Metal silver is widely used in our daily life and in medical care. Due to the breakthrough of nanotechnology, nano silver particles (hereinafter referred to as AgNPs) have gained more benefits. Silver Nanoparticle However, the increase in the use of AgNPs in various fields inevitably leads to an increase in the potential risk of nanoscale particles, which raise concerns about environmental safety and human health. In recent years, Silver Nanoparticle 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, Silver Nanoparticle nucleic acids, lipids, carbohydrates). The interaction of dynamics, dynamics, Silver Nanoparticle and heat exchange on this interface area can affect processes such as the formation of protein crowns, cell contact, plasma membrane entrapment, cell uptake and biocatalysis, all of which determine the presence of nanomaterials Biocompatibility and biohazardous.
Once AgNPs enter the body, some may remain in the original target tissue, but in principle they will be transported through the bloodstream or lymphatic system, distributed to the body's secondary target organ, causing a specific organ or systemic response. In rodents, AgNPs, given oral, intravenous, Silver Nanoparticle or intraperitoneal injection, have demonstrated that the brain, liver, spleen, kidney, Silver Nanoparticle and testis are predominantly secondary target organs throughout the body. Such organ distribution patterns suggest that the potential toxicity of AgNPs can cause neurotoxicity, immunotoxicity, nephrotoxicity, and reproductive toxicity in vivo.
Cytotoxicity, such as reactive oxygen species, DNA damage, 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 the cells are facing unfavorable conditions, 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, 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 are involved in active transport (ie, endocytosis) into cells. In contrast, the internalization of AgNPs, Silver Nanoparticle which are mainly exchanged into the lysosomal interval, is significantly toxic by endocytosis. Considering that AgNPs endocytosis is considered to be a sufficient and noninvasive 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.
"Autophonic tide" is used to indicate the autophagy after the dynamic process, first of all the formation and maturation of autophagosomes, followed by autophagylosin fusion, Silver Nanoparticle and finally hydrolyzed vesicle wrapped cell components and the release of macromolecules Cytoplasm. In this regard, any of the above steps in the process of interruption as a cell autophagic tide is flawed. AgNPs exposure increased LC3-I to LC3-II in a dose-dependent manner, and the accumulation of p62 protein was dose-dependent. This suggests that although AgNPs activate autophagy, they eventually lead to autophonic tide being blocked. In addition to autophagic dysfunction, RNP and apoptosis were also increased after AgNPs exposure.
More and more evidence suggests that post-translational modifications, Silver Nanoparticle especially phosphorylation, acetylation, and ubiquitination, determine the activity and / or aggregation of proteins involved in the implementation of 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, 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.