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dc.contributor.author
Mackenzie, Gerardo G.
dc.contributor.author
Salvador, Gabriela Alejandra
dc.contributor.author
Romero, Carolina
dc.contributor.author
Keen, Carl L.
dc.contributor.author
Oteiza, Patricia Isabel
dc.date.available
2016-07-12T19:56:14Z
dc.date.issued
2011-07
dc.identifier.citation
Mackenzie, Gerardo G.; Salvador, Gabriela Alejandra; Romero, Carolina; Keen, Carl L.; Oteiza, Patricia Isabel; A deficit in zinc availability can cause alterations in tubulin thiol redox status in cultured neurons and in the developing fetal rat brain; Elsevier; Free Radical Biology and Medicine; 51; 2; 7-2011; 480-489
dc.identifier.issn
0891-5849
dc.identifier.uri
http://hdl.handle.net/11336/6464
dc.description.abstract
Zinc (Zn) deficiency during early development can result in multiple brain abnormalities and altered neuronal functions. In rats, a gestational deficit of Zn can affect the fetal brain cytoskeleton, and signaling cascades involved in cellular processes that are central to brain development. In the current paper, we tested the hypothesis that oxidative stress is involved in Zn deficiency-induced altered tubulin dynamics and the associated dysregulation of transcription factor NF-êB.For this purpose, we used two cell culture models (rat cortical neurons, human IMR-32 neuroblastoma cells) and an animal model of Zn deficiency. A low rate of in vitro tubulin polymerization, an increase in tubulin oligomers and a higher protein cysteine oxidation were observed in the Zn deficient neuronal cells, and in gestation day 19 fetal brains obtained from dams fed marginal Zn diets throughout pregnancy. These alterations could be prevented by treating the Zn deficient cells with the reducing agen tris (2-carboxyethyl)phosphine, or the presence of N-acetyl cysteine (NAC) and á-lipoic acid (LA) Consistent with the above, Zn deficiency-induced tubulin-mediated alterations in transcription factor NF-êB nuclear translocation were prevented by treating IMR-32 cells with LA and NAC. Binding of the NF-êB protein p50, dynein and karyopherin alpha (components of the NF-êB transport complex) to â-tubulin as well as the expression of NF-êB dependent genes (bcl-2, cyclin D1 and c-myc) were also restored by the addition of LA and NAC to Zn deficient cells. In conclusion, a deficit in Zn viability could affect early brain development through: 1) an induction of oxidative stress; 2) tubulin oxidation; 3) altered tubulin dynamics, and 4) deregulation of signals (e.q. NF-êB) involved in critical developmental events.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Elsevier
dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
dc.subject
Zinc Deficiency
dc.subject
Oxidative Stress
dc.subject
Neuron Development
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Tubulin Oxidation
dc.subject.classification
Bioquímica y Biología Molecular
dc.subject.classification
Ciencias Biológicas
dc.subject.classification
CIENCIAS NATURALES Y EXACTAS
dc.title
A deficit in zinc availability can cause alterations in tubulin thiol redox status in cultured neurons and in the developing fetal rat brain
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2016-07-05T18:47:04Z
dc.journal.volume
51
dc.journal.number
2
dc.journal.pagination
480-489
dc.journal.pais
Países Bajos
dc.journal.ciudad
Amsterdam
dc.description.fil
Fil: Mackenzie, Gerardo G.. University Of California At Davis; Estados Unidos
dc.description.fil
Fil: Salvador, Gabriela Alejandra. Consejo Nacional de Investigaciones Cientificas y Técnicas. Centro Científico Tecnológico Bahia Blanca. Instituto de Investigaciones Bioquímicas Bahia Blanca (i); Argentina. Universidad Nacional del Sur; Argentina
dc.description.fil
Fil: Romero, Carolina. University Of California At Davis; Estados Unidos
dc.description.fil
Fil: Keen, Carl L.. University Of California At Davis; Estados Unidos
dc.description.fil
Fil: Oteiza, Patricia Isabel. University Of California At Davis; Estados Unidos
dc.journal.title
Free Radical Biology and Medicine
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/10.1016/j.freeradbiomed.2011.04.028
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3506427/
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/pmid/PMC3506427
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/http://www.sciencedirect.com/science/article/pii/S0891584911002553


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