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Theranostics 2020, Vol. 10, Issue 20 9020 Objects Animal In vitro/ model vivo — In vitro — In vivo — In vitro — In vitro Cell lines/Tissues Jurkat T, NCI-H460, HeLa cells, HepG2, MCF-7, Beas-2B Human lymphocytes and sperms Pk15 Zebrafish ovarian follicle cells Exposure Size; Shape 5–10 nm 8–10 nm 61.2±33.9 nm, nonunifor m 30–55 nm Dosages 0.2, 0.5 and 1 mg/L Density gradient: 1:9, 1:3, 1:1 50 mg/L 30 μg/mL Toxicity Route Incubation — Incubation Incubation Time 4, 12 and 24 h 30 and 60 mins 24 and 48 h 2h Effect DNA damage; p38 MAPK activation; cell arrest; apoptosis Cell viability decrease Genotoxicity in Pk15 cells Apoptosis of ovarian follicle cells; germinal vesicle breakdown Toxicity manners Time- and concentration- dependent Concentration- and time- dependent Dose- dependent Concentration- dependent References [27] [367] [342] [349] *NOTE: UMR 106, rat osteosarcoma cells; MDA-MB-231, triple negative breast cancer cell line; PMBC, peripheral blood mononuclear cell; HepG2, human liver cancer cell line; Jurkat T, human T lymphocyte cell line; NCI-H460, human lung cancer cell line; MCF-7, human breast cancer cell line; Beas-2B: human bronchial epithelial cells; SPD, surfactant protein-D; U937, human histiocytic lymphoma cell line; Pk15, pig kidney cell line; BV-2, murine microglial cell line; N2a cells, mouse neuroblastoma; HEKs, human embryonic kidney cells; A549, human lung carcinoma; BxPC-3, human pancreas adenocarcinoma cells; PC3, prostate adenocarcinoma cells; HepG2, hepatocellular carcinoma cells; ESCs, embryonic stem cell; CNE, nasopharyngeal carcinoma cells; AsPC-1, pancreas adenocarcinoma cells; U-87 MG, glioblastoma cells; SW480, colorectal adenocarcinoma cells; EC109, esophageal cancer cells; VSMC, vascular smooth muscle cells; HMEC, human microvascular endothelial cells; LO2, hepatocytes; 293FT, embryonic kidney cells. Eye Toxicity AgNPs agent may cause concentration- dependent acute conjunctival irritation, but there is still no reliable evidence for toxicological effects. Pattwat et al. [326] dripped 50 ppm and 2,5000 ppm colloidal AgNPs into the eyes of guinea pig and explored whether there were acute eye irritation or corrosion throughout the 78 hours observation period. Although transient mild conjunctival irritation, i.e. blood vessel hyperemia in conjunctivae, was observed within 24 hours after 5000 ppm AgNPs treatment, neither low-dose nor high-dose colloidal AgNPs caused any acute toxicological effects in guinea pigs. AgNPs may have developmental toxicity in the eyes of early-stage individuals, which can eventually result in multiple types of eye defects. Yuan Wu et al. [327] studied the developmental toxicity of AgNPs by using Japanese medaka at early-life stages as experimental models, including embryonic, larval and juvenile stages. The Japanese medaka was exposed to 100–1000 mg/mL AgNPs for 70 days and various morphological malformations weredescribedandanalyzed,suchasedema,visceral deformities, heart malformations, spinal abnormality , especially eye defects. AgNPs-treated group showed different eye defects, such as microphthalmia, exophthalmia, cyclopia and anophthalmia. Histopathological examinations of 2-day-old larvae showed increased thickness of retinal pigment epithelium and missing of the retina in inner segments. Interestingly, comparing with the high-dose groups, the types and numbers of eye malformations in the low-dose groups were significantly higher. These morphological abnormalities and non-linear dose-response pattern suggest that the developmental toxicity of AgNPs may exhibit complex toxicological mechanisms. Respiratory toxicity AgNPs can induce acute lung toxicity and therefore impair lung function, and the damage severity is related to particle accumulation and clearance. Akinori [328] et al. studied the pulmonary toxicity of nanometer particles in mouse models. Ultrafine particles may pass the air-blood barrier through the gap between alveolar epithelial cells, induce vacuolation and necrosis of bronchiolar epithelial cells, resulting in transient acute lung inflammation and tissue damage. The oxidative stress and apoptosis induced by ultrafine particles may contribute to lung damage. In addition, nanoparticles showed size-dependent pulmonary toxicity , i.e. the particles in smaller size exhibit higher capacity for inducing lung inflammation and tissue damage than larger size [36, 329]. On the other hand, AgNPs may induce dose-dependent lung toxicity. Kaewamatawong et al. [330] demonstrated dose- dependent acute lung toxicity in mice induced by AgNPs using a single intratracheal instillation of 0, 10, 100, 1000 or 10000 ppm of colloidal AgNPs. And they observed moderate to severe bronchitis and multifocal alveolitis in 100, 1000 and 10,000 ppm AgNPs treated groups. Proinflammatory cytokines such as IL-1β and TNF-α released by alveolar macrophages and airway epithelial cells might involve in the inflammatory lesions in mice. The aggregation of AgNPs had a direct effect on the basement membrane, and disrupted equilibrium between the synthesis and degradation of the extracellular matrix, thus may cause pulmonary fibrosis.Similarly,theyalsospeculatedthatAgNPs induced oxidative stress in the lung. Furthermore, they recognized that metallothionein (MT) expression induced by AgNPs might be regarded as one of the possible protective mechanisms of lung. Different concentrations of AgNPs, which induce lung damage, http://www.thno.orgPDF Image | Silver nanoparticles Synthesis medical applications safety
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