Abstract

AbstractInduction of the hepatic detoxification enzyme cytochrome P4501A has been observed in fish exposed to bleached‐kraft mill effluents (BKME). P4501A content was examined in three species of wild fish exposed to BKME in a western Canadian river as part of an extensive program that included chemical monitoring, fish population studies, and other fish biochemical and physiological measurements. The Rocky Mountain whitefish Prosopium williamsoni exhibited marked induction of P4501A compared to reference whitefish, as measured by both catalytic activity and immunoreactive protein content. Similar P4501A induction was observed 4 d after reference fish were treated with 20 mg/kg β‐naphthoflavone. Whitefish P4501A levels have declined from a peak in spring 1991, following mill process modifications and concurrent with reductions in body burdens of hydrophobic compounds. Whitefish collected near the mill, moved upstream of effluent discharges, and held for 8 d showed no significant loss of hepatic P4501A‐related (ethoxyresorufin O‐deethylase, EROD) enzyme activity or P4501A protein levels. For spring 1991, correlations were found between EROD activity and measures of chronic exposure to BKME (e.g., muscle 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin content), but not between EROD and measures of acute exposure (e.g., bile content of resin acids or chlorophenolic metabolites). These and other lines of evidence indicate that the P4501A‐inducing agent(s) at this site may be neither waterborne nor rapidly eliminated. A second species, longnose sucker (Catostomus catostomus), collected near the mill exhibited modest (two‐ to threefold) P4501A induction. For both species, no significant correlations between P4501A induction and trends in other biological responses were found, as described in a companion paper. Burbot (Lota lota) had hepatic EROD activities generally in the range of reference values, despite substantial exposure to mill‐related compounds. In contrast to studies at historically degraded pulp mill sites, P4501A induction is the only major biological response observed to date at this site. As P4501A induction is not related to adverse effects, it could be best classified as an indicator of exposure to BKME.

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