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缺乏加剧丙烯醛诱导的肺损伤通过线粒体氧化还原环境恶化。

Deficiency Exacerbates Acrolein-Induced Lung Injury through Mitochondrial Redox Environment Deterioration.

机构信息

Department of Food and Biotechnology, Korea University, Sejong, Republic of Korea.

School of Life Sciences and Biotechnology, BK21 Plus KNU Creative BioResearch Group, College of Natural Sciences, Kyungpook National University, Taegu, Republic of Korea.

出版信息

Oxid Med Cell Longev. 2017;2017:1595103. doi: 10.1155/2017/1595103. Epub 2017 Dec 31.

DOI:10.1155/2017/1595103
PMID:29456784
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5804324/
Abstract

Acrolein is known to be involved in acute lung injury and other pulmonary diseases. A number of studies have suggested that acrolein-induced toxic effects are associated with depletion of antioxidants, such as reduced glutathione and protein thiols, and production of reactive oxygen species. Mitochondrial NADP-dependent isocitrate dehydrogenase () regulates mitochondrial redox balance and reduces oxidative stress-induced cell injury via generation of NADPH. Therefore, we evaluated the role of in acrolein-induced lung injury using short hairpin RNA- (shRNA-) transfected Lewis lung carcinoma (LLC) cells and -deficient ( ) mice. Downregulation of expression increased susceptibility to acrolein via induction of apoptotic cell death due to elevated mitochondrial oxidative stress. deficiency also promoted acrolein-induced lung injury in knockout mice through the disruption of mitochondrial redox status. In addition, acrolein-induced toxicity in shRNA-transfected LLC cells and in knockout mice was ameliorated by the antioxidant, N-acetylcysteine, through attenuation of oxidative stress resulting from deficiency. In conclusion, deficiency leads to mitochondrial redox environment deterioration, which causes acrolein-mediated apoptosis of LLC cells and acrolein-induced lung injury in mice. The present study supports the central role of deficiency in inducing oxidative stress resulting from acrolein-induced disruption of mitochondrial redox status in the lung.

摘要

丙烯醛已知会引起急性肺损伤和其他肺部疾病。许多研究表明，丙烯醛诱导的毒性作用与抗氧化剂的耗竭有关，如还原型谷胱甘肽和蛋白质巯基减少，以及活性氧的产生。线粒体 NADP 依赖性异柠檬酸脱氢酶 () 调节线粒体氧化还原平衡，并通过生成 NADPH 减轻氧化应激诱导的细胞损伤。因此，我们使用短发夹 RNA- (shRNA-) 转染的 Lewis 肺癌 (LLC) 细胞和 -缺陷 () 小鼠评估了在丙烯醛诱导的肺损伤中的作用。由于线粒体氧化应激增加，下调表达会通过诱导细胞凋亡死亡增加对丙烯醛的敏感性。缺陷也通过破坏线粒体氧化还原状态促进 敲除小鼠中的丙烯醛诱导的肺损伤。此外，抗氧化剂 N-乙酰半胱氨酸通过减轻由于 缺陷导致的氧化应激，改善了 shRNA 转染的 LLC 细胞和 敲除小鼠中的丙烯醛诱导的毒性。总之，缺陷导致线粒体氧化还原环境恶化，导致 LLC 细胞中的丙烯醛介导的细胞凋亡和 小鼠中的丙烯醛诱导的肺损伤。本研究支持 缺陷在诱导由丙烯醛诱导的线粒体氧化还原状态破坏引起的氧化应激方面的核心作用在肺部。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0ff/5804324/011ad818c28a/OMCL2017-1595103.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0ff/5804324/44bd95a3525a/OMCL2017-1595103.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0ff/5804324/219a5e7be09a/OMCL2017-1595103.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0ff/5804324/039a18b8c596/OMCL2017-1595103.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0ff/5804324/08ee85cfb948/OMCL2017-1595103.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0ff/5804324/68183ee3ff89/OMCL2017-1595103.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0ff/5804324/011ad818c28a/OMCL2017-1595103.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0ff/5804324/44bd95a3525a/OMCL2017-1595103.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0ff/5804324/219a5e7be09a/OMCL2017-1595103.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0ff/5804324/039a18b8c596/OMCL2017-1595103.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0ff/5804324/08ee85cfb948/OMCL2017-1595103.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0ff/5804324/68183ee3ff89/OMCL2017-1595103.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f0ff/5804324/011ad818c28a/OMCL2017-1595103.006.jpg

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