EROD induction and biliary metabolite excretion following exposure to the water accommodated fraction of crude oil and to chemically dispersed crude oil

Citation
Rm. Gagnon et Da. Holdway, EROD induction and biliary metabolite excretion following exposure to the water accommodated fraction of crude oil and to chemically dispersed crude oil, ARCH ENV C, 38(1), 2000, pp. 70-77
Citations number
40
Categorie Soggetti
Environment/Ecology,"Pharmacology & Toxicology
Journal title
ARCHIVES OF ENVIRONMENTAL CONTAMINATION AND TOXICOLOGY
ISSN journal
00904341 → ACNP
Volume
38
Issue
1
Year of publication
2000
Pages
70 - 77
Database
ISI
SICI code
0090-4341(200001)38:1<70:EIABME>2.0.ZU;2-5
Abstract
Immature Atlantic salmon (Salmo salar) were exposed to water accommodated f raction (WAF) of Bass Strait crude oil or to Corexit 9527-dispersed crude o il for 6 days, followed by a depuration period of 29 days. Serum sorbitol d ehydrogenase (SDH) levels, indicator of liver damages, remained low during the experiment. Hepatic EROD activity was induced within 2 days following t he onset of the exposure in both treatments, and persisted for 2-4 and 4-6 days after transfer to clean sea water in the WAF and dispersed oil treatme nt, respectively. Naphthalene-type metabolites, determined by fixed-wavelen gth fluorescence detection, appeared in the bile of the fish with 2 days' d elay compared to EROD induction. In both treatments, EROD activity inductio n and levels of naphthalene-type metabolites in the bile were significantly related. The biliary levels of naphthalene-type metabolites were over 15 t imes higher in fish exposed to dispersed crude oil relative to fish exposed to the WAF of Bass Strait crude oil. BaP-type metabolites appeared only in the bile of the fish exposed to the WAF, possibly due to BaP-type compound s remaining associated with the dispersant in the water column or to an inh ibition of Phase II detoxification enzymes by the dispersant. Bile metaboli tes as determined by fixed-wavelength fluorescence and EROD induction appea r to be sensitive and complementary biomarkers of exposure to PAH.