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

It has previously been shown that trichloroethylene (TCE) soot extracts cau se dioxin-like toxic effects in medaka fish (Oryzias latipes) and primary l iver cell culture of rainbow trout (Oncorhynchus mykiss). This study examin es embryonic and larval induction of cytochrome P450 1A and stress proteins after exposure of medaka embryos to extracts and fractions of TCE combusti on-generated aerosols. Embryos were exposed to three concentrations of whol e soot extract (WE; 2.7, 7.2 and 18 mug l(-1) incomplete combustion byprodu cts), TCDD (2,3, 7,8-tetrachlorodibenzo-p-dioxin, 3 ng l(-1)) and four TCE fractions with different polarity (Fr 1-4; 18 mug l(-1)) for 8 days. Approx imately 50% of the embryos were then transferred to control water and allow ed to hatch. EROD activity in embryos was significantly higher than in cont rols after the 8 day-exposure to TCE soot extract (WE), with activity being highest at 2.7 mug l(-1) WE (5.6x control). Of TCE fractions, only fractio n 1 (Fr1, non-polar compounds) caused a significant increase in EROD activi ty. In larvae, significantly induced EROD activity was detected following t he 7. 2 mug l(-1) WE treatment (3.30 pmol min(-1) mg prot.(-1)). Dioxin tre atment did not result in increased embryonal or larval EROD activity. Larva l CYP 1A was localized mainly in liver, gut, kidney, cornea and chondrocyte s of cranium and tail. Hsp70 was induced in larvae but not in embryos. Stat istically significant induction over controls was observed in two WE groups (2. 7, 7.2 mug l(-1)) and in the group exposed to dioxin (WE 18 mug l(-1) not analysed). Mean hsp60 levels were not significantly higher than control s. Apparent bacterial contamination may have induced hsp70 in one control g roup including embryos and larvae (C/Fr3).