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[Phenolic antioxidant TS-13 regulating ARE-dependent genes induces tumor cell death by mitochondria-dependent

G G Martinovich, I V Martinovich, N K Zenkov

    Biofizika
    |April 15, 2015
    PubMed

    Insights

    Phenolic antioxidants show varied effects on tumor cells. ARE-inducing antioxidant TS-13 inhibits growth by triggering mitochondria-dependent apoptosis, while others stimulate proliferation.

    Area of Science:

    • Biochemistry
    • Cell Biology
    • Pharmacology

    Background:

    • Water-soluble phenolic antioxidants are investigated for their biological effects.
    • Tumor cell proliferation is influenced by redox and calcium signaling pathways.

    Purpose of the Study:

    • To evaluate the impact of specific phenolic antioxidants (TS-13, BEP-11-K, potassium phenosan) on tumor cell proliferation.
    • To elucidate the role of redox and calcium signaling in mediating tumor cell responses to these antioxidants.

    Main Methods:

    • Cell culture studies to assess tumor cell proliferation.
    • Measurement of intracellular reactive oxygen species (ROS) and calcium levels.
    • Inhibition studies using apocynin, antimycin A, and cyclosporine A.

    Main Results:

    • Potassium phenosan and BEP-11-K stimulated tumor cell proliferation.
    • ARE-inducing phenolic antioxidant TS-13 inhibited tumor cell growth.
    • TS-13 treatment transiently increased intracellular ROS and calcium, an effect blocked by cyclosporine A.
    • Tumor cell growth rate correlated with intracellular ROS production.

    Conclusions:

    • Phenolic antioxidant TS-13 induces mitochondria-dependent apoptosis in tumor cells via the opening of permeability transition pores.
    • Potassium phenosan and BEP-11-K promote tumor cell proliferation.
    • Redox and calcium signaling are critical in mediating antioxidant effects on tumor cells.

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