Developmental Neurotoxicity of Difenoconazole in Zebrafish Embryos

Yang, Qing; Deng, Peng; Xing, Dan; Liu, Haoling; Shi, Fang; Hu, Lian; Zou, Xi; Nie, Hongyan; Zuo, Junli; Zhuang, Zimeng; Pan, Meiqi; Chen, Juan; Li, Guangyu

doi:10.3390/toxics11040353

Cited by 9 publications

(1 citation statement)

References 73 publications

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“…When the exposure dose was EC 10 , difenoconazole exposure mainly affected the regulation of cell and nervous system development. A previous study indicated that the exposure of zebrafish to difenoconazole could initiate neurotoxicity [ 37 ]. Moreover, muscle contraction (seven downregulated DEGs, one upregulated DEG) and muscle system processes (seven downregulated DEGs, one upregulated DEG) were also significantly affected ( Tables S7 and S17 ).…”

Section: Resultsmentioning

confidence: 99%

Use of Transcriptomics to Reveal the Joint Immunotoxicity Mechanism Initiated by Difenoconazole and Chlorothalonil in the Human Jurkat T-Cell Line

Li,

Liu,

et al. 2023

Foods

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It is very important to evaluate the immunotoxicity and molecular mechanisms of pesticides. In this study, difenoconazole and chlorothalonil were evaluated for immunotoxicity by using the human Jurkat T-cell line, and the EC50 were 24.66 and 1.17 mg/L, respectively. The joint exposure of difenoconazole and chlorothalonil showed a synergistic effect at low concentrations (lower than 10.58 mg/L) but an antagonistic effect at high concentrations (higher than 10.58 mg/L). With joint exposure at a concentration of EC10, the proportion of late apoptotic cells was 2.26- and 2.91-fold higher than that with exposure to difenoconazole or chlorothalonil alone, respectively. A transcriptomics analysis indicated that the DEGs for single exposure are associated with immunodeficiency disease. Single exposure to chlorothalonil was mainly involved in cation transportation, extracellular matrix organization, and leukocyte cell adhesion. Single exposure to difenoconazole was mainly involved in nervous system development, muscle contraction, and immune system processes. However, when the joint exposure dose was EC10, the DEGs were mainly involved in the formation of cell structures, but the DEGs were mainly involved in cellular processes and metabolism when the joint exposure dose was EC25. The results indicated that the immunotoxicological mechanisms underlying joint exposure to difenoconazole and chlorothalonil are different under low and high doses.

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Section: Resultsmentioning

confidence: 99%