Embryonic exposure to butachlor in zebrafish (Danio rerio): Endocrine disruption, developmental toxicity and immunotoxicity
- Authors
- Tu, W., Niu, L., Liu, W., and Xu, C.
- ID
- ZDB-PUB-130110-31
- Date
- 2013
- Source
- Ecotoxicology and environmental safety 89: 189-195 (Journal)
- Registered Authors
- Keywords
- butchalor, innate immune, developmental toxicity, estrogen-responsive, zebrafish
- MeSH Terms
-
- Pericardium/drug effects
- Estrogen Receptor alpha/metabolism
- Zebrafish/embryology*
- Zebrafish/metabolism
- Yolk Sac/drug effects
- Immune System/drug effects*
- Interleukin-8/metabolism
- Acetanilides/toxicity*
- Embryo, Nonmammalian/drug effects*
- Animals
- Vitellogenins/metabolism
- Gene Expression Regulation, Developmental/drug effects
- Endocrine Disruptors/toxicity*
- Water Pollutants, Chemical/toxicity*
- Chemokines, CXC/metabolism
- Endocrine System/drug effects*
- PubMed
- 23294635 Full text @ Ecotoxicol. Environ. Saf.
Butachlor is a chloroacetanilide herbicide widely employed in weeding important crops. Recently, the study of the possible toxic effects of butachlor in non-target organisms has increased substantially. However, the endocrine disruption, developmental toxicity and immunotoxicity effects of butachlor in fish have not been fully investigated in previous studies. In the present study, zebrafish embryos were exposed to a range of butachlor concentrations from 4 to 20 μM to evaluate the embryonic toxicity of butachlor until 84 hours postfertilization (hpf). The results demonstrated that butachlor was highly toxic to zebrafish embryos, hindering the hatching process, resulting in a series of malformations and followed by mortality. The malformations observed included pericardial edema (PE) and yolk sac edema (YSE), which showed concentration-dependent responses. The analysis of endocrine gene transcription indicated that butachlor significantly induced the expression of the estrogen-responsive gene Vtg1 but had no effect on the expression of the ERα gene. The innate immune system appeared to be another possible target of butachlor. At 72 hpf, butachlor significantly up-regulated the innate immune system-related genes, including IL-1β, CC-chem, CXCL-C1c and IL-8. These data suggest that butachlor causes developmental toxicity, endocrine disruption and immune toxicity in the zebrafish embryo. Bidirectional interactions between the endocrine system and the immune system might be present, and further studies are needed to determine these possible pathways.