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抑制线粒体β-氧化可以选择性地降低大脑中非酶促氧化多不饱和脂肪酸代谢物的水平。

Inhibiting mitochondrial β-oxidation selectively reduces levels of nonenzymatic oxidative polyunsaturated fatty acid metabolites in the brain.

机构信息

Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada.

1] Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada [2] Nestlé Institute of Health Sciences SA, Lausanne, Switzerland.

出版信息

J Cereb Blood Flow Metab. 2014 Mar;34(3):376-9. doi: 10.1038/jcbfm.2013.221. Epub 2013 Dec 11.

Abstract

Schönfeld and Reiser recently hypothesized that fatty acid β-oxidation is a source of oxidative stress in the brain. To test this hypothesis, we inhibited brain mitochondrial β-oxidation with methyl palmoxirate (MEP) and measured oxidative polyunsaturated fatty acid (PUFA) metabolites in the rat brain. Upon MEP treatment, levels of several nonenzymatic auto-oxidative PUFA metabolites were reduced with few effects on enzymatically derived metabolites. Our finding confirms the hypothesis that reduced fatty acid β-oxidation decreases oxidative stress in the brain and β-oxidation inhibitors may be a novel therapeutic approach for brain disorders associated with oxidative stress.

摘要

舍恩菲尔德和赖泽尔最近假设脂肪酸β-氧化是大脑氧化应激的一个来源。为了验证这一假设,我们用甲基棕榈酸(MEP)抑制脑线粒体β-氧化,并测量大鼠脑中氧化多不饱和脂肪酸(PUFA)的代谢物。在 MEP 处理后,几种非酶自动氧化的 PUFA 代谢物的水平降低,而对酶衍生的代谢物影响很小。我们的发现证实了这样的假设,即减少脂肪酸β-氧化可降低大脑中的氧化应激,β-氧化抑制剂可能是治疗与氧化应激相关的大脑疾病的一种新方法。

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