Linked Life Data

6433187

Source:http://linkedlifedata.com/resource/pubmed/id/6433187

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1984-10-24
pubmed:abstractText
L-Ethionine is an ethyl analogue of the amino acid, methionine, well known as a carcinogen but not as a mutagen. Its activity is clearly related to its capacity to hypomethylate DNA and RNA. At a final concentration of 5 mM, L-ethionine completely inhibits DNA synthesis in PHA-stimulated human lymphocytes, probably acting on a methylation reaction critical for the initiation of the S phase. This block can be reversed. Utilizing this capacity of L-ethionine to block cell proliferation, we have studied the influence of G0 and G1 repair of premutational damage (PMD) (equivalent to liquid-holding recovery in bacteria) on spontaneous and MMC-induced SCEs in human lymphocytes. Our results clearly show that L-ethionine in our experimental conditions significantly increases the frequencies of spontaneous and MMC-induced SCEs. In view of the hypomethylating activity of the analogue, we hypothesize that this action at the replication fork level may increase the error-prone ligation of unrepaired lesions, thus influencing the frequency of occurrence of SCEs.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0027-5107
pubmed:author
pubmed:issnType
Print
pubmed:volume
128
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
153-9
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1984
pubmed:articleTitle
Effect of L-ethionine on spontaneous and MMC-induced SCEs in G0 and G1 human lymphocytes under liquid-holding recovery conditions.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't