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乙醇诱导由线粒体活性氧调节的自噬 于……(原文此处不完整)

Ethanol Induces Autophagy Regulated by Mitochondrial ROS in .

作者信息

Jing Hongjuan, Liu Huanhuan, Zhang Lu, Gao Jie, Song Haoran, Tan Xiaorong

机构信息

College of Biological Engineering, Henan University of Technology, Zhengzhou 450001, P.R. China.

出版信息

J Microbiol Biotechnol. 2018 Dec 28;28(12):1982-1991. doi: 10.4014/jmb.1806.06014.

DOI:10.4014/jmb.1806.06014
PMID:30394045
Abstract

Ethanol accumulation inhibited the growth of during wine fermentation. Autophagy and the release of reactive oxygen species (ROSs) were also induced under ethanol stress. However, the relation between autophagy and ethanol stress was still unclear. In this study, expression of the autophagy genes and and production of ROS under ethanol treatment in yeast were measured. The results showed that ethanol stress very significantly induced expression of and genes and the production of peroxide hydrogen (H₂O₂) and superoxide anion (O₂). Moreover, the and mutants aggregated more H₂O₂ and O₂ than the wild-type yeast. In addition, inhibitors of the ROS scavenging enzyme induced expression of the and genes by increasing the levels of H₂O₂ and O₂. In contrast, glutathione (GSH) and N-acetylcystine (NAC) decreased the and expression by reducing H₂O₂ and O₂ production. Rapamycin and 3-methyladenine also caused an obvious change in autophagy levels and simultaneously altered the release of H₂O₂ and O₂. Finally, inhibitors of mitochondrial electron transport chain (mtETC) increased the production of H₂O₂ and O₂ and also promoted expression levels of the and genes. In conclusion, ethanol stress induced autophagy which was regulated by H₂O₂ and O₂ derived from mtETC, and in turn, the autophagy contributed to the elimination H₂O₂ and O₂.

摘要

乙醇积累在葡萄酒发酵过程中抑制了酵母的生长。在乙醇胁迫下还诱导了自噬和活性氧(ROS)的释放。然而,自噬与乙醇胁迫之间的关系仍不清楚。在本研究中,测定了酵母在乙醇处理下自噬基因的表达以及ROS的产生。结果表明,乙醇胁迫非常显著地诱导了自噬基因的表达以及过氧化氢(H₂O₂)和超氧阴离子(O₂)的产生。此外,自噬基因的突变体比野生型酵母积累了更多的H₂O₂和O₂。另外,ROS清除酶的抑制剂通过增加H₂O₂和O₂的水平诱导了自噬基因的表达。相反,谷胱甘肽(GSH)和N - 乙酰半胱氨酸(NAC)通过减少H₂O₂和O₂的产生降低了自噬基因的表达。雷帕霉素和3 - 甲基腺嘌呤也引起了自噬水平的明显变化,同时改变了H₂O₂和O₂的释放。最后,线粒体电子传递链(mtETC)的抑制剂增加了H₂O₂和O₂的产生,也促进了自噬基因的表达水平。总之,乙醇胁迫诱导的自噬受mtETC产生的H₂O₂和O₂调控,反过来,自噬有助于清除H₂O₂和O₂。

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