Liver Oxidative Stress after Renal Ischemia-Reperfusion Injury is Leukocyte Dependent in Inbred Mice

Authors

  • Atefeh Najafi Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
  • Behjat Seifi Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
  • Hamid reza Sadeghipour Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
  • Hossein Khastar School of Medicine, Shahroud University of Medical Sciences, Shahroud, Iran
  • Jamshid Hadjati Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
  • Manoocher Soleimani Department of Medicine, University of Cincinnati, MSB G259 OH, United States
  • Mehri Kadkhodaee Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
Abstract:

Objective(s) There are some reports in recent years indicating that renal ischemia - reperfusion (IR) induces deleterious changes in remote organs such as liver. The aim of this study was to investigate whether leukocytes have a role on the induction of oxidative stress in liver after renal IR. Materials and Methods Inbred mice in IR donor group were subjected to renal IR injury. In sham donor group the procedure was almost the same except that ischemia was not induced. Then, mice were anesthetized and blood was collected. Leukocytes were isolated from donor groups and were then transferred to intact recipient mice (from IR donor mice to IR recipient mice and from sham donor mice to sham recipient mice). Results After 24 hr, hepatic superoxide dismutase (SOD) and catalase (CAT) activities decreased significantly in recipient mice that received leukocytes from IR donor mice in comparison to recipient mice received leukocytes from sham donor mice. Conclusion These findings indicate that leukocytes are one of the mediators that induce hepatic oxidative stress after renal IR.

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Journal title

volume 14  issue 6

pages  534- 539

publication date 2011-11-01

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