The so-called "Trojan-horse" mechanism, in which nanoparticles are internalized within cells and then release high levels of toxic ions, has been proposed as a behavior in the cellular uptake of Ag nanoparticles (AgNPs). While several reports claim to have proved this mechanism by measuring AgNPs and Ag ions (I) in cells, it cannot be fully proven without examining those two components in both intra- and extracellular media. In our study, we found that even though cells take up AgNPs similarly to (microglia (BV-2)) or more rapidly than (astrocyte (ALT)) Ag (I), the ratio of AgNPs to total Ag (AgNPs+Ag (I)) in both cells was lower than that in outside media. It could be explained that H2O2, a major intracellular reactive oxygen species (ROS), reacts with AgNPs to form more Ag (I). Moreover, the major speciation of Ag (I) in cells was Ag(cysteine) and Ag(cysteine)2, indicating the possible binding of monomer cysteine or vital thiol proteins/peptides to Ag ions. Evidence we found indicates that the Trojan-horse mechanism really exists.

No abstract

Silver nanoparticles (AgNPs) have antibacterial characteristics, and currently are applied in Ag-containing products. This study found neural cells can uptake 3-5 nm AgNPs, and investigated the potential effects of AgNPs on gene expression of inflammation and neurodegenerative disorder in murine brain ALT astrocytes, microglial BV-2 cells and neuron N2a cells. After AgNPs (5, 10, 12.5 μg/ml) exposure, these neural cells had obviously increased IL-1β secretion, and induced gene expression of C-X-C motif chemokine 13 (CXCL13), macrophage receptor with collagenous structure (MARCO) and glutathione synthetase (GSS) for inflammatory response and oxidative stress neutralization. Additionally, this study found amyloid-β (Aβ) plaques for pathological feature of Alzheimer's disease (AD) deposited in neural cells after AgNPs treatment. After AgNPs exposure, the gene expression of amyloid precursor protein (APP) was induced, and otherwise, neprilysin (NEP) and low-density lipoprotein receptor (LDLR) were reduced in neural cells as well as protein level. These results suggested AgNPs could alter gene and protein expressions of Aβ deposition potentially to induce AD progress in neural cells. It's necessary to take notice of AgNPs distribution in the environment.

No abstract

No abstract

Silver nanoparticles (AgNPs) are commonly used nanomaterials in consumer products. Previous studies focused on its effects on neurons; however, little is known about their effects and uptake mechanisms on glial cells under normal or activated states. Here, ALT astrocyte-like, BV-2 microglia and differentiated N2a neuroblastoma cells were directly or indirectly exposed to 10 nm AgNPs using mono- and co-culture system. A lipopolysaccharide (LPS) was pretreated to activate glial cells before AgNP treatment for mimicking NP exposure under brain inflammation. From mono-culture, ALT took up the most AgNPs and had the lowest cell viability within three cells. Moreover, AgNPs induced H O and NO from ALT/activated ALT and BV-2, respectively. However, AgNPs did not induce cytokines release (IL-6, TNF-α, MCP-1). LPS-activated BV-2 took up more AgNPs than normal BV-2, while the induction of ROS and cytokines from activated cells were diminished. Ca -regulated clathrin- and caveolae-independent endocytosis and phagocytosis were involved in the AgNP uptake in ALT, which caused more rapid NP translocation to lysosome than in macropinocytosis and clathrin-dependent endocytosis-involved BV-2. AgNPs directly caused apoptosis and necrosis in N2a cells, while by indirect NP exposure to bottom chamber ALT or BV-2 in Transwell, more apoptotic upper chamber N2a cells were observed. Cell viability of BV-2 also decreased in an ALT-BV-2 co-culturing study. The damaged cells correlated to NP-mediated H O release from ALT or NO from BV-2, which indicates that toxic response of AgNPs to neurons is not direct, but indirectly arises from AgNP-induced soluble factors from other glial cells.

No abstract

No abstract