THE CAPABILITIES OF FISH AND OTHER AQUATIC ORGANISMS FOR XENOBIOTIC METABOLISM

Abstract It is now recognized that marine and freshwater fish contain virtually all of the enzymatic pathways present in mammals for xenobiotic metabolism (1, 2). The cytochrome P-450-dependent monooxygenase system, essential for the oxidative metabolism of many pollutants, is present in the liver of every fish adequately studied, although activities are substantially lower for most substrates than in mammals. Administration of certain polycyclic aromatic hydrocarbons (PAH) to fish causes induction of the hepatic monooxygenase system although phenobarbital-type compounds apparently have no inductive effect in the fish studied. As in mammals, the large increases of hepatic monooxygenase activity after treatment with PAH-type chemicals are related to the presence of one or more novel forms of induced cytochrome P-450 in liver of the treated fish. Recent studies from our laboratory have demonstrated that large numbers (up to 84%) of feral winter flounder ( Pseudopleuronectes americanus ) from Maine have hepatic monooxygenase activities and properties indistinguishable from those of flounder treated with PAH-type inducers (1,2,3,4-dibenzanthracene, DBA; 5,6-benzoflavone, BNF). Thus, many of the fish had elevated 7-ethoxyresorufin deethylase and elevated benzo(a)pyrene hydroxylase (AHH) activities which were inhibited by in vitro 7,8-benzoflavone (ANF). Polyacrylamide gel electrophoresis of hepatic microsomes from flounder with elevated AHH activities, in the presence of SDS, showed a prominent band of approximate molecular weight 57,000; this band was absent or minor in fish with very low AHH activities. A major electrophoretic band of identical molecular weight (57 K) was also always present in hepatic microsomes from winter flounder treated with DBA or BNF. The data suggest that many feral winter flounder from Maine have induced monooxygenase activities because of exposure to certain chemicals in their environment. These pollutants could be of natural origin (flavonoids) or of anthropogenic origin (e.g., many PAH, certain PCB, PBB or chlorinated dioxin isomers) because chemicals in these classes are known to produce PAH-type induction of the hepatic monooxygenase system in fish.