Insights on the toxicity of selected rare earth elements in rainbow trout hepatocytes

The increasing extraction of rare earth elements (REEs) for technology applications raised concerns for contamination and toxicity in the environment. The purpose of this study was to examine the toxicity of the following REEs in primary cultures of rainbow trout hepatocytes: yttrium (Y), samarium (Sm), gadolinium (Gd), terbium (Tb) and lutetium (Lu). Hepatocytes were exposed to increasing concentrations of the above elements for 24 h at 15 degrees C and they were analyzed for viability, metallothioneins (MT), glutathione-S-transferase (GST) and arachidonate cyclooxygenase (COX) as markers of oxidative stress and inflammation. The results revealed that the cytoxicity of REEs were as follows in decreasing order: Y > Sm > Lu > Tb > Gd in concordance with published rainbow trout mortality data. While effects on GST and COX activities were marginal, MT levels were more strongly increased with the 2 most toxic REEs (Y and Sm) and Gd, while MT levels were decreased in the least toxic ones (Tb, Lu). While cell viability followed published trout mortality data, it also followed the redox potential and the glutathione affinity constant (log k). The capacity to induce/decrease MT levels was associated with ionic radius, log k (glutathione) and electronegativity. A proposed mechanism of toxicity for REEs is presented based on the chemical properties of REEs, namely the glutathione binding constant and ionic radius, in light of the observed effects in trout hepatocytes.

Automated summary

The study found that the toxicity of rare earth elements on rainbow trout hepatocytes followed the order of yttrium > samarium > lutetium > terbium > gadolinium, with metallothioneins (MT) levels closely associated with toxicity. Glutathione-S-transferase (GST) and arachidonate cyclooxygenase (COX) activities had minimal impact on toxicity.