Abstract
Nanosilver plays an important role in nanoscience and nanotechnology, and is becoming increasingly used for applications in nanomedicine. Nanosilver ranges from 1 to 100 nanometers in diameter. Smaller particles more readily enter cells and interact with the cellular components. The exposure dose, particle size, coating, and aggregation state of the nanosilver, as well as the cell type or organism on which it is tested, are all large determining factors on the effect and potential toxicity of nanosilver. A high exposure dose to nanosilver alters the cellular stress responses and initiates cascades of signalling that can eventually trigger organelle autophagy and apoptosis. This review summarizes the current knowledge of the effects of nanosilver on cellular metabolic function and response to stress. Both the causative effects of nanosilver on oxidative stress, endoplasmic reticulum stress, and hypoxic stress—as well as the effects of nanosilver on the responses to such stresses—are outlined. The interactions and effects of nanosilver on cellular uptake, oxidative stress (reactive oxygen species), inflammation, hypoxic response, mitochondrial function, endoplasmic reticulum (ER) function and the unfolded protein response, autophagy and apoptosis, angiogenesis, epigenetics, genotoxicity, and cancer development and tumorigenesis—as well as other pathway alterations—are examined in this review.
Highlights
Nanosilver is made up of extremely small particles of silver, with lengths of 1–100 nm in at least one dimension [1]
Since inflammation is an important step in the wound healing process, the initial short-term increase in inflammation due to the nanosilver treatment reported in the in vitro and in vivo studies leads to an increased speed of wound healing and a faster decrease in inflammation, which agrees with the results found in the wound healing studies
Copper deficiency was observed in the rats, as well as decreased mRNA expression of several genes such as the cuproenzyme cytochrome c oxidase subunit 4 isoform 1 (Cox4i1), and genes involved in copper homeodynamics such as Cu(I)/Ag(I)-transporter 1 (CTR1), Cu(I)/Ag(I)-transporter 2 (CTR2), Cu-chaperone for SOD1 (CCS), MT1A, and Cu(II) binding cytosol protein (Commd1); the protein expression of MT1A and Commd1 did not decrease [40]
Summary
Nanosilver is made up of extremely small particles of silver, with lengths of 1–100 nm in at least one dimension [1]. Human mesenchymal stem cells (hMSC) treated with non-toxic levels of 50 nm PVP-coated nanosilver took up the nanosilver through clathrin-dependent endocytosis and macropinocytosis. TEM images of human acute monocytic leukemia cells (THP-1) treated with cytotoxic levels of 20 nm nanosilver showed that the nanosilver was contained in endosomes or lysosomes within the cells, but not in the nucleus or mitochondria. Similar results were seen in Chinese hamster ovary subclone K1 (CHO-K1) cells and NIH 3T3 mouse embryonic fibroblast cells, where nanosilver was observed to be contained in endosomes or lysosomes, but not inside the nucleus, mitochondria, or Golgi apparatus [64,65], and non-toxic nanosilver (citrate-coated, 15.26 nm) treatment of U251 glioblastoma cells resulted in aggregates contained in endosomes [66]. Many different factors may be contributing to these results, including the methods used for detecting ROS, the exact ROS being measured, the relative sensitivities and unique responses of the various cells lines, and the nanosilver coating, size, dose, and treatment time that are used
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