Abstract
Abstract The increasing extraction of rare earth elements (REEs) and their subsequent release to freshwater ecosystems are expected to threaten aquatic organisms, yet little is known about the scope of this issue. The purpose of this study was to identify key molecular responses associated with exposure and toxicity of two data-poor REEs, terbium (Tb, heavy REE) and praesodymium (Pr, light REE) in rainbow trout juveniles. Fish were exposed for 96 h to increasing concentrations of Tb and Pr to determine impacts on survival and variation in biomarkers involved in oxidative stress, inflammation, DNA damage and metal homeostasis (metallothioneins). In surviving fish, a suite of 14 gene expression endpoints were also examined as well as genes associated with protein stability, calcium binding, immune response, protein damage, cell division, iron homeostasis and mitochondrial activity. The data showed that Tb was approximately two times more toxic than Pr, with estimated LC50 of 5.8 and 11 mg/L respectively. In addition, Tb and Pr exhibit respectively anti and pro-inflammatory responses relative to controls as demonstrated by the significant variation in the arachidonate cycloocygenase (COX) activity. However only Pr displayed a genotoxic effect due to the increase in the level of DNA strand breaks. Exposure to these two elements lead to the expression of genes involved in DNA repair activity, inflammation, protein denaturation, calcium binding, oxidative stress and divalent metal handling, ATP synthesis and hemoprotein activity. Based on the observed responses to both Tb and Pr, metal homeostasis, protein denaturation and DNA repair activity were commonly affected. The most toxic element (Tb) produced more important changes in the expression of genes involved in oxidative stress, calcium binding, hemoprotein activity and protein folding and turnover. These genes represents potential physiological targets involved in the mode of action for Tb and Pr in fish toxicity.
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