Abstract

This experimental study was designed to analyze the expression of heat shock protein (HSP) in hepatic tissue induced by acute and adaptive hypoxic hypoxia. Rabbits were exposed to 5000 m simulated altitude at 11% O(2) in a chamber. Total antioxidant status (TAS) plasma content showed a significant decrease in the acute and adaptive hypoxia groups compared with the control group. Regarding TAS, there was no statistically significant difference between the acute and adaptive hypoxia groups. Histopathological evidence of liver injury was observed in study groups. Immunohistochemical analysis showed diffuse HSP70 staining in the hepatocytes in acute hypoxia group. Staining was focal and prominent in pericentral hepatocytes in the adaptive hypoxia group. As HSP expression appeared increased, total injury score increased as well. There was an inverse correlation between HSP and TAS, but it did not reach statistical value. Our results confirmed the expression of HSP in hepatic tissue related to defense against cellular injury in a hypoxia model. It is an early response in acute hypoxia and may decrease in adaptive hypoxia. It seems that HSP is induced, rather than protectively, as an early marker of liver injury. HSP70 induction and overexpression seem to be, at least in part, explained by impaired antioxidant defense mechanisms.

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