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Effect of oxygen derived free radicals and glycine on sodium-potassium adenosine triphosphatase in the basolateral membrane of the kidney in ischemia-reperfusion.

OBJECTIVES
The aim of the present study was to examine the effect of exposing rats to ischemia-reperfusion while breathing 100% oxygen or room air, to find the effect of glycine on renal sodium-potassium adenosine triphosphatase (Na+-K+ATPase) and endogenous antioxidant enzymes, superoxide dismutase and catalase, also to ascertain the effect of ischemia-reperfusion on renal nitric oxide and lipid peroxides.


METHODS
This study was carried out at King Saud University, Riyadh, Kingdom of Saudi Arabia, over a period of 11 months, February to December 2001. All previous measurements were carried out on the renal homogenate after 60 minutes ischemia, then after reperfusion while animals breathed room air or 100% oxygen and also after glycine treatment.


RESULTS
The activity of Na+-K+ATPase, catalase and superoxide dismutase concentration was decreased significantly in the ischemic rats compared to the control, a further decrease was found after 20 minutes of reflow while breathing room air. Breathing 100% oxygen resulted in a significant decrease in catalase and Na+-K+ATPase activity and concentration of superoxide dismutase, glycine caused insignificant change of these enzymes after ischemia-index of lipid peroxidation and nitric oxide they were significantly elevated following reperfusion while rats breathed room air and further elevation was noticed after breathing 100% oxygen. However, potassium and creatinine did not change in all study groups, showed significant decrease after ischemia and ischemia-reperfusion may be due to marked Na+ loss in urine and lack of Na+ reabsorption. The inhibition of superoxide dismutase and catalase can be explained by increased reactive oxygen species during reperfusion and hyperoxia, also due to nitric oxide production and lipid peroxidation as shown by high malondialdehyde. Lack of Na+K+ATPase can be contributed to loss of antioxidant enzymes, nitric oxide production, and high reactive oxygen species.


CONCLUSION
Hyperoxia in ischemia-reperfusion induces severe damage to cellular defence mechanisms and enhances reactive oxygen species injury. Glycine, as antioxidant, is involved in kidney protection from massive injury induced by ischemia-reperfusion, protects renal antioxidant enzymes and Na+-K+ATPase, normalizes malondialdehyde, and nitric oxide levels. This data further supports the possible role of glycine therapy as an adjunct in the treatment of renal failure.