Waterborne exposure to clodinafop-propargyl disrupts the posterior and ventral development of zebrafish embryos.

Clodinafop-propargyl, an aryloxyphenoxypropionate herbicide, is widely used for the control of annual grasses. However, research focusing on the ecotoxicity of this herbicide is limited. The present study employed zebrafish (Danio rerio) as a model to investigate its developmental toxicity. Embryos were exposed to a range of concentrations from 0.2 µM to 5 µM starting at late cleavage stage (2 h postfertilization, [hpf]) or late gastrulation stage (10 hpf). The results showed that the two exposure strategies had the same minimum teratogenic concentration of 0.6 µM but caused different groups of morphogenetic malformations. When exposure was initiated at 2 hpf, clodinafop-propargyl caused various embryonic phenotypes, including embryos with a fin gap in the ventral tail and embryos with coiled tail. When exposure was initiated at 10 hpf, clodinafop-propargyl resulted in failure of the tail to detach, in which the ventral tissues failed to grow out but instead adhered to the yolk extension, and the defect differed to various degrees among embryos. Similar effects were observed for embryos exposed to clodinafop, the metabolite of clodinafop-propargyl. Because these defects were mainly confined to the posterior and ventral region that derived from ventral blastoderm cells, we have evaluated the expression of the ventral mesoderm marker gene gata-1 and ventral ectoderm marker gene gata-3. No significant alteration was seen in gata-1 expression except for the expanded blood islands, whereas the expression of gata-3 was significantly reduced. Our findings showed that clodinafop-propargyl exposure disturbed embryonic patterning and fate specification of ventrally derived gastrula ectoderm cells.