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Induction of tolerance to hypothermia and hyperthermia by a common mechanism in mammalian cells
Author(s) -
Glofcheski David J.,
Borrelli Michael J.,
Stafford Diane M.,
Kruuv Jack
Publication year - 1993
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041560115
Subject(s) - hyperthermia , hypothermia , chinese hamster , heat shock protein , trypsin , cell culture , chemistry , pharmacology , biology , microbiology and biotechnology , andrology , biochemistry , medicine , enzyme , genetics , physiology , gene
Pretreatment by hypothermic (25°C) cycling (PHC) of attached exponential‐phase V79 Chinese hamster cells by Method 4 (24 hr at 25°C + 1.5 hr at 37°C + 24 hr at 25°C + trypsin + 3 hr at 37°C) or by Method 3 (48 hr at 25°C + trypsin + 3 hr at 37°C) make mammalian V79 cells significantly more resistant to 43°C hyperthermia. There is no significant difference in the 43°C curves whether Method 3 or 4 is used for pre‐exposure. If pre‐exposure is at 15 or 10°C, the resistance to hyperthermia is significantly reduced. PHC by Method 4 significantly increases survival of cells exposed to 5°C and, to a lesser extent, to 10°C. The increase in hyper‐ and hypothermic survival after PHC cannot be accounted for by changes in cell cycle distribution. Heat‐shock protein synthesis is not induced by PHC; hence, protection does not result from newly synthesized proteins. When cells are made tolerant to hyperthermia by a pretreatment in 2% DMSO for 24 hr at 37°C (Method 8), the cells are not more resistant to subsequent exposures to hypothermia, either at 5 or 10°C. The results imply that there may be two mechanisms of inducing resistance to hyperthermia, only one of which also confers resistance to hypothermia. © 1993 Wiley‐Liss, Inc.