Document Detail


Inhibitors of endogenous nitrosation. Mechanisms and implications in human cancer prevention.
MedLine Citation:
PMID:  3057363     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Although the proof that N-nitroso compounds (NOC), a versatile class of carcinogens in animals, are also carcinogenic in man is lacking, humans are exposed through ingestion or inhalation to preformed NOC in the environment and through the endogenous nitrosation of amino precursors in the body. Activated macrophages can synthesize nitrate, nitrite and nitrosating agents that can form NOC. A number of bacterial strains isolated from human infections can produce NOC enzymatically from precursors at neutral pH. As a consequence endogenous nitrosation may occur at various sites of the body such as the oral cavity, stomach, urinary bladder, lungs, and at other sites of infection or inflammation. Since the demonstration by Mirvish et al. (1972) showing that ascorbate can reduce tumor formation in animals following feeding of nitrite plus amine, numerous substances to which humans are exposed have been identified and shown to inhibit formation of NOC in vitro, in animal models and in humans. Such inhibitors of nitrosation include vitamins C and E, phenolic compounds, and complex mixtures such as fruit and vegetable juices or other plant extracts. Nitrosation inhibitors normally destroy the nitrosating agents and thus act as competitors for the amino compound that serves as substrate for the nitrosating species. Independently, epidemiological studies have already established that fresh fruits and vegetables that are sources of vitamin C, other vitamins and polyphenols have a protective effect against cancers at various sites and in particular gastric cancer. Although the evidence that endogenously formed NOC are involved in human cancers is far from conclusive, it is suggestive and justifies preventive measures for reducing exposure to NOC. This article briefly reviews (i) the chemistry of NOC formation and inhibition, (ii) the studies in experimental animals which showed that inhibition of endogenous NOC synthesis leads to a reduction of toxic, mutagenic and carcinogenic effects, (iii) recent studies in humans where the degree of inhibition of endogenous NOC synthesis was directly quantified and lastly (iv) the contribution of nitrosation inhibitors to human cancer prevention.
Authors:
H Bartsch; H Ohshima; B Pignatelli
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Mutation research     Volume:  202     ISSN:  0027-5107     ISO Abbreviation:  Mutat. Res.     Publication Date:  1988 Dec 
Date Detail:
Created Date:  1989-01-05     Completed Date:  1989-01-05     Revised Date:  2004-11-17    
Medline Journal Info:
Nlm Unique ID:  0400763     Medline TA:  Mutat Res     Country:  NETHERLANDS    
Other Details:
Languages:  eng     Pagination:  307-24     Citation Subset:  IM    
Affiliation:
International Agency for Research on Cancer, Lyon, France.
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MeSH Terms
Descriptor/Qualifier:
Animals
Humans
Metabolic Detoxication, Drug
Neoplasms / chemically induced,  prevention & control*
Nitroso Compounds / antagonists & inhibitors*,  toxicity
Chemical
Reg. No./Substance:
0/Nitroso Compounds

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