1. Academic Validation
  2. Clethodim exposure induces developmental immunotoxicity and neurobehavioral dysfunction in zebrafish embryos

Clethodim exposure induces developmental immunotoxicity and neurobehavioral dysfunction in zebrafish embryos

  • Fish Shellfish Immunol. 2019 Mar;86:549-558. doi: 10.1016/j.fsi.2018.12.002.
Guanghua Xiong 1 Lufang Zou 2 Yunyun Deng 3 Yunlong Meng 2 Xinjun Liao 1 Huiqiang Lu 4
Affiliations

Affiliations

  • 1 College of Life Sciences, Jinggangshan University, Ji'an, Jiangxi, China; Jiangxi Engineering Laboratory of Zebrafish Modeling and Drug Screening for Human Diseases, Ji'an, Jiangxi, China; Jiangxi Key Laboratory of Developmental Biology of Organs, Ji'an, Jiangxi, China.
  • 2 College of Life Sciences, Jinggangshan University, Ji'an, Jiangxi, China.
  • 3 Jiangxi Engineering Laboratory of Zebrafish Modeling and Drug Screening for Human Diseases, Ji'an, Jiangxi, China; Jiangxi Key Laboratory of Developmental Biology of Organs, Ji'an, Jiangxi, China.
  • 4 College of Life Sciences, Jinggangshan University, Ji'an, Jiangxi, China; Jiangxi Engineering Laboratory of Zebrafish Modeling and Drug Screening for Human Diseases, Ji'an, Jiangxi, China; Jiangxi Key Laboratory of Developmental Biology of Organs, Ji'an, Jiangxi, China. Electronic address: luhq2@126.com.
Abstract

Clethodim is one of the most widely used herbicides in agriculture, but its potential negative effects on aquatic organisms are still poorly understood. This study examined the effects of clethodim on zebrafish at aspects of early stage embryonic development, immune toxicity, cell Apoptosis and locomotor behavior. Firstly, clethodim exposure markedly decreased the survival rate, body length, and heart rate and resulted in a series of morphological abnormalities, primarily spinal deformities (SD) and yolk sac edema, in zebrafish larvae. Secondly, the number of immune cells was substantially reduced but the levels of Apoptosis and oxidative stress were significantly increased in a dose-dependent manner upon clethodim exposure. Thirdly, we evaluated the expression of some key genes in TLR signaling including TLR4, MyD88, and NF-κB p65 and they were all up-regulated by exposure to 300 μg/L clethodim. Meanwhile, some proinflammatory cytokines such as TNF-α, IL-1β, IL8, and IFN-γ were also activated in both the mock and the TLR4-KD conditions. Moreover, the locomotor behaviors and the enzymatic activities of AChE were obviously inhibited but the levels of acetylated histone H3 were greatly increased by clethodim exposure. In addition, incubation of zebrafish larvae with acetylcholine receptor (AChR) agonist carbachol can partially rescue the clethodim-modulated locomotor behavior. Taken together, our results suggest that clethodim has the potential to induce developmental immunotoxicity and cause behavioral alterations in zebrafish larvae. The information presented in this study will help to elucidate the molecular mechanisms underlying clethodim exposure in aquatic ecosystems.

Keywords

Clethodim; Histone acetylation; Immunotoxicity; Locomotor behavior; TLR signaling.

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