Chemically induced resistance to heat treatment and stress protein synthesis in cultured mammalian cells.
Chemically induced resistance to heat treatment and stress protein synthesis in cultured mammalian cells.
复制标题
化学诱导培养的哺乳动物细胞对热处理和应激蛋白合成的抵抗力。
DOI：
10.1080/09553008614550441
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发表时间：
1986
期刊：
影响因子：
--
通讯作者：
Kipp,JB
中科院分区：
文献类型：
--
作者：
Haveman,J;Li,GC;Mak,JY;Kipp,JB
来源于可移植小鼠乳腺癌的培养细胞短时间暴露于亚砷酸钠、2,4-二硝基苯酚（DNP）、羰基氰化物-3-氯苯腙（CCP）或二硫仑，诱导对后续热处理产生抗性，类似于热诱导耐热性。在浓度为300µm的亚砷酸钠暴露后，在浓度为3mm的DNP暴露后，在浓度为300µm的CCP暴露后，在浓度为1-30µm的双硫仑暴露后，在45°C下对45 min的试验热处理的最佳抗性获得。将细胞暴露于CCP、亚砷酸钠或二硫仑会导致一些与“热休克”蛋白分子量相同的蛋白质合成增强。这些蛋白质合成增强的模式是药物特异性的。通过一维凝胶电泳，我们无法检测到DNP后蛋白质合成的显著增强。这些结果表明，增强的应激蛋白合成并不是耐热性发展的先决条件。
Short exposure (1–2h) of cultured cells, derived from a transplantable murine mammary carcinoma, to sodium arsenite, 2,4-dinitrophenol (DNP), carbonylcyanide-3-chlorophenylhydrazone (CCP) or disulfiram, induced resistance to a subsequent heat treatment, similar to heat-induced thermotolerance.Optimum resistance to a test heat treatment of 45 min at 45°C after sodium arsenite exposure was obtained at a concentration of 300 µm, after DNP exposure at 3mm, after CCP at 300 µmand after disulfiram exposure in the range 1–30 µm.Exposure of cells to CCP, sodium arsenite or disulfiram led to enhanced synthesis of some proteins with the same molecular weight as ‘heat shock’ proteins. The pattern of enhanced synthesis of these proteins was agent specific. We could not detect significantly enhanced synthesis of the proteins after DNP using one-dimensional gel electrophoresis. These results suggest that enhanced stress protein synthesis is not a prerequisite for the development of thermal resistance.