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dc.contributor.author
Kaufman, Z.
dc.contributor.author
Salvador, Gabriela Alejandra
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dc.contributor.author
Liu, X.
dc.contributor.author
Oteiza, Patricia Isabel
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dc.date.available
2021-04-06T18:52:09Z
dc.date.issued
2020-08
dc.identifier.citation
Kaufman, Z.; Salvador, Gabriela Alejandra; Liu, X.; Oteiza, Patricia Isabel; Zinc and the modulation of Nrf2 in human neuroblastoma cells; Elsevier Science Inc; Free Radical Biology and Medicine; 155; 8-2020; 1-9
dc.identifier.issn
0891-5849
dc.identifier.uri
http://hdl.handle.net/11336/129466
dc.description.abstract
Zinc plays a key role in the modulation of neuronal redox homeostasis. A decreased zinc availability is associated with neuronal NADPH oxidase and nitric oxide synthase activation, deregulation of redox signaling, and impaired glutathione synthesis. The present work tested the hypothesis that zinc is necessary in the neuronal defense response against dopamine (DA)-induced oxidative stress, in particular through heme oxygenase-1 (HO-1) upregulation. DA showed higher cytotoxicity when zinc availability was low. Human IMR-32 neuroblastoma cells responded to high DA concentrations (100 μM) by upregulating HO-1. This upregulation involved Nrf2 translocation to the nucleus, degradation of the Bach-1 repressor, and Nrf2-DNA binding, but it was independent of ERK1/2 activation. DA-mediated induction of HO-1 expression was dependent on the concentration of zinc in the medium. IMR-32 cells incubated in zinc deficient medium showed an impaired response to DA, with lower HO-1 mRNA and protein levels than control DA-challenged cells. This altered HO-1 upregulation was reversed by zinc supplementation. In the presence of DA, Nrf2 nuclear translocation and Bach-1 degradation were lower in zinc deficient cells. The mechanisms involved include: i) impaired Nrf2-tubulin interactions and ii) alterations in the proteasome-mediated degradation of Bach-1 secondary to a decreased ubiquitylation. Results suggest that zinc is crucial in the neuronal response to DA-induced oxidative stress in part through its role in the modulation of the Nrf2-and Bach-1-driven upregulation of HO-1 expression.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Elsevier Science Inc
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dc.rights
info:eu-repo/semantics/restrictedAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
BACH-1
dc.subject
DOPAMINE
dc.subject
HO-1
dc.subject
NRF-2
dc.subject
ZINC
dc.subject
ZINC DEFICIENCY
dc.subject.classification
Bioquímica y Biología Molecular
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dc.subject.classification
Ciencias Biológicas
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dc.subject.classification
CIENCIAS NATURALES Y EXACTAS
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dc.title
Zinc and the modulation of Nrf2 in human neuroblastoma cells
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2021-03-26T12:59:10Z
dc.journal.volume
155
dc.journal.pagination
1-9
dc.journal.pais
Estados Unidos
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dc.journal.ciudad
Nueva York
dc.description.fil
Fil: Kaufman, Z.. University of California at Davis; Estados Unidos
dc.description.fil
Fil: Salvador, Gabriela Alejandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina
dc.description.fil
Fil: Liu, X.. 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
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dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S0891584920307115
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1016/j.freeradbiomed.2020.05.010
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