Intestinal metaplasia induced by X-irradiation: its biological characteristics

摘要

The gastric regions of mice, Mongolian gerbils or different strains of rats were irradiated with a total dose of 20 Gy of X-rays given in two fractions. Intestinal metaplasia was induced in rats, however, not in mice or gerbils, and it was greatly influenced by the rat strains and sexes. Alkaline phosphatase (ALP)-positive metaplastic foci were increased by the administration of ranitidine, crude stomach antigens or the subtotal resection of the fundus and decreased by cysteamine, histamine or the removal of the submandibular gland. We suggest that an elevation in the pH of the gastric juice was due to the disappearance of the parietal cells and is one of the principal factors for the development of intestinal metaplasia, which may be reversible. When the gastric tissue was implanted into the duodenum, pepsinogen-positive chimeric glands with goblet cells appeared in the graft. Esophagus grafts were transplanted into the stomach or duodenum and newly differentiated into gastric or duodenal mucosa,respectively. In the gut, the microenvironment might thus be conducive to the development of metaplasia or to new differentiation. Intestinal metaplasia was found to possibly increase the sensitivity to the induction of tumors by carcinogens of the 1,2-dimethylhydrazine (DMH) or azoxymethane (AOM) type. This route, however, is relatively minor compared to the main route of the 7V-methyl-iVr-nitro-A/-nitrosoguanidine (MNNG) or N-methylnitrosourea (MNU) which was not affected.