Carbon Black CB-EDA Nanoparticles in Macrophages: Changes in the Oxidative Stress Pathway and in Apoptosis Signaling
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Otros documentos de la autoría: Rodolpho, Joice Margareth de Almeida; de Godoy, Krissia Franco; Brassolatti, Patricia; Dias de Lima Fragelli, Bruna; Camillo, Luciana; Castro, Cynthia Aparecida de; Assis, Marcelo de; Speglich, Carlos; Longo, Elson; Anibal, Fernanda de Freitas
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Mostrar el registro completo del ítemcomunitat-uji-handle:10234/9
comunitat-uji-handle2:10234/7013
comunitat-uji-handle3:10234/8638
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INVESTIGACIONMetadatos
Título
Carbon Black CB-EDA Nanoparticles in Macrophages: Changes in the Oxidative Stress Pathway and in Apoptosis SignalingAutoría
Fecha de publicación
2023-06Editor
MDPIISSN
2227-9059Cita bibliográfica
Rodolpho, J.M.d.A.; Godoy, K.F.d.; Brassolatti, P.; Fragelli, B.D.d.L.; Camillo, L.; Castro, C.A.d.; Assis, M.; Speglich, C.; Longo, E.; Anibal, F.d.F. Carbon Black CB-EDA Nanoparticles in Macrophages: Changes in the Oxidative Stress Pathway and in Apoptosis Signaling. Biomedicines 2023, 11, 1643. https://doi.org/10.3390/biomedicines11061643Tipo de documento
info:eu-repo/semantics/articleVersión de la editorial
https://www.mdpi.com/2227-9059/11/6/1643Versión
info:eu-repo/semantics/publishedVersionPalabras clave / Materias
Resumen
The influence of black carbon nanoparticles on J774.A1 murine cells was investigated with the objective of exploring the cytotoxicity of black carbon functionalized with ethylenediamine CB-EDA. The results showed that ... [+]
The influence of black carbon nanoparticles on J774.A1 murine cells was investigated with the objective of exploring the cytotoxicity of black carbon functionalized with ethylenediamine CB-EDA. The results showed that CB-EDA has a cytotoxic profile for J774.A1 macrophages in a time- and dose-dependent manner. When phagocytosed by the macrophage, CB-EDA triggers a mechanism that leads to apoptosis. In this process, there is an increase in oxidative stress pathways due to the activation of nitric oxide and then ROS. This causes an imbalance in redox function and a disruption of membrane integrity that occurs due to high levels of LDH, in addition to favoring the release of the pro-inflammatory cytokines IL-6, IL-12, and tumor necrosis factor (TNF) in an attempt to modulate the cell. However, these stimuli are not sufficient to repair the cell and the level of mitochondrial integrity is affected, causing a decrease in cell viability. This mechanism may be correlated with the activation of the caspasse-3 pathway, which, when compromised, cleaves and induces cells death via apoptosis, either through early or late apoptosis. In view of this, the potential for cell damage was investigated by analyzing the oxidative and inflammatory profile in the macrophage lineage J774.A1 and identifying potential mechanisms and metabolic pathways connected to these processes when cells were exposed to NP CB-EDA for both 24 h and 48 h. [-]
Publicado en
Biomedicines, 2023, vol. 11, no 6Entidad financiadora
PETROBRAS | European Union-Next Generation EU | Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) | Financiadora de Estudos e Projetos (FINEP) | Coordenação de Aperfeiçoamento de Pessoal de Nível Superior(CAPES) | Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
Código del proyecto o subvención
2017/00010-7 | MGS/2021/21 (UP2021-021) | 2013/07296-2 | 001
Derechos de acceso
info:eu-repo/semantics/openAccess
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