Trophic transfer of copper decreases the condition index in Crassostrea gigas spat in concomitance with a change in the microalgal fatty acid profile and enhanced oyster energy demand.

Due to new usages and sources, copper (Cu) concentrations are increasing in the Arcachon Basin, an important shellfish production area in France. In the present paper, the trophic transfer of Cu was studied between a microalga, Tetraselmis suecica, and Crassostrea gigas (Pacific oyster) spat. An experimental approach was developed to assess Cu exposure, transfer and toxicity on both phytoplankton and spat. Exposure of microalgal cultures to Cu for 7-8 days (3.1 ± 0.1, 15.7 ± 0.2 and 50.4 ± 1.0 µg Cu·L-1 for the control, Cu15 and Cu50 conditions, respectively) led to concentrations in microalgae (28.3 ± 0.9 and 110.7 ± 11.9 mg Cu·kg dry weight-1 for Cu15 and Cu50, respectively) close to those measured in the field. Despite Cu accumulation, the physiology of the microalgae remained poorly affected. Exposed cultures could only be discriminated from controls by a higher relative content in intracellular reactive oxygen species, and a lower relative content in lipids together with a reduced metabolic activity. By contrast, the fatty acid profile of microalgae was modified, with a particularly relevant lower content of the essential polyunsaturated fatty acid 22:6n-3 (docosahexaenoic acid [DHA]). Following 21 days of spat feeding with Cu15 and Cu50 microalgal cultures, trophic transfer of Cu was observed with a high initial Cu concentration in spat tissues. No effect was observed on oxidative stress endpoints. Cu exposure was responsible for a decrease in the spat condition index, an outcome that could be related to an insufficient DHA supply and extra energy demand as suggested by the overexpression of genes involved in energy metabolism, ATP synthesis and glycogen catabolism.

Dietary exposure of juvenile common sole (Solea solea L.) to polybrominated diphenyl ethers (PBDEs): Part 1. Bioaccumulation and elimination kinetics of individual congeners and their debrominated metabolites.

The uptake and elimination of six PBDE congeners (BDE-28, -47, -99, -100, -153, -209) were studied in juvenile common sole (Solea solea L.) exposed to spiked contaminated food over a three-month period, then depurated over a five-month period. The results show that all of the studied PBDEs accumulate in fish tissues, including the higher brominated congener BDE-209. Several additional PBDE congeners were identified in the tissues of exposed fish, revealing PBDE transformation, mainly via debromination. The identified congeners originating from PBDE debromination include BDE-49 and BDE-202 and a series of unidentified tetra-, penta-, and hepta- BDEs. Contaminant assimilation efficiencies (AEs) were related to their hydrophobicity (log Kow) and influenced by PBDE biotransformation. Metabolism via debromination appears to be a major degradation route of PBDEs in juvenile sole in comparison to biotransformation into hydroxylated metabolites.

Relationship between PAH biotransformation as measured by biliary metabolites and EROD activity, and genotoxicity in juveniles of sole (Solea solea).

Polycylic aromatic hydrocarbons (PAHs) are ubiquitous contaminants in the marine environment. Their toxicity is mainly linked to the ability of marine species to biotransform them into reactive metabolites. PAHs are thus often detected at trace levels in animal tissues. For biomonitoring purposes, this findings have two main consequences, (i) the determination of the PAH tissue concentration is not suitable for the evaluation of individual exposure to PAHs (ii) it can explain sometimes the lack of correlations obtained with relevant markers of toxicity such as genotoxicity biomarkers. The aim of the present study was to better investigate the link between PAH exposure and genotoxicity in marine flatfish. During a laboratory experiment, juvenile soles were exposed for four weeks to a mixture of three PAHs, namely benzo[a]pyrene, fluoranthene and pyrene, followed by one week of depuration. Fish were exposed via the trophic route to a daily PAH concentration of 120 µg/g food. Fish were sampled at different time points. The bioavailability and the biotransformation of PAHs were assessed by the measurement of biliary metabolites using a sensitive UPLC MS/MS method. The 7-ethoxyresorufine-O-deethylase was also measured in liver subcellular fractions as a biomarker of phase I biotransformation activities. Genotoxicity was assessed in parallel by the measurement of DNA strand breaks in fish erythrocytes by the alkaline comet assay. During this study, the high amount of PAH metabolites produced in sole demonstrated the bioavailability of PAHs and their biotransformation by fish enzymes. A positive correlation was observed between the level of hydroxylated PAH metabolites and genotoxicity as measured by the alkaline comet assay.

Acute toxicity of fluorescein to turbot (Scophthalmus maximus).

Some land-based marine fish-farms situated on the Atlantic coastline of France use high volumes of underground sea water. Studies of the available quantities and movements of this underground resource became necessary, using fluorescent dyes such as fluorescein. As fluorescein may reach reared fish, it became important to assess its toxicity to fish. Acute fluorescein toxicity to turbot (Scophthalmus maximus) was investigated by exposing fish to different fluorescein concentrations (0.5, 0.7, 0.9, 1.1 and 1.3 milligrams) at 14.0 C for 24, 48 or 96 h. The lethal concentration inducing 50% fish mortality (LC50) was 997.1 +/- 11.4 mg/l (mean +/- standard deviation) after a 24, 48 or 96 h exposure. Toxicity affected the central nervous system. Early postmortem findings were a brown-green coloring of some tissues and encephalon congestion. The fluorescein LC50 was much higher than the recommended concentration in field applications (1 mg/l), indicating that fluorescein toxicity to turbot will not be expected when used at the recommended concentration.