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Effects of sodium nitrite and catechol, 3-methoxycatechol, or butylated hydroxyanisole in combination in a rat
M Hirose1, H Tanaka, S Takahashi
1First Department of Pathology, Nagoya City University Medical School, Japan.
Abstract:
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.
Insights
Sodium nitrite (NaNO2) altered the effects of phenolic antioxidants like catechol and 3-methoxycatechol in a rat cancer model. NaNO2 enhanced forestomach tumors but inhibited glandular stomach tumors, particularly in the upper digestive tract.
Area of Science:
- Toxicology
- Carcinogenesis
- Gastrointestinal Health
Background:
- Phenolic antioxidants are widely used, but their interaction with other compounds in biological systems requires further investigation.
- Sodium nitrite (NaNO2) is a common food additive and its potential role in modulating carcinogenesis is of significant interest.
- Understanding the complex interplay between dietary components and carcinogens is crucial for public health.
Purpose of the Study:
- To investigate the effects of simultaneous treatment with NaNO2 and phenolic antioxidants (butylated hydroxyanisole, catechol, 3-methoxycatechol) on rat carcinogenesis.
- To determine how NaNO2 influences the carcinogenic or chemopreventive effects of these phenolic compounds.
- To examine the impact on specific organs, particularly the forestomach, glandular stomach, and esophagus.
Main Methods:
- A rat multiorgan carcinogenesis model was employed using multiple carcinogens including diethylnitrosamine, N-methylnitrosourea, dimethylhydrazine, N-butyl-N-(4-hydroxybutyl)nitrosamine, and 2,2'-dihydroxy-di-n-propylnitrosamine.
- Animals received diets containing butylated hydroxyanisole, catechol, 3-methoxycatechol, or basal diet, with or without 0.3% NaNO2, starting after carcinogen exposure.
- Histological examination of organs was performed at week 28 to assess lesion development.
Main Results:
- NaNO2 strongly enhanced forestomach lesions but inhibited glandular stomach lesions when co-administered with catechol or 3-methoxycatechol.
- 3-Methoxycatechol promoted esophageal carcinogenesis regardless of NaNO2 presence; catechol's promotion was evident only with NaNO2.
- Post-carcinogen exposure treatment with NaNO2 enhanced forestomach carcinogenesis.
Conclusions:
- NaNO2 can significantly modify the effects of phenolic antioxidants on cell proliferation and carcinogenesis.
- The interaction primarily impacts the upper digestive tract, highlighting organ-specific effects.
- These findings suggest a complex role for NaNO2 in modulating diet-related cancer risks.