Stress proteins tolerance induction

For future research in this field, in addition to physiological and biochemical approaches, genetic analysis will be essential in the establishment of causal relationships between the induction of a stress protein and the establishment of tolerance to the stress condition. In most cases it is not difficult to detect the induction of new proteins during stress. However, the induction of new proteins does not necessarily establish stress tolerance it may well be the consequence of damage caused by stress conditions. Thus, genetic mutants will be necessary to test the physiological role of a stress protein. 

Gerner and Schneider (1975) were the first to demonstrate that heat shock induces a transient state of heat resistance in mammalian cells. Subsequent research has demonstrated that cells or embryos given a sublethal heat shock sufficient to induce hsp synthesis exhibit tolerance to an otherwise lethal heat shock (Li and Laszlo 1985 Mirkes 1987 Johnston and Kucey 1988 Riabowol et al. 1988). This phenomenon has been termed acquired thermotolerance, and is defined for the purposes of this review as selftolerance. Data from numerous studies demonstrate that the acquisition of thermotolerance is attributable to the induction and expression of stress proteins (Landry et al. 1982 Welch and Mizzen 1988). Many investigations, including those of Landry et al. (1982), Li and Werb (1982), and Lavoie et al. (1993), have demonstrated that the kinetics of thermotolerance induction and decay are correlated with stress protein synthesis and degradation, respectively. 

A considerable number of stress protein inducers, such as cadmium, ethanol, and sodium arsenite, are as effective as heat in conditioning the cell to become thermotolerant. This type of tolerance, where the inducing and stress stimulus are different, is termed cross-tolerance. Induction of cross-... 

Because of the diversity of the stress response in various organisms in response to different stressors, it is difficult to make generalities regarding the involvement of any specific stress protein in the establishment of tolerance to metals and other xenobiotics. Additional research is needed to determine which of these stress proteins, if any, are essential for the induction of self- and cross-tolerance to metals and other stressors, and to elucidate other physiologic mechanisms which may be involved in this phenomenon. 

Prior induction of stress proteins by heat or metals has been shown to protect cells or organisms against toxic injury by metals, such as arsenite or cadmium, as was discussed in more detail in Sect. D. The mechanism for this tolerance is believed to occur via protein-protein interactions, which involves the salvaging of damaged proteins or targeting damaged proteins for proteolysis. 

Carson-Jurica MA, Lee AT, Dobson AW, Conneely OM, Schrader WT, O Malley BW (1989) Interaction of the chicken progesterone receptor with heat shock protein (hsp) 90. J Steroid Biochem 34 1-9 Cervera J (1985) Induction of self-tolerance and enhanced stress protein synthesis in L-132 cells by cadmium chloride and by hyperthermia. Cell Biol Int Rep 9 131-141... 

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