Alcohol scavenges nitric oxide in gastric lumen

The biological activities of endogenously produced nitric oxide (NO; nitrogen monoxide) can be affected not only by NO itself but also by relatively stable NO-derived substances or by-products of NO. It is well known that NO-derived nitrosation at the center of nitrogen, sulfur, and carbon (N-, S-, and C-nitrosation) have a great biological significance, while that at oxygen center (O-nitrosation) remains to be detected. During the course of a physiologic study on ethanol-induced gastric injury employing an ex vivo gastric chamber system of rats, we found that ethanol could be nitrosated by endogenously produced NO. Luminal nitrite and nitrate (NOx) levels in gastric lumen were decreased sharply about 70% during ethanol saline solution infusion to the chamber and then immediately returned to the basal levels by infusion of ethanol-free saline solution. On the other hand, NO levels in gastric mucosa were slightly increased during the infusion of ethanol saline solution, suggesting that ethanol never inhibits NO biosynthesis. These results demonstrate that ethanol perfused in gastric lumen can scavenge gastric tissue-derived NO and ethanol may react with NO-derived species (probably, N(2)O(3)) to form an ethylnitrite in oxygen-containing luminal solution. Alkyl nitrites including ethylnitrite have been not only widely used as a nitrovasodilator but also shown to act as a nitrosating agent. Thus, in vivo O-nitrosation also has important biological meaning in the same manner as N-, S-, and C-nitrosation.