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Carcinogenesis forestomach

Both l-nitroso-3,5-dimethylpiperazine and l-nitroso-3,4,5-trimethylpiperazine induced a high incidence of thymic leukemia in rats within 6 months (23). The 4-acetyl derivative of the former induced esophageal tumors in the same time, while the 4-benzoyl derivative was a very much weaker carcinogen, giving rise to only a few tumors of the forestomach after almost 2 years. These contrasting results are difficult to reconcile with any simple mechanism of carcinogenesis. [Pg.98]

Luo, X.M., H.J. Wei, and S.P. Yang. 1983. Inhibitory effects of molybdenum on esophageal and forestomach carcinogenesis in rats. Jour. Natl. Cancer Inst. 71 75-80. [Pg.1575]

Ghanayem Bl, Maronpot RR, Matthews HB. 1986. Association of chemically-induced forestomach cell proliferation and carcinogenesis. Cancer Lett 32 271-278. [Pg.119]

J,l/mouse, twice a week for 25 weeks, to female ICR mice produced forestomach tumors (squamous cell carcinoma and papilloma), lung tumors (adenocarcinoma and adenoma), and tumors of the hematopoietic system (thymic lymphosarcoma and lymphatic leukemia), with dose-related response by 18 months. It was concluded that the target organ of benzotrichloride carcinogenesis in mice is the local tissue that is primarily exposed and the lung and hematopoietic tissue when administered systemically. [Pg.78]

Berenblum I, Haran N The influence of croton oil and of polyethylene glycol-400 on carcinogenesis in the forestomach of the mouse. Cancer Res 15 510-516, 1955... [Pg.210]

Lifetime cancer bioassays using orally exposed animals were not located. In a shorter-term study, exposure to p-cresol in the feed for 20 weeks produced an increased incidence of forestomach hyperplasia in hamsters, suggesting that this cresol isomer may have the potential to act as a promoter of forestomach carcinogenesis in this species (Hirose et al. 1986). However, promotion potential was not tested directly. p-Cresol did not produce forestomach hyperplasia in rats (Altmann et al. 1986), but rats are generally less sensitive than hamsters to inducers of forestomach lesions. [Pg.44]

Hirose M, Inoue T, Asamoto M, et al. 1986. Comparison of the effects of 13 phenolic compounds in induction of proliferative lesions of the forestomach and increase in the labeling indices of the glandular stomach and urinary bladder epithelium of Syrian golden hamsters. Carcinogenesis 7(8)... [Pg.152]

CLA, the acronym for a series of conjugated dienoic isomers of linoleic acid, occurs naturally in many foods, particularly dairy products and other foods derived from ruminant animals (6). Synthetically prepared CLA inhibits chemically-induced mouse epidermal and forestomach neoplasia (7,8) and rat mammary neoplasia (9). Hence, the effect of CLA on carcinogenesis is opposite that of linoleic acid. [Pg.262]

Ghanayem, B.I., Elwell, M.R. Eldridge, S.R. (1997) Effeets of the eareinogen, acrylonitrile, on forestomach cell proliferation and apoptosis in the rat comparison with methacrylonitrile. Carcinogenesis, 18, 675-680... [Pg.97]

Groups of 10-20 male Fischer 344 rats, seven weeks of age, received catechol (> 99.8% pure) in the diet at concentrations of 0 or 1.5% for four weeks followed by 0.8% for 47 weeks either with no other exposure or one week after exposure to A-mcthyl-A"-nitro-A -nitrosoguanidinc to initiate stomach carcinogenesis. With catechol alone, the incidence of forestomach papillomas was 1/15 compared with 0/10 in untreated controls. Glandular stomach adenocarcinomas were found in 3/15 rats compared with 0/10 in controls. Catechol increased the incidence of squamous-cell carcinomas of the forestomach induced by the initiator from 5/19 to 19/19 (p < 0.001). In the glandular stomach, the incidence of adenocarcinomas in the pyloric region was 18/19 (p < 0.001) compared with none in rats given only the initiator (Hirose et al., 1987). [Pg.436]

Shibata, M.A., Hirose, M., Yamada, M., Tatematsu, M., Uwagawa, S. Ito, N. (1990a) Epithelial cell proliferation in rat forestomach and glandular stomach mucosa induced by catechol and analogous dihydroxybenzenes, Carcinogenesis, 11, 997-1000... [Pg.450]

Hirose, M., Yamaguchi, S., Fukushima, S., Hasegawa, R., Takahashi, S. Ito, N. (1989) Promotion by dihydroxybenzene derivative of V-methyl-V -nitro-A-nitrosoguanidine-induced F344 rat forestomach and glandular stomach carcinogenesis. Cancer Res., 49, 5143-5147... [Pg.714]

Garlic oil also exhibits an antagonistic effect on benzo[a]pyrene by inhibiting benzo[a]pyrene-induced skin carcinogenesis in Swiss mice during the initiation phase (Sadhana et al. 1988). A primary constituent of garlic oil. allyl methyl trisulfide (ATM), has also demonstrated an inhibitory effect on benzo[a]pyrene induced neoplasia of the forestomach in mice (Sparnins et al. 1986). [Pg.192]


See other pages where Carcinogenesis forestomach is mentioned: [Pg.311]    [Pg.169]    [Pg.307]    [Pg.40]    [Pg.438]    [Pg.438]    [Pg.439]    [Pg.695]    [Pg.937]    [Pg.183]    [Pg.490]    [Pg.171]    [Pg.37]    [Pg.47]    [Pg.177]    [Pg.180]    [Pg.180]    [Pg.187]    [Pg.189]    [Pg.189]    [Pg.532]    [Pg.536]    [Pg.585]    [Pg.386]    [Pg.583]    [Pg.504]    [Pg.505]   
See also in sourсe #XX -- [ Pg.180 ]




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