Disturbed mitochondrial quality control involved in hepatocytotoxicity induced by silica nanoparticles

Qi, Yi; Ma, Ru; Li, Xueyan; Lv, Songqing; Li, Xiaoying; Abulikemu, Alimire; Zhao, Xinying; Li, Yanbo; Guo, Caixia; Sun, Zhiwei

doi:10.1039/d0nr01893g

Cited by 40 publications

(16 citation statements)

References 71 publications

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“…However, their tendency to accumulate in the liver for long periods after repeated exposure has raised some concerns on the potential hepatotoxicity observed in some in vitro and in vivo studies. 69 Their possibility to cross the different biological barriers existing in every route of entrance, and to reach specific organs and tissues such as the lung alveoli or the intestinal epithelia, as for any other nanomaterial, will mainly depend on the size. 68,70 Moreover, independently of the route of entrance, some nanomaterials can reach the blood or the lymph and have a broad biodistribution.…”

Section: Cytotoxicity and Health Effects Of Silica Nanomaterialsmentioning

confidence: 99%

Insights on toxicity, safe handling and disposal of silica aerogels and amorphous nanoparticles

Vareda

García‐González

Valente

et al. 2021

Environ. Sci.: Nano

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Section: Cytotoxicity and Health Effects Of Silica Nanomaterialsmentioning

confidence: 99%

Insights on toxicity, safe handling and disposal of silica aerogels and amorphous nanoparticles

Vareda

García‐González

Valente

et al. 2021

Environ. Sci.: Nano

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“…Although, most of the histopathological findings in the positive studies in Table 1 do not demonstrate a definitive, irreversible adverse outcome such as liver fibrosis (or any effects at all), these findings can potentially progress to liver fibrosis due to further prolonged exposure. However, the exact mechanism of hepatic toxicity caused by SAS is unknown and a topic of present research (Kermanizadeh, Powell, and Stone 2020;Medina-Reyes et al 2020;Murugadoss et al 2017;Qi et al 2020). Yet, as SAS is present in many everyday products, humans will be exposed to SAS on a daily basis over a prolonged period.…”

Section: Mode Of Actionmentioning

confidence: 99%

Issues currently complicating the risk assessment of synthetic amorphous silica (SAS) nanoparticles after oral exposure

et al. 2021

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Synthetic amorphous silica (SAS) is applied in food products as food additive E 551. It consists of constituent amorphous silicon dioxide (SiO 2 ) nanoparticles that form aggregates and agglomerates. We reviewed recent oral toxicity studies with SAS. Some of those report tissue concentrations of silicon (Si). The results of those studies were compared with recently determined tissue concentrations of Si (and Si-particles) in human postmortem tissues. We noticed inconsistent results of the various toxicity studies regarding toxicity and reported tissue concentrations, which hamper the risk assessment of SAS. A broad range of Si concentrations is reported in control animals in toxicity studies. The Si concentrations found in human postmortem tissues fall within this range. On the other hand, the mean concentration found in human liver is higher than the reported concentrations causing liver effects in some animal toxicity studies after oral exposure to SAS. Also higher liver concentrations are observed in other, negative animal studies. Those inconsistencies could be caused by the presence of other Si-containing chemical substances or particles (which potentially also includes background SAS) and/or different sample preparation and analytical techniques that were used. Other factors which could explain the inconsistencies in outcome between the toxicity studies are the distinct SAS used and different dosing regimes, such as way of administration (dietary, via drinking water, oral gavage), dispersion of SAS and dose. More research is needed to address these issues and to perform a proper risk assessment for SAS in food. The current review will help to progress research on the toxicity of SAS and the associated risk assessment.

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“…-Dose-dependent decrease in cell viability - Mitochondrial ROS production -Suppressed mitochondrial biogenesis -Induction of mitophagy Mitochondrial dysfunction and oxidative stress (Qi et al 2020) SiO2NPs 20, 30, 50, 300, 1000 (TEM) BALB/c mice 1040 mg/kg (IV)…”

Section: Silicamentioning

confidence: 99%

“…Moreover, oral intake of SiO2NPs caused hepatic ballooning, infiltration of inflammatory cells in the liver, liver fibrosis and deoxyribonucleic acid (DNA) damage in mice. These data suggest that the mitochondrion is a main target for the initiation of the hepatotoxic outcomes, possibly by disturbing the mitochondrial quality control leading to imbalanced mitochondria dynamics and mitochondrial dysfunction (Qi et al 2020). Short-term (24h) exposure of primary rat Kupffer cells to SiO2NPs resulted in their activation, as indicated by increased ROS amounts, and release of tumor necrosis factor alpha (TNF), hydrogen peroxide and nitric oxide (Chen et al 2013).…”

Section: Silicamentioning

confidence: 99%

Hepatotoxicity induced by nanomaterials: mechanisms and in vitro models

Vilas-Boas

Vinken

2020

Arch Toxicol

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The unique physicochemical properties of materials at nanoscale have opened a plethora of opportunities for applications in the pharmaceutical and medical field, but also in consumer products from food and cosmetics industries. As a consequence, daily human exposure to nanomaterials through distinct routes is considerable and therefore may raise health concerns. Many nanomaterials have been described to accumulate and induce adversity in the liver. Among these, silica and some types of metallic nanoparticles are the most broadly used in consumer products and, therefore, the most studied and reported. The reviewed literature was collected from PubMed.gov during the month of March 2020 using the search words "nanomaterials induced hepatotoxicity", which yielded 181 papers. This present paper reviews the hepatotoxic effects of nanomaterials described in in vitro and in in vivo studies, with emphasis on the underlying mechanisms. The induction of oxidative stress and inflammation are the manifestations of toxicity most frequently reported following exposure of cells or animal models to different nanomaterials. Furthermore, the available in vitro models for the evaluation of the hepatotoxic effects of nanomaterials are discussed, highlighting the continuous interest in the development of more advanced and reliable in vitro models for nanotoxicology.

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Disturbed mitochondrial quality control involved in hepatocytotoxicity induced by silica nanoparticles

Abstract: SiNPs triggered hepatocytotoxicity through interfering mitochondrial quality control process, including imbalanced mitochondrial dynamics, disturbed mitophagy and suppressed biogenesis, leading to mitochondrial dysfunction and ensuing cell damage.

Cited by 40 publications

References 71 publications

Insights on toxicity, safe handling and disposal of silica aerogels and amorphous nanoparticles

Insights on toxicity, safe handling and disposal of silica aerogels and amorphous nanoparticles

Issues currently complicating the risk assessment of synthetic amorphous silica (SAS) nanoparticles after oral exposure

Hepatotoxicity induced by nanomaterials: mechanisms and in vitro models

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