title: Increasing development of pepsinogen-altered pyloric glands and adenocarcinoma in glandular stomach of analbuminemic rats.
abstract: The susceptibility of pepsinogen-altered pyloric glands (PAPG) and neoplastic glandular stomach lesions induced by N-methyl-N-nitro-N-nitrosoguanidine (MNNG) and catechol or sodium cholate in Nagase analbuminemic rats (NAR) was compared to Sprague-Dawley rats (SD). Male NAR and SD rats were given a single dose of 80 mg/kg body weight of MNNG by gastric intubation and, 2 weeks later, fed basal diet containing 0.8% catechol or 0.3% sodium cholate for 18 weeks. The animals were killed at the end of week 20 or after maintenance on basal diet at week 60. The number of pepsinogen-altered pyloric glands at week 20 was significantly (P < 0.001) higher in NAR fed either catechol or sodium cholate compared with SD rats. At week 60, adenomatous hyperplasias and adenocarcinomas were observed in 7 (88%; P < 0.01) and 3 (38%; P < 0.01) of 8 NAR fed catechol and in 4 (22%) and 0 of 18 SD rats, respectively. The results show that the frequency of PAPG in NAR and SD rats is related to the susceptibility to glandular stomach carcinoma. PAPG is a useful endpoint lesion for evaluation of gastric carcinogenicity in a 20-week carcinogenicity test, and NAR are sensitive for glandular stomach carcinogenesis.
authors.affiliation: First Department of Pathology, Nagoya City University Medical School, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Ogawa
authors.forename: Y
authors.initials: Y
authors.lastname: Shichino
authors.forename: M
authors.initials: M
authors.lastname: Tatematsu
authors.forename: C
authors.initials: C
authors.lastname: Furihata
authors.forename: M
authors.initials: M
authors.lastname: Asamoto
authors.forename: S
authors.initials: S
authors.lastname: Nagase
authors.forename: T
authors.initials: T
authors.lastname: Shirai
authors.forename: N
authors.initials: N
authors.lastname: Ito
mesh_terms: D000230:Adenocarcinoma / Q000139:chemically induced / Q000473:pathology*; D000818:Animals; D002273:Carcinogens; D002396:Catechols / Q000633:toxicity*; D019826:Cholic Acid; D002793:Cholic Acids / Q000633:toxicity*; D005753:Gastric Mucosa / Q000187:drug effects* / Q000201:enzymology / Q000473:pathology; D006965:Hyperplasia; D008297:Male; D008769:Methylnitronitrosoguanidine; D010435:Pepsinogens / Q000378:metabolism*; D011706:Pyloric Antrum; D051381:Rats; D011922:Rats, Mutant Strains; D017207:Rats, Sprague-Dawley; D012709:Serum Albumin / Q000172:deficiency* / Q000235:genetics; D013045:Species Specificity; D013274:Stomach Neoplasms / Q000139:chemically induced / Q000473:pathology*
chemical_list: D002273:Carcinogens; D002396:Catechols; D002793:Cholic Acids; D010435:Pepsinogens; D012709:Serum Albumin; D008769:Methylnitronitrosoguanidine; D019826:Cholic Acid; C034221:catechol