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Chronic retene exposure causes sustained induction of CYP1A activity and protein in rainbow trout ( Oncorhynchus mykiss )
Author(s) -
Fragoso Nuno M.,
Parrott Joanne L.,
Hahn Mark E.,
Hodson Peter V.
Publication year - 1998
Publication title -
environmental toxicology and chemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.1
H-Index - 171
eISSN - 1552-8618
pISSN - 0730-7268
DOI - 10.1002/etc.5620171127
Subject(s) - rainbow trout , effluent , paper mill , chemistry , pulp (tooth) , pulp mill , environmental chemistry , phenanthrene , toxicity , pulp and paper industry , biology , fish <actinopterygii> , environmental science , fishery , environmental engineering , organic chemistry , medicine , pathology , engineering
The removal of persistent chlorinated organic compounds from pulp mill effluents has not eliminated mixed function oxygenase (MFO) induction by these effluents. Therefore, continuous MFO induction downstream of pulp mills may be due to exposure to more labile compounds, such as retene (an alkyl‐substituted phenanthrene), which typically cause transient induction after a single brief exposure. Because fish are exposed continuously to pulp mill effluents, we have tested, and rejected, the null hypothesis that continuous exposure of fish to retene does not cause sustained MFO induction. Rainbow trout exposed continuously to retene, a component of some pulp mill effluents and sediments downstream of pulp mills, showed concentration‐dependent increases in hepatic ethoxyresorufin‐ O ‐deethylase (EROD) activity. The increase in EROD activity was sustained over 32 d of continuous exposure, but it diminished to background levels within 4 d after transfer to clean water. The enzymatic response was confirmed by measuring changes in the content of immunodetectable cytochrome P4501A (CYP1A) protein. These data support a role for labile, nonhalogenated compounds in chronic effects of pulp mill effluents on fish.