Effect of Vitamin C (Ascorbic Acid) as an Antioxidant in Reducing Cellular Injury Following Renal Reperfusion in Wistar Rats

Abstract

Renal ischemia-reperfusion (I/R) injury occurs as a result of the production of reactive oxygen species (ROS) and reactive nitrogen species (RNS). ROS cause oxidative stress, which results in an imbalance between oxidants such as ROS and antioxidants. The objective of this study was to evaluate the protective effect of the antioxidant vitamin C compared to the effect of vitamin E on renal I/R. Wistar albino rats were divided into six groups. There were three control groups: Group 1—normal control; Group 2—sham control; Group 3—untreated experimental control. There were three experimental groups where rats were pretreated with a vitamin for 30 days: Group 4—pretreated with vitamin E; Group 5—pretreated with vitamin C; Group 6—pretreated with a combination of vitamins E and C. On day 31, all groups except normal and sham control underwent 60 minutes of renal ischemia followed by reperfusion for 10 minutes. After this, the kidney was removed and homogenized. The homogenate was used for the biochemical estimations of lipid peroxidation, glutathione (GSH) and superoxide dismutase (SOD). Ischemia followed by reperfusion led to a significant increase in tissue lipid peroxidation and a decrease in GSH and SOD levels (Group 3). However, in Groups 4, 5 and 6, where the rats were pretreated with vitamin C or E or a combination of both, there was a decrease in lipid peroxidation, and an increase in GSH and SOD levels. Though a decrease in lipid peroxidation was observed in all three vitamin-pretreated groups, it was not as low as in the normal control group. There were no statistically significant differences among the three vitaminpretreated groups. Both antioxidants, singly and in combination, showed equal beneficial effects in reducing renal injury.