In many aquatic organisms including Mytilus edulis, the role of temperature on bioaccumulation of metals is still not clearly understood. In this study, uptake and accumulation of Cu, Co, Cd and Pb in mussels were investigated at different temperatures (6-26 degrees C). Results from exposure of isolated gills showed a positive relationship between temperature and metal uptake. But in whole organism experiments, only the accumulations of non-essential metals (Cd, Pb) showed a similar trend while the two essential metals Co and Cu were independent and inversely related to temperature, respectively. With exception of Cu, elimination process appeared to be independent of temperature. The study also showed that neither changes in scope for growth (SFG) of mussels nor chemical speciation could fully account for the observed temperature-effects. Overall, these results suggest that fundamentally (i.e. at epithelial membranes), temperature-effects on uptake are largely due to changes in solution chemistry and physical kinetics, which favours higher uptake at high temperature. But at whole organism level, complex physiological responses appears to mask the relationship, particularly for biologically essential metals like copper.

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The effects of humic acids (HA) on Cu uptake by the blue mussel (Mytilus edulis) were studied in chemically defined seawater. Short-term uptake by excised gills was studied and compared with whole-mussel Cu accumulation. Copper uptake in gills is not a saturable process within the time frame and concentration range tested, being a linear function of time (0-120 min) and Cu concentration (0-150 microg/L). For the whole mussel, Cu uptake is not linear with time (0-72 h) and Cu concentration (0-130 microg/L). The presence of HA (0-10 mg/L) clearly reduced Cu uptake by gills, but it did not have such an effect on whole-animal uptake. A simple complexation model obtained from voltammetric measurements was used to determine the noncomplexed (labile) fraction of Cu in the presence of HA to test the effect of speciation on Cu uptake. In most cases, Cu uptake by gills was better explained by labile Cu concentrations than by total Cu exposure concentrations, which is in agreement with the free-ion activity model. In whole-animal experiments, Cu uptake was not related to labile Cu concentrations in the presence of HA, indicating that Cu-HA complexes are at least partially available for uptake by the mussels.

Lanthanum carbonate is a new phosphate binder that is poorly absorbed from the gastrointestinal tract and eliminated largely by the liver. After oral treatment, we and others had noticed 2-3 fold higher lanthanum levels in the livers of rats with chronic renal failure compared to rats with normal renal function. Here we studied the kinetics and tissue distribution, absorption, and subcellular localization of lanthanum in the liver using transmission electron microscopy, electron energy loss spectrometry, and X-ray fluorescence. We found that in the liver lanthanum was located in lysosomes and in the biliary canal but not in any other cellular organelles. This suggests that lanthanum is transported and eliminated by the liver via a transcellular, endosomal-lysosomal-biliary canicular transport route. Feeding rats with chronic renal failure orally with lanthanum resulted in a doubling of the liver levels compared to rats with normal renal function, but the serum levels were similar in both animal groups. These levels plateaued after 6 weeks at a concentration below 3 microg/g in both groups. When lanthanum was administered intravenously, thereby bypassing the gastrointestinal tract-portal vein pathway, no difference in liver levels was found between rats with and without renal failure. This suggests that there is an increased gastrointestinal permeability or absorption of oral lanthanum in uremia. Lanthanum levels in the brain and heart fluctuated near its detection limit with long-term treatment (20 weeks) having no effect on organ weight, liver enzyme activities, or liver histology. We suggest that the kinetics of lanthanum in the liver are consistent with a transcellular transport pathway, with higher levels in the liver of uremic rats due to higher intestinal absorption.

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