Silver Nanoparticle Interaction

- Jul 21, 2017 -

Metal silver is widely used in our daily life and in medical care. Silver Nanoparticle Due to the breakthrough of nanotechnology, Silver Nanoparticle nano silver particles (hereinafter referred to as AgNPs) have gained more benefits. However, the increase in the use of AgNPs in various fields inevitably leads to an increase in the potential risk of nanoscale particles, raising concerns about environmental safety and human health. Silver Nanoparticle In recent years, researchers have evaluated the toxicities of AgNPs and sought to explore their cellular and molecular toxicity mechanisms.

After the nanomaterials enter the biological system, a series of nanoparticle-biomolecule interfaces are established with cells, subcellular organelles and macromolecules (such as proteins, nucleic acids, Silver Nanoparticle lipids, carbohydrates). The interaction of dynamics, dynamics, and heat exchange on this interface area can affect processes such as protein crown formation, cell contact, plasma membrane entrapment, Silver Nanoparticle cell uptake and biocatalysis, all of which determine the presence of nanomaterials Biocompatibility and biohazardability.

Cytotoxicity, such as reactive oxygen species, DNA damage, Silver Nanoparticle changes in intracellular enzyme activity, and the occurrence of apoptosis and necrosis, have been associated with liver toxicity induced by AgNPs in vivo. Basically, when cells are facing unfavorable conditions, Silver Nanoparticle several steady-state processes will begin to sustain cell survival, one of which is autophagy. Autophagy can act as a cell defense process that is essential to counteract the toxicity of AgNPs, but does not maintain autophagic activity, Silver Nanoparticle accompanied by reduced energy, which may contribute to the onset of apoptosis and subsequent liver function damage.

There is no obvious cytotoxic effect on AgNPs that enter the cells by means of active transport (ie, endocytosis). In contrast, internalization of AgNPs, which are predominantly exchanged into the lysosomal interval through endocytosis, has a significant toxic effect on cells. Considering that AgNPs endocytosis is considered to be a sufficient and non-essential condition for inducing cytotoxicity. In addition, Silver Nanoparticle AgNPs may destroy the integrity of the cell membrane by inducing lipid peroxidation and thus penetrate directly into the cell membrane.

More and more evidence suggests that post-translational modifications, especially phosphorylation, acetylation, and ubiquitination, determine the activity and / or aggregation of proteins involved in performing autophagy and fine-tuning autophagous tide development. Silver Nanoparticle Increased cellular stress can lead to the collapse of the post-translational modification system or cause nonspecific modification that does not occur under physiological conditions.

Ubiquitination has long been considered the key to controlling the fate of proteins, Silver Nanoparticle which is the process of labeling proteins to be degraded by proteasomes. Silver Nanoparticle More recently, there is growing evidence that conjugated ubiquitin chains determine the selectivity of autophagy.

Autophagy dysfunction has been delineated as autophagic hyperactivity or autophagic tide is blocked, and the results are manifested as autophagic transport and / or lysosomal dysfunction, which has been recognized as apoptosis and autophagy The potential impetus for cell death is also known as type II programmed cell death. Recent in vitro studies have shown that AgNPs also in turn block subsequent autophonic tide (which may be the consequence of lysosomal dysfunction), which may interfere with normal cell physiology. Silver Nanoparticle In addition, the accumulation of p62, on the surface, P62 seems to be conducive to maintaining normal cell physiology.


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