Pollutants that occur at sublethal concentrations in water may lead to chronic exposure in aquatic organisms. These organisms can accumulate high metal concentrations, which may result in the trophic transfer of such pollution to predators. Trophic transfer can thus become a major source of exposure to metals 1–5. For this reason, attention has recently been focused on the relative importance of dietary uptake in assessing toxicity. A number of aquatic organisms, including fishes, can accumulate metals via aqueous and dietary exposure routes 6. Certain authors have emphasized the need for toxicological tests that focus on the trophic transfer of metals in aquatic animals, to assess the importance of food as a source of metal toxicity 7. Thus, awareness is growing among regulators concerning the suitability of water quality guidelines established for dissolved metals, and whether these are sufficiently protective 4, 5.
Ecological risk assessments often focus on the relationship between direct exposure and the associated effects, but many standard toxicology tests do not take trophic exposure into account, even though trophic exposure in controlled conditions is easy to reproduce and interpret as direct exposure standardized tests 8.
In parallel with the use of the biotic ligand model 9, the intention of the present study is to express the chronic toxic effects as a function of accumulated dose. This is referred to as the critical body residues approach 7, 10–14, which focuses on the characterization of metal distribution in organisms. Even if the relationship between bioaccumulation expressed by the metal-available fraction and toxicity remains complex 15–17, toxicity is now seen to depend partly on the biological model, the metal, and more accurately, chemical binding of the metal within cells 17, 18.
To adopt such an approach, additional knowledge about the cellular distribution of metals after dietary or direct exposures is required to assess potential toxic effects attributable to these two different routes of exposure.
Uranium is an element of interest: its concentration in freshwater ecosystems (from 12 µg/L to 2 mg/L) is currently increasing because of anthropogenic activities 19, 20. Although uranium is a radionuclide, its toxic effects and uptake are controlled by its chemical properties. The accumulation levels and toxic effects of this element have been evaluated in several biological models 21–24. In crayfish, uranium can impair mitochondrial function and induce oxidative stress 23. Very few studies have focused on its accumulation and associated toxic effects after trophic exposure 8, 25–27. The ecotoxicological profile of uranium is not yet fully understood, and the major pathway responsible for its accumulation levels has not yet been determined.
Various species of crayfish have been found to be suitable candidates for evaluating the importance of routes of exposure to uranium. These are often used as indicators of freshwater metal pollution, because they tend to rapidly accumulate metals and radionuclides (uranium) in their tissues via direct and trophic routes 23, 26, 28–32. Short-term exposure has been used to evaluate the transfer capability of direct and dietary exposure pathways. As prey for trophic exposure experiments, we selected the Asiatic clam, C. fluminea, which is well known for its high capacity for metal bioaccumulation 33–36.
The aim of the present study was to compare the uranium bioaccumulation rate at tissue and subcellular concentrations and its micro-localization in the gills and the hepatopancreas of the crayfish Orconectes limosus after 10 d. Two exposure treatments were adopted: direct exposure (with three uranium concentrations), and trophic exposure (with five treatments).