6533b82afe1ef96bd128b8ac

RESEARCH PRODUCT

Cytochrome P450 1A- and stress protein-induction in early life stages of medaka (Oryzias latipes) exposed to trichloroethylene (TCE) soot and different fractions

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It has previously been shown that trichloroethylene (TCE) soot extracts cause dioxinlike toxic effects in medaka fish (Oryzias latipes) and primary liver cell culture of rainbow trout (Oncorhynchus mykiss). This study examines embryonic and larval induction of cytochrome P450 1A and stress proteins after exposure of medaka embryos to extracts and fractions of TCE combustien-generated aerosols. Embryos were exposed to three concentrations of whole soot extract (WE; 2.7, 7.2 and 18 μg l -1 incomplete combustion by-products), TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin, 3 ng l -1 ) and four TCE fractions with different polarity (Fr 1-4; 18 μg l -1 ) for 8 days. Approximately 50% of the embryos were then transferred to control water and allowed to hatch. EROD activity in embryos was significantly higher than in controls after the 8 day-exposure to TCE soot extract (WE), with activity being highest at 2.7 μg l -1 WE (5.6× control). Of TCE fractions, only fraction 1 (Fr1, non-polar compounds) caused a significant increase in EROD activity. In larvae, significantly induced EROD activity was detected following the 7.2 μg l -1 WE treatment (3.30 pmol min -1 mg prot. -1 ). Dioxin treatment did not result in increased embryonal or larval EROD activity. Larval CYP 1A was localized mainly in liver, gut, kidney, cornea and chondrocytes of cranium and tail. Hsp70 was induced in larvae but not in embryos. Statistically significant induction over controls was observed in two WE groups (2.7, 7.2 μg l -1 ) and in the group exposed to dioxin (WE 18 μg l -1 not analysed). Mean hsp60 levels were not significantly higher than controls. Apparent bacterial contamination may have induced hsp70 in one control group including embryos and larvae (C/Fr3).