铜蓝蛋白作为低密度脂蛋白氧化酶：被抗坏血酸和脱氢抗坏血酸激活。

Ceruloplasmin as low-density lipoprotein oxidase: activation by ascorbate and dehydroascorbate.

作者信息

Feichtenhofer S, Fabjan J S, Abuja P M

机构信息

Institute of Molecular Biology, Biochemistry and Microbiology, SFB Biomembrane Research Centre, University of Graz, Schubertstrasse 1, A-8010, Graz, Austria.

出版信息

FEBS Lett. 2001 Jul 13;501(1):42-6. doi: 10.1016/s0014-5793(01)02623-0.

DOI:10.1016/s0014-5793(01)02623-0

PMID:11457453

Abstract

The ability of ceruloplasmin (Cp) to oxidize low-density lipoproteins (LDL) in the presence of water-soluble antioxidants was investigated and a reaction mechanism proposed. Ascorbate strongly enhanced LDL oxidation, but only after its rapid consumption. Dehydroascorbate enhanced Cp-mediated LDL oxidation even more strongly. Lipid-soluble antioxidants and water-soluble peroxides did not show noticeable activation. However, loading of LDL with lipid hydroperoxides increased the initial oxidation rate. We conclude that Cp mediates a localized redox cycle, where reduction of Cp-Cu2+ is effected by water-soluble reductants and reoxidation by liposoluble hydroperoxides.

摘要

研究了在水溶性抗氧化剂存在下铜蓝蛋白（Cp）氧化低密度脂蛋白（LDL）的能力，并提出了一种反应机制。抗坏血酸强烈增强LDL氧化，但仅在其快速消耗之后。脱氢抗坏血酸更强烈地增强了Cp介导的LDL氧化。脂溶性抗氧化剂和水溶性过氧化物未表现出明显的活化作用。然而，用脂质氢过氧化物加载LDL会提高初始氧化速率。我们得出结论，Cp介导一个局部的氧化还原循环，其中Cp-Cu2+的还原由水溶性还原剂实现，而再氧化由脂溶性氢过氧化物实现。