Mabrey S, Powis G, Schenkman J B, Tritton T R
J Biol Chem. 1977 May 10;252(9):2929-33.
Differential scanning calorimetric measurements of normal rat liver microsomes reveal a single thermal transition at about 50 degrees. This transition is assigned to irreversible prorein denaturation. There is no evidence for a reversible lipid phase transition at any temperature above 0 degrees, indicating that the microsomal membrane is in teh fluid state under these conditions. Rats fed a fat-free diet which increases the degree of saturation of fatty acids in the membrane lipids do produce microsomal membranes exhibiting a reversible lipid phase transition. The NADH=dependent and NADPH-dependent enzymatic reductions of cytochrome c show linear Arrhenius behavior in the normal rat liver microsomes but reveal discontinuities and breaks in the Arrhenius plots at approximately the calorimetrically determined phase transition temperatures in microsomes from rats fed the fat-free diet. Hence, the fluidity of cell membranes can be altered by diet with consequent effects on membrane-supported functions. The data further show that the lipid organization of the membrane is not independent of the protein component and supports models of membrane structure where a separate class of lipids forms a boundary between the bulk phase and the proteins.
对正常大鼠肝脏微粒体进行差示扫描量热法测量，结果显示在约50摄氏度处有一个单一的热转变。此转变归因于不可逆的蛋白质变性。在0摄氏度以上的任何温度下，均无证据表明存在可逆的脂质相变，这表明在这些条件下微粒体膜处于流体状态。喂食无脂饮食的大鼠，其膜脂中脂肪酸饱和度增加，确实会产生表现出可逆脂质相变的微粒体膜。细胞色素c的NADH依赖性和NADPH依赖性酶促还原在正常大鼠肝脏微粒体中呈线性阿伦尼乌斯行为，但在喂食无脂饮食的大鼠的微粒体中，在大约量热法测定的相变温度处，阿伦尼乌斯图出现不连续和断点。因此，饮食可改变细胞膜的流动性，进而影响膜支持的功能。数据还表明，膜的脂质组织并非独立于蛋白质成分，支持了膜结构模型，即一类独特的脂质在本体相和蛋白质之间形成边界。
