|Document Type:||Contract Report|
|Title:||Interactive effects of aromatic hydrocarbons, their derivatives, and heavy metals in marine fish|
|Author/Editor:||Edward H. Gruger, Joyce W. Hawkes, Donald C. Malins|
|Publisher:||National Marine Fisheries Service|
|Contracting Agency:||U.S. Environmental Protection Agency. Washington, D.C|
|Keywords:||combined toxins, aromatic hydrocarbons, PCBs, lead, salmon,|
Marine organisms living in environments containing toxic chemicals are often exposed simultaneously to many different classes of compounds, which collectively pose a different threat of toxicological effects than is posed separately by the individual compounds. The present research was directed toward elucidating the effect of xenobiotics which alter the metabolism and toxicity of aromatic hydrocarbons by marine fish, as evinced through biochemical changes and altered cellular morphology. The xenobiotics used included petroleum aromatic hydrocarbons, chlorinated biphenyls, p-cresol, cadmium, and lead.
Coho salmon Oncorhynchus kisutch, maintained in seawater at 7°C and fed model mixtures containing chlorobiphenyls, petroleum hydrocarbons, and a mixture of the two classes of compounds, were examined for uptake of these chemicals in liver, kidney, and residual body tissues comprised of eviscerated, headless and tailless carcass; and for possible changes in the activities of hepatic microsomal aryl hydrocarbon hydroxylase (AHH). Analyses of the coho salmon tissues indicated that the concentrations of individual chlorobiphenyls were highly variable; the concentrations of the hydrocarbons were below detection limits, suggesting that they were metabolized and/or excreted by the fish. In addition, the activities of hepatic AHH were induced by mixtures of the chlorobiphenyls and petroleum hydrocarbons, but not by the chlorobiphenyls alone or hydrocarbons alone. An apparent synergism, reflected by increased AHH activities, occurred when the chlorobiphenyls and hydrocarbons were administered together.
Chinook salmon Oncorhynchus tshawytscha, maintained in seawater at 13°C and fed mixtures of chlorobiphenyls and petroleum hydrocarbons separately and together, were examined for changes in hepatic microsomal AHH activity and for alterations in the morphology of liver, kidney, intestine, gill and skin tissues. The data suggested that the AHH activity was affected differently for chinook than for coho salmon. Using chinook salmon microsomes, AHH activities were found depressed for all fish treated with either the chlorobiphenyls or the hydrocarbon mixture. In addition, morphological changes relating to inclusions in the cells of the intestinal mucosa were observed for chinook salmon fed either hydrocarbons or chlorobiphenyls; whereas, considerable sloughing of the mucosal epithelium occurred in fish treated with the combined mixtures. The latter finding also indicated an interactive effect of the two classes of xenobiotics. Additional alterations were found in some hepatocytes, but not in the other tissues.
The differences for the coho and chinook salmon in terms of the responses of the hepatic AHH systems to petroleum hydrocarbons and chlorobiphenyls may have been caused by differences due to seasonal parameters between the two experiments. Hence, depending on the temperatures, normal biotransformations of petroleum in exposed marine organisms may be enhanced or retarded, assuming no species differences. These xenobiotic effects may be influential factors in marine environments.
Coho salmon and starry flounder Platichthys stellatus, exposed to 200 ppb of cadmium or lead in seawater at l0°C, were fed a model mixture of polycyclic aromatic hydrocarbons (PAHs) consisting of 2-nethylnaphthalene, 2,6-dimethylnaphthalene, and phenanthrene. The effects of the metals were determined on the AHH activity of liver microsomes. (Concentrations of cadmium and lead in livers were not determined.) The results suggest that hepatic hydroxylations of PAHs, using naphthalene as a substrate, are not affected by exposure of fish to these metals at 200 ppb. Addition of 4–5 ppm cadmium to reaction mixtures containing liver microsomes caused 82–98% inhibition of AHH activity