On the metabolic activation of benz[a]acridine and benz[c]acridine by rat liver and lung microsomes.
Cancer Lett
; 16(3): 297-306, 1982 Sep.
Article
em En
| MEDLINE
| ID: mdl-7151049
ABSTRACT
The metabolism of benz[a]- and benz[c]acridine by liver and lung microsomes from untreated, phenobarbital (PB)-treated and benzo[k]fluoranthene (BkF)-treated rats has been studied by gas chromatography/mass spectrometry (GC/MS). Epoxidation and hydrolysis of the epoxides to dihydrodiols were found to be the predominant pathways for all substrates. N-Oxidation is likely to occur in the case of benz[c]acridine. However, no unequivocal evidence could be obtained for the formation of the ultimate carcinogens--the t-3,4-dihydrodiol-1,2-epoxides--in case of both benz[a]- and benz[c]acridine. K-Region oxidation was induced by phenobarbital, whereas the formation of non-K-region metabolites increased after BkF treatment in the case of benz[c]acridine.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Acridinas
/
Microssomos Hepáticos
/
Carcinógenos
/
Pulmão
/
Microssomos
Limite:
Animals
Idioma:
En
Revista:
Cancer Lett
Ano de publicação:
1982
Tipo de documento:
Article