A new silicone-based agent was developed to treat and recover oil slicks and various floating oily residues that are often observed in marinas and harbors. As part of its ecotoxicologic assessment, the fate of the treating agent alone or combined with crude oil, and the effects on natural microbial communities were studied in estuarine mesocosms (3.5 m 3 ) over a 9-week period. The ability of the in situ formed silicone layer to trap an oil slick at the water surface was highlighted by a significative reduction in the volatilization, natural dispersion, and sedimentation of the treated oil. The treatment favored the dissolution of light aromatic hydrocarbons such as methyl-naphthalenes but these compounds were rapidly biodegraded in the water column. The agent alone, as well as the treated or untreated oil, had no effect on the biomass and photosynthetic ability of the phytoplankton community entrapped in the mesocosms. A significant stimulation of oil-degrading bacteria was noted in mesocosms containing treated and untreated oil slicks. On the basis of these results, we conclude that the use of a silicone-based treating agent could be an effective countermeasure to an oil spill, with neither deleterious effects to natural microbial communities nor to long-term biodegradation of the unrecovered oil residues.
Abstract-Tributyltin (TBT), an organometal used as an antifouling biocide, has been reported to inhibit cytochrome P450 (P450) 1A isozyme. Benzo [a]pyrene (BaP), a widespread carcinogenic polycyclic aromatic hydrocarbon, is both metabolized and bioactivated to carcinogenic BaP diol-epoxide (BPDE) metabolites primarily by hepatic P450 1A. Hence, TBT may inhibit the metabolism and bioactivation of BaP. This study was therefore designed to examine the potential in vivo interactions between BaP and TBT in a model fish. Male brook trout (Salvelinus fontinalis) were given a single intraperitoneal injection of either BaP (10 mg/kg), TBT (10 mg/kg), or both in combination. After 48 h, blood, bile, and liver samples were collected and analyzed for a suite of biomarkers associated with P450 activity, BaP metabolism and bioactivation, and TBT metabolism. The results showed that TBT significantly ( p Ͻ 0.05; two-way analysis of variance) inhibited (a) the induction of hepatic P450 1A-mediated ethoxyresorufin Odeethylase (EROD) and P450-mediated 3-cyano-7-ethoxycoumarin-O-deethylase (CN-ECOD) activities by BaP, (b) the formation of biliary BaP metabolites, and (c) the formation of (ϩ)-anti-BPDE-plasma albumin adducts as measured by high-performance liquid chromatography/fluorescence. Notably, TBT alone did not inhibit EROD activity but induced CN-ECOD activity ( p Ͻ 0.05). Gas chromatography/mass spectrometry analysis indicated that the combined BaP ϩ TBT dose resulted in higher levels of dibutyltin metabolites in the bile ( p Ͻ 0.05). The present study supports the hypothesis that a single, high dose of TBT can antagonize the metabolism and bioactivation of BaP at least by inhibiting the induction of P4501A. On the other hand, BaP unexpectedly potentiated the metabolism of TBT, suggesting that hepatic isoforms other than P4501A may be responsible for TBT metabolism. Finally, this study supports the utility of a biomarker approach to screen potential xenobiotic interactions in aquatic organisms and to obtain mechanistic insights.
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