Oxidative damage induced by the fullerene C60 on photosensitization in rat liver microsomes
Oxidative damage induced by the fullerene C60 on photosensitization in rat liver microsomes
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DOI：
10.1016/s0009-2797(98)00047-7
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发表时间：
1998-07-24
影响因子：
5.1
通讯作者：
Mittal, JP
中科院分区：
文献类型：
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作者：
Kamat, JP;Devasagayam, TPA;Mittal, JP
我们已经研究了一种常用的富勒烯，C-60，诱导氧化损伤的光敏作用，以大鼠肝微粒体作为模型膜的能力。当C-60以其环糊精复合物的形式掺入大鼠肝微粒体中并暴露于紫外线或可见光时，它诱导了显著的氧化损伤：（1）通过硫代巴比妥酸反应物质（TBARS）、脂质氢过氧化物和共轭二烯测定的脂质过氧化，和（2）通过蛋白质羰基和膜结合酶损失评估的蛋白质损伤。诱导的氧化损伤具有时间和浓度依赖性。单线态氧（O-1（2））、β-胡萝卜素和叠氮化钠的猝灭剂以及缓冲液增强的过氧化反应的氘代反应均能显著抑制C-60加光诱导的脂质过氧化反应。这些观察结果表明，C-60是一种有效的过氧化诱导剂，主要是由于O-1（2）。生物抗氧化剂，如谷胱甘肽，抗坏血酸和α-生育酚显着不同的能力，以抑制过氧化诱导的C-60。因此，我们的研究表明，C-60在光敏作用下可以诱导生物膜中显着的脂质过氧化和其他形式的氧化损伤，并且这种现象可以通过内源性抗氧化剂和活性氧清除剂进行很大程度的调节。(C)1998爱思唯尔科学爱尔兰有限公司保留所有权利。
We have examined the ability of a commonly used fullerene, C-60, to induce oxidative damage on photosensitization using rat liver microsomes as model membranes. When C-60 was incorporated into rat liver microsomes in the form of its cyclodextrin complex and exposed to UV or visible light, it induced significant oxidative damage in terms of (1) lipid peroxidation as assayed by thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides and conjugated dienes, and (2) damage to proteins as assessed by protein carbonyls and loss of the membrane-bound enzymes. The oxidative damage induced was both time- and concentration-dependent. C-60 plus light-induced lipid peroxidation was significantly inhibited by the quenchers of singlet oxygen (O-1(2)), beta-carotene and sodium azide, and deuteration of the buffer-enhanced peroxidation. These observations indicate that C-60 is an efficient inducer of peroxidation and is predominantly due to O-1(2). Biological antioxidants such as glutathione, ascorbic acid and alpha-tocopherol significantly differ in their ability to inhibit peroxidation induced by C-60. Our studies, hence, indicate that C-60, on photosensitization, can induce significant lipid peroxidation and other forms of oxidative damage in biological membranes and that this phenomenon can be greatly modulated by endogenous antioxidants and scavengers of reactive oxygen species. (C) 1998 Elsevier Science Ireland Ltd. All rights reserved.