Toxic effect of palladium on embryonic development of zebrafish

Abstract

Since palladium (Pd) is now increasingly used in modern industry, it progressively accumulates in the environment, especially in aquatic ecosystem. The potential toxicity of Pd has therefore caused extensive concern worldwidely. In the present study, we investigated the toxic effect of Pd on zebrafish development. Acute Pd exposure significantly decreased both the survival rate (LC50: 292.6 μg/L, viz. 2.75 μM) and hatching rate (IC50: 181.5 μg/L, viz. 1.71 μM) of zebrafish during embryonic development. The most common developmental defect observed in Pd treated embryos is pericardiac edema, which occurs in a dose-dependent manner. Whole mount immunostaining and histological studies revealed that Pd exposure would produce the elongated, string-like heart. The heartbeat rate of zebrafish embryos was also decreased after Pd exposure. Consistently, mRNA expression levels of several cardiac-related genes were affected by Pd, suggesting a potential molecular mechanism of Pd-induced cardiac malformation of zebrafish embryo. Moreover, similar to other metals, Pd exposure resulted in the elevated expression of general metal-inducible genes. It was also found that the expression of several antioxidant enzymes was significantly down-regulated in the presence of Pd. Taken together, our study investigated the effects of Pd on zebrafish embryonic development and its potential molecular mechanisms, paving the way for the full understanding of Pd toxicity.

Keywords: Cardiac malformation; Embryonic toxicity; Palladium; Zebrafish.