ALTERATIONS IN MITOCHONDRIAL-MEMBRANE FLUIDITY BY LIPID-PEROXIDATION PRODUCTS

ALTERATIONS IN MITOCHONDRIAL-MEMBRANE FLUIDITY BY LIPID-PEROXIDATION PRODUCTS
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DOI:
10.1016/0891-5849(94)90167-8
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发表时间:
1994-11-01
影响因子:
7.4
通讯作者:
YU, BP
YU, BP
中科院分区:
医学1区
文献类型:
--
作者:
CHEN, JJ;YU, BP

文献摘要

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线粒体膜的线粒体相关损伤,包括膜流动性降低,已归因于自由基反应。我们以前的研究指出,脂质过氧化作为一个主要原因,在与年龄有关的变化,膜流动性。这份报告提供了新的证据,脂质过氧化调节膜流动性的降低是通过两种植物脂质过氧化产物,4-羟基壬烯醛(HNE)和丙二醛(MDA)介导的。从不同年龄的自由进食(AL)和饮食限制(DR)大鼠中分离肝线粒体。醛类物质的引入使线粒体膜流动性降低,但HNE引起的膜流动性降低比MDA引起的膜流动性降低更明显。HNE似乎可能通过与膜磷脂的直接相互作用来改变膜流动性,如HNE和膜磷脂之间产生荧光复合物所示。最后,在线粒体中分离和定量HNE和MDA。它们的水平在不同年龄和饮食组的动物之间存在明显差异。这些数据表明,脂质过氧化反应产物,尤其是HNE,可能在介导衰老动物线粒体膜流动性降低中起重要作用。
Age-related damage to the mitochondrial membrane, including decreased membrane fluidity, has been attributed to free radical reactions. Our previous studies point to lipid peroxidation as a primary cause in age-related changes in membrane fluidity. This report offers new evidence that lipid peroxidation-modulated decreases in membrane fluidity are mediated through two aldehydic lipid peroxidation products, 4-hydroxynonenal (HNE) and malondialdehyde (MDA). Hepatic mitochondria were isolated from both ad libitum fed (AL) and dietary restricted (DR) rats of different ages. Introduction of the aldehydes was found to decrease mitochondrial membrane fluidity, although the fluidity decrease induced by HNE was more pronounced than that induced by MDA. It seems likely that HNE modifies membrane fluidity by direct interaction with membrane phospholipids, as shown by the generation of a fluorescent complex between HNE and membrane phospholipids. Finally, HNE and MDA were isolated and quantitated in mitochondria. Their levels clearly differentiated between animals of different age and dietary groups. These data indicate that the reactive products of lipid peroxidation, especially HNE, may play an important role in mediating the decreased mitochondrial membrane fluidity observed in aging animals.