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Metals and Stress Proteins

  • Chapter
Toxicology of Metals

Part of the book series: Handbook of Experimental Pharmacology ((HEP,volume 115))

Abstract

Prokaryotic and eukaryotic cells respond to physical and chemical stressors or stress by increasing the transcription of specific genes that encode for a small class of proteins termed heat shock proteins (hsps). This response is believed to represent a transient reprogramming of gene expression and biological activity which serves to protect sensitive cellular components from irreversible damage and assists in the rapid recovery after the stress is removed or ceases. The changes in gene expression associated with this response following exposure to a stimulus are rapid, and result in both increased de novo synthesis and accumulation of stress proteins. Originally termed the heat shock response because of the induction of these proteins following hyperthermia (RItossa 1962), the signaling mechanism involved in its initiation is sensitive to a variety of physical and chemical insults, including metals (NOver 1991). Because the response can be initiated by a variety of stressors it is generically referred to as the “stress response.” In this review, for convention and to avoid confusion, we have adopted the use of the term “stress proteins” when referring to classic hsps and other stress proteins. Therefore, the hsps will be considered as a subset of the stress proteins, and reference to hsps will be used only when deemed necessary, e.g., when referring to specific references and studies describing specific hsps.

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Goering, P.L., Fisher, B.R. (1995). Metals and Stress Proteins. In: Goyer, R.A., Cherian, M.G. (eds) Toxicology of Metals. Handbook of Experimental Pharmacology, vol 115. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-79162-8_11

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