Xenobiotics in gametes of Lake Michigan lake trout ( Salvelinus namaycush) induce hepatic monooxygenase activity in their offspring

• Published in: Fundamental and applied toxicology 1984-12, Vol.4 (6), p.1042-1054
• Main Authors: Binder, Robert L., Lech, John J.
• Format: Article
• Language: English
• Subjects: Animals; Aroclors - toxicity; Aryl Hydrocarbon Hydroxylases - metabolism; Benzoflavones - toxicity; Chlorodiphenyl (54% Chlorine); Cytochrome P-450 Enzyme System - metabolism; Embryo, Nonmammalian - drug effects; Enzyme Induction - drug effects; Female; In Vitro Techniques; Liver - enzymology; Microsomes, Liver - metabolism; Mixed Function Oxygenases - metabolism; Ovum - metabolism; Salmonidae - metabolism; Trout - metabolism; Water Pollutants - toxicity; Water Pollutants, Chemical - toxicity
• ISSN: 0272-0590; 1095-6832
• DOI: 10.1016/0272-0590(84)90244-6

Eggs spawned from Lake Michigan lake trout contain a number of xenobiotic compounds, including polychlorinated biphenyls (PCBs). To assess whether this contamination is sufficient to induce hepatic cytochrome P-450-dependent monooxygenase (MO) activity during early development, the hepatic MO systems of laboratory-cultured offspring of Lake Michigan, Green Bay, and Marquette Hatchery lake trout were compared. Additionally, the induction of hepatic cytochrome P-450 systems in developing lake trout by the commercial PCB mixture, Aroclor 1254 (A1254), was characterized. During late embryonic development and at the swim-up stage, the hepatic MO systems of the feral lake trout offspring appeared induced, based on levels of aryl hydrocarbon hydroxylase (AHH) activity that were 3.5- to 8.6-fold higher than the hatchery control levels. Furthermore, at the swim-up stage the feral trout offspring resembled A1254-treated hatchery fry with regard to the degree of inhibition of hepatic AHH activity by α-naphthoflavone, and the presence of an inducible M r = 58,000 polypeptide in hepatic microsomes. The levels of aminopyrine N-demethylase activity, which was relatively unresponsive to inducers, were moderately lower in the Lake Michigan and Green Bay swim-up fry compared to the hatchery control levels. After 7 months of posthatching laboratory culture, when residues of xenobiotics present at fertilization were greatly diluted by growth, the hepatic MO systems of the Lake Michigan and hatchery trout offspring appeared essentially indistinguishable with regard to a number of parameters. These results indicate that the differences observed between the hatchery and feral trout offspring at earlier stages were not likely to have a genetic basis, but rather were due to a xenobiotic-type induction. Dose-response experiments and residue analysis data indicated that residues of commercial PCB mixtures were at least partially responsible for the effects described here. Overall, these data provide very strong evidence that contamination of Lake Michigan lake trout gametes by PCBs and possibly other xenobiotics caused induction of hepatic MO activity in their progeny. Fish embryos and fry with induced MO systems may have an increased sensitivity to the toxicity of certain environmental contaminants that are metabolically activated by cytochrome P-450.