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Extraction of Aqueous Metabolites from Cultured Adherent Cells for Metabolomic Analysis by Capillary Electrophoresis-Mass Spectrometry
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Extraction of Aqueous Metabolites from Cultured Adherent Cells for Metabolomic Analysis by Capillary Electrophoresis-Mass Spectrometry

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Effects of 6-aminonicotinamide on cell growth, poly(ADP-ribose) synthesis and nucleotide metabolism

D Hunting, B Gowans, J F Henderson

    Biochemical Pharmacology
    |November 15, 1985
    PubMed

    Insights

    6-aminonicotinamide inhibits cell growth by disrupting nucleotide metabolism, not solely by blocking poly(ADP-ribose) synthesis. This finding clarifies its cytotoxic mechanism in cancer research.

    Area of Science:

    • Biochemistry
    • Cell Biology
    • Pharmacology

    Background:

    • Poly(ADP-ribose) synthesis is a crucial cellular process involved in DNA repair and cell survival.
    • 6-aminonicotinamide (6-AN) is known to inhibit poly(ADP-ribose) synthesis, but its precise cytotoxic mechanisms are not fully understood.
    • 3-aminobenzamide (3-AB) is a well-established inhibitor of poly(ADP-ribose) synthesis used for comparison.

    Purpose of the Study:

    • To investigate whether the cytotoxic effects of 6-aminonicotinamide are exclusively due to the inhibition of poly(ADP-ribose) synthesis.
    • To compare the effects of 6-AN and 3-AB on cell growth, poly(ADP-ribose) synthesis, and nucleotide concentrations in L1210 and CHO cells.

    Main Methods:

    • Comparative analysis of cell growth inhibition by 6-AN and 3-AB.
    • Measurement of poly(ADP-ribose) synthesis using NAD+ depletion assay induced by N-methyl N-nitrosourea.
    • Quantification of purine and pyrimidine ribonucleotide concentrations, NAD+, and ATP/ADP ratio.

    Main Results:

    • 3-AB, a potent inhibitor of poly(ADP-ribose) synthesis, showed minimal inhibition of L1210 cell growth.
    • 6-AN significantly inhibited the growth of L1210 and CHO cells at low concentrations.
    • 6-AN caused a pronounced depletion of nucleotides and NAD+, and reduced the ATP/ADP ratio, indicating widespread metabolic disruption.

    Conclusions:

    • Inhibition of poly(ADP-ribose) synthesis alone contributes minimally to growth inhibition.
    • The cytotoxic effects of 6-AN are primarily mediated by its profound impact on nucleotide metabolism.
    • Disruption of nucleotide metabolism by 6-AN is sufficient to inhibit both cell growth and DNA repair processes.

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