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红细胞脂质的选择性联合丢失。

The selective and conjoint loss of red cell lipids.

作者信息

Cooper R A, Jandl J H

出版信息

J Clin Invest. 1969 May;48(5):906-14. doi: 10.1172/JCI106049.

Abstract

The pattern of lipid loss from the membrane of red cells incubated in serum is influenced by the availability of glucose. Under homeostatic conditions with respect to glucose, cholesterol alone is lost. This results from esterification of free cholesterol in serum by the serum enzyme, lecithin:cholesterol acyltransferase, and is associated with a proportional decrease in membrane surface area, reflected by an increased osmotic fragility. This selective loss of membrane cholesterol also occurs in hereditary spherocytosis (HS) red cells, even after incubation for 65 hr in the presence of glucose. The loss of free cholesterol from red cells relative to its loss from serum, under these conditions, is greatest at higher hematocrits, similar to those found in the spleen. Although the selective loss of membrane cholesterol increases the spherodicity of normal red cells, it does not lead to a change in their rate of glucose consumption, and both the loss of cholesterol and the increase in osmotic fragility are reversible in vitro. Moreover, normal red cells made osmotically fragile by cholesterol depletion in vitro rapidly become osmotically normal and survive normally after their reinfusion in vivo.In contrast to this selective loss of membrane cholesterol, red cells incubated in the absence of glucose lose both cholesterol and phospholipid. This occurs more rapidly in HS than normal red cells and is followed by a disruption of cation gradients and then by hemolysis. Cholesterol and phospholipid lost under these conditions is not restored during subsequent incubations in vitro. Selective loss of membrane cholesterol is a physiologic event secondary to an altered state of serum lipids. It is reversible both in vitro and in vivo and neither influences cellular metabolism nor impairs viability. Conjoint loss of phospholipid and cholesterol, however, results from intrinsic injury to the red cell membrane which results from prolonged metabolic depletion.

摘要

在血清中孵育的红细胞膜脂质损失模式受葡萄糖可用性的影响。在葡萄糖稳态条件下,仅胆固醇会流失。这是由于血清中的卵磷脂胆固醇酰基转移酶将血清中的游离胆固醇酯化所致,并且与膜表面积的成比例减少相关,这通过渗透脆性增加得以体现。这种膜胆固醇的选择性流失也发生在遗传性球形红细胞增多症(HS)的红细胞中,即使在有葡萄糖存在的情况下孵育65小时后也是如此。在这些条件下,相对于血清中胆固醇的流失,红细胞中游离胆固醇的流失在较高的血细胞比容下最大,类似于在脾脏中发现的情况。尽管膜胆固醇的选择性流失增加了正常红细胞的球形度,但它不会导致其葡萄糖消耗速率发生变化,并且胆固醇的流失和渗透脆性的增加在体外都是可逆的。此外,在体外因胆固醇耗竭而变得渗透脆性增加的正常红细胞在体内重新输注后会迅速恢复渗透正常并正常存活。与这种膜胆固醇的选择性流失相反,在无葡萄糖条件下孵育的红细胞会同时流失胆固醇和磷脂。这种情况在HS红细胞中比正常红细胞发生得更快,随后会破坏阳离子梯度,进而导致溶血。在这些条件下流失的胆固醇和磷脂在随后的体外孵育过程中不会恢复。膜胆固醇的选择性流失是血清脂质状态改变继发的生理事件。它在体外和体内都是可逆的,既不影响细胞代谢也不损害活力。然而,磷脂和胆固醇的联合流失是由于红细胞膜的内在损伤所致,这种损伤是由长期的代谢消耗引起的。

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Hereditary spherocytosis.遗传性球形红细胞增多症
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