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首页> 外文期刊>Journal of applied toxicology >Oxidative stress-mediated developmental toxicity induced by isoniazide in zebrafish embryos and larvae
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Oxidative stress-mediated developmental toxicity induced by isoniazide in zebrafish embryos and larvae

机译：在斑马鱼胚胎和幼虫中异氧化物诱导的氧化胁迫介导的发育毒性

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摘要

Isoniazide (INH) is an important first-line drug that is used to treat tuberculosis. However, the effect of INH on fetal growth has not yet been elucidated, and the mechanism of INH-induced developmental toxicity is still unknown. In the present study, we employed zebrafish embryos and larvae to investigate the developmental toxicity of INH. The survival rates of the embryos and larvae as well as the hatching rates of embryos were significantly reduced. Morphological abnormalities, including spinal curvature, yolk retention, swimming bladder absence, tail bending and shorter body lengths were induced by INH. Histopathological analysis showed loose cell-to-cell contacts and large vacuoles in the larval hepatocytes. Thin intestinal walls, frayed gut villi and widespread cell lysis were observed in the intestines of the larvae in the higher concentration (8, 16mM) exposure groups. In addition, exposure to high doses (>= 6mM) of INH significantly reduced the locomotor capacity of the zebrafish larvae. INH significantly increased the levels of reactive oxygen species and malondialdehyde and decreased the superoxide dismutase activity in zebrafish larvae, which suggested that oxidative stress was induced and that the antioxidant capacity was inhibited. Superoxide dismutase 1 and liver fatty acid-binding protein mRNA levels were significantly downregulated, while the GSTP2 and cytochrome P450 3A mRNA levels were significantly upregulated in the INH-exposed zebrafish larvae. The overall results indicated that INH caused a dose-and time-dependent increase in developmental toxicity and that oxidative stress played an important role in the developmental toxicity induced by INH in zebrafish larvae. Copyright (C) 2017 John Wiley & Sons, Ltd.
机译：异嗪（INH）是一种重要的一线药物，用于治疗结核病。然而，INH对胎儿生长的影响尚未阐明，INH诱导的发育毒性的机制仍然未知。在本研究中，我们使用斑马鱼胚胎和幼虫来研究侵权的发育毒性。胚胎和幼虫的存活率以及胚胎的孵化率显着降低。通过侵权，包括脊柱曲率，卵黄卷，游泳膀胱，尾部弯曲和较短的体长等形态异常。组织病理学分析显示幼虫肝细胞中松散的细胞 - 细胞接触和大型液泡。在幼虫的肠道中较高浓度（8,16mm）曝光基团，观察到薄肠壁，磨损的肠绒毛和广泛的细胞裂解。此外，暴露于高剂量（> = 6mm）的INH显着降低了斑马鱼幼虫的运动能力。 INH显着提高了活性氧物质和丙二醛水平，并降低了斑马鱼幼虫中的超氧化物歧化酶活性，这表明诱导氧化应激并抑制抗氧化能力。超氧化物歧化酶1和肝脏脂肪酸结合蛋白mRNA水平显着下调，而GSTP2和细胞色素P450 3A mRNA水平在INH暴露的斑马鱼幼虫中显着上调。总结果表明INH导致发育毒性的剂量和时间依赖性增加，并且氧化应激在Zebrafish幼虫inh诱导的发育毒性中发挥着重要作用。版权所有（c）2017 John Wiley＆Sons，Ltd。

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  • 来源
    《Journal of applied toxicology》 |2017年第8期|共11页
  • 作者

    Zou Yu; Zhang Yun; Han Liwen; He Qiuxia; Hou Hairong; Han Jian; wang Ximin; Li Chengyun; Cen Juan; Liu Kechun;

  • 作者单位

    Henan Univ Key Lab Nat Med &

    Immunoengn Kaifeng 475004 Henan Province Peoples R China;

    Shandong Acad Sci Biol Inst 19 Keyuan Rd Jinan 250014 Shandong Peoples R China;

    Shandong Acad Sci Biol Inst 19 Keyuan Rd Jinan 250014 Shandong Peoples R China;

    Shandong Acad Sci Biol Inst 19 Keyuan Rd Jinan 250014 Shandong Peoples R China;

    Shandong Acad Sci Biol Inst 19 Keyuan Rd Jinan 250014 Shandong Peoples R China;

    Shandong Acad Sci Biol Inst 19 Keyuan Rd Jinan 250014 Shandong Peoples R China;

    Shandong Acad Sci Biol Inst 19 Keyuan Rd Jinan 250014 Shandong Peoples R China;

    Shandong Acad Sci Ecol Inst 19 Keyuan Rd Jinan 250014 Shandong Peoples R China;

    Henan Univ Key Lab Nat Med &

    Immunoengn Kaifeng 475004 Henan Province Peoples R China;

    Shandong Acad Sci Biol Inst 19 Keyuan Rd Jinan 250014 Shandong Peoples R China;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 毒物学（毒理学）;
  • 关键词

    Isoniazide; developmental toxicity; zebrafish embryos; zebrafish larvae; swimming behavior; oxidative stress;

    机译：异尼嗪;发育毒性;斑马鱼胚胎;斑马鱼幼虫;游泳行为;氧化应激;

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