Frickenhaus S, Herrmann A, Heinrich R
Humboldt-University Berlin, Institute of Biology, Germany.
Mol Membr Biol. 1998 Oct-Dec;15(4):213-20. doi: 10.3109/09687689709044323.
By a combined kinetic and thermodynamic model on the transbilayer dynamics and asymmetric distribution of lipids in the red blood cell, compensating lipid fluxes to the exoplasmic leaflet have been analysed, counterbalancing the active transport of aminophospholipids to the cytoplasmic monolayer by the aminophospholipid translocase. The compensating fluxes are assumed to be of passive nature generated by forces of lateral mechanical stress and of lipid concentration differences between the two monolayers. These forces are shown to be caused and maintained by the operation of the aminophospholipid translocase. Simulations reveal that a reduction of the compensating fluxes upon ATP-depletion can be attributed to the inhibition of the aminophospholipid translocase. Thus, a Mg(2+)- and ATP-dependence of the outward movement of phospholipid analogues in the plasma membrane of red blood cells can be expected independent of the existence and operation of an ATP-dependent 'floppase' activity.
通过一个关于红细胞中脂质跨膜动力学和不对称分布的联合动力学与热力学模型,分析了向细胞外小叶的补偿性脂质通量,以平衡氨基磷脂转运酶将氨基磷脂主动转运至细胞质单层的过程。补偿通量被假定为是由横向机械应力和两个单层之间的脂质浓度差异所产生的被动性质的通量。这些力被证明是由氨基磷脂转运酶的运作所引起和维持的。模拟结果表明,ATP耗竭时补偿通量的减少可归因于氨基磷脂转运酶的抑制。因此,可以预期红细胞质膜中磷脂类似物向外移动对Mg(2+)和ATP的依赖性,而与ATP依赖性“翻转酶”活性的存在和运作无关。