Abstract
For the last few years, we have been Interested in the interactions between oxygen free radicals (OFR) and the heat shock, or stress response. Oxidative injury participates in a variety of pathological conditions such as inflammation and ischemia. During inflammation, OFR are generated by the phagocytic cells (polymorphonuclear leukocytes, monocytes-macrophages) infiltrating the inflamed tissues, whereas after ischemia and during reperfusion, OFR are generated by a xanthine-xanthine oxidase system. In vitro, we have investigated in human monocytes-macrophages the effects of exogenous addition, as well as of endogenous production (during phagocytosis) of OFR. These cells respond to oxidative injury by the synthesis of the classical heat shock proteins (HSPs) and of oxidation-specific stress proteins such as heme oxygenase or superoxide dismutase (SOD). HSPs may thus be part of a physiological response to injury during inflammation. In animal models, HSPs are induced during reperfusion injuiy in the ischemic organs.
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© 1991 Springer-Verlag Berlin Heidelberg
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Polla, B.S., Mili, N., Kantengwa, S. (1991). Heat Shock and Oxidative Injury in Human Cells. In: Maresca, B., Lindquist, S. (eds) Heat Shock. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-76679-4_30
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DOI: https://doi.org/10.1007/978-3-642-76679-4_30
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