Uptake of cerium oxide nanoparticles and its influence on functions of mouse leukemic monocyte macrophages

Abstract

Exposure of the CeO 2 nanoparticles (NPs) causes a public concern on their potential health risk due to their wide applications in the fields of fuel additive, commodities, pharmaceutical, and other industries. In this study, the interactions between two commercial CeO 2 NPs (D-CeO 2 from Degussa and PC-CeO 2 from PlasmaChem) and mouse leukemic monocyte macrophage Raw264.7 cells were investigated to provide a fast and in-depth understanding of the biological influences of the NPs. Both types of the CeO 2 NPs had a negative surface charge around -12 mV and showed a tendency to form aggregates with sizes of 191 ± 5.9 and 60.9 ± 2.8 nm in cell culture environment, respectively. The cellular uptake of the CeO 2 NPs increased along with the increase of feeding dosage and prolongation of the culture time. The PC-CeO 2 NPs had a faster uptake rate and reached higher cellular loading amount at the highest feeding concentration (200 lg/mL). In general, both types of the CeO 2 NPs had rather small cytotoxicity even with a dosage as high as 200 lg/mL. The D-CeO 2 NPs showed a relative stronger cytotoxicity especially at higher concentrations and longer incubation time. The NPs were dispersed in vacuoles (most likely endosomes and lysosomes) and cytoplasm. Although both types of the CeO 2 NPs could suppress the production of reactive oxygen species, they impaired the mitochondria membrane potential to some extent. The cytoskeleton organization was altered and consequently the cell adhesion ability decreased after uptake of both types of the CeO 2 NPs.

Immune-regulating strategy against rheumatoid arthritis by inducing tolerogenic dendritic cells with modified zinc peroxide nanoparticles

“…Hence, various pharmacological inhibitors (amantadine, genistein, amiloride and cytochalasin D) were used. Amantadine prevented the budding of clathrin-coated pits; genistein retarded the activation of the Src family of tyrosine kinases; amiloride inactivated Na + /H + channels; and cytochalasin D destroyed the cytoskeleton to inhibit NP transportation [ 40 ]. Figure 2 d showed that cytochalasin D significantly suppressed the internalization efficiency of ZnCM NPs compared to amantadine, genistein and amiloride after 2 h of incubation, indicating the feasible participation of the DC cytoskeleton in the process of ZnCM NP ingestion, which was independent of clathrin-caveolin-mediated endocytosis.…”

ROS-Responsive Nanoparticles for Suppressing the Cytotoxicity and Immunogenicity Caused by PM2.5 Particulates

“…In addition, the extraneous particles may evoke some inflammatory cells such as monocytes to migrate to the affected area and differentiate into macrophages or dendritic cells, triggering immune response . RAW264.7 cells, which are undifferentiated mononuclear macrophage with a strong phagocytic ability and a potential to initiate immune response, have been widely used in the in vitro model to study the toxicity and inflammatory response of nanomaterials. , Therefore, A549 lung epithelial cells and RAW264.7 cells were assayed in terms of viability and inflammatory response challenged by PM2.5 and remedied by PPADT NPs.…”

“…59 RAW264.7 cells, which are undifferentiated mononuclear macrophage with a strong phagocytic ability and a potential to initiate immune response, have been widely used in the in vitro model to study the toxicity and inflammatory response of nanomaterials. 60,61 Therefore, A549 lung epithelial cells and RAW264.7 cells were assayed in terms of viability and inflammatory response challenged by PM2.5 and remedied by PPADT NPs.…”