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Theranostics 2020, Vol. 10, Issue 20 may also accumulate in peripheral organs and cause potential health risks. Joanna et al. [46] found that AgNPs disrupted the blood/alveolar epithelial permeability barrier, elicited oxidative stress, activated eosinophils and promoted the release of multiple cytokines. Most importantly, their results showed that AgNPs induced eosinophilic and neutrophilic inflammation, which was an important pathological change in asthma. This might suggest that exposure to AgNPs could trigger asthma. Hepatobiliary System Toxicity Part of the ingested nanoparticles tend to be sequestered, degraded and accumulated in the liver, which means the liver may be responsible for the metabolism of nanoparticles as well as one of the most frequently attacked organs. On the other hand, the gallbladder collects, stores and excretes bile or biological waste to the intestine. Various metal nanoparticles, including AgNPs, are recognized to be exported from the liver through this pathway. Therefore, hepatocytes are widely studied in the liver toxicity of AgNPs. Maglie et al. [48] found that AgNPs induced severe hepatobiliary damage in mice, including significant hepatocyte necrosis and gallbladder hemorrhage. In this study, AgNPs exhibited size- and dose-dependent hepatobiliary toxicity, i.e. AgNPs in smaller size produced more serious toxic effects, and higher dose of AgNPs induced severer hepatobiliary damages. Camilla et al. [331] observed multi-system acute toxicities in mice with a single intravenous injection of AgNPs. First of all, significant hepatobiliary damages were recognized, including hepatocyte necrosis, micro- hemorrhage around the biliary tract, and portal vein injury. Secondly, they also observed that AgNPs could induce acute tubular necrosis and apoptosis, and moderate splenomegaly. The results of Mohammad et al. [332] showed that AgNPs penetrating via the skin induced time-dependent liver damage such as hyperemia, dilatation in central venous, swelling hepatocytes and increased inflammatory cells. Besides hepatocytes, Kupffer cells (KCs) are also responsible for the removal of AgNPs [333]. KCs are macrophages that reside in the hepatic sinusoids and have the active ability of phagocytosis, maintaining the normal immune response and removing nanoparticles from organisms [333, 334]. Therefore, KCs become the focus of research on liver toxicity and metabolism of AgNPs. Central Nervous System Toxicity The central nervous system consists of two parts: the brain and the spinal cord. Lots of supporting non-nervous cells, i.e. neuroglial cells fill the 9021 interneuronal space within the central nervous system. In recent years, some articles point out that AgNPs may penetrate the brain and subsequently induce neuronal death. Due to the limited self-repairing ability of nerve cells, the potential neurotoxicity of AgNPs is receiving more attention. Different exposure patterns can lead to the accumulation of AgNPs in the brain. Injected AgNPs cross blood-brain barrier (BBB) and then penetrate the brain, while inhaled AgNPs reach the central nervous system through the olfactory and/or BBB [335, 336]. Due to the unique physicochemical properties of AgNPs, deposited AgNPs in nerve cells, astrocytes and extravascular lymphocytes may cause and aggravate neurotoxicity and inflammation, and increase the permeability of BBB. In the study of the cytotoxicity of AgNPs on rat cerebral astrocytes, Cheng et al. [337] investigated the neurotoxicological effects of AgNPs and Ag+ and compared the mechanisms. Both AgNPs and Ag+ exposure could internalize silver in astrocytes in dose- and time-dependent manners. The AgNPs had higher bioaccumulation ability than Ag+ after 24 h treatment. Afterthesametreatmenttime,theyfoundthatAgNPs might induce intracellular ROS generation in rat cerebral astrocytes and caused cell apoptosis, however, there were undetectable alterations in Ag+ group. More importantly, they confirmed that AgNPs could increase the level of phosphorylated JNK, a kind of kinase involved in mediating apoptosis. The non-cytotoxic dose of AgNPs, rather than Ag+, might induce neuroinflammation by promoting the secretion of multiple cytokines of astrocytes, including CINC-2a/b, CINC-3, IL-10, IP-10, L-selectin and thymus chemokine. Liming et al. [38] investigated the neurotoxicity of AgNPs in the rat after intragastric administration of low-dose (1 mg/kg, body weight) orhigh-dose(10mg/kg,bodyweight)fortwoweeks. They observed a variety of cell morphological changes in the nervous system, including neuron shrinkage, astrocytes swelling and extravascular lymphocytes. They also observed significantly increased inflammatory factors such as IL-4 in the serum. These data supported the proinflammatory effects of AgNPs in the nervous system. Then they focused on the possible mechanisms for AgNPs or Ag+ transporting across the blood-brain barrier. AgNPs or released Ag+ might cross through the blood-brain barrier via ionic pores or channels and subsequently damage the nerve cells. Besides, AgNPs could enter the central nervous system via vesicular transport of endothelial cells and subsequently induced neuroinflammation. At the same time, they demonstrated the increased permeability of the blood-brain barrier in a rat model after AgNPs treatment. They also observed that http://www.thno.orgPDF Image | Silver nanoparticles Synthesis medical applications safety
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