Abstract

In order to assess the differences in the ability of fish and rat liver to metabolize carcinogenic polycyclic aromatic hydrocarbons (PAHs), we have investigated the metabolism of dibenzo[a,l]pyrene (DB[a,l]P), a highly potent carcinogenic PAH, by liver microsomes from 3-methylcholanthrene-treated Shasta rainbow trout ( Oncorhynchus mykiss) and rats. Rat liver microsomes metabolized DB[a,l]P at a slightly higher rate (1.3-fold) than trout liver microsomes. 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 the microsomes from the two species metabolized DB[a,l]P to qualitatively similar metabolites, they showed significant differences in the profile of the 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 greater (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 forming the proximate carcinogenic metabolite of DB[a,l]P but less efficient in producing its K-region diol, a non-carcinogenic metabolite.

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