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12（S）-氢过氧化二十碳四烯酸（12-HETE）通过增加线粒体内钙含量来增加线粒体一氧化氮。

12(S)-hydroperoxyeicosatetraenoic acid (12-HETE) increases mitochondrial nitric oxide by increasing intramitochondrial calcium.

作者信息

Nazarewicz Rafal R, Zenebe Woineshet J, Parihar Arti, Parihar Mordhwaj S, Vaccaro Michael, Rink Cameron, Sen Chandan K, Ghafourifar Pedram

机构信息

Department of Surgery, Davis Heart and Lung Research Institute, Institute of Mitochondrial Biology, The Ohio State University, 460 West 12th Avenue, Columbus, OH 43210, USA.

出版信息

Arch Biochem Biophys. 2007 Dec 1;468(1):114-20. doi: 10.1016/j.abb.2007.09.018. Epub 2007 Sep 29.

DOI:10.1016/j.abb.2007.09.018
PMID:17963719
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2210014/
Abstract

12(S)-hydroxyeicosatetraenoic acid (12-HETE) is one of the metabolites of arachidonic acid involved in pathological conditions associated with mitochondria and oxidative stress. The present study tested effects of 12-HETE on mitochondrial functions. In isolated rat heart mitochondria, 12-HETE increases intramitochondrial ionized calcium concentration that stimulates mitochondrial nitric oxide (NO) synthase (mtNOS) activity. mtNOS-derived NO causes mitochondrial dysfunctions by decreasing mitochondrial respiration and transmembrane potential. mtNOS-derived NO also produces peroxynitrite that induces release of cytochrome c and stimulates aggregation of mitochondria. Similarly, in HL-1 cardiac myocytes, 12-HETE increases intramitochondrial calcium and mitochondrial NO, and induces apoptosis. The present study suggests a novel mechanism for 12-HETE toxicity.

摘要

12（S）-羟基二十碳四烯酸（12-HETE）是花生四烯酸的代谢产物之一，参与与线粒体和氧化应激相关的病理状况。本研究测试了12-HETE对线粒体功能的影响。在分离的大鼠心脏线粒体中，12-HETE增加线粒体内游离钙浓度，刺激线粒体一氧化氮（NO）合酶（mtNOS）活性。mtNOS衍生的NO通过降低线粒体呼吸和跨膜电位导致线粒体功能障碍。mtNOS衍生的NO还产生过氧亚硝酸盐，诱导细胞色素c释放并刺激线粒体聚集。同样，在HL-1心肌细胞中，12-HETE增加线粒体内钙和线粒体NO，并诱导细胞凋亡。本研究提出了12-HETE毒性的新机制。

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本文引用的文献

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Hypoxia/reoxygenation of isolated rat heart mitochondria causes cytochrome c release and oxidative stress; evidence for involvement of mitochondrial nitric oxide synthase.
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