GLUTAMINE PRESERVES GUT GLUTATHIONE LEVELS DURING INTESTINAL ISCHEMIAREPERFUSION/

Intestinal ischemia/reperfusion (I/R) causes formation of reactive oxy gen intermediates (ROI) which lead to mucosal cell injury. Glutathione (GSH), an ROI scavenger, protects tissues from ROI-mediated cell inju ry. Since GSH biosynthesis is partially dependent on glutamine (Gin) l evels, we tested the hypothesis that intravenous Gin infusion will ass ist in maintaining mucosal cell GSH levels and decrease membrane lipid peroxidation during intestinal I/R. The external jugular vein of male Sprague-Dawley rats was cannulated and infused with normal saline (NS ) at 2 cc/hr. After 3 days, matched pairs of rats received either NS a lone or NS + 3% Gin for an additional 24 hr. Next, mucosal GSH levels were measured after a sham I/R in 6 rats and after either 30 or 60 min of ischemia/60 min of reperfusion in a group of 8 and 12 rats, respec tively. Finally, conjugated diene (CD), a byproduct of membrane lipid peroxidation, was measured following 60 min of ischemia/ 60 min of rep erfusion in a separate group of 12 rats. Control rats had the highest GSH levels and there was no difference between NS vs NS + 3% G;ln rats (2.50 +/- 0.48 vs 2.50 +/- 0.43, P = NS). With 30 and 60 min of ische mia/60 min of reperfusion, GSH levels were significantly lower in NS-i nfused rats compared to those in NS + 3% Gin-infused rats (30 min: 1.5 4 +/- 0.14 vs 1.80 +/- 0.16, P < 0.05; 60 min: 1.27 +/- 0.15 vs 1.52 /- 0.20, P ( 0.04). In addition, CD levels were lower in NS + 3% Gin-i nfused rats compared to those in NS alone-infused rats (5.58 +/- 0.87 vs 7.94 +/- 0.55, P < 0.04). In conclusion, Gin supplementation partia lly maintains gut GSH levels during bowel I/R, which in turn lessens I /R-induced cell membrane lipid peroxidation. (C) 1994 Academic Press,I nc.