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Updated: Aug 21, 2026

An Effective Mouse Model of Unilateral Renal Ischemia-Reperfusion Injury
Published on: July 15, 2021
[Oxidative stress in experimental acute glomerulonephritis]
Grazyna Wójcicka1, Andrzej Marciniak, Jerzy Bełtowski
1Katedra i Zakład Patofizjologii, Akademii Medycznej w Lublinie.
Abstract:
The aim of this study was to estimate the concentration of lipid peroxidation products (TBARS -thiobarbituric acid reactive substances) in serum and in renal cortex, and erythrocytes superoxide dismutase (SOD), glutathione peroxidase (GPx) activity in blood during the development of experimental acute glomerulonephritis. Total antioxidant capacity of plasma and some of plasma nonenzymatic antioxidants, such as total protein level and uric acid were also measured. Acute glomerulonephritis was induced by intravenous injection of bovine serum albumin (BSA) in rabbits, at a dose of 250 mg/kg. Blood and tissues for analysis were taken from animals on the 2nd, 4th, 8th and 12th day after antigen administration. Morphologic changes in kidneys were verified by light and electron microscope. Injection of the BSA resulted in diffuse endocapillary proliferative glomerulonephritis with transient proteinuria with peak on the 8th day after antigen administration. Morphological alterations were associated with marked increase of TBARS in serum (on the 2nd, 4th, and 12th day) and renal cortex (on the 2nd, 4th and 8th day). In immunized rabbits we observed an increase in SOD activity (after 8 and 12 days of BSA injection). Activity of GPx was elevated throughout the observation period. We also noted an exhaustion of nonenzymatic antioxidants in plasma expressed as the decrease of total plasma antioxidant capacity (on the 2nd, 4th, 8th and 12th day), uric acid and total plasma protein level (8th day). We conclude, that during development of experimental acute glomerulonephritis, oxidative stress occurs which manifests as an increase of lipid peroxidation products, changes in antioxidant enzymes and exhaustion of nonenzymatic scavengers. The oxidant-antioxidant imbalance may contribute in the development of pathogenic changes in this model of glomerulonephritis.
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