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首页> 外文期刊>Journal of Agricultural and Food Chemistry >Acrylamide Induces Abnormal mtDNA Expression by Causing Mitochondrial ROS Accumulation, Biogenesis, and Dynamics Disorders
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Acrylamide Induces Abnormal mtDNA Expression by Causing Mitochondrial ROS Accumulation, Biogenesis, and Dynamics Disorders

机译：丙烯酰胺通过引起线粒体ROS累积，生物发生和动力学疾病来诱导异常的MTDNA表达

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摘要

Acrylamide, a well-documented neurotoxicant, is commonly found as a byproduct of the Maillard reaction in carbohydrate-rich foods. Numerous studies have indicated that acrylamide-induced apoptosis accompanied by mitochondrial dysfunction contributes to its neurotoxicity. However, the mechanisms of how acrylamide causes mitochondrial impairment is not well understood. In this study, we observed destroyed redox balance, accumulated mitochondrial reactive oxygen species (ROS), damaged mitochondrial structures, and activated apoptosis in astrocytes following acrylamide treatment. Furthermore, acrylamide decreased the expression of mitochondrial biogenesis- and dynamics-related genes, including PGC-1 alpha, TFAM, Mfn2, and Opa1, and altered the expression of mitochondrial DNA (mtDNA)-encoded mitochondrial respiratory chain complexes, along with the inhibited mitochondrial respiration. Pretreatment with a mitochondrial ROS scavenger mitoquinone dramatically restored the expressions of PGC-1 alpha, TFAM, Mfn2, and Opa1; protected the mitochondrial structure; and decreased acrylamide-induced apoptosis. Further in vivo experiments confirmed that acrylamide decreased the expressions of PGC-1 alpha, TFAM, Mfn2, and Opa1 in rat brain tissues. These results revealed that acrylamide triggered the mitochondrial ROS accumulation to interfere with mitochondrial biogenesis and dynamics, causing mtDNA damage and finally resulting in mitochondrial dysfunction and apoptosis.
机译：丙烯酰胺是一种公认的神经毒性物质，在富含碳水化合物的食物中通常被发现是美拉德反应的副产物。大量研究表明，丙烯酰胺诱导的细胞凋亡伴随线粒体功能障碍是其神经毒性的原因之一。然而，丙烯酰胺导致线粒体损伤的机制尚不清楚。在这项研究中，我们观察到丙烯酰胺处理后星形胶质细胞的氧化还原平衡被破坏，线粒体活性氧（ROS）积累，线粒体结构受损，细胞凋亡被激活。此外，丙烯酰胺降低了线粒体生物发生和动力学相关基因的表达，包括PGC-1α、TFAM、Mfn2和Opa1，并改变了线粒体DNA（mtDNA）编码的线粒体呼吸链复合物的表达，同时抑制了线粒体呼吸。线粒体活性氧清除剂米托醌预处理可显著恢复PGC-1α、TFAM、Mfn2和Opa1的表达；保护线粒体结构；减少丙烯酰胺诱导的细胞凋亡。进一步的体内实验证实，丙烯酰胺降低了大鼠脑组织中PGC-1α、TFAM、Mfn2和Opa1的表达。这些结果表明，丙烯酰胺触发线粒体活性氧的积累，干扰线粒体的生物发生和动力学，导致线粒体DNA损伤，最终导致线粒体功能障碍和凋亡。

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  • 作者

    Yang Liuqing; Dong Li; Zhang Lujia; Bai Jie; Chen Fang; Luo Yinghua;

  • 作者单位

    China Agr Univ Coll Food Sci &

    Nutr Engn Minist Educ Natl Engn Res Ctr Fruits &

    Vegetables Proc Minist Engn Res Ctr Fruits &

    Vegetables Proc Key Lab Sto Beijing 100083 Peoples R China;

    China Agr Univ Coll Food Sci &

    Nutr Engn Minist Educ Natl Engn Res Ctr Fruits &

    Vegetables Proc Minist Engn Res Ctr Fruits &

    Vegetables Proc Key Lab Sto Beijing 100083 Peoples R China;

    China Agr Univ Coll Food Sci &

    Nutr Engn Minist Educ Natl Engn Res Ctr Fruits &

    Vegetables Proc Minist Engn Res Ctr Fruits &

    Vegetables Proc Key Lab Sto Beijing 100083 Peoples R China;

    China Agr Univ Coll Food Sci &

    Nutr Engn Minist Educ Natl Engn Res Ctr Fruits &

    Vegetables Proc Minist Engn Res Ctr Fruits &

    Vegetables Proc Key Lab Sto Beijing 100083 Peoples R China;

    China Agr Univ Coll Food Sci &

    Nutr Engn Minist Educ Natl Engn Res Ctr Fruits &

    Vegetables Proc Minist Engn Res Ctr Fruits &

    Vegetables Proc Key Lab Sto Beijing 100083 Peoples R China;

    China Agr Univ Coll Food Sci &

    Nutr Engn Minist Educ Natl Engn Res Ctr Fruits &

    Vegetables Proc Minist Engn Res Ctr Fruits &

    Vegetables Proc Key Lab Sto Beijing 100083 Peoples R China;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 营养卫生、食品卫生;农业科学;
  • 关键词

    acrylamide; mitochondrial ROS; mitochondrial dynamics; mitochondrial biogenesis; neurotoxicity;

    机译：丙烯酰胺;线粒体ROS;线粒体动力学;线粒体生物发生;神经毒性;

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