首页> 外文期刊>Environmental Science & Technology >Zn Stimulates the Phospholipids Biosynthesis via the Pathways of Oxidative and Endoplasmic Reticulum Stress in the Intestine of Freshwater Teleost Yellow Catfish
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Zn Stimulates the Phospholipids Biosynthesis via the Pathways of Oxidative and Endoplasmic Reticulum Stress in the Intestine of Freshwater Teleost Yellow Catfish

机译:锌通过淡水硬骨鱼Cat肠中的氧化和内质网应激途径刺激磷脂的生物合成。

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摘要

The hypothesis of our study was that waterborne Zn exposure evoked phospholipids (PL) biosynthesis to compensate for the loss of membrane integrity, and the pathways of oxidative stress and endoplasmic reticulum (ER) stress mediated the Zn-evoked changes of PL biosynthesis. Thus, we conducted RNA sequencing to analyze the differences in the intestinal transcriptomes between the control and Zn-treated P. fulvidraco. The 56-day Zn exposure increased the intestinal Zn accumulation, and mRNA levels of 816 genes were markedly up-regulated, while that of 263 genes were down-regulated. Many differentially expressed genes in the pathways of PL biosynthesis and protein processing in ER were identified. Their expression profiles indicated that waterborne Zn exposure injured protein metabolism, induced PL biosynthesis caused oxidative stress and ER stress, and activated the unfolded protein response. Then, using the primary enterocytes, we identified the mechanism of oxidative and ER stress mediating Zn-induced PL biosynthesis, and indicated that the activation of these pathways constituted adaptive mechanisms to reduce Zn toxicity. Our study demonstrated that Zn exposure via the water increased Zn accumulation and PL biosynthesis, and that oxidative stress and ER stress were interdependent and mediated the Zn-induced PL biosynthesis of the intestine in the freshwater teleost.
机译:我们研究的假设是,水性锌暴露引起磷脂(PL)的生物合成,以补偿膜完整性的损失,而氧化应激和内质网(ER)应激的途径介导了Zn引起的PL生物合成的变化。因此,我们进行了RNA测序,以分析对照和经Zn处理的黄萎病菌之间肠道转录组的差异。锌暴露56天增加了肠道锌的积累,816个基因的mRNA水平显着上调,而263个基因的mRNA水平下调。在ER的PL生物合成和蛋白质加工途径中鉴定了许多差异表达基因。他们的表达谱表明,水接触锌会损害蛋白质代谢,诱导PL生物合成会引起氧化应激和ER应激,并激活展开的蛋白质反应。然后,使用原代肠上皮细胞,我们确定了氧化和内质网应激介导锌诱导的PL生物合成的机制,并表明这些途径的激活构成了降低锌毒性的适应性机制。我们的研究表明,通过水接触锌会增加锌的积累和PL的生物合成,氧化应激和ER应激是相互依赖的,并介导了Zn诱导的淡水硬骨鱼肠的PL生物合成。

著录项

  • 来源
    《Environmental Science & Technology》 |2018年第16期|9206-9214|共9页
  • 作者单位

    Huazhong Agr Univ, Minist Agr PRC, Fishery Coll, Key Lab Freshwater Anim Breeding, Wuhan 430070, Hubei, Peoples R China;

    Huazhong Agr Univ, Minist Agr PRC, Fishery Coll, Key Lab Freshwater Anim Breeding, Wuhan 430070, Hubei, Peoples R China;

    Kings Coll London, Sch Med, Diabet & Nut Sci Div, Franklin Wilkins Bldg,150 Stamford St, London SE1 9NH, England;

    Huazhong Agr Univ, Minist Agr PRC, Fishery Coll, Key Lab Freshwater Anim Breeding, Wuhan 430070, Hubei, Peoples R China;

    Huazhong Agr Univ, Minist Agr PRC, Fishery Coll, Key Lab Freshwater Anim Breeding, Wuhan 430070, Hubei, Peoples R China;

    Huazhong Agr Univ, Minist Agr PRC, Fishery Coll, Key Lab Freshwater Anim Breeding, Wuhan 430070, Hubei, Peoples R China;

  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
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  • 入库时间 2022-08-17 13:56:44

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