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锌通过氧化和内质网应激途径刺激淡水鱼类黄颡鱼肠道中磷脂的生物合成。

Zn Stimulates the Phospholipids Biosynthesis via the Pathways of Oxidative and Endoplasmic Reticulum Stress in the Intestine of Freshwater Teleost Yellow Catfish.

机构信息

Key Laboratory of Freshwater Animal Breeding, Ministry of Agriculture of P.R.C., Fishery College , Huazhong Agricultural University , Wuhan 430070 , China.

Collaborative Innovation Center for Efficient and Health Production of Fisheries in Hunan Province , Changde 415000 , China.

出版信息

Environ Sci Technol. 2018 Aug 21;52(16):9206-9214. doi: 10.1021/acs.est.8b02967. Epub 2018 Aug 13.

Abstract

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.

摘要

本研究的假设是,水传播的锌暴露会引发磷脂(PL)生物合成以补偿膜完整性的丧失,而氧化应激和内质网(ER)应激途径介导了锌诱发的 PL 生物合成变化。因此,我们进行了 RNA 测序,以分析对照组和 Zn 处理的黄颡鱼肠道转录组之间的差异。56 天的 Zn 暴露增加了肠道 Zn 积累,816 个基因的 mRNA 水平显著上调,而 263 个基因的 mRNA 水平下调。在 PL 生物合成和 ER 中蛋白质加工的途径中鉴定出许多差异表达的基因。它们的表达谱表明,水传播的 Zn 暴露损伤了蛋白质代谢,诱导了导致氧化应激和 ER 应激的 PL 生物合成,并激活了未折叠蛋白反应。然后,使用原代肠细胞,我们确定了氧化应激和 ER 应激介导 Zn 诱导的 PL 生物合成的机制,并表明这些途径的激活构成了减少 Zn 毒性的适应性机制。本研究表明,通过水摄入的 Zn 暴露增加了 Zn 积累和 PL 生物合成,并且氧化应激和 ER 应激是相互依存的,并介导了淡水硬骨鱼肠道中 Zn 诱导的 PL 生物合成。

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