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首页> 外文期刊>Journal of applied toxicology >Cadmium exposure induces endothelial dysfunction via disturbing lipid metabolism in human microvascular endothelial cells
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Cadmium exposure induces endothelial dysfunction via disturbing lipid metabolism in human microvascular endothelial cells

机译：镉暴露通过扰乱人微血管内皮细胞中的脂质代谢诱导内皮功能障碍

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摘要

Cadmium (Cd) is an occupational and environmental heavy metal pollutant derived from many sources that is linked to endothelial homeostasis. The endothelium is an important site of Cd deposition, while increasing evidence has revealed there is a close relationship between endothelial dysfunction and abnormal lipid metabolism. However, the effects of the alterations in lipid metabolism on endothelial cells (ECs) after Cd exposure still remain unclear. In our study, human microvascular endothelial cells (HMEC-1) were exposed to 40-mu M Cd for 6, 12, or 24 h or 10-, 20-, or 40-mu M Cd for 24 h, respectively. The Cd exposure accelerated the decomposition of triglyceride (TG) and resulted in the accumulation of free fatty acids (FFAs). These changes stimulated cytotoxicity, impaired fatty acid oxidation (FAO), induced reactive oxygen species (ROS) generation, altered the mitochondrial membrane potential (MMP), and decreased the ATP content, which eventually led to endothelial dysfunction and cell death. In summary, exposure to cadmium caused endothelial dysfunction by disrupting lipid metabolism in HMEC-1. These changes were mainly due to FFA accumulation and FAO inhibition, which further induced ROS generation and mitochondrial dysfunction. Moreover, our results provide novel insight into understanding the alterations of lipid metabolism induced by Cd exposure in ECs.
机译：镉（Cd）是一种职业性和环境性重金属污染物，来源于多种与内皮细胞稳态相关的来源。内皮细胞是Cd沉积的重要部位，而越来越多的证据表明内皮功能障碍与脂质代谢异常密切相关。然而，镉暴露后脂质代谢的改变对内皮细胞（EC）的影响仍不清楚。在我们的研究中，人类微血管内皮细胞（HMEC-1）分别暴露于40μM Cd中6、12或24小时，或暴露于10、20或40μM Cd中24小时。镉暴露加速了甘油三酯（TG）的分解，导致游离脂肪酸（FFA）的积累。这些变化刺激细胞毒性，损害脂肪酸氧化（FAO），诱导活性氧（ROS）生成，改变线粒体膜电位（MMP），降低ATP含量，最终导致内皮功能障碍和细胞死亡。总之，镉暴露通过扰乱HMEC-1中的脂质代谢而导致内皮功能障碍。这些变化主要是由于FFA积累和FAO抑制，进一步诱导ROS生成和线粒体功能障碍。此外，我们的结果为理解镉暴露引起的内皮细胞脂质代谢改变提供了新的见解。

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  • 来源
    《Journal of applied toxicology》 |2021年第6期|共14页
  • 作者

    Liang Hao; Yue Rongchuan; Zhou Chao; Liu Mengyu; Yu Xi; Lu Shengzhong; Zeng Jing; Yu Zhengping; Zhou Zhou; Hu Houxiang;

  • 作者单位

    North Sichuan Med Coll Affiliated Hosp Dept Cardiovasol Nanchong 637000 Sichuan Peoples R China;

    North Sichuan Med Coll Affiliated Hosp Dept Cardiovasol Nanchong 637000 Sichuan Peoples R China;

    Third Mil Med Univ Dept Occupat Hlth Chongqing Peoples R China;

    Third Mil Med Univ Dept Occupat Hlth Chongqing Peoples R China;

    Zhejiang Univ Sch Med Dept Occupat &

    Environm Med Hangzhou Peoples R China;

    North Sichuan Med Coll Affiliated Hosp Dept Cardiovasol Nanchong 637000 Sichuan Peoples R China;

    North Sichuan Med Coll Affiliated Hosp Dept Cardiovasol Nanchong 637000 Sichuan Peoples R China;

    Third Mil Med Univ Dept Occupat Hlth Chongqing Peoples R China;

    Zhejiang Univ Sch Med Dept Occupat &

    Environm Med Hangzhou Peoples R China;

    North Sichuan Med Coll Affiliated Hosp Dept Cardiovasol Nanchong 637000 Sichuan 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

    cadmium; endothelial dysfunction; lipid droplet; lipogenesis; lipolysis;

    机译：镉;内皮功能障碍;脂质液滴;脂肪生成;脂解;

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