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富勒烯C60对大鼠肝微粒体光致敏作用诱导的氧化损伤。

Oxidative damage induced by the fullerene C60 on photosensitization in rat liver microsomes.

作者信息

Kamat J P, Devasagayam T P, Priyadarsini K I, Mohan H, Mittal J P

机构信息

Cell Biology Division, Bhabha Atomic Research Centre, Mumbai, India.

出版信息

Chem Biol Interact. 1998 Jul 24;114(3):145-59. doi: 10.1016/s0009-2797(98)00047-7.

DOI:10.1016/s0009-2797(98)00047-7
PMID:9839628
Abstract

We have examined the ability of a commonly used fullerene, C60, to induce oxidative damage on photosensitization using rat liver microsomes as model membranes. When C60 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. C60 plus light-induced lipid peroxidation was significantly inhibited by the quenchers of singlet oxygen ((1)O2), beta-carotene and sodium azide, and deuteration of the buffer-enhanced peroxidation. These observations indicate that C60 is an efficient inducer of peroxidation and is predominantly due to (1)O2. Biological antioxidants such as glutathione, ascorbic acid and alpha-tocopherol significantly differ in their ability to inhibit peroxidation induced by C60. Our studies, hence, indicate that C60, 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.

摘要

我们以大鼠肝微粒体作为模型膜,研究了常用富勒烯C60在光致敏作用下诱导氧化损伤的能力。当C60以其环糊精复合物的形式掺入大鼠肝微粒体并暴露于紫外线或可见光下时,它在以下方面诱导了显著的氧化损伤:(1)通过硫代巴比妥酸反应性物质(TBARS)、脂质氢过氧化物和共轭二烯测定的脂质过氧化;(2)通过蛋白质羰基和膜结合酶的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(1O2)猝灭剂β-胡萝卜素和叠氮化钠可显著抑制C60加光诱导的脂质过氧化,缓冲液的氘化增强了过氧化作用。这些观察结果表明,C60是一种有效的过氧化诱导剂,主要归因于1O2。生物抗氧化剂如谷胱甘肽、抗坏血酸和α-生育酚在抑制C60诱导的过氧化能力方面存在显著差异。因此,我们的研究表明,C60在光致敏作用下可在生物膜中诱导显著的脂质过氧化和其他形式的氧化损伤,并且这种现象可被内源性抗氧化剂和活性氧清除剂大大调节。

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