ASSESSMENT OF THE BIOACTIVITY OF CREOSOTE-CONTAMINATED SEDIMENT OF LIVER BIOTRANSFORMATION SYSTEM OF RAINBOW TROUT LIVER
Tarja Hyötyläinen and Aimo Oikari
Department of Biology and Environmental Sciences, University of Jyväskylä, P.O. Box 35, FIN-40351 Jyväskylä, Finland
Cytochrome p-450 (CYP) superfamily comprises of an array of mono-oxygenases with various metabolic functions, including biotransformations of xenobiotic chemicals. CYP-system modifies the chemical structure of compounds by hydroxylation and related reactions, often making them more water soluble and excretable. Certain compounds, however, e.g. polycyclic aromatic hydrocarbons (PAH) may also be activated into products with ultimately toxic, mutagenic or carcinogenic properties. PAHs are readily absorbed by fish and other aquatic animals during exposure to contaminated water, sediment and food.
A sediment area in the Lake Jämsänvesi (municipality of Petäjävesi) contaminated by creosote has been investigated to assess possible ecotoxicological risks it may cause to benthic animals, including those which may evolve due to physical measures in remediating the contaminated site. We earlier determined the concentrations of PAHs in whole sediments and their elutriates (1 : 4 vol/vol), and measured the acute toxicity of the elutriates and pore waters by bacterial bioluminescence inhibition test and with water flea (Daphnia magna). The highest total concentration of PAHs in the sediment was 3.3 mg/g d.w. at the uppermost 0 - 10 cm layer, corresponding 1.7 mg/l in the elutriate. There was a distinct association between toxicities of elutriates and pore waters with highest concentrations of PAHs in the sediments (Chemosphere, in press). We can expect that when sediment and water mix with each others, like during dredging operations, toxic compounds spread from the sediment to the water column and impact the fish.
In order to further assess toxicological risks to fish, juvenile rainbow trout were exposed by intraperitoneal dosing to extracts of creosote-contaminated sediments from Lake Jämsänvesi and their elutriates. This was compared to pristine lake sediment spiked with creosote (6g creosote / 100g w.w reference sediment). Activity of CYP1A1 in trout liver was measured as ethoxyresorufin O deethylase, suggesting to indicate the sum bioactivity of creosote related PAHs mediated by aryl hydrocarbon receptor (AhR) in this organ. When compared to vechicle controls and pristine reference sediment (0.9 - 1.3 pmol/min/mg PMS protein), the extract of creosote-contaminated sediment of Lake Jämsänvesi induced EROD activity up to 20 û 30 times with dose 100 mg/kg (total PAHs (mg) / fish (kg)). With the dose 50 mg/kg, however, there was only minor tendency to increase EROD (2.1 pmol/min/mg prot.). Instead, the elutriate of this most-contaminated sediment site did not induce EROD. The creosote-spiked clean sediment, serving as positive control, revealed similar results with contaminated Lake Jõmsõnvesi sediment and its elutriates. Next the data on CYP1A1 responses in the liver will be further associated with metabolites of PAHs in the bile of trout. We conclude, this far, that although the creosote-contaminated sediment represents a potential threat to benthic animals at that site, there appears to develop only minor further toxicological impacts - as judged by AhR mediated bioactivity - due to particulate material which may become suspended with water under dredging operations.