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dc.contributor.author
Piloni, Natacha Estefanía  
dc.contributor.author
Puntarulo, Susana Ángela  
dc.contributor.other
Berhardt, Leon V.  
dc.date.available
2023-01-04T10:44:59Z  
dc.date.issued
2021  
dc.identifier.citation
Piloni, Natacha Estefanía; Puntarulo, Susana Ángela; Iron homeostasis and oxidative balance in the context of endotoxemia; Nova Science Publishers; 189; 2021; 37-59  
dc.identifier.isbn
978-1-68507-234-6  
dc.identifier.uri
http://hdl.handle.net/11336/183233  
dc.description.abstract
This chapter intends to contribute to a deeper understanding of the main pathways playing a role in the complex mechanisms triggered in Fe-treated organisms. It has been shown that Fe overload causes an increase, as compared to values in control animals, in serum Fe content, and in hepatic ferritin (Ft) content, Fe content in Ft, labile Fe pool (LIP), and protein carbonyl content. High levels of LIP are harmful in tissues, especially through redox damage that can lead to fibrosis. High levels of Ft can occur in several diseases including hemophagocytic lymphohistiocytosis, macrophage activation syndrome, adult-onset Still?s disease, catastrophic antiphospholipid syndrome and septic shock. Lipopolysaccharide (LPS) treatment by itself significantly decreased Fe content in serum, and increased blood NO content. Numerous studies have demonstrated the immunomodulatory effects of Ft and its association with mortality and sustained inflammatory process. A pathogenic role of Ft and Fe has even been described during SARS-CoV-2 infection. Inflammatory responses involving microglia and astrocytes contribute to the pathogenesis of neurodegenerative diseases (NDs). Ferroptosis is a Reactive Oxygen Species (ROS)-and Fe-dependent form of regulated cell death, playing a critical role in organ injury. Ferroptosis participates in the development of cardiomyopathy including cardiac hypertrophy, diabetic cardiomyopathy and doxorubicin-induced cardiotoxicity. However, the role of ferroptosis in sepsis-induced injury remains unclear. Even though inflammation is tightly linked to Fe metabolism dysregulation, it is not clear whether the dysregulation of Fe metabolism induced by brain inflammation contributes to the pathogenesis of NDs or, depending on the doses and duration of the exposure, if it leads to hormesis (beneficial effects). The protective strategy against endotoxemia of sequestering serum Fe content is not fully operative under Fe-overload conditions, even though endogenous mechanisms are able to regulate the amount of catalytically active Fe. Information linked to these aspects of LPS exposure in several organs is updated here, but further studies are necessary to wholly identify the mechanisms involved.  
dc.format
application/pdf  
dc.language.iso
eng  
dc.publisher
Nova Science Publishers  
dc.rights
info:eu-repo/semantics/restrictedAccess  
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/  
dc.subject
Fe overload  
dc.subject
Ferroptosis  
dc.subject
Inflammation  
dc.subject
Oxidative stress  
dc.subject.classification
Bioquímica y Biología Molecular  
dc.subject.classification
Ciencias Biológicas  
dc.subject.classification
CIENCIAS NATURALES Y EXACTAS  
dc.title
Iron homeostasis and oxidative balance in the context of endotoxemia  
dc.type
info:eu-repo/semantics/publishedVersion  
dc.type
info:eu-repo/semantics/bookPart  
dc.type
info:ar-repo/semantics/parte de libro  
dc.date.updated
2022-10-04T17:53:19Z  
dc.journal.volume
189  
dc.journal.pagination
37-59  
dc.journal.pais
Estados Unidos  
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: 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.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://doi.org/10.52305/XSGI7651  
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://novapublishers.com/shop/advances-in-medicine-and-biology-volume-189/  
dc.conicet.paginas
242  
dc.source.titulo
Advances in Medicine and Biology