Linked Life Data

6120542

Source:http://linkedlifedata.com/resource/pubmed/id/6120542

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1982-4-22
pubmed:abstractText
Incubation of hepatic microsomes from phenobarbital treated rats, 1,1,1-trichloropropene-2,3-oxide (TCPO) (3 mM), EDTA (0.2 mM) and NADPH-gene-rating system in vitro decreased the levels of cytochrome P-450 by 40% and equivalently decreased microsomal heme. Appreciable losses of cytochrome P-450 were not observed [1] if metyrapone (2.3 mM) or CO:O2 (80:20; v/v) were included in incubation mixtures, [2] if the TCPO or NADPH-gene-rating system were omitted from reaction mixtures, or [3] if microsomes from untreated or beta-naphthoflavone treated rats were utilized. The time course for the TCPO mediated loss of hepatic microsomal cytochrome P-450 showed a time lag of 5 min, before the levels of cytochrome P-450 were significantly altered, followed by a 10-15 min period in which the levels of cytochrome P-450 rapidly decreased to a non-zero plateau level. The concentration of TCPO required for half maximal loss of cytochrome P-450 was ca. 0.5 mM. In the absence of cytochrome P-450 degradation, TCPO (2 mM) was an effective inhibitor of aminopyrine demethylase and benzpyrene-3-hydroxylase but not of p-nitroanisole demethylase or ethoxyresorufin deethylase. In contrast, the degradation of cytochrome P-450 by TCPO strikingly decreased ethoxyresorufin deethylase and to a lesser extent p-nitroanisole demethylase. A reaction mechanism is proposed for the TCPO mediated degradation of cytochrome P-450 in vitro.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0034-5164
pubmed:author
pubmed:issnType
Print
pubmed:volume
35
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
111-20
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1982
pubmed:articleTitle
1,1,1-Trichloropropene-2,3-oxide: an alternate mechanism for its inhibition of cytochrome P-450.
pubmed:publicationType
Journal Article, In Vitro