Involvement of NO Generation in Aluminum-Induced Cell Death

  • Satoh Eiko
    Department of Clinical Chemistry, Faculty of Pharmaceutical Sciences, Hokuriku University
  • Yasuda Iho
    Department of Clinical Chemistry, Faculty of Pharmaceutical Sciences, Hokuriku University
  • Yamada Tomoko
    Department of Clinical Chemistry, Faculty of Pharmaceutical Sciences, Hokuriku University
  • Suzuki Yasuyuki
    Department of Clinical Chemistry, Faculty of Pharmaceutical Sciences, Hokuriku University
  • Ohyashiki Takao
    Department of Clinical Chemistry, Faculty of Pharmaceutical Sciences, Hokuriku University

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Abstract

Previously, we have reported that the exposure of PC12 cells to the aluminum–maltolate complex (Al(maltol)3) results in decreased cell viability via the apoptotic cell death pathway. In this study, we have used several nitric oxide synthase (NOS) inhibitors and the NO generator diethylenetriamine NONOate (DETA NONOate) to examine whether or not intracellular nitric oxide (NO) generation is involved in the onset mechanism of Al(maltol)3-induced cell death. Cell viability was assessed by measuring lactate dehydrogenase (LDH) release and caspase-3 activity. Treatment of the cells with 150 μM Al(maltol)3 for 48 h resulted in intracellular NO generation. Exposure of the cells to DETA NONOate also induced a marked decrease in cell viability. Pre-treatment of the cells with a general NOS inhibitor or with a selective inducible NOS (iNOS) inhibitor effectively prevented Al(maltol)3-induced cell death. However, a neuronal NOS (nNOS) inhibitor did not exhibit any protective effect against Al(maltol)3-induced cell death. In addition, ascorbic acid markedly inhibited Al(maltol)3- and DETA NONOate-induced cell death. Based on these results, we discussed the involvement of intracellular NO generation in the onset mechanisms of Al(maltol)3-induced cell death.

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