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哒螨灵抑制斑马鱼(Danio rerio)细胞周期进程并延迟早期胚胎发育。

Pyridaben inhibits cell cycle progression and delays early embryonic development in zebrafish (Danio rerio).

机构信息

College of Medicine, Huanghuai University, Zhumadian 463000, China; Department of Scientific Research Section, Zhumadian Central Hospital, Affiliated Hospital of Huanghuai University, Zhumadian 463000, China.

The Second Affiliated Hospital of Jiaxing University, Jiaxing 314000, China.

出版信息

Ecotoxicol Environ Saf. 2024 Sep 15;283:116857. doi: 10.1016/j.ecoenv.2024.116857. Epub 2024 Aug 12.

DOI:10.1016/j.ecoenv.2024.116857
PMID:39137465
Abstract

Pyridaben is a broad-spectrum, contact-killing acaricide that can be used to control a variety of harmful food and plant mites. Pyridaben displays cardiotoxicity and liver toxicity toward fish, but the effects on fish embryonic development have not been characterized. We exposed early zebrafish embryos to 20, 30, and 40 μg/L concentrations of pyridaben. The exposure caused developmental abnormalities, including delayed embryonic shield formation, yolk sac resorption, decreases in body length, reduced pigmentation, and delays in hatching. Pyridaben caused a significant increase in the transcription level of the endoderm marker foxa2, but the transcription levels of the ectoderm development marker foxb1a and the mesoderm development marker snaila were not significantly altered. The transcription levels of the genes SOX17 in early embryos were significantly reduced. After exposure to pyridaben, catalase (CAT) activity and glutathione (GSH) content were increased, and cyclin D1, that is involved in early embryonic development, was abnormally expressed. This study shows that pyridaben causes anomalous development in zebrafish embryos by interfering with the cell cycle order of early embryonic development and inducing excessive oxidative stress. Colivelin, an agonist of the STAT3 signaling pathway, acted as a salvage drug to restore the cell cycle order during embryonic development following exposure to pyridaben. Thus, the toxic effects may be caused by pyridaben's regulation of the STAT3 signaling pathway.

摘要

哒螨灵是一种广谱、触杀性杀螨剂,可用于防治多种果蔬害螨。哒螨灵对鱼类具有心脏毒性和肝脏毒性,但尚未对其对鱼类胚胎发育的影响进行特征描述。我们将早期斑马鱼胚胎暴露于 20、30 和 40μg/L 的哒螨灵浓度下。暴露导致发育异常,包括胚胎盾形成延迟、卵黄囊吸收、体长减少、色素沉着减少和孵化延迟。哒螨灵导致内胚层标志物 foxa2 的转录水平显著增加,但外胚层发育标志物 foxb1a 和中胚层发育标志物 snaila 的转录水平没有显著改变。早期胚胎中 SOX17 基因的转录水平显著降低。暴露于哒螨灵后,过氧化氢酶(CAT)活性和谷胱甘肽(GSH)含量增加,参与早期胚胎发育的细胞周期蛋白 D1 异常表达。本研究表明,哒螨灵通过干扰早期胚胎发育的细胞周期顺序和诱导过度氧化应激,导致斑马鱼胚胎发育异常。STAT3 信号通路的激动剂 Colivelin 作为一种挽救药物,在暴露于哒螨灵后恢复胚胎发育过程中的细胞周期顺序。因此,毒性作用可能是哒螨灵对 STAT3 信号通路的调节所致。

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