However, the significant up-regulation of CYP2B
and CYP3A by BDE-47 was also achieved at high doses of 4.
Given that berberine metabolism involves CYP3A and CYP2B
in the rat (Liu et al.
1997) were as follows: Wolff group 1A, potentially estrogenic, weak phenobarbital inducers, not persistent congeners (PCB-52); Wolff group 2A, potentially antiestrogenic and immunotoxic, dioxin-like, non-ortho--and mono-ortho-substituted, moderately persistent congeners (PCB-74, PCB-105, PCB-118); Wolff group 2B, limited dioxin activity, di-ortho substituted, persistent congeners (PCB-138, PCB-170) and Wolff group 3, phenobarbital inducers, CYPlA and CYP2B
inducers, and persistent congeners (PCB-153, PCB-180, PCB-203).
In the current study, researchers grouped congeners on the basis of their reported abilities to induce the enzymes UDP-GT, CYP1A, and CYP2B
Although tolbutamide hydroxylation has been shown to be increased following phenobarbital (an inducer of CYP2B
in rat liver) pretreatment (Veronese et al.
Other PCB congeners have a phenobarbital-like induction pattern which is characterized by the induction of CYP2B
and UGT1A1 (Sugatani et al.
Although only the phenobarbital treated group showed a significant increase in CYP1 and CYP2-3 activities, bergamottine and isopimpinellin treated animals showed an increase in CYP2B
In the dietary-restricted group administered 100 mg/kg CH, of the enzymes associated with PPAR[alpha] agonism (total CYP, CYP2B
isoform, CYP4A, or lauric acid [omega]-hydroxylase activity), only CYP4A and lauric acid [omega]-hydroxylase activity were increased at 15 months of exposure.
Chronic administration of P1G10 into rats does not seem to alter the activity of several microsomal P450 enzymes (unpublished results), while omeprazole enhances the activity of CYPA1/2, CYP2B
and CYP3A1/2 and the activity of NADP-dependent cytochrome reductase (Masubuchi et al.
1988) hypothesized that cetaceans do not possess a group of cytochrome P450 enzymes (known as CYP2B
isoenzymes) responsible for the oxidation and activation of halogenated aromatic hydrocarbons, suggesting that these species accumulate some of the toxic PCB congeners and are therefore more susceptible to their long-term effects (Boon et al.
The three structure-activity groups of PCBs were, for group 1, potentially estrogenic and weak phenobarbital inducers (PCB congeners 44, 49, 52, 101, 187, 174, 177, and 157/201); group 2, potentially antiestrogenic and dioxin-like PCBs (PCB congeners 95/66, 74, 77/110, 105/141, 118, 156, 167, 128, 138, and 170); and group 3, phenobarbital and CYP1A and CYP2B
inducers (PCB congeners 99, 153, 180, 196/203, and 183).
This binding induces phase I and phase II metabolic enzymes; mono-ortho PCBs may therefore induce CYP1A and CYP2B
enzymes that, in the absence of substrate, can produce reactive oxygen species.