Interaction of Amorphous Silica Nanoparticles with Erythrocytes<b><i>in Vitro</i></b>: Role of Oxidative Stress

Nemmar, Abderrahim; Beegam, Sumaya; Yuvaraju, Priya; Yasin, Javed; Shahin, Allen; Ali, Badreldin H.

doi:10.1159/000362996

Cited by 56 publications

(58 citation statements)

References 41 publications

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“…41 Such condition was not observed in our study as there was no obvious change with the data about RBCs. Platelet aggregation was demonstrated by Corbalan et al 42 applying SiNPs to isolated human platelets, and they also stated that the effects on platelet aggregation were inversely proportional to the nanoparticle size.…”

Section: Discussioncontrasting

confidence: 57%

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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Section: Discussioncontrasting

confidence: 57%

In vivo toxicologic study of larger silica nanoparticles in mice

Chan¹,

Liu²,

Chiau³

et al. 2017

IJN

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“…32 Indeed, previous studies have reported oxidative stress as the toxic mechanism of SiNPs in various cell types. [33][34][35] Oxidative stress arises from a significant increase in concentrations of ROS to levels that are toxic to biomolecules like DNA, proteins, and lipids. Subsequently, the abnormal accumulation of intracellular ROS could induce oxidative stress and cause oxidative damage, followed by the production of lipid peroxidation and inhibition of antioxidant activities, resulting in cells failing to maintain normal physiological redox-regulated functions.…”

Section: Discussionmentioning

confidence: 99%

Silica nanoparticles induce oxidative stress, inflammation, and endothelial dysfunction in vitro via activation of the MAPK/Nrf2 pathway and nuclear factor-κB signaling

Guo¹,

Xia²,

Niu³

et al. 2015

IJN

204

125

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Despite the widespread application of silica nanoparticles (SiNPs) in industrial, commercial, and biomedical fields, their response to human cells has not been fully elucidated. Overall, little is known about the toxicological effects of SiNPs on the cardiovascular system. In this study, SiNPs with a 58 nm diameter were used to study their interaction with human umbilical vein endothelial cells (HUVECs). Dose- and time-dependent decrease in cell viability and damage on cell plasma-membrane integrity showed the cytotoxic potential of the SiNPs. SiNPs were found to induce oxidative stress, as evidenced by the significant elevation of reactive oxygen species generation and malondialdehyde production and downregulated activity in glutathione peroxidase. SiNPs also stimulated release of cytoprotective nitric oxide (NO) and upregulated inducible nitric oxide synthase (NOS) messenger ribonucleic acid, while downregulating endothelial NOS and ET-1 messenger ribonucleic acid, suggesting that SiNPs disturbed the NO/NOS system. SiNP-induced oxidative stress and NO/NOS imbalance resulted in endothelial dysfunction. SiNPs induced inflammation characterized by the upregulation of key inflammatory mediators, including IL-1β, IL-6, IL-8, TNFα, ICAM-1, VCAM-1, and MCP-1. In addition, SiNPs triggered the activation of the Nrf2-mediated antioxidant system, as evidenced by the induction of nuclear factor-κB and MAPK pathway activation. Our findings demonstrated that SiNPs could induce oxidative stress, inflammation, and NO/NOS system imbalance, and eventually lead to endothelial dysfunction via activation of the MAPK/Nrf2 pathway and nuclear factor-κB signaling. This study indicated a potential deleterious effect of SiNPs on the vascular endothelium, which warrants more careful assessment of SiNPs before their application.

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“…However, further on the silicon content in the body of Danio rerio decreased, probably due to homeostasis activity [25]. In g/g addition, SiO 2 NPs do not prevent the regeneration of tissues [23], but can cause both prothrombotic effects and increased concentrations of fibrinogen, as well as of anti-inflammatory cytokines in the blood plasma [22,31]. Moreover, the markers of oxidative stress (SOD, CT) are not affected [22].…”

Section: The Catalasementioning

confidence: 99%

“…In g/g addition, SiO 2 NPs do not prevent the regeneration of tissues [23], but can cause both prothrombotic effects and increased concentrations of fibrinogen, as well as of anti-inflammatory cytokines in the blood plasma [22,31]. Moreover, the markers of oxidative stress (SOD, CT) are not affected [22]. An interesting explanation of the death of the test organism after the contact with NPs was proposed by S.N.…”

Section: The Catalasementioning

confidence: 99%

“…Thus, contact of the SiO 2 NPs with the test object manifested in a decreased survival of Danio rerio by 7 %, and by 33 % at the end of the experiment, although the total loss of the test object was not observed. Previously, against application of the SiO 2 NPs chromosomal aberrations were identified, as well as the development of the oxidative stress [21,22]. In a model of Carassius auratus gibelio (crucian carp), the ability of the Si/SiO 2 nanoparticles to induce an inflammatory response was demonstrated [23].…”

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confidence: 99%

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ASSESSMENT OF GENERAL TOXICITY AND PROOXIDANT EFFECTS OF CeO2 AND SiO2 NANOPARTICLES ON Danio rerio

Miroshnikova¹,

Kosyan²,

Arizhanov³

et al. 2016

S-h. biol.

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A b s t r a c tA diversified use of nanomaterials leads to their accumulation in the environment and involvement into remediation. In water biocoenosis, nanomaterials influence fishes. Lipid peroxidation (LPO) in aquatic bioindicators is considered the parameters generally used to assess an impact of man-caused water pollution. It should be taken into account that the level of LPO products can be due not only to anthropogenic pollution, but also to the presence of peroxide substrates in fish tissues. We firstly showed the effect of silica and cerium nanoparticles in water environment with direct assay of the enzyme activity of the bioindiator used. Our purpose was to evaluate the prooxidant effects of CeO 2 (15.8 nm) and SiO 2 (40.9 nm) nanoparticles (NPs) on the Danio rerio model, to study LPO as influenced by the NPs doses, and to find out if there are any adaptive mechanisms in Danio rerio to withstand the NPs in the habitat. Complete death of the test objects occurred on days 80 and 84 when CeO 2 NPs used. The first signs of the CeO 2 NPs toxic effect at a dose of 10 mg/dm 3 in the feed appeared on day 45, on day 56 the test-organism number was 33 % lower, and on day 65 a more than 54 % decline occurred. SiO 2 NPs led to 33 % reduced survival. The presence of the nanoparticles in the habitat depressed the antioxidant system of Danio rerio but the signs of adaptation were manifested by the end of week 2, and a significant increase in catalase (CAT) and superoxide dismutase (SOD) activity proceeded by the end of the test. At 10 and 100 mg/dm 3 of CeO 2 NPs the malonic dialdehyde (MDA) level decreased by 11.0 % and 61.0 %, respectively. For SiO 2 NPs the changes were similar with the MDA level decrease of 50.0 and 41.5 % at 10 and 100 mg/dm 3 dosage, respectively. SOD activity when influenced by CeO 2 NPs (10 mg/dm 3 and 100 mg/dm 3 ) decreased by 75 and 69 %, respectively, and for SiO 2 NPs the indexes were 50 and 26 % lower as compared to control. Similar changes were characteristic of CAT activity. Thus, the investigated nanoparticles possess sufficient toxic properties that necessitates their further study.

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Interaction of Amorphous Silica Nanoparticles with Erythrocytesin Vitro: Role of Oxidative Stress

Cited by 56 publications

References 41 publications

In vivo toxicologic study of larger silica nanoparticles in mice

In vivo toxicologic study of larger silica nanoparticles in mice

Silica nanoparticles induce oxidative stress, inflammation, and endothelial dysfunction in vitro via activation of the MAPK/Nrf2 pathway and nuclear factor-κB signaling

ASSESSMENT OF GENERAL TOXICITY AND PROOXIDANT EFFECTS OF CeO2 AND SiO2 NANOPARTICLES ON Danio rerio

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Interaction of Amorphous Silica Nanoparticles with Erythrocytesin Vitro: Role of Oxidative Stress

Cited by 56 publications

References 41 publications

In vivo toxicologic study of larger silica nanoparticles in mice

In vivo toxicologic study of larger silica nanoparticles in mice

Silica nanoparticles induce oxidative stress, inflammation, and endothelial dysfunction in vitro via activation of the MAPK/Nrf2 pathway and nuclear factor-&kappa;B signaling

ASSESSMENT OF GENERAL TOXICITY AND PROOXIDANT EFFECTS OF CeO2 AND SiO2 NANOPARTICLES ON Danio rerio

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Silica nanoparticles induce oxidative stress, inflammation, and endothelial dysfunction in vitro via activation of the MAPK/Nrf2 pathway and nuclear factor-κB signaling