Glutathione Reduction in Liver Tissue after Renal Ischemia Reperfusion
DOI:
https://doi.org/10.22100/jkh.v9i3.325Keywords:
Renal ischemia, Remote organs, Liver damage, Leukocyte, Oxidative stress.Abstract
Introduction: Renal ischemia reperfusion (IR) is a common cause of acute renal failure. Renal IR induces remote organ dysfunction such as lung, heart and liver. The aim of this study was to assess the role of leukocytes on the hepatic tissue glutathione as a liver antioxidant index after renal IR injury.
Methods: Inbred mice were subjected to either sham operation (sham donor) or bilateral renal IR injury that undergoes 50 min ischemia followed by 3h reperfusion (IR donor). Mice were then anesthetized for collection of blood and liver samples. Leukocytes isolated from blood and then were transferred to two recipient groups: recipient mice that received leukocytes from sham-operated control mice and intact recipient mice that received leukocytes from IR mice. After 24h, recipient mice were anesthetized and blood and liver samples were collected.
Results: Hepatic glutathione (GSH) decreased significantly in intact recipient mice that received leukocytes from IR mice in comparison to intact recipient mice received leukocytes from sham-operated control mice.
Conclusion: These results suggest that leukocytes are one of the possible factors that contribute to liver damage after renal IR injury and this damage is partly due to the induction of oxidative stress.
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