HYDROGEN-PEROXIDE OXIDATION INDUCES THE TRANSFER OF PHOSPHOLIPIDS FROM THE MEMBRANE INTO THE CYTOSOL OF HUMAN ERYTHROCYTES
HYDROGEN-PEROXIDE OXIDATION INDUCES THE TRANSFER OF PHOSPHOLIPIDS FROM THE MEMBRANE INTO THE CYTOSOL OF HUMAN ERYTHROCYTES
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DOI：
10.1021/bi00181a013
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发表时间：
1994-04-19
期刊：
影响因子：
2.9
通讯作者：
HUESTIS, WH
中科院分区：
文献类型：
--
作者：
BRUNAUER, LS;MOXNESS, MS;HUESTIS, WH
在人红细胞中检测了氧化损伤对膜磷脂组织的影响。暴露于H2O2诱导这些细胞的形状变化，正常的椎间盘细胞成为棘细胞，和外来磷脂酰丝氨酸掺入产生的口细胞恢复到盘状形态。H2O2处理也抑制磷脂酰丝氨酸运输从外到内膜单层，与早期报道的氧化敏感性的氨基磷脂转运。形态学变化与内层单层脂质向外层单层的移动一致，这可能是氨基磷脂螯合受损的预期结果。然而，脂质提取和凝血酶原酶激活试验表明，没有增加暴露的磷脂酰丝氨酸的细胞表面。相反，磷脂酰丝氨酸被发现与H2O2处理的细胞的胞质组分。这些观察结果表明，氧化损伤改变了红细胞膜的脂质组织，而不是通过随机化的脂质类内的双层，但通过诱导提取内单层成分到胞质溶胶。
The effects of oxidative damage on membrane phospholipid organization were examined in human erythrocytes. Exposure to H2O2 induced shape changes in these cells; normal discocytes became echinocytic, and stomatocytes generated by foreign phosphatidylserine incorporation reverted to discoid morphology. H2O2 treatment also inhibited phosphatidylserine transport from the outer to inner membrane monolayer, consistent with earlier reports on oxidative sensitivity of the aminophospholipid translocator. The morphological changes are consistent with movement of inner monolayer lipids to the outer monolayer, as might be expected if aminophospholipid sequestration is compromised. However, lipid extraction and prothrombinase activation assays showed no increased exposure of phosphatidylserine on the cell surface. Instead, phosphatidylserine was found associated with the cytosolic fraction of H2O2-treated cells. These observations suggest that oxidative damage alters the lipid organization of erythrocyte membranes, not by randomizing the lipid classes within the bilayer, but by inducing extraction of inner monolayer components into the cytosol.