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紫外线B诱导的人低密度和高密度脂蛋白脂质的光过氧化。色氨酸残基的可能作用。

UVB-induced photoperoxidation of lipids of human low and high density lipoproteins. A possible role of tryptophan residues.

作者信息

Salmon S, Maziere J C, Santus R, Morliere P, Bouchemal N

机构信息

Muséum National d'Histoire Naturelle, INSERM U312, Paris, France.

出版信息

Photochem Photobiol. 1990 Sep;52(3):541-5. doi: 10.1111/j.1751-1097.1990.tb01797.x.

DOI:10.1111/j.1751-1097.1990.tb01797.x
PMID:2126629
Abstract

Ultraviolet radiation of the UVB region readily destroy tryptophan (Trp) residues of low (LDL) and high (HDL) density lipoproteins. The photooxidation of tryptophan residues is accompanied by the peroxidation of low and high density lipoproteins unsaturated fatty acids, as measured by the thiobarbituric acid assay. Moreover, low and high density lipoproteins are natural carriers of vitamin E and carotenoids. These two antioxidants are also rapidly bleached by UVB. The UVA radiation promotes neither tryptophan residue destruction nor lipid photoperoxidation. The redox cycling Cu2+ ions considerably increase lipid photoperoxidation. The synergistic action of photo and auto (Cu2(+)-induced) peroxidation induces marked post-irradiation modifications of apolipoproteins as illustrated by the degradation of most tryptophan residues after overnight incubation in the dark of pre-irradiated samples.

摘要

UVB区域的紫外线辐射很容易破坏低密度脂蛋白(LDL)和高密度脂蛋白(HDL)中的色氨酸(Trp)残基。通过硫代巴比妥酸测定法可知,色氨酸残基的光氧化伴随着低密度和高密度脂蛋白不饱和脂肪酸的过氧化。此外,低密度脂蛋白和高密度脂蛋白是维生素E和类胡萝卜素的天然载体。这两种抗氧化剂也会被UVB迅速漂白。UVA辐射既不会促进色氨酸残基的破坏,也不会促进脂质光过氧化。氧化还原循环的Cu2+离子会显著增加脂质光过氧化。光过氧化和自动(Cu2+诱导)过氧化的协同作用会诱导载脂蛋白发生明显的辐照后修饰,如预辐照样品在黑暗中过夜孵育后,大多数色氨酸残基降解所示。

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