Linked Life Data

7394317

Source:http://linkedlifedata.com/resource/pubmed/id/7394317

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1980-9-23
pubmed:abstractText
Acute or chronic treatment of Sprague-Dawley rats with N-2-fluorenylacetamide (2-FAA) significantly increased the capacity of hepatic microsomes for N-hydroxylation of 2-FAA. The optimal increases, 11- and 16-fold, were measured in hepatic microsomes of male and female rats, respectively, 24 hr after a single intraperitoneal injection of 0.67 mmole 2-FAA/kg of body weight. The increases in 2-FAA N-hydroxylating activity were not paralleled by any appreciable changes in the content of cytochrome P-450. After oral intake of 2-FAA, small increases in the content of cytochrome b5 and of total heme were measured. Gel electrophoresis showed the presence of a new protein, staining for heme, in the MW region of 46,000 as soon as 24 hr after treatment of rats with at least 0.34 mmole 2-FAA/kg of body weight. The intensity of this protein band was enhanced by prolonged treatment of rats with 2-FAA, but was not paralleled by the extent of induction of N-hydroxylation of 2-FAA. This protein was induced in hepatic microsomes of rats both susceptible (male) and nonsusceptible (female) to hepatocarcinogenesis by 2-FAA. The data suggest that the 2-FAA-induced protein may not be a specific marker of early preneoplastic changes in rat liver.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0034-5164
pubmed:author
pubmed:issnType
Print
pubmed:volume
28
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
53-64
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1980
pubmed:articleTitle
Effects of acute or chronic treatment of rats with N-2-fluorenylacetamide on its N-hydroxylation and on hemoproteins of hepatic microsomes.
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.