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Abstract: FR-PO1037

The Effect of Ischemia-Reperfusion Injury on Mitochondrial Reduced Glutathione Levels in Kidney Cortex and Medulla from Aging Female Lewis Rats

Session Information

Category: CKD (Non-Dialysis)

  • 2303 CKD (Non-Dialysis): Mechanisms


  • Zamlauski-Tucker, Marianna J., Ball State University, Muncie, Indiana, United States
  • Ye, Bingwei, Ball State University, Muncie, Indiana, United States

The purpose of the study was to determine the effect of ischemia-reperfusion injury (IRI) on changes in the mitochondrial reduced glutathione (GSH) levels in kidney cortex and medulla from old rats. GSH is the major antioxidant inside cells, and a decrease in GSH levels would result in oxidative stress and damage due to increased generation of free radicals in IRI.


Anesthetized female Lewis rats (22 months of age) were used. Both renal pedicles were clamped for 60 min, followed by 60 min of reperfusion in the Experimantal Group (n =5). The kidneys were then harvested, separated into cortex and medulla, and homogenized. Kidneys in the Control Sham Group (n=5) were not subjected to IRI before being harvested. The mitochondrial fractions were isolated by differential centrifugation, and GSH levels were measured using a spectrophometric assay. The water contents of the cortex and medulla were determined to allow GSH levels to be expressed as nmol/g kidney dry weight. A Student's T Test was used to compare groups, and statistical significance was determined at p< 0.05. All data reported as X ± SEM.


There was a significant 58% decrease in mitochondrial GSH levels in the kidney cortex, from 388 ± 19 nmol/g kidney dry wt in the Control Group to 163 ± 6 nmol/g kidney dry wt in the Experimental Group. There was also a significant 40 % decrease in mitochondrial GSH levels in the kidney medulla, from 531 ± 32 nmol/kidney dry wt in the Control Group to 318 ± 22 nmol/ g kidney dry wt in the Experimental Group.


Mitochondrial GSH levels in rat kidney cortex and medulla did not return to normal levels after one hour of reperfusion following 60 minutes of ischemia. This finding suggests that mitochondria in both the kidney cortex and medulla are experiencing major oxidative stress, and this may be contributing to the renal dysfunction seen in IRI.