Linked Life Data

3057367

Source:http://linkedlifedata.com/resource/pubmed/id/3057367

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1989-1-5
pubmed:abstractText
We briefly review current concepts with regard to the nature of oxygen-derived oxidants in biological systems. Of these substances, hydroxyl radicals derived from hydrogen peroxide seem most likely to be involved in the various stages of carcinogenesis. Hydrogen peroxide detoxification, primarily through glutathione activity, is essential in preventing hydroxyl-radical formation. Transition metals such as iron play a central role in this latter process. Alterations in cellular macromolecules are most likely to take place if hydroxyl-radical formation is directed toward specific intramolecular sites by appropriately sequestered metals. For this reason, repair and turnover events are apt to be more important protective devices than are the actions of molecules which scavenge hydroxyl radicals. Although many cellular constituents are potential targets in free-radical and oxidant attacks leading to carcinogenesis, nucleic acids have been most extensively studied in this connection. On the basis of these investigations, it is a facile conclusion that oxidants might be involved in the early events of carcinogenesis as well as in transformation or promotion. The literature on antioxidants in chemoprevention in animals is supportive of such a role. However, other biochemical effects of antioxidants should raise a note of caution in the interpretation of animal experiments.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0027-5107
pubmed:author
pubmed:issnType
Print
pubmed:volume
202
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
363-75
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1988
pubmed:articleTitle
The nature of oxidants and antioxidant systems in the inhibition of mutation and cancer.
pubmed:affiliation
Institute for Toxicology, University of Southern California, Los Angeles 90033.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review