Basic FGF, NGF, and IGFs protect hippocampal and cortical neurons against iron-induced degeneration

Ying Zhang, Tohru Tatsuno, John M. Carney, Mark P. Mattson

Research output: Contribution to journalArticlepeer-review

Abstract

Iron is believed to contribute to the process of cell damage and death resulting from ischemic and traumatic insults by catalyzing the oxidation of protein and lipids. Exposure of cultured rat hippocampal neurons to iron (FeSO4) caused a dose-dependent reduction in neuronal survival, which was potentiated by ascorbate. Damage to neurons was associated with a significant level of oxygen radical in the culture medium. The iron chelator desferal prevented both the neuronal degeneration caused by FeSO4 and the production of oxygen radical, demonstrating that ionic iron was responsible for the cell damage. Iron neurotoxicity was associated with an elevation of [Ca2+]i and was attenuated by NMDA receptor antagonists. Since recent findings demonstrated neuroprotec tive effects of growth factors in cell culture and in vivo models of ischemia, we examined the effects of growth factors on iron-induced damage. Basic fibroblast growth factor (bFGF), nerve growth factor (NGF), and insulin-like growth factors (IGF-I and IGF-II) each protected neurons against iron-induced damage. Both rat hippocampal and human cortical neurons were protected by these growth factors. Taken together, the data suggest that the neuroprotective effects of growth factors against excitotoxic/ischemic insults may result, in part, from a prevention or attenuation of oxidative damage.

Original languageEnglish (US)
Pages (from-to)378-388
Number of pages11
JournalJournal of Cerebral Blood Flow and Metabolism
Volume13
Issue number3
StatePublished - 1993
Externally publishedYes

Keywords

  • Calcium
  • Desferal
  • Free radical
  • Glutamate
  • Insulin-like growth factor
  • Ischemia
  • Nerve growth factor

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism
  • Neuroscience(all)

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