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[Cancer Research 53, 32-37, January 1, 1993]
© 1993 American Association for Cancer Research

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Effects of Sodium Nitrite and Catechol, 3-Methoxycatechol, or Butylated Hydroxyanisole in Combination in a Rat Multiorgan Carcinogenesis Model1

Masao Hirose2, Hikaru Tanaka, Satoru Takahashi, Mitsuru Futakuchi, Shoji Fukushima3 and Nobuyuki Ito

First Department of Pathology, Nagoya City University Medical School, 1 Kawasumi, Mizuho-cho, Mizuho-ku, Nagoya 467, Japan

Effects of simultaneous treatment with NaNO2 and butylated hydroxyanisole, catechol, or 3-methoxycatechol were examined in a rat multiorgan carcinogenesis model. Groups of 15 animals were given a single i.p. injection of 100 mg/kg of body weight diethylnitrosamine, 4 i.p. injections of 20 mg/kg of body weight N-methylnitrosourea, 4 s.c. injections of 40 mg/kg of body weight dimethylhydrazine, p.o. treatment with 0.05% N-butyl-N-(4-hydroxybutyl)nitrosamine in the drinking water for the first 2 weeks and p.o. treatment with 0.1% 2,2'-dihydroxy-di-n-propylnitrosamine in the drinking water for the next 2 weeks of the initial 4-week initiation period. Starting 3 days after the completion of these carcinogen treatments, animals were given diets containing 2% butylated hydroxyanisole, 0.8% catechol, 2% 3-methoxycatechol, or basal diet either alone or in combination with 0.3% sodium nitrite until week 28, when complete autopsy was performed.

Histological examination showed that NaNO2 strongly enhanced development of forestomach lesions but inhibited that of glandular stomach lesions in rats simultaneously given catechol or 3-methoxycatechol with or without prior carcinogen exposure. 3-Methoxycatechol promoted esophageal carcinogenesis either with or without NaNO2, but promoting effects of catechol were evident only in the presence of NaNO2. In addition, treatment with NaNO2 after carcinogen exposure enhanced forestomach carcinogenesis. These results indicate that NaNO2 can modify phenolic antioxidant-induced cell proliferation and/or carcinogenesis, particularly in the upper digestive tract.

1 This work was supported by a Grant-in-Aid for Cancer Research from the Ministry of Education, Science and Culture, a grant from the Ministry of Health and Welfare, and a grant from the Society for Promotion of Pathology of Nagoya.

2 To whom requests for reprints should be addressed.

3 Present address: First Department of Pathology, Osaka City University Medical School, 1-4-54, Asahi-machi, Abeno-ku, Osaka, 545, Japan.

Received 6/29/92. Accepted 10/19/92.




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HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 1993 by the American Association for Cancer Research.