The influence of membrane lipid composition and procaine on hyperthermic death of cells.
The influence of membrane lipid composition and procaine on hyperthermic death of cells.
复制标题
膜脂成分和普鲁卡因对细胞高温死亡的影响。
DOI：
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发表时间：
1977
期刊：
影响因子：
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通讯作者：
M. Yatvin
中科院分区：
文献类型：
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作者：
M. Yatvin
作为某些癌症治疗的组成部分，高温杀死的机制尚不清楚。高温暴露过程中的细胞存活曲线可用于阐明膜修饰程序对细胞死亡的影响。设计实验以测试所报道的增加膜流动性的程序是否也导致高温暴露时的杀伤增加。大肠大肠杆菌K12突变体K1060用于可预测地改变掺入膜中的不饱和脂肪酸的程度和量。从18：1到18：3不饱和脂肪酸的变化增加了杀伤力。通过增加生长温度来减少不饱和脂肪酸细胞的掺入量会降低杀伤力。普罗帕酮，一种已知的降低膜粘度的药物，增加了热杀伤。这些数据最简单的解释是假设膜解体发生的结果，温度升高到一个点，脂质转变引起膜结构的变化，这导致细胞死亡。
The mechanism of hyperthermic killing, a component of some cancer therapy, is not known. Cell-survival curves during hyperthermic exposure can be used to elucidate the effects of membrane modifying procedures on cell death. Experiments were designed to test whether procedures that were reported to increase membrane fluidity also resulted in increased killing on hyperthermic exposure. An E. coli K12 mutant, K1060, is used to predictably alter the degree and amount of unsaturated fatty acids incorporated into membranes. Changing from an 18:1 to an 18:3 unsaturated fatty acid increases killing. Decreasing the amount of unsaturated fatty acid cells incorporated by increasing growth temperature decreases killing. Procaine, a drug known to decrease membrane viscosity, increases heat killing. These data are most simply explained by the hypothesis that membrane disorganization occurs as a result of temperature increasing to a point where a lipid transition causes a membrane structural change, which results in cell-death.