Preventive effect of fermented brown rice and rice bran on N-methyl-N'-nitro-N-nitrosoguanidine-induced gastric carcinogenesis in rats.
A number of possible preventive agents for cancers in different organs have been reported, however, little information is available regarding the effective agents for the development of gastric cancers. The rice components are known to be effective for the prevention of the development of cancers. Our group has demonstrated that fermented brown rice by Aspergillus Orzae (FBRA) has chemopreventive potentials in several organs. In this study, we investigated the modifying effects of FBRA exposed during the initiation or post-initiation phase of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced gastric carcinogenesis in rats. Five-week-old male ACI rats were divided into 7 groups. Groups 1-5 were given oral administration of MNNG (100 mg/l in distilled water) for 24 weeks starting at 6 weeks of age. Groups 2 and 3 were fed a diet containing 5 and 10% FBRA during the initiation phase, respectively, whereas groups 4 and 5 were fed these diets during the post-initiation phase. Group 6 was given a diet containing 10% FBRA throughout the experiment. Group 7 was kept on the basal diet alone and served as an untreated control. Rats were sacrificed at 52 weeks after the start, and the epithelium of the stomach was investigated in detail. Incidence and multiplicity of gastric proliferative lesions of group 1 (MNNG alone) were 61% and 1.67+/-1.57/rat, respectively. Those of group 5 (25%, 0.35+/-0.67) which were given FBRA at a dose of 10% during the post-initiation phase were significantly less than those of group 1. Furthermore, the same group expressed a significantly decreased Ki67-labeling index in the non-lesional gastric epithelium when compared to that of group 1. These results indicate that FBRA inhibits MNNG-induced development of gastric tumors by administration during the post-initiation phase in rats. FBRA is regarded as a promising dietary agent for the prevention of human gastric cancer.
Tomita
Hiroyuki
H
Department of Tumor Pathology, Gifu University Graduate School of Medicine, Gifu 501-1194, Japan. j2111706@edu.gifu-u.ac.jp
Kuno
Toshiya
T
Yamada
Yasuhiro
Y
Oyama
Takeru
T
Asano
Nami
N
Miyazaki
Yasuo
Y
Baba
Seiji
S
Taguchi
Ayako
A
Hara
Akira
A
Iwasaki
Teruaki
T
Kobayashi
Hiroshi
H
Mori
Hideki
H
D000230:Adenocarcinoma / Q000473:pathology / Q000517:prevention & control*; D000818:Animals; D016588:Anticarcinogenic Agents / Q000627:therapeutic use*; D017209:Apoptosis / Q000187:drug effects; D002273:Carcinogens / Q000633:toxicity; D049109:Cell Proliferation / Q000187:drug effects; D007150:Immunohistochemistry; D008297:Male; D008769:Methylnitronitrosoguanidine / Q000633:toxicity; D012275:Oryza / Q000737:chemistry*; D008517:Phytotherapy; D051381:Rats; D013274:Stomach Neoplasms / Q000473:pathology / Q000517:prevention & control*
D016588:Anticarcinogenic Agents; D002273:Carcinogens; D008769:Methylnitronitrosoguanidine