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Phenanthrene-lnduced Apoptosis and Its Underlying Mechanism

机译：菲诱导的细胞凋亡及其潜在机制

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摘要

Phenanthrene (Phe) is one of the most abundant low-molecular-weight polycyclic aromatic hydrocarbons, (PAHs). Widespread human and aquatic organism exposure to Phe has been reported, but the toxic effects of Phe and potential mechanisms are unclear. We focused on the chronic hepatotoxicity of Phe in adult Chinese rare minnows (Gobiocypris rants) and the underlying mechanisms. The chronic effects of exposing Chinese rare minnows to 8.9, 82.3, or 510.0 mu g/L Phe for 30 days were examined by histopathological observation, TUNEL assays, caspase activity assays, and gene expression profiles. The liver lesion frequency and hepatocyte apoptosis were increased in Phe-exposed groups. Caspase 9 and caspase 3 enzyme activity in liver tissues was markedly increased. The expression of miR-17/92 cluster members was significantly increased in the 82.3 and 510.0 mu g/L groups. Moreover, the response of primary hepatocytes indicated a significant decrease in the mitochondria' membrane potential (MMP) after a 48 h exposure to Phe. Interestingly, miR-18a was significantly decreased in primary hepatocytes in all treatments. Moreover, molecular docking indicated that Phe might have the same binding domain as pri-miR-18a, forming pi-pi and pi-sigma interactions with heterogeneous nuclear ribonucleoprotein (hnRNP) Al. Given the above, Phe caused liver lesions and induced hepatocyte apoptosis through the intrinsic apoptosis pathway, and the interaction of Phe with hnRNP Al contributes to the suppression of miR-18a expression and hepatocyte apoptosis.
机译：菲（Phe）是最丰富的低分子量多环芳烃（PAHs）之一。据报道，人类和水生生物广泛接触Phe，但是Phe的毒性作用和潜在机制尚不清楚。我们集中研究了成年中国稀有min鱼（Gobiocypris rants）中苯丙氨酸的慢性肝毒性及其潜在机制。通过组织病理学观察，TUNEL分析，胱天蛋白酶活性分析和基因表达谱，研究了将中国稀有小鱼暴露于8.9、82.3或510.0μg / L Phe 30天的慢性影响。 Phe暴露组肝损伤频率和肝细胞凋亡增加。肝组织中的胱天蛋白酶9和胱天蛋白酶3酶活性明显增加。在82.3和510.0μg / L组中，miR-17 / 92簇成员的表达显着增加。此外，原发性肝细胞的反应表明，暴露于Phe 48小时后，线粒体的膜电位（MMP）明显降低。有趣的是，在所有处理中，miR-18a在原代肝细胞中均显着降低。此外，分子对接表明Phe可能具有与pri-miR-18a相同的结合结构域，与异质核糖核蛋白（hnRNP）A1形成pi-pi和pi-sigma相互作用。鉴于以上所述，Phe通过内在的凋亡途径引起肝损伤并诱导肝细胞凋亡，并且Phe与hnRNP A1的相互作用有助于抑制miR-18a表达和肝细胞凋亡。

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  • 来源
    《Environmental Science & Technology》 |2017年第24期|14397-14405|共9页
  • 作者

    Hong Xiangsheng; Qin Jianhui; Chen Rui; Yuan Lilai; Zha Jinmiao; Huang Chao; Li Na; Ji Xiaoya; Wang Zijian;

  • 作者单位

    Chinese Acad Sci, Res Ctr Ecoenvironm Sci, Key Lab Drinking Water Sci & Technol, Beijing 100085, Peoples R China;

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

    Chinese Acad Sci, Res Ctr Ecoenvironm Sci, Key Lab Drinking Water Sci & Technol, Beijing 100085, Peoples R China;

    Chinese Acad Sci, Res Ctr Ecoenvironm Sci, Key Lab Drinking Water Sci & Technol, Beijing 100085, Peoples R China;

    Chinese Acad Sci, Res Ctr Ecoenvironm Sci, Key Lab Drinking Water Sci & Technol, Beijing 100085, Peoples R China;

    Chinese Acad Sci, Res Ctr Ecoenvironm Sci, Key Lab Drinking Water Sci & Technol, Beijing 100085, Peoples R China;

    Chinese Acad Sci, Res Ctr Ecoenvironm Sci, Key Lab Drinking Water Sci & Technol, Beijing 100085, Peoples R China;

    Chinese Acad Sci, Res Ctr Ecoenvironm Sci, Key Lab Drinking Water Sci & Technol, Beijing 100085, Peoples R China;

    Chinese Acad Sci, Res Ctr Ecoenvironm Sci, Key Lab Drinking Water Sci & Technol, Beijing 100085, 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);
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