In order to assess the differences in the ability of fish and rat liver to
metabolize carcinogenic polycyclic aromatic hydrocarbons (PAHs), we have in
vestigated the metabolism of dibenzo[a,l]pyrene (DB[a,l]P), a highly potent
carcinogenic PAH, by liver microsomes from 3-methylcholanthrene-treated Sh
asta rainbow trout (Oncorhynchus mykiss) and rats. Rat liver microsomes met
abolized DB[a,l]P at a slightly higher rats (1.3-fold) than trout liver mic
rosomes. Compared to benzo[a]pyrene (B[a]P), DB[a.l]P was metabolized at a
significantly lower rate by both rat and trout liver microsomes. Although t
he microsomes from the two species metabolized DB[a.l]P to qualitatively si
milar metabolites, they showed significant differences in the profile of th
e metabolites formed. The proportion of DB[a,l]P-11,12-diol, the proximate
carcinogen of DB[a,l]P, formed by trout microsomes was over two-fold greate
r (32.6%:) than the corresponding value for rat microsomes (15.6%). Unlike
rat microsomes, trout microsomes metabolized DB[a,l]P to its K-region diol
(8.9-diol) to a small extent (26.1 vs 3.6%). As previously noted with B[a]P
, trout liver, compared to rat liver, appears to be more efficient in formi
ng the proximate carcinogenic metabolite of DB[a.l]P but less efficient in
producing its K-region diol, a non-carcinogenic metabolite. (C) 1999 Elsevi
er Science B.V. All rights reserved.