Thallium (Tl) is a rare trace metal element but increasingly detected in wastewater produced by coal-burning, smelting, and more recently, high-tech manufacturing industries. However, the adverse effects of Tl, especially cardiotoxicity, on aquatic biota remain unclear. In this study, zebrafish model was used to elucidate the effects and mechanisms of Tl(I) cardiotoxicity in developing embryos. Exposure of embryonic zebrafish to low-dose Tl(I) (25-100 μg/L) decreased heart rate and blood flow activity, and subsequently impaired swim bladder inflation and locomotive behavior of larvae. Following high-level Tl(I) administration (200-800 μg/L), embryonic zebrafish exhibited pericardial edema, incorrect heart looping, and thinner myocardial layer. Based on RNA-sequencing, Tl(I) altered pathways responsible for protein folding and transmembrane transport, as well as negative regulation of heart rate and cardiac jelly development. The gene expression of nppa, nppb, ucp1, and ucp3, biomarkers of cardiac damage, were significantly upregulated by Tl(I). Our findings demonstrate that Tl(I) at environmentally relevant concentrations interfered with cardiac development with respect to anatomy, function, and transcriptomic alterations. The cardiotoxic mechanisms of Tl(I) provide valuable information in the assessment of Tl-related ecological risk in freshwater environment.
Keywords: Cardiotoxicity; Developmental toxicity; Embryonic zebrafish model; Thallium; Transcriptomic profiling.
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