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dc.contributor.author
Piloni, Natacha Estefanía  
dc.contributor.author
Caro, Andres A.  
dc.contributor.author
Puntarulo, Susana Ángela  
dc.date.available
2019-11-08T18:42:54Z  
dc.date.issued
2018-08  
dc.identifier.citation
Piloni, Natacha Estefanía; Caro, Andres A.; Puntarulo, Susana Ángela; Iron overload prevents oxidative damage to rat brain after chlorpromazine administration; Springer; Biometals; 31; 4; 8-2018; 561-570  
dc.identifier.issn
0966-0844  
dc.identifier.uri
http://hdl.handle.net/11336/88375  
dc.description.abstract
The hypothesis tested is that Fe administration leads to a response in rat brain modulating the effects of later oxidative challenges such as chlorpromazine (CPZ) administration. Either a single dose (acute Fe overload) or 6 doses every second day (sub-chronic Fe overload) of 500 or 50 mg Fe-dextran/kg, respectively, were injected intraperitoneally (ip) to rats. A single dose of 10 mg CPZ/kg was injected ip 8 h after Fe treatment. DNA integrity was evaluated by quantitative PCR, lipid radical (LR · ) generation rate by electron paramagnetic resonance (EPR), and catalase (CAT) activity by UV spectrophotometry in isolated brains. The maximum increase in total Fe brain was detected after 6 or 2 h in the acute and sub-chronic Fe overload model, respectively. Mitochondrial and nuclear DNA integrity decreased after acute Fe overload at the time of maximal Fe content; the decrease in DNA integrity was lower after sub-chronic than after acute Fe overload. CPZ administration increased LR · generation rate in control rat brain after 1 and 2 h; however, CPZ administration after acute or sub-chronic Fe overload did not affect LR · generation rate. CPZ treatment did not affect CAT activity after 1–4 h neither in control rats nor in acute Fe-overloaded rats. However, CPZ administration to rats treated sub-chronically with Fe showed increased brain CAT activity after 2 or 4 h, as compared to control values. Fe supplementation prevented brain damage in both acute and sub-chronic models of Fe overload by selectively activating antioxidant pathways.  
dc.format
application/pdf  
dc.language.iso
eng  
dc.publisher
Springer  
dc.rights
info:eu-repo/semantics/openAccess  
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/  
dc.subject
ANTIOXIDANT  
dc.subject
BRAIN  
dc.subject
CHLORPROMAZINE  
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ELECTRON PARAMAGNETIC RESONANCE  
dc.subject
FE  
dc.subject
OXIDATIVE STRESS  
dc.subject.classification
Otras Ciencias Médicas  
dc.subject.classification
Otras Ciencias Médicas  
dc.subject.classification
CIENCIAS MÉDICAS Y DE LA SALUD  
dc.title
Iron overload prevents oxidative damage to rat brain after chlorpromazine administration  
dc.type
info:eu-repo/semantics/article  
dc.type
info:ar-repo/semantics/artículo  
dc.type
info:eu-repo/semantics/publishedVersion  
dc.date.updated
2019-10-23T20:58:36Z  
dc.journal.volume
31  
dc.journal.number
4  
dc.journal.pagination
561-570  
dc.journal.pais
Alemania  
dc.journal.ciudad
Berlin  
dc.description.fil
Fil: Piloni, Natacha Estefanía. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad Medicina. Instituto de Bioquímica y Medicina Molecular; Argentina  
dc.description.fil
Fil: Caro, Andres A.. Hendrix College, Conway; Estados Unidos  
dc.description.fil
Fil: Puntarulo, Susana Ángela. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad Medicina. Instituto de Bioquímica y Medicina Molecular; Argentina  
dc.journal.title
Biometals  
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/http://link.springer.com/10.1007/s10534-018-0104-8  
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1007/s10534-018-0104-8  
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6800076/