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Induction of heat shock proteins in short‐term cultured hepatocytes derived from normal and chronically griseofulvin‐treated mice
Author(s) -
Zatloukal Kurt,
Sohar Ruth,
Lackinger Elisabeth,
Denk Helmut
Publication year - 1988
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.1840080328
Subject(s) - sodium arsenite , griseofulvin , heat shock protein , arsenite , hepatocyte , in vivo , ethanol , hsp70 , shock (circulatory) , chemistry , heat shock , protein biosynthesis , in vitro , biochemistry , pharmacology , biology , medicine , pathology , arsenic , organic chemistry , gene , microbiology and biotechnology
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.