The process of erosion formation in the glandular stomach of the rat given single and multiple intragastric doses of 100 mg N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)/kg body weight, was studied histologically, histochemically, and ultramicroscopically and compared with erosion induced by other gastric carcinogens and erosion-forming chemicals. The acute effect of several nongastric carcinogens on the glandular mucosa was also studied. The earliest degenerative transformation, fatty change, was found in the surface mucous cells within 1 hour a one-pulse intragastric dose of 100 mg MNNG/kg body weight; the change gradually progressed into deeper glandular cells and after three successive doses, erosion was complete in every rat. Ultrastructurally, four main glandular cells showed essentially similar degenerative alterations. Fatty change was also induced by other gastric caricnogens such as 4-nitroquinoline-1-oxide, methylnitrosocyanamide, methylnitrosourea, N-2-fluorenylacetamide, and iodacetamide, a noncarcinogenic alkylating agent. Mucosal damage induced by acetylsalicylic acid and thermal burn did not show fatty change. Nongastric carcinogens failed to induce mucosal damage. The relationship of the carcinogen-induced fatty change and mucosal damage to carcinogenesis was discussed.