Role of nitric oxide in prevention of ethanol-induced gastric damage by CuNSN a copper-chelating compound.

CuNSN a bis (2-benzimidazolyl)thiother complex with copper, has been shown to prevent the formation of acute gastric mucosal lesions induced by acetylsalicylic acid and ethanol. In the present study we have investigated the role of NO in CuNSN protection from ethanol-induced gastric damage. For this purpose we have used the inhibitor of NO biosynthesis, NG-nitro-L-arginine (L-NNA) as well as L- or D-arginine. Gastric mucosal damage caused by ethanol was dose-dependently increased by i.v. administration of graded dose of L-NNA. The effect of L-NNA was completely antagonized by the administration of L-arginine while D-arginine did not cause a reduction in the damage. Treatment with CuNSN has shown a significant protection against the damage produced by ethanol. This protection was not reversed by L-NNA and was significant as compared to the corresponding control group. The combination of L-NNA plus L-arginine potentiates this protection. These results suggest that NO synthesis is not involved in the protection afforded by CuNSN.