Soto M A, Sotomayor C P, Lissi E A
Facultad de Ciencias Básicas y Matemáticas, Instituto de Química, Universidad Católica de Valparaíso, Avenida Brasil 2950, Valparaíso, Chile.
Chem Phys Lipids. 2003 Mar;123(1):77-86. doi: 10.1016/s0009-3084(02)00163-9.
Gramicidin incorporation to DPPC or lecithin-PC large unilamellar vesicles (LUVs) leads to pore formation that, under hyper-osmotic conditions, produces a noticeable increase in the rate of trans-membrane water flow. This pore formation is more efficient in the more fluid lecithin-PC LUVs. Exposure of these vesicles to peroxyl radicals generated in the aerobic thermolysis of 2,2'-azo-bis(2-amidinopropane) (AAPH), changes the physical properties of the bilayer (as sensed employing fluorescent probes), modifies gramicidin molecules (as sensed by the decrease in Trp fluorescence) and notably reduces the transbilayer rate of water outflow. In order to evaluate if this reduced water-transport capacity is due to changes in the membrane due to lipid-peroxidation and/or direct damage to gramicidin channels, results obtained in the oxidable vesicles (lecithin-PC) were compared to those obtained in DPPC vesicles. The data obtained show that most of the water transport efficiency loss can be ascribed to a direct disruption of gramicidin channels by AAPH derived peroxyl radicals.
将短杆菌肽掺入二棕榈酰磷脂酰胆碱（DPPC）或卵磷脂-磷脂酰胆碱（lecithin-PC）大单层囊泡（LUVs）会导致孔形成，在高渗条件下，跨膜水流速率会显著增加。这种孔形成在流动性更强的卵磷脂-磷脂酰胆碱LUVs中更有效。将这些囊泡暴露于2,2'-偶氮二（2-脒基丙烷）（AAPH）有氧热解产生的过氧自由基中，会改变双层膜的物理性质（通过荧光探针检测），修饰短杆菌肽分子（通过色氨酸荧光降低检测），并显著降低水流出跨膜速率。为了评估这种水运输能力的降低是否是由于脂质过氧化导致的膜变化和/或对短杆菌肽通道的直接损伤，将可氧化囊泡（卵磷脂-磷脂酰胆碱）中获得的结果与DPPC囊泡中获得的结果进行了比较。所获得的数据表明，大部分水运输效率的损失可归因于AAPH衍生的过氧自由基对短杆菌肽通道的直接破坏。
