Peroxidation-induced perturbations of erythrocyte lipid organization.
Peroxidation-induced perturbations of erythrocyte lipid organization.
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过氧化诱导的红细胞脂质组织扰动。
DOI：
10.1016/0005-2736(90)90132-8
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发表时间：
1990
期刊：
影响因子：
--
通讯作者：
Schlegel,RA
中科院分区：
文献类型：
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作者：
Pradhan,D;Weiser,M;Lumley-Sapanski,K;Frazier,D;Kemper,S;Williamson,P;Schlegel,RA
过氧化氢使红细胞膜脂质过氧化，扰乱脂质双层，增加巨噬细胞的吞噬能力。这项研究阐述了这些过程的潜在机制，特别是丙二醛的作用，丙二醛是脂质过氧化的主要副产物。当红细胞用过氧化氢或抗坏血酸/铁处理产生丙二醛，或用丙二醛本身处理时，只有那些用过氧化氢处理的细胞显示磷脂间距增加和吞噬能力增强。这一结果表明，所观察到的变化是过氧化氢处理所独有的，丙二醛在诱导这些表面性质变化中不起作用。对人脐静脉内皮细胞的黏附和吞噬作用的比较表明，吞噬作用的增加并不能通过增强黏附来反映。这一结果表明，两种不同的信号可能介导了巨噬细胞和内皮细胞对红细胞的识别。
Peroxidation of erythrocyte membrane lipids by hydrogen peroxide perturbs the lipid bilayer and increases phagocytosis by macrophages. This study addresses the underlying mechanism of these processes, and in particular the role of malondialdehyde, a major byproduct of lipid peroxidation. When erythrocytes were treated with hydrogen peroxide or ascorbate/iron to generate malondialdehyde, or with malondialdehyde itself, only those cells treated with hydrogen peroxide showed increased phospholipid spacing and enhanced phagocytosis. This result indicates that the alterations observed are unique to hydrogen peroxide treatment, and that malondialdehyde does not play a role in inducing these changes in surface properties. Comparison of adherence to human umbilical vein endothelial cells and phagocytosis showed that increased phagocytosis was not mirrored by enhanced adherence. This result suggests that two different signals may mediate recognition of erythrocytes by macrophages and by endothelial cells.