Acute respiratory and systemic toxicity of pulmonary exposure to rutile Fe-doped TiO2 nanorods

Melghit, Khaled; Al-Salam, Suhail; Zia, Shaheen; Dhanasekaran, Subramanian; Attoub, Samir; Al-Amri, Issa; Ali, Badreldin H.

doi:10.1016/j.tox.2010.10.007

Cited by 46 publications

(39 citation statements)

References 41 publications

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“…This increase is suggestive of cytolysis, and has been described following exposure to nanoparticles in vivo 27 and in vitro. 40 We have recently reported the occurrence of oxidative stress in the DEP-induced acute thrombotic tendency in pial venules and activation of circulating blood platelets in mice.…”

supporting

confidence: 52%

“…25,26 Moreover, it represents about 10% of the dose of nanoparticles intratracheally instilled in experimental animals. [27][28][29][30] In the present study, we have assessed the effect of SiNPs on coagulation events by measuring a set of relevant indices: ie, thrombosis assessment in pial venules in vivo; platelet numbers and aggregation in vitro; and measurement of circulating fibrinogen, PAI-1, and soluble vWF. It has been recently demonstrated that in vitro exposure of human platelets to amorphous SiNPs causes platelet aggregation and high nitroxidative/oxidative stress.…”

mentioning

confidence: 99%

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Amorphous silica nanoparticles impair vascular homeostasis and induce systemic inflammation

Nemmar¹,

Albarwani²,

Beegam³

et al. 2014

IJN

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Amorphous silica nanoparticles (SiNPs) are being used in biomedical, pharmaceutical, and many other industrial applications entailing human exposure. However, their potential vascular and systemic pathophysiologic effects are not fully understood. Here, we investigated the acute (24 hours) systemic toxicity of intraperitoneally administered 50 nm and 500 nm SiNPs in mice (0.5 mg/kg). Both sizes of SiNPs induced a platelet proaggregatory effect in pial venules and increased plasma concentration of plasminogen activator inhibitor-1. Elevated plasma levels of von Willebrand factor and fibrinogen and a decrease in the number of circulating platelets were only seen following the administration of 50 nm SiNPs. The direct addition of SiNPs to untreated mouse blood significantly induced in vitro platelet aggregation in a dose-dependent fashion, and these effects were more pronounced with 50 nm SiNPs. Both sizes of SiNPs increased lactate dehydrogenase activity and interleukin 1β concentration. However, tumor necrosis factor α concentration was only increased after the administration of 50 nm SiNPs. Nevertheless, plasma markers of oxidative stress, including 8-isoprostane, thiobarbituric acid reactive substances, catalase, and glutathione S-transferase, were not affected by SiNPs. The in vitro exposure of human umbilical vein endothelial cells to SiNPs showed a reduced cellular viability, and more potency was seen with 50 nm SiNPs. Both sizes of SiNPs caused a decrease in endothelium-dependent relaxation of isolated small mesenteric arteries. We conclude that amorphous SiNPs cause systemic inflammation and coagulation events, and alter vascular reactivity. Overall, the effects observed with 50 nm SiNPs were more pronounced than those with 500 nm SiNPs. These findings provide new insight into the deleterious effect of amorphous SiNPs on vascular homeostasis.

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supporting

confidence: 52%

mentioning

confidence: 99%

Amorphous silica nanoparticles impair vascular homeostasis and induce systemic inflammation

Nemmar¹,

Albarwani²,

Beegam³

et al. 2014

IJN

Self Cite

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“…and splenocyte apoptosis [41,42]. In another study, treatment of female mice with TNPs (5 g/kg) by oral gavage caused hepatic injury, nephrotoxicity, and pathological changes in the kidneys [32].…”

Section: Respiratory Systemmentioning

confidence: 96%

The potential health risk of titania nanoparticles

Zhang

Bai

Zhang

et al. 2012

Journal of Hazardous Materials

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“…Sections of 3 μm were prepared from paraffin blocks and stained with hematoxylin and eosin. 22,23 The stained sections were In plasma (n=6-8 per group), besides measuring TNFα level and catalase activity as described earlier, the levels of CRP (GenWay Biotech, Inc., San Diego, CA, USA), fibrinogen (Molecular Innovation, Southfield, MI, USA), and PAI-1 (Molecular Innovation) were measured by using ELISA kits. The total antioxidant activity was quantified with a colorimetric assay kit (Cayman Chemicals, Ann Arbor, MI, USA).…”

Section: Histopathologymentioning

confidence: 99%

“…36 Previous reports showed that pulmonary exposure to pollutant particles and some engineered NPs induce systemic and cardiovascular events. 22,24,37,38 The latter effects were explained by the capacity of NPs to induce lung inflammation, which causes systemic inflammation and oxidative stress, and/or the aptitude of NPs to traverse the air-blood barrier to enter the blood and affect cardiovascular endpoints. 5,18 It has been reported that IV administration of CeO 2 NPs induce liver injury and oxidative stress.…”

mentioning

confidence: 99%

The acute pulmonary and thrombotic effects of cerium oxide nanoparticles after intratracheal instillation in mice

Al-Salam¹,

Beegam²,

Yuvaraju³

et al. 2017

IJN

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Cerium oxide nanoparticles (CeO 2 NPs), used as a diesel fuel catalyst, can be emitted into the ambient air, resulting in exposure to humans by inhalation. Recent studies have reported the development of lung toxicity after pulmonary exposure to CeO 2 NPs. However, little is known about the possible thrombotic effects of these NPs. The present study investigated the acute (24 hours) effect of intratracheal (IT) instillation of either CeO 2 NPs (0.1 or 0.5 mg/kg) or saline (control) on pulmonary and systemic inflammation and oxidative stress and thrombosis in mice. CeO 2 NPs induced a significant increase of neutrophils into the bronchoalveolar lavage (BAL) fluid with an elevation of tumor necrosis factor α (TNFα) and a decrease in the activity of the antioxidant catalase. Lung sections of mice exposed to CeO 2 NPs showed a dose-dependent infiltration of inflammatory cells consisting of macrophages and neutrophils. Similarly, the plasma levels of C-reactive protein and TNFα were significantly increased, whereas the activities of catalase and total antioxidant were significantly decreased. Interestingly, CeO 2 NPs significantly and dose dependently induced a shortening of the thrombotic occlusion time in pial arterioles and venules. Moreover, the plasma concentrations of fibrinogen and plasminogen activator inhibitor-1 were significantly elevated by CeO 2 NPs. The direct addition of CeO 2 NPs (1, 5, or 25 μg/mL) to mouse whole blood, collected from the inferior vena cava, in vitro neither caused significant platelet aggregation nor affected prothrombin time or partial thromboplastin time, suggesting that the thrombotic events observed in vivo may have resulted from systemic inflammation and/or oxidative stress induced by CeO 2 NPs. This study concludes that acute pulmonary exposure to CeO 2 NPs induces pulmonary and systemic inflammation and oxidative stress and promotes thrombosis in vivo.

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Acute respiratory and systemic toxicity of pulmonary exposure to rutile Fe-doped TiO2 nanorods

Cited by 46 publications

References 41 publications

Amorphous silica nanoparticles impair vascular homeostasis and induce systemic inflammation

Amorphous silica nanoparticles impair vascular homeostasis and induce systemic inflammation

The potential health risk of titania nanoparticles

The acute pulmonary and thrombotic effects of cerium oxide nanoparticles after intratracheal instillation in mice

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