Linked Life Data

12889515

Source:http://linkedlifedata.com/resource/pubmed/id/12889515

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5-6
pubmed:dateCreated
2003-7-31
pubmed:abstractText
Genetic regulation of acetyl coenzyme A-dependent N-acetyltransferase (NAT)and O-acetyltransferase (OAT) activities may play an important role in the metabolic activation of arylamine chemicals and carcinogens. N-acetylation is thought to be the first step in arylamine metabolism. The enzyme responsible for N-acetylation is called NAT. In this study, synthetic non-steroidal antiestrogen tamoxifen was selected for determining the inhibition of arylamine NAT activity, gene expression (NAT mRNA) and DNA-2-aminofluorene adduct formation in human leukemia HL-60 cell line. The results demonstrated that tamoxifen did not affect the level of NAT mRNA in HL-60 cells. But the results also showed that NAT activity and 2-Aminofluorene-DNA adduct formation in HL-60 cells were inhibited and decreased by tamoxifen in a dose-dependent manner when the doses of tamoxifen up to 100 micro M. We also examined the standard steady-state kinetic analysis, and the data showed that tamoxifen may be an uncompetitive inhibitor to NAT activity in cytosols based on the decrease apparent values of Km and Vmax. This report is the first finding that tamoxifen inhibited human leukemia HL-60 cells NAT activity and DNA-2-aminofluorene on adduct formation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1078-0297
pubmed:author
pubmed:issnType
Print
pubmed:volume
109
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
319-31
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Tamoxifen inhibits arylamine N-acetyltransferase activity and DNA-2-aminofluorene adduct in human leukemia HL-60 cells.
pubmed:affiliation
Institute of Medicine, Chung Shan Medical & Dental College, Taichung, Taiwan, ROC.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't