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The relationship between gastric neoplasia and intestinal metaplasia, a process whose incidence increases with age, remains controversial. In the present experiment, we therefore investigated induction of both intestinal metaplasia and gastric cancers in the Senescence-accelerated mouse (SAMP3/Aicc) treated with N-methyl-N-nitrosourea (MNU). Seven-week-old animals of both sexes received the carcinogen in their drinking water at 120 or 60 ppm on alternative weeks for 10 weeks, or continuously at 30 ppm for the same period, then maintained without further treatment until sacrificed at week 50. The incidences of adenocarcinomas in the 120, 60, and 30 ppm MNU treated and control groups were 6/10 (60%), 5/16 (31.3%), 1/17 (5.9%), and 0/6 (0%) in males, and 2/7 (28.6%), 3/13 (23.1%), 1/6 (16.7%), and 0/9 (0%) in females, respectively. All neoplasms were of well-differentiated type, mainly consisting of gastric epithelial type cells. With immuno- and enzyme-histochemistry, intestinal alkaline phosphatase (I-ALP) positive intestinal absorptive cell-like elements were observed in regions of hyperplasia, adenomas, and adenocarcinomas of MNU treated mice, but no phenotypic expression of goblet or Paneth cells was found. In the control mice, gastric mucosa showed no intestinal epithelium phenotype. Since the degree of appearance of I-ALP positive cells in the lesions in SAMP3/Aicc mice was not different from that found for six other strains mice in our previous work, the results suggest that Senescence-acceleration may not influence intestinalization in the gastric mucosa or induction of gastric carcinomas.

Gastric Carcinogenesis and Intestinalization Induced by N-methyl-N-nitrosourea in the Senescence-Accelerated Mouse(SAMP3).