need to correlate clinical evidence of acetaldehyde central nervous cytotoxicity with the incidence of different types of cognitive defect.
Authors:
O E Pratt; H K Rooprai; G K Shaw; A D Thomson
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Alcohol and alcoholism (Oxford, Oxfordshire)     Volume:  25     ISSN:  0735-0414     ISO Abbreviation:  Alcohol Alcohol.     Publication Date:  1990  
Date Detail:
Created Date:  1990-09-05     Completed Date:  1990-09-05     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  8310684     Medline TA:  Alcohol Alcohol     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  217-30     Citation Subset:  IM    
Affiliation:
Department of Neuropathology, Institute of Psychiatry, London, U.K.
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MeSH Terms
Descriptor/Qualifier:
Acetaldehyde / blood
Alcoholism / complications*
Animals
Brain / drug effects
Brain Damage, Chronic / etiology*
Ethanol / pharmacokinetics
Free Radicals
Humans
Liver / drug effects
Liver Diseases, Alcoholic / etiology
Substance-Related Disorders / etiology*
Chemical
Reg. No./Substance:
0/Free Radicals; 64-17-5/Ethanol; 75-07-0/Acetaldehyde

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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