Document Detail


Possible cellular and molecular mechanisms for asbestos carcinogenicity.
MedLine Citation:
PMID:  1536158     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Asbestos fibers may exert their carcinogenic effects on mesothelial cells and bronchial epithelial cells by direct and indirect mechanisms. Direct effects can occur following the physical interaction of fibers with target cells or by the generation of free radicals from the fiber surface; indirect effects, following the interaction of fibers with inflammatory cells can result in the production of cellular mediators such as cytokines and various reactive oxygen species. As a result, target cells may be induced to proliferate and/or sustain genetic alterations, which lead to tumor development.
Authors:
C Walker; J Everitt; J C Barrett
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  American journal of industrial medicine     Volume:  21     ISSN:  0271-3586     ISO Abbreviation:  Am. J. Ind. Med.     Publication Date:  1992  
Date Detail:
Created Date:  1992-03-23     Completed Date:  1992-03-23     Revised Date:  2006-02-27    
Medline Journal Info:
Nlm Unique ID:  8101110     Medline TA:  Am J Ind Med     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  253-73     Citation Subset:  IM    
Affiliation:
Chemical Industry Institute for Toxicology, Research Triangle Park, North Carolina 27709.
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MeSH Terms
Descriptor/Qualifier:
Animals
Asbestos / adverse effects*,  metabolism
Carcinoma, Bronchogenic / etiology*,  genetics
Cell Transformation, Neoplastic / chemically induced,  genetics
Chromosome Aberrations / chemically induced
Chromosome Disorders
Cricetinae
Growth Substances / metabolism
Humans
Mesocricetus
Mesothelioma / etiology*,  genetics
Mutation
Oxidants / metabolism
Rats
Smoking / adverse effects,  metabolism
Chemical
Reg. No./Substance:
0/Growth Substances; 0/Oxidants; 1332-21-4/Asbestos
Comments/Corrections
Comment In:
Am J Ind Med. 1992;21(2):137-9   [PMID:  1536150 ]

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


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