On the Biochemical Background of Cysteamine-Induced Duodenal Ulceration in the Rat

Abstract

In cysteamine-induced duodenal ulceration the endogenous prostacyclin level initially showed an elevation. This elevation later disappeared, and the endogenous prostacyclin level dropped to zero—that is, below the detection limit. During ulceration the mucosal DNA level decreased, a phenomenon that was directly proportional to ulceration. In the course of the ulcerative process in the duodenal mucosa a de novo protein synthesis took place. This process was most probably a mucus secretion and served as a protective reaction against damaging noxae. The mucosal cyclic adenosine 5′-monophosphate (cAMP) content increased in the so-called pre-ulcerative phase but later returned to the normal (physiologic) level. The changes in the cyclic guanosine 5′-monophosphate (cGMP) level were more pronounced than those of cAMP, and the final result was a decrease in the mucosal cAMP/cGMP ratio. In accordance with our previous results we conclude that a positive cAMP/cGMP ‘shift’ indicates antiulcerogenic, cytoprotective, reparative processes in the mucosa, whereas its decrease is connected to damaging noxae.

Key Words:

• Biochemistry
• cyclic adenosine 5′-monophosphate
• cyclic guanosine 5′-monophosphate
• cysteamine
• DNA
• duodenal ulceration
• prostacyclin
• rat