propyl-n--nitro-n-nitrosoguanidine and Stomach-Neoplasms

Topics: Animals; Carcinogens; Cell Transformation, Neoplastic; Disease Models, Animal; Epithelium; Gastric Mucosa; Humans; Methylnitronitrosoguanidine; Mice; Mucus; Precancerous Conditions; Rats; Stomach; Stomach Neoplasms

N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and N-propyl-N'-nitro-N-nitrosoguanidine (PNNG) were administered to male F344 rats at a single dose of 200 mg/kg by gavage and the animals were observed for 110 weeks. The results revealed that PNNG was a weaker carcinogen for the stomach than MNNG under these conditions. After MNNG, the mortality of animals was higher and their average survival time was shorter than after PNNG. Neoplasms were induced in both the forestomach and glandular stomach by both agents. The incidence of forestomach tumors was high: 85% with MNNG, 64% with PNNG, but with PNNG a greater proportion of the forestomach neoplasms were benign. The incidence of neoplasms of the glandular stomach was 18% with PNNG as compared to 65% with MNNG. Intestinal metaplasia appeared in the glandular stomach after exposure to either MNNG or PNNG. There was also a high incidence in untreated control rats. Most glandular stomach neoplasms were composed of both gastric-type and intestinal-type epithelial elements. Only 3 cases of adenocarcinomas were composed solely of intestinal-type cells. These findings suggest that intestinal metaplasia may not necessarily be a preneoplastic stage.

Topics: Animals; Gastric Mucosa; Hyperplasia; Male; Metaplasia; Methylnitronitrosoguanidine; Precancerous Conditions; Rats; Rats, Inbred F344; Stomach Neoplasms

Sequential studies were made on the histopathologic changes in the glandular stomach of rats induced by a weak carcinogen. N-propyl-N'-nitro-N-nitrosoguanidine (PNNG). Fiftyfour rats were given 100 micrograms/ml of PNNG in their drinking water for 44 weeks, and then normal tap water until the end of the experiment. Rats were killed at intervals between week 1 and week 88. No marked atrophy or ulceration of the mucosa was found between week 1 and the end of the experiment. Focal intestinal metaplasia was found in week 19 and its incidence increased during the experiment. Adenocarcinoma in situ with extreme cellular atypia was found in mucosa with a normal appearance in week 67. An adenocarcinoma invading the submucosa was found in week 69, and one invading the serosa in week 88. All these pathological lesions were found on the anal side of the pyloric region. No pathologic changes were found in the fundic region. The sequential changes of the mucosa of the glandular stomach induced by this weak gastric carcinogen, PNNG, were very different from those induced by the potent gastric carcinogen, N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). Gastric carcinoma induced by PNNG seems to be more similar to human gastric cancer than that induced by MNNG.

Topics: Adenocarcinoma; Animals; Carcinogens; Gastric Mucosa; Male; Methylnitronitrosoguanidine; Rats; Stomach Neoplasms; Time Factors

Topics: Adenocarcinoma; Animals; Intestines; Male; Metaplasia; Methylnitronitrosoguanidine; Neoplasms, Experimental; Precancerous Conditions; Rats; Stomach Neoplasms

Topics: Animals; Male; Metaplasia; Methylnitronitrosoguanidine; Neoplasms, Experimental; Nitrosoguanidines; Rats; Stomach; Stomach Neoplasms