The paradoxical effect of 1,4-naphthoquinone on the process of cell death induced by hydrogen peroxide in rat thymocytes

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著者

    • Ohtani Hana
    • Laboratory of Cell Signaling, Institute of Socio-Arts and Sciences, The University of Tokushima
    • Fukunaga Eri
    • Laboratory of Cell Signaling, Institute of Socio-Arts and Sciences, The University of Tokushima
    • Oyama Yasuo
    • Laboratory of Cell Signaling, Institute of Socio-Arts and Sciences, The University of Tokushima

抄録

1,4-Naphthoquinone (NAPH) is found in diesel exhaust particles and it is an active metabolite of naphthalene, a fumigant insecticide. This compound is known to cause oxidative stress. Therefore, it is plausible to suggest that NAPH increases cell vulnerability to oxidative stress in an additive or synergistic manner. We tested this possibility using rat thymocytes with flow-cytometric techniques and appropriate fluorescent probes. NAPH attenuated the increase in cell lethality induced by hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>). The combination of NAPH and H<sub>2</sub>O<sub>2</sub> promoted the transition from normal cells to apoptotic living cells, but attenuated further transition to cell death. Thus, the process of cell death induced by H<sub>2</sub>O<sub>2</sub> was not completed in the presence of NAPH. However, NAPH did not attenuate certain lethal cellular events such as decrease in the cellular content of non-protein thiols and increases in intracellular Ca<sup>2+</sup> and Zn<sup>2+</sup> levels, induced by H<sub>2</sub>O<sub>2</sub>. The inhibitory effect of NAPH on the increase in cell lethality induced by H<sub>2</sub>O<sub>2</sub> was also observed when caspase activity was suppressed. In the present study, the mechanism underlying the NAPH-induced attenuation of cell death in cells affected by H<sub>2</sub>O<sub>2</sub>-generated oxidative stress was, however, not fully elucidated. Since both H<sub>2</sub>O<sub>2</sub> and NAPH elevated intracellular Ca<sup>2+</sup> and Zn<sup>2+</sup> levels, and since Zn<sup>2+</sup> is known to partly attenuate Ca<sup>2+</sup>-dependent cell death, the intracellular interaction between Ca<sup>2+</sup> and Zn<sup>2+</sup> may complicate the process of cell death induced by oxidative stress.

収録刊行物

  • Fundamental Toxicological Sciences

    Fundamental Toxicological Sciences 1(4), 123-129, 2014

    一般社団法人 日本毒性学会

各種コード

  • NII論文ID(NAID)
    130005083349
  • 本文言語コード
    ENG
  • データ提供元
    J-STAGE 
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