Carbon Black CB-EDA Nanoparticles in Macrophages: Changes in the Oxidative Stress Pathway and in Apoptosis Signaling
Joice Margareth de Almeida Rodolpho,
Krissia Franco de Godoy,
Patricia Brassolatti,
Bruna Dias de Lima Fragelli,
Luciana Camillo,
Cynthia Aparecida de Castro,
Marcelo Assis,
Carlos Speglich,
Elson Longo,
Fernanda de Freitas Anibal
Affiliations
Joice Margareth de Almeida Rodolpho
Laboratório de Inflamação e Doenças Infecciosas, Departamento de Morfologia e Patologia, Universidade Federal de São Carlos, São Carlos 13565-905, Brazil
Krissia Franco de Godoy
Laboratório de Inflamação e Doenças Infecciosas, Departamento de Morfologia e Patologia, Universidade Federal de São Carlos, São Carlos 13565-905, Brazil
Patricia Brassolatti
Laboratório de Inflamação e Doenças Infecciosas, Departamento de Morfologia e Patologia, Universidade Federal de São Carlos, São Carlos 13565-905, Brazil
Bruna Dias de Lima Fragelli
Laboratório de Inflamação e Doenças Infecciosas, Departamento de Morfologia e Patologia, Universidade Federal de São Carlos, São Carlos 13565-905, Brazil
Luciana Camillo
Laboratório de Inflamação e Doenças Infecciosas, Departamento de Morfologia e Patologia, Universidade Federal de São Carlos, São Carlos 13565-905, Brazil
Cynthia Aparecida de Castro
Laboratório de Inflamação e Doenças Infecciosas, Departamento de Morfologia e Patologia, Universidade Federal de São Carlos, São Carlos 13565-905, Brazil
Marcelo Assis
Department of Analytical and Physical Chemistry, University Jaume I (UJI), 12006 Castelló, Spain
Carlos Speglich
Centro de Pesquisa Leopoldo Américo Miguez de Mello CENPES/Petrobras, Rio de Janeiro 21941-915, Brazil
Elson Longo
Centro de Desenvolvimento de Materiais Funcionais, Departamento de Química, Universidade Federal de São Carlos, São Carlos 13565-905, Brazil
Fernanda de Freitas Anibal
Laboratório de Inflamação e Doenças Infecciosas, Departamento de Morfologia e Patologia, Universidade Federal de São Carlos, São Carlos 13565-905, Brazil
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.