Phenolic antioxidant TS-13 regulating ARE-driven genes induces tumor cell death by a mitochondria-dependent pathway

被引：0
作者：
Martinovich G.G. [1 ]
Martinovich I.V. [1 ]
Zenkov N.K. [2 ]
Menshchikova E.B. [2 ]
Kandalintseva N.V. [3 ]
Cherenkevich S.N. [1 ]
机构：
[1] Belarusian State University, ul. Nezavisimosti 4, Minsk
[2] Scientific Center of Clinical and Experimental Medicine, Siberian Branch, Russian Academy of Medical Sciences, ul. Timakova 2, Novosibirsk
[3] Novosibirsk State Pedagogical University, ul. Vilyuiskaya 28, Novosibirsk
来源：
Biophysics | 2015年 / 60卷 / 1期
基金：
俄罗斯基础研究基金会;
关键词：
mitochondria-dependent apoptosis; reactive oxygen species; tumor cell growth; water-soluble phenolic antioxidants;
D O I：
10.1134/S0006350915010194
中图分类号：
学科分类号：
摘要：
Effects of water-soluble phenolic antioxidant sodium 3-(3′-tert-butyl-4′-hydroxyphenyl)-propyl thiosulfonate (TS-13), potassium 3,5-dimethyl-4-hydroxybenzyl thioethanoate (BEP-11-K), and potassium 3-(3′,5′-di-tert-butyl-4′-hydroxyphenyl)-propionate (potassium phenosan) on the proliferative activity of tumor cells and the role of redox-dependent and calcium-dependent signaling mechanisms in realization of tumor cell response to antioxidants were studied. Potassium phenosan and BEP-11-K were found to stimulate proliferation, whereas the ARE-inducing phenolic antioxidant TS-13 inhibited tumor cell growth in culture. The rate of tumor cell growth depended on the rate of intracellular reactive oxygen species production and was suppressed by apocynin (a NADPH oxidase inhibitor) and antimycin A (an ubiquinol-cytochrome c oxidoreductase inhibitor). The action of TS-13 on tumor cells was accompanied by a transient increase in the intracellular production of reactive oxygen species and the intracellular calcium concentration, whereas cell incubation with potassium phenosan and BEP-11-K did not influence the level of reactive oxygen species and intracellular calcium ions. Cyclosporin A blocked the inhibitory effect of TS-13. Thus, it can be reasonably speculated that phenolic antioxidant TS-13 triggers mitochondria-dependent apoptosis in tumor cells by opening mitochondrial permeability transition pores. © 2015, Pleiades Publishing, Inc.
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页码：94 / 100
页数：6
相关论文
共 31 条
  • [1] Zenkov N.K., Menshchikova E.B., Kandalintseva N.V., Et al., Biochemistry (Moscow), 72, 6, (2007)
  • [2] Zenkov N.K., Menshchikova E.B., Tkachev V.O., Biochemistry (Moscow), 78, 1, (2013)
  • [3] Turpaev K.T., Biochemistry (Moscow), 78, 2, (2013)
  • [4] Menshchikova E.B., Tkachev V.O., Zenkov N.K., Et al., Bull. Exp. Biol. Med., 155, 3, (2013)
  • [5] Menshchikova E.B., Zenkov N.K., Tkachev V.O., Et al., Bull. Exp. Biol. Med., 155, 3, (2013)
  • [6] Weisman N.Y., Menshchikova E.B., Zenkov N.K., Et al., Adv. Gerontol., 2, 3, (2012)
  • [7] Martinovich G.G., Cherenkevich S.N., Usp. Fiziol. Nauk, 39, 3, (2008)
  • [8] Yamamoto T., Hsu S., Lewis J., Et al., J. Pharmacol. Exp. Ther., 307, 1, (2003)
  • [9] Martinovich G.G., Martinovich I.V., Golubeva E.N., Et al., Izv. Nats. Akad. Nauk Belarusi, Ser. Med. Nauk, 2, (2012)
  • [10] Trachootham D., Alexandre J., Huang P., Nat. Rev. Drug. Discov., 8, 7, (2009)
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