Oral Exposure to Silver Nanoparticles or Silver Ions May Aggravate Fatty Liver Disease in Overweight Mice

Jia, Jianbo; Li, Feifei; Zhou, Hongyu; Bai, Yan; Liu, Sijin; Jiang, Yanni; Jiang, Guibin; Yan, Bing

doi:10.1021/acs.est.7b02752

Cited by 94 publications

(57 citation statements)

References 60 publications

(86 reference statements)

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“…24 Similarly, oral exposure to silver NPs promoted progression from steatosis to steatohepatitis in overweight mice. 25 In contrast, cerium oxide NPs were found to reduce steatosis and display anti-inflammatory properties in liver-fibrosis rats. 26 However, the possible mechanisms of steatosis induced by NPs were unclear.…”

Section: Discussionmentioning

confidence: 99%

Silica nanoparticles trigger hepatic lipid-metabolism disorder in vivo and in vitro

Duan¹,

Liang²,

Lin³

et al. 2018

IJN

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BackgroundAs a promising nanocarrier in biomedical fields, silica nanoparticles (SiNPs) could transfer from the circulatory system to multiple organs. Among these, blood–liver molecular exchange is a critical factor in biological response to NPs. However, the potential effect of SiNPs on hepatic lipid metabolism is unclear. In this study, we employed three models to attempt discover whether and how SiNPs disturb hepatic lipid metabolism in vivo and in vitro.MethodsFirstly we used ICR mice models to evaulated the effects of SiNPs on the serum and hepatic lipid levels through repeated intravenous administration, meanwhile, the protein expressions of protein markers of lipogenesis (ACC1 and FAS), the key enzyme of fatty acid β-oxidation, CPT1A,and leptin levels in liver were detected by western blot. For verification studies, the model organism zebrafish and cultured hepatic L02 cells were further performed. The TLR5 and adipocytokine-signaling pathway were verified.ResultsInflammatory cell infiltration and mild steatosis induced by SiNPs were observed in the liver. Cholesterol, triglyceride, and low-density lipoprotein cholesterol levels were elevated significantly in both blood serum and liver tissue, whereas the ratio of high-density:low-density lipoprotein cholesterol was markedly decreased. Protein markers of lipogenesis (ACC1 and FAS) were elevated significantly in liver tissue, whereas the key enzyme of fatty acid β-oxidation, CPT1A, was decreased significantly. Interestingly, leptin levels in the SiNP-treated group were also elevated markedly. In addition, SiNPs caused hepatic damage and steatosis in zebrafish and enhanced hyperlipemia in high-cholesterol diet zebrafish. Similarly, SiNPs increased the release of inflammatory cytokines (IL1β, IL6, IL8, and TNFα) and activated the TLR5-signaling pathway in hepatic L02 cells.ConclusionIn summary, our study found that SiNPs triggered hyperlipemia and hepatic steatosis via the TLR5-signaling pathway. This suggests that regulation of TLR5 could be a novel therapeutic target to reduce side effects of NPs in living organisms.

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Section: Discussionmentioning

confidence: 99%

Silica nanoparticles trigger hepatic lipid-metabolism disorder in vivo and in vitro

Duan¹,

Liang²,

Lin³

et al. 2018

IJN

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“…The authors concluded that hypertension intensified AgNP-induced cardiotoxicity due to an observed reduction in NO and an increase in oxidative stress, leading to increased vasoconstriction and myocardial contractility. Jia et al [210] studied the effect of orally-exposed PVP-AgNPs (30 nm) in overweight mice and showed the progression of fatty liver disease from steatosis to steatohepatitis. The mechanisms proposed in the latter study were the activation of Kupffer cells, the enhancement of hepatic inflammation, and the suppression of fatty acid oxidation.…”

Section: Knowledge Gaps In Human and Environmental Risk Assessmentmentioning

confidence: 99%

Health Impact of Silver Nanoparticles: A Review of the Biodistribution and Toxicity Following Various Routes of Exposure

Ferdous

Nemmar

2020

IJMS

641

354

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Engineered nanomaterials (ENMs) have gained huge importance in technological advancements over the past few years. Among the various ENMs, silver nanoparticles (AgNPs) have become one of the most explored nanotechnology-derived nanostructures and have been intensively investigated for their unique physicochemical properties. The widespread commercial and biomedical application of nanosilver include its use as a catalyst and an optical receptor in cosmetics, electronics and textile engineering, as a bactericidal agent, and in wound dressings, surgical instruments, and disinfectants. This, in turn, has increased the potential for interactions of AgNPs with terrestrial and aquatic environments, as well as potential exposure and toxicity to human health. In the present review, after giving an overview of ENMs, we discuss the current advances on the physiochemical properties of AgNPs with specific emphasis on biodistribution and both in vitro and in vivo toxicity following various routes of exposure. Most in vitro studies have demonstrated the size-, dose- and coating-dependent cellular uptake of AgNPs. Following NPs exposure, in vivo biodistribution studies have reported Ag accumulation and toxicity to local as well as distant organs. Though there has been an increase in the number of studies in this area, more investigations are required to understand the mechanisms of toxicity following various modes of exposure to AgNPs.

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“…Recently, dissolved and nano-silver had been quantitated in organ lysates [ 18 ]. These studies suggested that after intravenous application, Ag-NP were mostly, but not exclusively, gathered in the liver [ 19 ], from where they were released into other organs where they were detectable as ions. Due to a disturbed liver metabolism, the authors suggested that silver NP toxicity was related to Ag-NP rather than to silver ions, a view substantiated by the finding that damage of endothelial cells and subsequent permeation through epithelial barriers is caused by Ag-NP rather than Ag ions [ 18 ].…”

Section: Introductionmentioning

confidence: 99%

Silver Nanoparticles in the Lung: Toxic Effects and Focal Accumulation of Silver in Remote Organs

Wiemann¹,

Vennemann²,

Blaske

et al. 2017

Nanomaterials

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The distribution of silver (Ag) into remote organs secondary to the application of Ag nanoparticles (Ag-NP) to the lung is still incompletely understood and was investigated in the rat with imaging methods. Dose-finding experiments were carried out with 50 nm- or 200 nm-sized polyvinyl pyrrolidine (PVP)-coated Ag-NP using alveolar macrophages in vitro and female rats, which received Ag-NP via intratracheal instillation. In the main study, we administered 37.5–300 µg per rat lung of the more toxic Ag50-PVP and assessed the broncho-alveolar lavage fluid (BALF) for inflammatory cells, total protein and fibronectin after three and 21 days. In parallel, lung tissue was analysed for DNA double-strand breaks and altered cell proliferation. While 75–150 µg Ag50-PVP per rat lung caused a reversible inflammation, 300 µg led to DNA damage, accelerated cell proliferation and progressively increasing numbers of neutrophilic granulocytes. Ag accumulation was significant in homogenates of liver and other peripheral organs upon lung dose of ≥75 µg. Quantitative laser-ablation inductively-coupled plasma mass spectrometry (LA-ICP-MS) combined with enhanced dark field microscopy and autometallography revealed focal accumulations of Ag and/or Ag-NP in sections of peripheral organs: mediastinal lymph nodes contained Ag-NP especially in peripheral macrophages and Ag in argyrophilic fibres. In the kidney, Ag had accumulated within proximal tubuli, while renal filter structures contained no Ag. Discrete localizations were also observed in immune cells of liver and spleen. Overall, the study shows that concentrations of Ag-NP, which elicit a transient inflammation in the rat lung, lead to focal accumulations of Ag in peripheral organs, and this might pose a risk to particular cell populations in remote sites.

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Oral Exposure to Silver Nanoparticles or Silver Ions May Aggravate Fatty Liver Disease in Overweight Mice

Cited by 94 publications

References 60 publications

Silica nanoparticles trigger hepatic lipid-metabolism disorder in vivo and in vitro

Silica nanoparticles trigger hepatic lipid-metabolism disorder in vivo and in vitro

Health Impact of Silver Nanoparticles: A Review of the Biodistribution and Toxicity Following Various Routes of Exposure

Silver Nanoparticles in the Lung: Toxic Effects and Focal Accumulation of Silver in Remote Organs

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