Zinc deficiency in neuronal biology

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

Research output: Contribution to journalArticle

23 Citations (Scopus)

Abstract

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
Volume59
Issue number4-5
DOIs
StatePublished - 2007

Fingerprint

Zinc
Availability
Infant Behavior
Oxidative stress
Transcription Factor AP-1
Cell proliferation
Neurology
Cytoskeleton
Malnutrition
Nervous System
Plasticity
Oxidative Stress
Cell Proliferation
Modulation

Keywords

  • 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

Cite this

Mackenzie, G., Zago, M. P., Aimo, L., & Oteiza, P. I. (2007). Zinc deficiency in neuronal biology. IUBMB Life, 59(4-5), 299-307. https://doi.org/10.1080/15216540701225966

Zinc deficiency in neuronal biology. / Mackenzie, Gerardo; Zago, M. Paola; Aimo, Lucila; Oteiza, Patricia I.

In: IUBMB Life, Vol. 59, No. 4-5, 2007, p. 299-307.

Research output: Contribution to journalArticle

Mackenzie, G, Zago, MP, Aimo, L & Oteiza, PI 2007, 'Zinc deficiency in neuronal biology', IUBMB Life, vol. 59, no. 4-5, pp. 299-307. https://doi.org/10.1080/15216540701225966
Mackenzie, Gerardo ; Zago, M. Paola ; Aimo, Lucila ; Oteiza, Patricia I. / Zinc deficiency in neuronal biology. In: IUBMB Life. 2007 ; Vol. 59, No. 4-5. pp. 299-307.
@article{1ae16d6e758941358f9f9f2935718c2a,
title = "Zinc deficiency in neuronal biology",
abstract = "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.",
keywords = "AP-1, Apoptosis, Cytoskeleton, Microtubules, NF-κB, NFAT, Nuclear transport, Reactive oxygen species, Zinc, Zinc deficiency",
author = "Gerardo Mackenzie and Zago, {M. Paola} and Lucila Aimo and Oteiza, {Patricia I.}",
year = "2007",
doi = "10.1080/15216540701225966",
language = "English (US)",
volume = "59",
pages = "299--307",
journal = "IUBMB Life",
issn = "1521-6543",
publisher = "Wiley-Blackwell",
number = "4-5",

}

TY - JOUR

T1 - Zinc deficiency in neuronal biology

AU - Mackenzie, Gerardo

AU - Zago, M. Paola

AU - Aimo, Lucila

AU - Oteiza, Patricia I.

PY - 2007

Y1 - 2007

N2 - 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.

AB - 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.

KW - AP-1

KW - Apoptosis

KW - Cytoskeleton

KW - Microtubules

KW - NF-κB

KW - NFAT

KW - Nuclear transport

KW - Reactive oxygen species

KW - Zinc

KW - Zinc deficiency

UR - http://www.scopus.com/inward/record.url?scp=34248545720&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=34248545720&partnerID=8YFLogxK

U2 - 10.1080/15216540701225966

DO - 10.1080/15216540701225966

M3 - Article

C2 - 17505969

AN - SCOPUS:34248545720

VL - 59

SP - 299

EP - 307

JO - IUBMB Life

JF - IUBMB Life

SN - 1521-6543

IS - 4-5

ER -