Abstract

Introduction: Glutathione (GSH) protects the tissue and cell from oxidative injury. Objectives: In the current study, we investigated the possible effects of GSH on liver markers, oxidative stress and inflammatory indices in rat with renal ischemia reperfusion (RIR) injury. Materials and Methods: Twenty-four adult male Wistar rats were divided into 3 groups (n=8). Group I (the control group), group II (the RIR group) received saline (0.25 mL/d, intraperitoneally; i.p.), group III as the RIR group that received GSH (100 mg/kg/d, i.p.). The treatment with saline or GSH began daily 14 days before RIR induction. RIR was induced by clamping renal pedicles for 45 minutes and 24 hours of reperfusion. Results: RIR significantly increased the serum level of nitric oxide (NO), the serum activities of aspartate aminotransferase (AST), alkaline phosphatase (ALP), gamma-glutamyltransferase (GGT), the serum and renal levels of malondialdehyde (MDA), and the serum activity of myeloperoxidase (MPO). However, RIR significantly decreased the serum and renal levels of GSH, serum paraoxonase 1 (PON1) activity, and the serum and renal activities of catalase (CAT) and glutathione peroxidase (GPX). GSH administration could significantly improve the serum activities of AST, GGT, MPO, GPX and PON1 and serum levels of NO, renal MDA, GSH levels, and serum and also renal CAT activities. Conclusion: Our study indicated that GSH administration ameliorated RIR injury in rats by improving the activities of liver markers and antioxidant enzymes, the levels of MDA, NO, GSH and MPO activity.

Highlights

  • Glutathione (GSH) protects the tissue and cell from oxidative injury

  • Implication for health policy/practice/research/medical education: Our study indicated that glutathione could ameliorate lipid peroxidation, the activities of liver markers, antioxidant enzymes, and the levels of glutathione, nitric oxide, and myeloperoxidase activity in ischemia reperfusion injury treated group

  • GSH (23.22%) reduced alkaline phosphatase (ALP) activity in the treatment group compared to the untreated Renal ischemia reperfusion (RIR) group

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Summary

Introduction

Renal ischemia reperfusion (RIR) injury is one of the causes of acute kidney failure (AKF). It may be induced by some conditions such as sepsis, trauma, and kidney transplantation. Renal ischemia begins a series of incidents that can cause cell dysfunction and cell death. The restoration of blood to tissues, which underwent ischemia, can make the recovery of the normal tissue function, while the tissue injury is induced by the reperfusion [1,2]. The precise mechanisms of the pathogenesis of ischemia reperfusion (IR) injury have not been fully demonstrated. Acute ischemia modulates an acute inflammation which is demonstrated by neutrophil

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