Dibenzofluoranthene-12,13-dihydrodiol (DBF-12,13-DHD) is six times more mutagenic in Salmonella TA100 than dibenzofluoranthene-3,4-dihydrodiol (DBF-3,4-DHD). However, these two major dibenzo[a,e]fluoranthene (DBF) proximate metabolites, which are immediate precursors of the corresponding diolepoxides, showed on an equimolar basis nearly identical initiation activities on mouse
The production by dibenzo[a,e]fluoranthene (DBF) of DNA-protein cross-links in cultured mouse fibroblasts is probably mediated by the activation of proximate metabolites of DBF and not by the DBF molecule itself. In order to test this hypothesis, several agents that enhance
Metabolic activation of dibenzo(a,e)fluoranthene, a nonalternant carcinogenic polycyclic hydrocarbon, in liver homogenates.
Quantitative and qualitative changes in the inhibition of DNA adduct formation in the presence of increasing concentrations of norharman (NH) were investigated in vivo in mouse fibroblasts treated with dibenzo[a,e]fluoranthene (DBF), a potent carcinogen in mice. The nuclease P1 modification
In vivo binding of dibenzo[a,e]fluoranthene (DBF) to mouse embryo fibroblast DNA was compared with that observed previously in vitro on calf thymus DNA incubated with mouse liver microsomes. The h.p.l.c. elution patterns of the adducts formed by DBF metabolites with
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