Zinc deficiency in neuronal biology.
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-betaB 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.
Mackenzie
Gerardo G
GG
Department of Nutrition, University of California Davis, California 95616, USA.
Zago
M Paola
MP
Aimo
Lucila
L
Oteiza
Patricia I
PI
D000818:Animals; D017209:Apoptosis / Q000502:physiology; D003599:Cytoskeleton / Q000378:metabolism; D006801:Humans; D016328:NF-kappa B / Q000378:metabolism; D050778:NFATC Transcription Factors / Q000378:metabolism; D009474:Neurons / Q000166:cytology / Q000378:metabolism*; D018384:Oxidative Stress; D015398:Signal Transduction / Q000502:physiology; D018808:Transcription Factor AP-1 / Q000378:metabolism; D015032:Zinc / Q000172:deficiency*
D016328:NF-kappa B; D050778:NFATC Transcription Factors; D018808:Transcription Factor AP-1; D015032:Zinc