Time-course effects of systemically administered diesel exhaust particles in rats

Nemmar, Abderrahim; Al-Salam, Suhail; Zia, Shaheen; Dhanasekaran, Subramanian; Shudadevi, Munjusha; Ali, Badreldin H.

doi:10.1016/j.toxlet.2010.02.001

Cited by 52 publications

(41 citation statements)

References 46 publications

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“…The prothrombin time (PT) was measured [21][22][23] on freshly collected, platelet-poor plasma with human relipidated recombinant thromboplastin (RecombiPlasTin; Instrumentation Laboratory, Orangeburg, NY, USA) in combination with a Merlin coagulometer (MC 1 VET; Merlin Medical, Lemgo, Germany)]. Activated partial thromboplastin time (aPTT) was measured [21][22][23] with automated aPTT reagent (bioMerieux, Inc., Durham, NC, USA) using a Merlin coagulometer (MC 1 VET; Merlin Medical). Normal plasma used as reference for both the PT and aPTT was prepared by pooling equal portions of platelet-poor plasmas from the blood of six untreated mice.…”

Section: In Vitro Measurement Of Prothrombin Time and Activated Partimentioning

confidence: 99%

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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Section: In Vitro Measurement Of Prothrombin Time and Activated Partimentioning

confidence: 99%

Amorphous silica nanoparticles impair vascular homeostasis and induce systemic inflammation

Nemmar¹,

Albarwani²,

Beegam³

et al. 2014

IJN

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“…The SOD activity was measured using a commercial kit (Cayman Chemical, Ann Arbor, MI, USA) (Nemmar et al 2010). …”

Section: Measurement Of Sod In Plasmamentioning

confidence: 99%

Thromboembolic injury and systemic toxicity induced by nicotine in mice

Fahim

Al‐Salam²,

Dhanasekaran³

et al. 2014

gpb

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Abstract. Nicotine is involved in the pathogenesis of hematological and cardiopulmonary diseases. However, the understanding of the pathophysiological mechanisms underlying these undesirable effects is unclear. Cigarette smoking, nicotine gums and patches are common sources for nicotine ingestion. We have investigated the nicotine's effect on cerebral microvessel thrombosis and systemic toxicity. Mice received either nicotine (1 mg/kg, i.p.) or saline (control), once a day for 21 days. Briefly, after bolus intravenous fluorescein injection, a photo insult of cerebral microvessel was done. The platelet aggregation in microvessels was video recorded and analyzed. In conjunction, the plasma levels of superoxide dismutase (SOD), lactate dehydrogenase (LDH), liver enzymes, creatinine and blood urea nitrogen (BUN), and histopathological studies were carried out. Our results revealed a significant prothrombotic effect following nicotine exposure. Significant decrease in SOD indicates the occurrence of oxidative stress involved in the tissue damages and increase in the LDH emphasize the systemic toxicity. Substantial rise in the liver aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels were observed. Lungs histology showed intra-vascular hemorrhagic infarction with necrosis, macrophage and neutrophils infiltration. Liver histology showed intravascular thrombosis and portal inflammation. We conclude that the sub-acute nicotine exposure causes an increase in thrombosis in cerebral microvessels and systemic, hepatic and pulmonary toxicity.

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“…Therefore, the early prothrombotic tendency appears not to result from pulmonary inflammation, but possibly from direct effects of systemically translocated particles on the blood platelets and/or the (pulmonary) vessel wall (Nemmar et al 2003c). The direct activating effect of PM on blood platelets was shown by the addition of as little as 0.5 μg/mL DEPs to untreated hamster blood, significantly shortenening the PAF-100 closure time (Nemmar et al 2003a), as well as by a dose-dependent (0.1-1 μg/mL) effect of PM on in vitro platelet aggregation in rat blood (Nemmar et al 2010), although similar experiments in human blood were negative (Rudez et al 2009). In agreement with these results, 1 hour after intratracheal instillation, well-defined positively charged ultrafine (60 nm) polystyrene particles significantly enhanced plateletrich thrombus formation, while 400 nm particles, incapable of systemic translocation, did not affect thrombus formation, despite similar increases in neutrophils, lactate dehydrogenase and histamine levels in the bronchoalveolar lavage fluid (Nemmar et al 2003b).…”

Section: Fig 1 Biological Pathways Linking Pm Exposure and Arterialmentioning

confidence: 99%

Air Pollution and Cardiovascular Disease

Emmerechts¹,

Jacobs²,

Hoylaerts³

2011

The Impact of Air Pollution on Health, Economy, Environment and Agricultural Sources

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Time-course effects of systemically administered diesel exhaust particles in rats

Cited by 52 publications

References 46 publications

Amorphous silica nanoparticles impair vascular homeostasis and induce systemic inflammation

Amorphous silica nanoparticles impair vascular homeostasis and induce systemic inflammation

Thromboembolic injury and systemic toxicity induced by nicotine in mice

Air Pollution and Cardiovascular Disease

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