Thermotropic lipid and protein transitions in chinese hamster lung cell membranes: relationship to hyperthermic cell killing.
Thermotropic lipid and protein transitions in chinese hamster lung cell membranes: relationship to hyperthermic cell killing.
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中国仓鼠肺细胞膜中的热致脂质和蛋白质转变：与高温细胞杀伤的关系。
DOI：
10.1139/o83-057
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发表时间：
1983
期刊：
影响因子：
--
通讯作者：
J. Kruuv
中科院分区：
文献类型：
--
作者：
J. Lepock;K. Cheng;H. Al;J. Kruuv
将哺乳动物细胞暴露于高温（约100 ℃）。41-45摄氏度）似乎作为一个直接或触发效应，产生一些后来的反应，如细胞死亡，耐热性，或热休克蛋白合成。细胞杀伤的高活化能表明，对于这种特定的反应，高温的直接效应可能是某些细胞成分的向热转变。高温存活和生长数据均表明，对于中国仓鼠肺V79细胞，开始高温细胞杀伤的温度为40-41.5 ℃。使用电子自旋共振标记物2，2-二甲基-5-十二烷基-5-甲基恶唑烷-N-氧化物和荧光探针1，6-二苯基-1，3，5-己三烯的研究表明，线粒体和全细胞匀浆中在约7-8 ℃和23-36 ℃（或这些温度之间的宽转变）存在脂质转变，这与生长和低温杀伤的变化密切相关。在40-41.5摄氏度附近没有检测到脂质转变，这可能与线粒体或质膜中的高温杀死相关，但内在蛋白质荧光和蛋白质荧光团向反式对苯二甲酸能量转移的测量表明，在高于约40- 41.5摄氏度的温度下，蛋白质结构或排列存在不可逆转变。线粒体和质膜的温度都是40摄氏度。这种转变是由于蛋白质重排和（或）解折叠，使得蛋白质色氨酸和酪氨酸残基暴露于极性基团和对苯二甲酸的程度增加。这种转变的强度意味着总膜蛋白的显著部分参与这种转变，这可能类似于水溶性蛋白质的热诱导变性。这种膜结构的改变。40摄氏度可能会导致质膜和线粒体功能的许多观察到的变化，这可能进一步参与细胞对高温的反应。
Exposure of mammalian cells to hyperthermic temperatures (ca. 41-45 degrees C) appears to act as a direct or triggering effect to produce some later response such as cell death, thermotolerance, or heat-shock protein synthesis. The high activation energy of cell killing indicates that the direct effect of hyperthermia might be a thermotropic transition in some cellular component, for this particular response. Both hyperthermic survival and growth data imply that the temperature for the onset of hyperthermic cell killing is 40-41.5 degrees C for Chinese hamster lung V79 cells. Studies using the electron spin resonance label 2,2-dimethyl-5-dodecyl-5-methyloxazolidine-N-oxide and the fluorescent probe 1,6-diphenyl-1,3,5-hexatriene show the existence of lipid transitions at approximately 7-8 and 23-36 degrees C (or a broad transition between these temperatures) in mitochondria and whole cell homogenates, that correlate well with changes in growth and hypothermic killing. No lipid transition was detected near 40-41.5 degrees C that could correlate with hyperthermic killing in either mitochondrial or plasma membranes, but measurements of intrinsic protein fluorescence and protein fluorophore to trans-paranaric acid energy transfer demonstrate the existence of an irreversible transition in protein structure or arrangement above ca. 40 degrees C in both mitochondrial and plasma membranes. This transition is due to protein rearrangement and (or) unfolding such that there is increased exposure of protein tryptophan and tyrosine residues to polar groups and to paranaric acid. The strength of the transition implies that a significant fraction of total membrane protein is involved in this transition, which may be analogous to the heat-induced denaturation of water-soluble proteins. This alteration in membrane structure above ca. 40 degrees C could cause many of the observed changes in plasma membrane and mitochondrial function, which may further be involved in cellular responses to hyperthermia.
酒精、普鲁卡因和热疗对细胞核和染色质蛋白质含量的影响。
DOI：
10.1080/09553008414551031
发表时间：
1984
期刊：
International journal of radiation biology and related studies in physics, chemistry, and medicine
影响因子：
--
作者：
RotiRoti,JL;Wilson,CF
通讯作者：
Wilson,CF