Abstract

Nickel is occurs naturally in the geophysical environment. It has become a common byproduct of industrialization. Nickel is released into the atmosphere and coal-burning power plants and trash incinerators, and is also discharged into waste water by industries which convert scrap or new nickel into alloys. The effluent that spreads to streams, rivers, and lakes may disrupt the integrity of the aquatic environment. Excess nickel contamination is hazardous to aquatic ecosystems due to its existence and bioaccumulation. While the adverse health effects associated with nickel exposure have been extensively examined in mammalian systems, very little is known concerning nickel's effects on aquatic organisms. Although trace amounts of nickel are necessary for maintaining the metabolic homeostasis of some vertebrate species, larger amounts of nickel have been shown to be toxic. In addition to being both genotoxic and carcinogenic, nickel modulates immunological functions in a variety of mammalian species. The toxic effects of nickel on the numbers, activity, and ultrastructure of macrophages (M[o]) have been well-studied. A number of other toxic metals such as copper, manganese, and cadmium modulate the immune responses of fish. To appraise the immunomodulating potential of nickel on fish, and to begin to establish baseline parameters of alteredmore » immune function as potential biomarkers of in vivo nickel exposure, elicited peritoneal macrophages from rainbow trout (Oncorhynchus mykiss) were treated in vitro with increasing concentrations of nickel sulfate (NiSO[sub 4]). Following exposure, M[o] activities important for maintaining host immunocompetence were evaluated and these include; mobility (random and stimulus-directed), production of reactive oxygen intermediates (ROI), acid phosphatase activity, and phagocytosis. 20 refs., 3 figs.« less

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