| Literature DB >> 28002765 |
Kang Li1, Jia-Qi Wu1, Ling-Ling Jiang1, Li-Zhen Shen1, Jian-Ying Li2, Zhi-Heng He3, Ping Wei1, Zhuo Lv4, Ming-Fang He5.
Abstract
2,4-Dichlorophenoxyacetic acid (2,4-D) is widely used in agriculture as herbicide/pesticide, plant growth regulator and fruit preservative agent. It progressively accumulates in the environment including surface water, air and soil. It could be detected in human food and urine, which poses great risk to the living organisms. In the present study, we investigated the developmental toxicity of 2,4-D on zebrafish (Danio rerio) embryo. 2,4-D exposure significantly decreased both the survival rate (LC50 = 46.71 mg/L) and hatching rate (IC50 = 46.26 mg/L) of zebrafish embryos. The most common developmental defect in 2,4-D treated embryos was pericardial edema. 2,4-D (25 mg/L) upregulated marker genes of cardiac development (vmhc, amhc, hand2, vegf, and gata1) and downregulated marker genes of oxidative stress (cat and gpx1a). Whole mount in situ hybridization confirmed the vmhc and amhc upregulation by 2,4-D treatment. LC/MS/MS showed that the bioaccumulation of 2,4-D in zebrafish embryos were increased in a time-dependent manner after 25 mg/L of 2,4-D treatment. Taken together, our study investigated the toxic effects of 2,4-D on zebrafish embryonic development and its potential molecular mechanisms, gave evidence for the full understanding of 2,4-D toxicity on living organisms and shed light on its environmental impact.Entities:
Keywords: 2,4-Dichlorophenoxyacetic acid; Cardiac toxicity; Developmental toxicity; Embryonic toxicity; Zebrafish
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Year: 2016 PMID: 28002765 DOI: 10.1016/j.chemosphere.2016.12.032
Source DB: PubMed Journal: Chemosphere ISSN: 0045-6535 Impact factor: 7.086