Histological analysis of 70-nm silica particles-induced chronic toxicity in mice

Nishimori, Hikaru; Kondoh, Masuo; Isoda, Katsuhiro; Tsunoda, Shin-ichi; Tsutsumi, Yasuo; Yagi, Kiyohito

doi:10.1016/j.ejpb.2009.03.007

Cited by 78 publications

(55 citation statements)

References 10 publications

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“…However, when administered intravenously, only scanty amount of SiNPs was deposited in mice brain 59 and no studies reported brain damage in the tested animals. 31,51 All the histopathological abnormal findings in our study were nonspecific, and the incidence did not correlate to the dosage of the SiNPs administered proportionally.…”

mentioning

confidence: 87%

“…40,49,51 It had been reported that SiNPs induced cardiotoxicity to zebrafish embryo because these particles inhibited angiogenesis and disturbed heart formation and development; 52 neutrophil-mediated cardiac inflammation 53 was assumed to be the cause. However, no definite cardiac injury was noted in the studies 40,49,51 of mature mice. Studies investigating the adverse effects about inhalation or intratracheal instillation with SiNPs had been performed, and pulmonary inflammation was common.…”

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confidence: 99%

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In vivo toxicologic study of larger silica nanoparticles in mice

Chan¹,

Liu²,

Chiau³

et al. 2017

IJN

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Silica nanoparticles (SiNPs) are being studied and used for medical purposes. As nanotechnology grows rapidly, its biosafety and toxicity have frequently raised concerns. However, diverse results have been reported about the safety of SiNPs; several studies reported that smaller particles might exhibit toxic effects to some cell lines, and larger particles of 100 nm were reported to be genotoxic to the cocultured cells. Here, we investigated the in vivo toxicity of SiNPs of 150 nm in various dosages via intravenous administration in mice. The mice were observed for 14 days before blood examination and histopathological assay. All the mice survived and behaved normally after the administration of nanoparticles. No significant weight change was noted. Blood examinations showed no definite systemic dysfunction of organ systems. Histopathological studies of vital organs confirmed no SiNP-related adverse effects. We concluded that 150 nm SiNPs were biocompatible and safe for in vivo use in mice.

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confidence: 87%

mentioning

confidence: 99%

In vivo toxicologic study of larger silica nanoparticles in mice

Chan¹,

Liu²,

Chiau³

et al. 2017

IJN

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“…The hepatotoxic effect after either single or repeated silica nanoparticle administration has also been reported by others. 29,30 Differences in hepatotoxic effects, apart from other factors, might be accounted for by the distinct characteristics of particle size 31 or surface charge, 32 or both. Noteworthy, in our study, the liver silicon content in the silica nanoparticle-treated animals was documented to be at least six-fold higher than in the controls for up to 30 days after administration.…”

Section: Discussionmentioning

confidence: 99%

Passive targeting of ischemic-reperfused myocardium with adenosine-loaded silica nanoparticles

Galagudza¹,

Королев²,

Постнов³

et al. 2012

IJN

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Pharmacological agents suggested for infarct size limitation have serious side effects when used at cardioprotective doses which hinders their translation into clinical practice. The solution to the problem might be direct delivery of cardioprotective drugs into ischemic-reperfused myocardium. In this study, we explored the potential of silica nanoparticles for passive delivery of adenosine, a prototype cardioprotective agent, into ischemic-reperfused heart tissue. In addition, the biodegradation of silica nanoparticles was studied both in vitro and in vivo. Immobilization of adenosine on the surface of silica nanoparticles resulted in enhancement of adenosine-mediated infarct size limitation in the rat model. Furthermore, the hypotensive effect of adenosine was attenuated after its adsorption on silica nanoparticles. We conclude that silica nanoparticles are biocompatible materials that might potentially be used as carriers for heart-targeted drug delivery.

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“…Similarly, Cho et al 5 described how nanosized SiO 2 particles (50 nm, 100 nm, and 200 nm) aggregated and caused acute inflammation in the liver. In a chronic toxicity study, Nishimori et al 6 found that administration of nanoparticles with a diameter of 70 nm induced elevated serum alanine aminotransferase levels in blood and liver fibrosis, among other effects. In in vitro systems, SiO 2 nanoparticles with diameters of 20-80 nm have been shown to induce apoptosis via activation of p53, Bax, and Bcl-2, all of which are involved in the mitochondrial-dependent pathway in certain cell lines, including human hepatocytes and human lung fibroblasts.…”

Section: Introductionmentioning

confidence: 99%

SiO2 nanoparticle-induced impairment of mitochondrial energy metabolism in hepatocytes directly and through a Kupffer cell-mediated pathway in vitro

Yang¹,

Chen²,

Ding³

et al. 2014

IJN

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The liver has been shown to be a primary target organ for SiO 2 nanoparticles in vivo, and may be highly susceptible to damage by these nanoparticles. However, until now, research focusing on the potential toxic effects of SiO 2 nanoparticles on mitochondria-associated energy metabolism in hepatocytes has been lacking. In this work, SiO 2 nanoparticles 20 nm in diameter were evaluated for their ability to induce dysfunction of mitochondrial energy metabolism. First, a buffalo rat liver (BRL) cell line was directly exposed to SiO 2 nanoparticles, which induced cytotoxicity and mitochondrial damage accompanied by decreases in mitochondrial dehydrogenase activity, mitochondrial membrane potential, enzymatic expression in the Krebs cycle, and activity of the mitochondrial respiratory chain complexes I, III and IV. Second, the role of rat-derived Kupffer cells was evaluated. The supernatants from Kupffer cells treated with SiO 2 nanoparticles were transferred to stimulate BRL cells. We observed that SiO 2 nanoparticles had the ability to activate Kupffer cells, leading to release of tumor necrosis factor-α, nitric oxide, and reactive oxygen species from these cells and subsequently to inhibition of mitochondrial respiratory chain complex I activity in BRL cells.

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Histological analysis of 70-nm silica particles-induced chronic toxicity in mice

Cited by 78 publications

References 10 publications

In vivo toxicologic study of larger silica nanoparticles in mice

In vivo toxicologic study of larger silica nanoparticles in mice

Passive targeting of ischemic-reperfused myocardium with adenosine-loaded silica nanoparticles

SiO2 nanoparticle-induced impairment of mitochondrial energy metabolism in hepatocytes directly and through a Kupffer cell-mediated pathway in vitro

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