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Both clinical and experimental evidence suggest that the kidney may acquire resistance to injury when rechallenged with toxins such as aminoglycosides, heavy metals, glycerol (11). In addition, this acquired resistance may exhibit crossover between specific nephrotoxins. Yoshioka et al. (34) have recently repted that the rat kidney acquired resistance to ischemic oxidative injury after an initial episode of transient and attributed this resistance to enhanced antioxidant activity. In their study, s were not specifically evaluated (34). Several of the toxic stimuli associated with acquired resistance to cellular injury also induce members of the 70 gene family (16, 18, 25, 27) including 72, raising the possibility that these proteins are imptant cytoprotectants. This concept is suppted by indirect evidence in an animal model in which pri ameliated myocardial injury produced by transient conary occlusion (7). Because a cytoprotectant function has been ascribed to 72 (7,13,20,22,25,32), it was of interest to determine whether other es such as transient might induce this protein. The present study characterizes the induction of 72 that accompanies either sublethal in vivo to transient in situ using a specific protein 70; protein 72; shock; monoclonal anti- 72 antibody. We find that both hypoperfusion injury; hyperthermia; and
AJP - Renal Physiology – The American Physiological Society
Published: Apr 1, 1991
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