Mortality, bioaccumulation and physiological responses in juvenile freshwater mussels (Lampsilis siliquoidea) chronically exposed to copper.

Several studies have indicated that the early life stages of freshwater mussels are among the most sensitive aquatic organisms to inorganic chemicals, including copper. However, little is known about the toxic mode of action and sub-lethal effects of copper exposure in this group of imperiled animals. In this study, the physiological effects of long-term copper exposure (survival, growth, copper bioaccumulation, whole-body ion content, oxygen consumption, filtration rate, ATPase activities, and biomarkers of oxidative stress) were evaluated in juvenile (6 month old) mussels (Lampsilis siliquoidea). The mussels' recovery capacity and their ability to withstand further acute copper challenge were also evaluated in secondary experiments following the 28 day exposure by assessing survival, copper bioaccumulation and whole-body ion content. Mussels chronically exposed to 2 and 12 μg Cu/L showed significantly higher mortality than those held under control conditions (mortality 20.9, 69.9 and 12.5%, respectively), indicating that juvenile L. siliquoidea is underprotected by the U.S. Environmental Protection Agency (USEPA) biotic ligand model (BLM)-derived chronic water quality criteria (WQC) (2.18 μg Cu/L) and the hardness-derived USEPA WQC (12.16 μg Cu/L). Soft tissue copper burden increased equally for both copper exposures, suggesting that chronic toxicity is not associated with copper bioaccumulation. Several physiological disturbances were also observed during chronic copper exposure. Most relevant was a decrease in whole-body sodium content paralleled by an inhibition of Na(+) K(+)-ATPase activity, indicating a metal-induced ionoregulatory disturbance. Filtration and oxygen consumption rates were also affected. Redox parameters (reactive oxygen production, antioxidant capacity against peroxyl radicals, glutathione-S-transferase (GST) activity, and glutathione (GSH) concentration) did not show clear responses, but membrane damage as lipid peroxidation (LPO) was observed in both copper exposures. Mussels previously held in control conditions or pre-exposed to 2 μg dissolved Cu/L were able to maintain their ionic homeostasis and did not experience mortality after the 4-d recovery period. In contrast, those previously exposed to 12 μg dissolved Cu/L exhibited 50% mortality indicating that they had already reached a 'point of no return'. Pre-exposure to copper did not influence mussel response to the copper challenge test. As observed for the chronic exposure, mortality of mussels held in the absence of copper and submitted to the challenge test was also associated with an ionoregulatory disturbance. These results indicate that ionoregulatory disruption in freshwater mussels chronically exposed to copper is the main mechanism of toxicity and that redox parameters do not appear to be useful as indicators of sub-lethal copper toxicity in these animals.