Zinc deficiency in neuronal biology

Gerardo Mackenzie, M. Paola Zago, Lucila Aimo, Patricia I. Oteiza

Research output: Contribution to journalArticlepeer-review

24 Scopus citations


Adverse nutritional and environmental conditions during early development can irreversibly affect the nervous system. Zinc (Zn) deficiency associated with inadequate Zn intake and undernutrition is frequent throughout the world. Increasing evidence indicates that developmental Zn deficiency can lead to alterations in neonate and infant behavior, cognitive and motor performance that persist into adulthood. This review will address current knowledge on the events that are triggered in neuronal cells when Zn availability decreases and discuss their consequences on neuronal function and development. In neuronal cells, Zn deficiency induces oxidative stress, alters the normal structure and dynamics of the cytoskeleton, affects the modulation of transcription factors AP-1, NF-κB and NFAT and induces a decreased cell proliferation and increased apoptotic death. Thus, these closely associated events can affect neuronal function and critical developmental events (neuronal proliferation, differentiation, plasticity and survival) when Zn availability decreases.

Original languageEnglish (US)
Pages (from-to)299-307
Number of pages9
JournalIUBMB Life
Issue number4-5
StatePublished - 2007


  • AP-1
  • Apoptosis
  • Cytoskeleton
  • Microtubules
  • NF-κB
  • NFAT
  • Nuclear transport
  • Reactive oxygen species
  • Zinc
  • Zinc deficiency

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Genetics
  • Cell Biology


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