Stibler H, Beaugé F, Leguicher A, Borg S
Department of Neurology, Karolinska Hospital, Stockholm, Sweden.
Scand J Clin Lab Invest. 1991 Jun;51(4):309-19. doi: 10.3109/00365519109091621.
Erythrocyte membranes from healthy controls and alcoholic patients, examined within 24 h of abstinence, were studied for basal membrane fluidity and membrane sensitivity to ethanol by fluorescence polarization of the apolar probe 1,6-diphenyl-1, 3,5-hexatriene (DPH) and its cationic derivative 1,4(trimethylammonium phenyl)-6-phenyl-1,3,5-hexatriene (TMA-DPH). The membrane partition (Kp) of ethanol and phenobarbital, and the concentrations of membrane-bound sialic acid and galactose, were also determined. The apolar hydrocarbon region of the membrane (DPH) was less fluid, in the alcoholics than in the controls (p less than 0.005). In the patients this membrane layer, as well as the polar lipid head group region (TMA-DPH), showed reduced fluidizing effect of ethanol (p less than 0.01). This resistance or tolerance to ethanol correlated with a markedly impaired (-59%, p less than 0.025) partition of ethanol into the membrane. The low Kp of ethanol in turn was partly related to reduced concentrations of polar carbohydrates such as sialic acid and galactose (p less than 0.01) at the membrane surface. The Kp of phenobarbital was reduced in the patients (-59%, p less than 0.005) but, apparently unrelated to the carbohydrate changes. These results indicate that in man, chronic alcohol abuse is associated with complex changes of membrane properties at different membrane levels e.g. at the charged surface, in the polar lipid head group region and in the hydrocarbon core. A partial basis for biophysical membrane tolerance to ethanol is suggested, implying that apart from phospholipid alterations, structural changes in membrane-bound glycoconjugates participate in this adaptive process.
对戒酒24小时内的健康对照者和酒精性肝病患者的红细胞膜，通过非极性探针1,6 - 二苯基 - 1,3,5 - 己三烯（DPH）及其阳离子衍生物1,4 -（三甲基铵苯基）-6 - 苯基 - 1,3,5 - 己三烯（TMA - DPH）的荧光偏振，研究了基础膜流动性和膜对乙醇的敏感性。还测定了乙醇和苯巴比妥的膜分配系数（Kp）以及膜结合唾液酸和半乳糖的浓度。与对照组相比，酒精性肝病患者膜的非极性烃区域（DPH）流动性较低（p < 0.005）。在这些患者中，该膜层以及极性脂质头部基团区域（TMA - DPH）对乙醇的流化作用降低（p < 0.01）。这种对乙醇的抗性或耐受性与乙醇进入膜的明显受损（-59%，p < 0.025）分配相关。乙醇的低Kp又部分与膜表面极性碳水化合物如唾液酸和半乳糖浓度降低（p < 0.01）有关。患者中苯巴比妥的Kp降低（-59%，p < 0.005），但显然与碳水化合物变化无关。这些结果表明，在人类中，慢性酒精滥用与不同膜水平如带电表面、极性脂质头部基团区域和烃核心处的膜性质复杂变化有关。提示了生物物理膜对乙醇耐受性的部分基础，这意味着除了磷脂改变外，膜结合糖缀合物的结构变化也参与了这一适应性过程。
