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Biochem J. 1988 Dec 15;256(3):861-5. doi: 10.1042/bj2560861.
2
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本文引用的文献

1
Unsaturated lipide oxidation catalyzed by hematin compounds.血红素化合物催化的不饱和脂质氧化。
J Biol Chem. 1955 Dec;217(2):721-33.
2
Inhibition of lipid peroxidation by the iron-binding protein lactoferrin.铁结合蛋白乳铁蛋白对脂质过氧化的抑制作用。
Biochem J. 1981 Oct 1;199(1):259-61. doi: 10.1042/bj1990259.
3
Hemopexin-mediated transport of heme into isolated rat hepatocytes.血红素结合蛋白介导血红素转运至分离的大鼠肝细胞中。
J Biol Chem. 1981 Nov 10;256(21):10902-9.
4
Interactions of the histidine-rich glycoprotein of serum with metals.血清富含组氨酸糖蛋白与金属的相互作用。
Biochemistry. 1981 Mar 3;20(5):1054-61. doi: 10.1021/bi00508a002.
5
Superoxide dismutase in extracellular fluids.细胞外液中的超氧化物歧化酶。
Clin Chim Acta. 1982 Nov 24;126(1):41-51. doi: 10.1016/0009-8981(82)90360-6.
6
Fate of oxygen free radicals in extracellular fluids.细胞外液中氧自由基的归宿
Biochem Soc Trans. 1982 Apr;10(2):72-3. doi: 10.1042/bst0100072.
7
Caeruloplasmin: physiological and pathological perspectives.铜蓝蛋白:生理与病理视角
Crit Rev Clin Lab Sci. 1981;14(4):257-329. doi: 10.3109/10408368109105866.
8
The acute phase response of mouse liver. Genetic analysis of the major acute phase reactants.小鼠肝脏的急性期反应。主要急性期反应物的遗传分析。
J Biol Chem. 1984 Jan 10;259(1):566-73.
9
Hemin-mediated DNA strand scission.血红素介导的DNA链断裂。
J Biol Chem. 1983 Oct 10;258(19):12069-72.
10
The inactivation of hemostatic factors by hematin.血红素对止血因子的灭活作用。
J Lab Clin Med. 1983 Sep;102(3):361-9.

血红素结合蛋白对血红素刺激的脂质过氧化的抗氧化保护作用。

Antioxidant protection by haemopexin of haem-stimulated lipid peroxidation.

作者信息

Gutteridge J M, Smith A

机构信息

Division of Chemistry, National Institute for Biological Standards and Control, Potters Bar, Herts, U.K.

出版信息

Biochem J. 1988 Dec 15;256(3):861-5. doi: 10.1042/bj2560861.

DOI:10.1042/bj2560861
PMID:3223958
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1135495/
Abstract

Haem (ferrous protoporphyrin IX) is a reactive low-molecular-mass form of iron able to participate in oxygen-radical reactions that can lead to the degradation of proteins, lipids, carbohydrates and DNA. Oxygen-radical reactions are likely to occur upon tissue damage. Extracellular fluids rely on antioxidant mechanisms different from those found inside the cell, and circulating proteins limit radical reactions by converting pro-oxidant forms of iron into less-reactive forms. Of the compounds tested, only apohaemopexin and the chain-breaking antioxidant butylated hydroxytoluene inhibited (by more than 90%) haemin-stimulated peroxidation as measured by formation of conjugated dienes, thiobarbituric acid-reactive material from linolenic acid or peroxidation-induced phospholipid fluorescence. Haptoglobin, the haemoglobin-binding serum protein, was ineffective. Conversely, only haptoglobin significantly inhibited haemoglobin-stimulated lipid peroxidation. Iron-salt-induced lipid peroxidation was inhibited only by apotransferrin and the iron-chelator desferrioxamine. All lipid peroxidations were inhibited by the radical scavengers butylated hydroxytoluene and propyl gallate. These findings support the concept that transport and conservation of body iron stores are closely linked to antioxidant protection.

摘要

血红素(亚铁原卟啉IX)是一种具有反应活性的低分子量铁形式,能够参与氧自由基反应,这些反应可导致蛋白质、脂质、碳水化合物和DNA的降解。组织损伤时可能会发生氧自由基反应。细胞外液依赖于与细胞内不同的抗氧化机制,循环蛋白通过将铁的促氧化形式转化为反应性较低的形式来限制自由基反应。在所测试的化合物中,只有脱辅基血红蛋白结合蛋白和链断裂抗氧化剂丁基羟基甲苯抑制(超过90%)了血红素刺激的过氧化反应,这通过共轭二烯的形成、亚麻酸产生的硫代巴比妥酸反应性物质或过氧化诱导的磷脂荧光来测定。结合珠蛋白,即结合血红蛋白的血清蛋白,没有效果。相反,只有结合珠蛋白显著抑制了血红蛋白刺激的脂质过氧化。铁盐诱导的脂质过氧化仅被脱铁转铁蛋白和铁螯合剂去铁胺抑制。所有脂质过氧化反应均被自由基清除剂丁基羟基甲苯和没食子酸丙酯抑制。这些发现支持了体内铁储存的运输和保存与抗氧化保护密切相关的概念。