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Involvement of NO generation in aluminum-induced cell death

Eiko Satoh1, Iho Yasuda, Tomoko Yamada

  • 1Department of Clinical Chemistry, Faculty of Pharmaceutical Sciences, Hokuriku University, Kanagawa-machi, Kanazawa 920-1181, Japan.

Biological & Pharmaceutical Bulletin
|August 2, 2007
PubMed

Insights

Aluminum-maltol complex induces cell death by increasing nitric oxide (NO) production. Inhibiting inducible nitric oxide synthase (iNOS) protected cells, suggesting NO

Area of Science:

  • Neuroscience
  • Toxicology
  • Cell Biology

Background:

  • Aluminum-maltol complex (Al(maltol)(3)) exposure decreases PC12 cell viability through apoptosis.
  • The role of intracellular nitric oxide (NO) in this cell death pathway remains unclear.

Purpose of the Study:

  • To investigate the involvement of intracellular NO generation in Al(maltol)(3)-induced cell death.
  • To determine the specific nitric oxide synthase (NOS) isoforms involved.

Main Methods:

  • PC12 cells were treated with Al(maltol)(3) or a NO generator (DETA NONOate).
  • Cell viability was assessed using lactate dehydrogenase (LDH) release and caspase-3 activity assays.
  • NOS inhibitors (general, iNOS-selective, nNOS-selective) and ascorbic acid were used for pre-treatment.

Main Results:

  • Al(maltol)(3) treatment led to intracellular NO generation and decreased cell viability.
  • A general NOS inhibitor and an iNOS-selective inhibitor significantly protected cells from Al(maltol)(3)-induced death.
  • A neuronal NOS (nNOS) inhibitor had no protective effect.
  • Ascorbic acid inhibited cell death induced by both Al(maltol)(3) and DETA NONOate.

Conclusions:

  • Intracellular NO generation, particularly via inducible NOS (iNOS), plays a critical role in the mechanism of Al(maltol)(3)-induced PC12 cell death.
  • Ascorbic acid demonstrates a protective effect against NO-mediated cytotoxicity.

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