Effects of SiC nanoparticles orally administered in a rat model: Biodistribution, toxicity and elemental composition changes in feces and organs

Lozano, Omar; Laloy, Julie; Alpan, Lütfiye; Mejia, Jorge; Rolin, Stéphanie; Toussaint, Olivier; Dogné, Jean‐Michel; Lucas, Stéphane; Masereel, Bernard

doi:10.1016/j.taap.2012.08.004

Cited by 28 publications

(19 citation statements)

References 38 publications

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“…Lozano et al (2012) found that in acute toxicity study of silicon carbide there are no changes on liver and kidney functions by measuring level of ALT, AST, ALP, BUN and Cr. Furthermore they did not see any damages on kidney, liver, stomach and intestines which was referred to Sic (Lozano et al, 2012). Moreover, Park et al (2009) compared iron oxide nanosphere and nanorods.…”

Section: Investigated Thementioning

confidence: 96%

Investigating the cytotoxicity of iron oxide nanoparticles in in vivo and in vitro studies

Ghasempour

Shokrgozar

Ghasempour

et al. 2015

Experimental and Toxicologic Pathology

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Section: Investigated Thementioning

confidence: 96%

Investigating the cytotoxicity of iron oxide nanoparticles in in vivo and in vitro studies

Ghasempour

Shokrgozar

Ghasempour

et al. 2015

Experimental and Toxicologic Pathology

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“…Li et al reported that nano TiO 2 could enter into the blood and induce liver injury by intratracheal instillation in rats. Titanium carbide (39.6 nm) and silicon carbide (36.2 nm) could penetrate the intestinal barrier to the rat liver …”

Section: Discussionmentioning

confidence: 99%

Nickel oxide nanoparticles induce hepatocyte apoptosis via activating endoplasmic reticulum stress pathways in rats

Chang

Liu

Tian

et al. 2017

Environmental Toxicology

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Nickel oxide nanoparticles (nano NiO) could induce hepatocyte apoptosis, while its potential mechanisms are unclear. This study aimed to explore the role of endoplasmic reticulum (ER) stress pathways in hepatocyte apoptosis induced by nano NiO. Male Wistar rats were administrated with nano NiO (0.015, 0.06, and 0.24 mg/kg b.w.) and micro NiO (0.24 mg/kg b.w.) by intratracheal instillation twice a week for 6 weeks. We measured the hepatocyte apoptosis levels by TdT-mediated dUTP nick-end labeling (TUNEL) staining, ER stress related gene and protein expression levels in rat liver. The results showed that the TUNEL positive cells increased after exposure nano NiO, hinting hepatocyte apoptosis. The up-regulated gene and protein levels of 78 kD glucose regulated protein and CCAAT/enhancer binding protein homologous protein suggested that nano NiO triggered ER stress. Nano NiO exposure contributed to the increased protein contents of inositol-requiring enzyme 1 (IRE-1)α, p-IRE-1α, X box protein-1S, pancreatic ER kinase (PERK), p-PERK, eukaryotic initiation factor-2 alpha (eIF-2α), p-eIF-2α, caspase-12, -9, and -3, implicating that nano NiO can activate the pathways of ER stress-mediated apoptosis. These findings indicate that the ER stress pathways may play an important role in hepatocyte apoptosis induced by nano NiO.

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“…The trace elements of the diet ingested by rats were measured by PIXE [31] . From the average diet ingested by rats, 16.9 mg, mineral Ti in the diet accounts for 11.26 mg. For administered doses of 0.5 and 50 mg kg −1 , Ti content accounts for 0.091–0.122 mg and 9.1–12.2 mg (average rat weight: 182 g at day 1, 244 g at day 28), respectively.…”

Section: Methodsmentioning

confidence: 99%

Can TiC nanoparticles produce toxicity in oral administration to rats?

et al. 2014

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BackgroundTitanium carbide (TiC) is used for ceramic metal composites in several industries and is regarded as a nanomaterial for catalyst and battery applications. However, there are very few studies in regard to the toxicological potential of TiC nanoparticles (NPs).ObjectiveTo study the toxicodynamics and toxicokinetics of TiC NPs in Sprague Dawley rats in acute (24 h) and subacute (28 days) oral administrations. The acute doses were 0.5, 5, 50, 300 and 1000 mg kg−1; the subacute doses were 0.5 and 50 mg kg−1.ResultsOrgan histopathological examination (esophagus, stomach, intestines, spleen, liver, and kidneys) indicates the absence of damage at all applied doses, in both assessments. In the acute administration, alkaline phosphatases increased (5, 300 and 1000 mg kg−1), ASAT increased (1000 mg kg−1) and bile salts decreased (0.5 mg kg−1). No alterations in urine parameters (sodium, potassium, osmolarity) were found. Acute administration of TiC caused mineral changes in organs (liver, spleen, kidneys). TiC was mostly cleared by feces excretion 24 h after administration, in subacute administration causing variations in mineral absorption (Mg, Al, P, S, Ca, Zn). TiC could pass the intestinal barrier as TiC traces were detected in urine.ConclusionNo sign of toxicity was found after oral administration. TiC was excreted mostly in feces producing mineral absorption alterations. Low traces were retrieved in urine, indicating that TiC can cross the intestinal barrier.

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Effects of SiC nanoparticles orally administered in a rat model: Biodistribution, toxicity and elemental composition changes in feces and organs

Cited by 28 publications

References 38 publications

Investigating the cytotoxicity of iron oxide nanoparticles in in vivo and in vitro studies

Investigating the cytotoxicity of iron oxide nanoparticles in in vivo and in vitro studies

Nickel oxide nanoparticles induce hepatocyte apoptosis via activating endoplasmic reticulum stress pathways in rats

Can TiC nanoparticles produce toxicity in oral administration to rats?

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