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胆固醇氢过氧化物及其降解机制。

Cholesterol hydroperoxides and their degradation mechanism.

作者信息

Terao Junji

机构信息

Institute of Health Biosciences, University of Tokushima Graduate School, Tokushima, 770-8503, Japan,

出版信息

Subcell Biochem. 2014;77:83-91. doi: 10.1007/978-94-007-7920-4_7.

DOI:10.1007/978-94-007-7920-4_7
PMID:24374920
Abstract

Cholesterol is one of the oxidizable lipids constituting biomembranes and plasma lipoproteins. Cholesterol hydroperoxides (Chol-OOH) are the primary products if cholesterol is subjected to attack by reactive oxygen species. In particular, singlet molecular oxygen reacts with cholesterol to yield cholesterol 5α-hydroperoxide as the major hydroperoxide species. Chol-OOH may accumulate in biological systems because of its resistance to glutathione-dependent enzymatic detoxification reactions. Their degradation products (including hydroxycholesterol and 7-ketocholesterol) participate in the pathophysiological functions of oxysterols. Highly reactive cholesterol 5,6-secosterol present in atherosclerotic lesions can be derived from the degradation of cholesterol 5α-hydroperoxide. Chol-OOH themselves may affect the lipid rafts of biomembranes, thereby leading to the modification of signal transduction pathways.

摘要

胆固醇是构成生物膜和血浆脂蛋白的可氧化脂质之一。如果胆固醇受到活性氧的攻击,胆固醇氢过氧化物(Chol-OOH)是主要产物。特别是,单线态分子氧与胆固醇反应生成胆固醇5α-氢过氧化物作为主要的氢过氧化物种类。Chol-OOH可能因其对谷胱甘肽依赖性酶解毒反应的抗性而在生物系统中积累。它们的降解产物(包括羟基胆固醇和7-酮胆固醇)参与氧化甾醇的病理生理功能。存在于动脉粥样硬化病变中的高反应性胆固醇5,6-断胆甾醇可源自胆固醇5α-氢过氧化物的降解。Chol-OOH本身可能会影响生物膜的脂筏,从而导致信号转导途径的改变。

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Cholesterol hydroperoxides and their degradation mechanism.胆固醇氢过氧化物及其降解机制。
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2
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