Silver Nanoparticle Metallic silver is widely used in our daily life as well as in various medical treatments, as a result of nanotechnology breakthroughs, silver nanoparticles (hereinafter called AGNPS) have gained greater benefits. But the growth of AGNPS applications in various fields inevitably leads to increased potential risk of nanoparticles, causing concern for environmental safety and human health. In recent years, Silver Nanoparticle researchers have assessed the toxicity of AGNPS and sought to explore their cellular and molecular toxicity mechanisms.
Nano-Materials Enter the biological system, with cells, organelles and macromolecules (such as protein, nucleic acids, lipids, carbohydrates) to establish a series of nanoparticles-biomolecules interface. The dynamic physical-chemical interaction, kinetics, and heat transfer in this interfacial area affect some processes, such as the formation of protein crowns, cell contact, Silver Nanoparticle membrane-encapsulated particles, cell uptake and biocatalysis, all of which determine the biocompatibility and biological hazards of nanomaterials.
Agnps once in the human 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 organs, causing specific organs or systems to respond. Silver Nanoparticle In rodents, the brain, liver, spleen, kidney, and testis are the main secondary target organs of the whole body, regardless of whether oral, intravenous or intraperitoneal injections are given to Agnps. This pattern of organ distribution suggests that the potential toxicity of AGNPS can cause neurotoxicity, immune toxicity, nephrotoxicity and reproductive toxicity in vivo.
Bypassing active transport (i.e., swallowing) into the cells of the Agnps has no obvious cytotoxicity. In contrast, Agnps, which is mainly exchanged with internal swallowing to the internal lysosomal interval, has a significant toxicity to the cells. In general, Silver Nanoparticle Agnps is considered to be a sufficient and necessary condition for inducing cytotoxicity. In addition, Agnps may destroy the integrity of the cell membrane by inducing lipid peroxidation, thus directly infiltrating into the cell membrane.
There is growing evidence that the translation of post modifications, especially phosphorylation, acetylation, and ubiquitin, determines the activity and/or aggregation of proteins that perform autophagy and fine-tune autophagy development. The increase in cell stress can lead to the collapse of the modified system, or the nonspecific modification that does not occur under physiological conditions.
Ubiquitin has been regarded as the key to control the fate of proteins, which is the process of degrading the protein by protease. More recently, there is growing evidence that the conjugate ubiquitin chain determines the selectivity of autophagy.
Autophagy has been defined as autophagy-activated or autophagy is interrupted, the results showed that the transport and/or lysosomal functional defects of autophagy had been recognized as a potential driving force for apoptosis and autophagy, and were also known as type II programmed cell death. Recent studies in vitro have shown that Agnps also in turn blocks subsequent autophagy (possibly the consequence of lysosomal dysfunction), which may interfere with normal cellular physiology. In addition, the accumulation of p62, Silver Nanoparticle on the surface, P62 seems to be conducive to maintaining normal cellular physiology. In the early studies, it was found that the formation of ubiquitin containing proteins was a pathologic phenomenon, a pathological phenomenon that caused liver injury and neurodegenerative degeneration, which occurred simultaneously with the accumulation of p62 in the mice with autophagy deficiency. Surprisingly, the ablation of the P62 gene not only inhibited the presence of the protein inclusion body but also significantly reduced liver damage.