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Ascorbate is detectably mutagenic in the L5178Y TK+/- cell mutation assay

D E Amacher, S C Paillet

    Cancer Letters
    |November 1, 1981
    PubMed
    Summary

    Sodium ascorbate and ascorbic acid did not induce gene mutations in mouse lymphoma cells. Ascorbate toxicity resulted from in vitro reactions, preventable with catalase, suggesting it

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    Area of Science:

    • Toxicology
    • Genetics
    • Cell Biology

    Background:

    • Ascorbic acid (vitamin C) is an antioxidant with potential roles in cellular health.
    • Investigating the mutagenicity and cytotoxicity of ascorbic acid and its salt, sodium ascorbate, is crucial for understanding its safety profile.
    • Previous studies have yielded mixed results regarding the genotoxic potential of ascorbic acid.

    Purpose of the Study:

    • To evaluate the potential of sodium ascorbate and ascorbic acid to induce gene mutations and cytotoxicity in mouse lymphoma cells.
    • To determine if hydrogen ion concentration contributes to ascorbic acid toxicity.
    • To identify the source of observed ascorbate toxicity and explore mitigation strategies.

    Main Methods:

    • Mouse lymphoma L5178Y TK+/- cells were exposed to millimolar concentrations of sodium ascorbate and ascorbic acid.
    • Cytotoxicity was assessed by cell viability.
    • Gene mutations at the thymidine kinase locus were measured by trifluorothymidine resistance.
    • The role of hydrogen ion concentration and in vitro reaction products was investigated.
    • The effect of catalase co-incubation on ascorbate toxicity was examined.

    Main Results:

    • Neither sodium ascorbate nor ascorbic acid induced dose-related increases in trifluorothymidine resistance, even at toxic concentrations.
    • Increased hydrogen ion concentration did not account for ascorbic acid toxicity.
    • Ascorbate toxicity was attributed to reactive products formed in vitro via reactions with medium components.
    • Co-incubation with catalase prior to cell addition prevented the formation or persistence of these toxic substances.

    Conclusions:

    • Ascorbic acid and sodium ascorbate do not appear to be mutagens in mouse lymphoma cells under the tested conditions.
    • Ascorbate-induced cytotoxicity is mediated by in vitro reaction products, not the ascorbate molecule itself.
    • These findings suggest that ascorbic acid is unlikely to be a mammalian cell mutagen under normal physiological conditions, especially when reactive byproducts are managed.

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