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Diet and exposure to N-nitroso compounds.

S R Tannenbaum

    Princess Takamatsu Symposia
    |January 1, 1985
    PubMed
    Summary

    Nitrate intake may increase cancer risk by forming carcinogenic N-nitroso compounds in the body. Certain foods like beans and fermented soy products can generate these mutagens under simulated gastric conditions.

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    Area of Science:

    • Food Science
    • Toxicology
    • Oncology

    Background:

    • The link between nitrate consumption and cancer risk is hypothesized to involve endogenous reduction to nitrite and subsequent formation of carcinogenic N-nitroso compounds.
    • Investigating the potential of various foods and biological materials to generate mutagens or carcinogens under simulated gastric conditions in the presence of nitrite is crucial.

    Purpose of the Study:

    • To review the current knowledge on nitrate, nitrite, and N-nitroso compound formation in relation to cancer risk.
    • To discuss the chemistry of nitrosation for specific chemicals of interest.
    • To identify foods that may act as sources of genotoxic agents through nitrosation.

    Main Methods:

    • Examination of a wide range of foods and biological materials.
    • Simulated gastric conditions with nitrite exposure to assess mutagen/carcinogen generation.
    • Review of existing literature on N-nitroso compound chemistry and epidemiological evidence.

    Main Results:

    • A limited number of foods, including beans, salt-preserved fish, fermented soy products, and moldy foods, were found to generate mutagens upon nitrosation.
    • A potential association exists between N-nitroso compound formation in these foods and epidemiological data suggesting increased risk for specific cancers.
    • The chemistry of nitrosation for relevant compounds was discussed.

    Conclusions:

    • Certain foods can generate genotoxic agents through nitrosation, potentially linking dietary nitrate/nitrite to cancer risk.
    • Demonstrating in vivo formation of N-nitroso compounds and their interaction with cellular targets in at-risk populations remains a significant future challenge.

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