Metallic silver is widely used in our daily life as well as in various medical treatments, as a result of nanotechnology breakthroughs, Silver Nanoparticle 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, Silver Nanoparticle and heat transfer in this interfacial area affect some processes, such as the formation of protein crowns, cell contact, 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. In rodents, the brain, liver, spleen, Silver Nanoparticle 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.
Cytotoxic reactions, such as reactive oxygen, DNA damage, changes in intracellular enzyme activity, and apoptosis and necrosis, have been associated with liver toxicity caused by Agnps in vivo. Basically, when the cells are facing unfavorable conditions, several steady-state processes will begin to sustain the survival of the cell, one of which is autophagy. Autophagy can be used as a critical cell defense process to counteract AGNPS toxicity, but it does not maintain autophagy activity, with reduced energy, Silver Nanoparticle and may promote apoptosis and subsequent liver damage.
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), Silver Nanoparticle which may interfere with normal cellular physiology. In addition, the accumulation of p62, on the surface, P62 seems to be conducive to maintaining normal cellular physiology.