Zatloukal K, Sohar R, Lackinger E, Denk H
Division of Molecular Pathology, University of Graz School of Medicine, Austria.
Hepatology. 1988 May-Jun;8(3):607-12. doi: 10.1002/hep.1840080328.
Freshly isolated mouse hepatocytes were tested with respect to the induction of heat shock (stress) proteins by elevated temperature, sodium arsenite and ethanol treatment. With heat, arsenite and ethanol treatments, the synthesis of a protein with a molecular weight of 68 kD (heat shock protein 68) was predominantly elevated; arsenite and ethanol exerted their effects on heat shock protein synthesis in a dose-dependent manner. Hepatocytes derived from livers of chronically griseofulvin-pretreated mice differed in their response from normal hepatocytes in that ethanol was ineffective in these cells. These results indicate that different modes and pathways of the stress response exist, depending on the nature of the inducing agent but also on pretreatment conditions. In vivo, pathologic alterations of cells and organs (e.g., in the course of chronic diseases) can, therefore, be expected to modulate the stress response.
对刚分离出的小鼠肝细胞进行了测试，以研究升高温度、亚砷酸钠和乙醇处理对热休克（应激）蛋白诱导的影响。经加热、亚砷酸钠和乙醇处理后，分子量为68kD的蛋白质（热休克蛋白68）的合成显著增加；亚砷酸钠和乙醇对热休克蛋白合成的影响呈剂量依赖性。来自长期接受灰黄霉素预处理小鼠肝脏的肝细胞与正常肝细胞的反应不同，因为乙醇对这些细胞无效。这些结果表明，应激反应存在不同的模式和途径，这不仅取决于诱导剂的性质，还取决于预处理条件。因此，在体内，可以预期细胞和器官的病理改变（例如在慢性疾病过程中）会调节应激反应。
