Monooxygenase induction and lethality as endpoints in aquatic toxicology

Spot, Leiostomus xanthurus, were exposed to suspended sediments (&\approx&20 mg/L) contaminated with polycyclic aromatic hydrocarbons (PAH) in a laboratory flow-through system to evaluate the applicability of hepatic ethoxyresorufin O-deethylase (EROD) induction as an indicator of PAH exposure. PAH sources tested were coal-tar creosote (CTC), a low molecular weight fraction of creosote (LMWF), and a high molecular weight fraction of creosote (HMWF). A standard 96-h acute toxicity test was conducted to ensure that PAH concentrations tested in induction studies were sub-acutely toxic. The 96-h LC50 for spot was 1740 &\mu&g PAH/L (95% confidence interval = 1480-2060 &\mu&g PAH/L). The lowest concentration producing an observable effect in 96 h was 560 &\mu&g PAH/L; no effects were observed for spot exposed to 250 &\mu&g PAH/L for 96 h. Induction of hepatic EROD activity occurred rapidly in fish exposed to high environmentally realistic concentrations of CTC or the HMWF, but not the LMWF. Maximal induction (30-fold) occurred in fish exposed for 48 h to 150 &\mu&g PAH/L. Induction was concentration-dependent up to 150 &\mu&g PAH/L; at 320 &\mu&g PAH/L induction was 14-fold. EROD activity decreased upon further exposure; by day 7, EROD activity was not significantly different than that on day 0. EROD activity in fish exposed to 16 &\mu&g PAH/L was not consistently higher than that in control fish. Spot exposed to at least 70 &\mu&g PAH/L from CTC or the HMWF experienced severe fin erosion, epidermal lesions, and mortality beginning a few days after maximal EROD induction occurred. No relationship between EROD induction and whole animal responses is implied, only that EROD induction did precede any high order effects. These results indicate complications to the use of EROD activity as a sensitive, reliable indicator of PAH exposure. The toxicity of CTC may inhibit or interfere with continued induction of EROD activity, but neither the toxicity nor inducing capability is associated with the LMWF. The lack of exposure-dependent EROD induction indicate there could be difficulties in interpreting field studies, where fish have unknown exposure histories

Effects of Dose, Administration Route, and/or Vehicle on Decabromodiphenyl Ether Concentrations in Plasma of Maternal, Fetal, and Neonatal Rats and in Milk of Maternal Rats

The effects of route and vehicle on blood and milk levels of decabromodiphenyl ether (DecaBDE; CASRN 1163-19-5) were investigated in the rat to assist in the design and conduct of a developmental neurotoxicity study. Blood plasma and/or milk concentrations were determined in dams, fetuses, and/or nursing pups after repeated DecaBDE administration by gavage throughout gestation or gestation and lactation using corn oil (CO) or soyaphospholipon/Lutrol F 127-water (SPL) as the vehicle. The impact of vehicle on plasma levels was also investigated in pups derived from naive dams after a single postnatal dose. This study reports for the first time fetal and neonatal plasma concentrations concurrent with those of maternal plasma and/or milk. Higher concentrations of DecaBDE were achieved in plasma and in milk with CO than with SPL. Furthermore, pups derived from dams treated with only SPL were lower in body weight, compared with those from dams treated with either CO, CO and DecaBDE, or SPL and DecaBDE. The study further shows that exposure to DecaBDE is relatively consistent across the dose range of 100 to 1000 mg/(kg . day) when administered in CO