Iron overload triggers redox-sensitive signals in human IMR-32 neuroblastoma cells

Gabriela A. Salvador, Patricia I. Oteiza

Research output: Contribution to journalArticlepeer-review

33 Scopus citations


Excessive neuronal iron has been proposed to contribute to the pathology of several neurodegenerative diseases including Alzheimer's and Parkinson's diseases. This work characterized human neuroblastoma IMR-32 cells exposure to ferric ammonium citrate (FAC) as a model of neuronal iron overload and neurodegeneration. The consequences of FAC treatment on neuronal oxidative stress and on the modulation of the oxidant-sensitive transcription factors AP-1 and NF-κB were investigated. Incubation with FAC (150 μM) resulted in a time (3-72. h)-dependent increase in cellular iron content, and was associated with cell oxidant increase. FAC caused a time-dependent (3-48. h) increase in nuclear AP-1- and NF-κB-DNA binding. This was associated with the upstream activation of the mitogen activated kinases ERK1/2, p38 and JNK and of IκBα phosphorylation and degradation. After 72. h incubation with FAC, cell viability was 40% lower than in controls. Iron overload caused apoptotic cell death. After 48-72. h of incubation with FAC, caspase 3 activity was increased, and chromatin condensation and nuclear fragmentation were observed. In summary, the exposure of IMR-32 cells to FAC is associated with increased oxidant cell levels, activation of redox-sensitive signals, and apoptosis.

Original languageEnglish (US)
Pages (from-to)75-82
Number of pages8
Issue number1
StatePublished - Jan 2011


  • AP-1
  • Iron
  • Neurotoxicity
  • NF-κB
  • Oxidative stress

ASJC Scopus subject areas

  • Neuroscience(all)
  • Toxicology


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