Abstract
Exposure to sublethal heat stress activates a complex cascade of signaling events, such as activators (NO), signal molecules (PKCε), and mediators (HSP70 and COX-2), leading to implementation of heat preconditioning, an adaptive mechanism which makes the organism more tolerant to additional stress. We investigated the time frame in which these chemical signals are triggered after heat stress (41 ± 0.5°С/45 min), single or repeated (24 or 72 h after the first one) in heart tissue of male Wistar rats. The animals were allowed to recover 24, 48 or 72 h at room temperature. Single heat stress caused a significant increase of the concentration of HSP70, NO, and PKC level and decrease of COX-2 level 24 h after the heat stress, which in the next course of recovery gradually normalized. The second heat stress, 24 h after the first one, caused a significant reduction of the HSP70 levels, concentration of NO and PKCɛ, and significant increase of COX-2 concentration. The second exposure, 72 h after the first heat stress, caused more expressive changes of HSP70 and NO in the 24 h-recovery groups. The level of PKCɛ was not significantly changed, but there was significantly increased COX-2 concentration during recovery. Serum activity of AST, ALT, and CK was reduced after single exposure and increased after repeated exposure to heat stress, in both time intervals. In conclusion, a longer period of recovery (72 h) between two consecutive sessions of heat stress is necessary to achieve more expressive changes in mediators (HSP70) and triggers (NO) of heat preconditioning.
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Acknowledgments
We thank prof. Michal Horowitz (Laboratory of Environmental Physiology, The Hebrew University, Hadassah Medical Center, Jerusalem, Israel) for advice and critical comments during writing the paper.
The research was performed at the Department of Experimental Physiology and Biochemistry, Institute of Biology, Faculty of Natural Sciences and Mathematics, University “Ss Cyril and Methodius”, Skopje, R. Macedonia.
This research did not receive any specific grant from funding agencies in the public, commercial or non-profit sectors.
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Ilievska, G., Dinevska-Kjovkarovska, S. & Miova, B. Effect of single and repeated heat stress on chemical signals of heat shock response cascade in the rat’s heart. Cell Stress and Chaperones 23, 561–570 (2018). https://doi.org/10.1007/s12192-017-0863-0
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DOI: https://doi.org/10.1007/s12192-017-0863-0