Acute exposure to zinc oxide nanoparticles does not affect the cognitive capacity and neurotransmitters levels in adult rats

Amara, Salem; Benslama, I.; Mrad, Imen; Rihane, Naima; Jeljeli, Mustapha; El-Mir, Lassaad; Ben-Rhouma, Khemais; Rachidi, Walid; Sève, Michel; Abdelmelek, Hafedh; Sakly, Mohsen

doi:10.3109/17435390.2013.879342

Cited by 52 publications

(34 citation statements)

References 41 publications

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“…This finding was further confirmed by the results from another toxicity study 67 in which zinc concentrations in rat brains increased significantly after an intravenous injection of a suspension of ZnO NPs for 14 consecutive days. The study also found that the concentration of neurotransmitters in the brain, such as norepinephrine and epinephrine, remained unchanged.…”

Section: In Vivo Studies On the Potential Toxicity Of Nanomaterials Osupporting

confidence: 77%

Application of dental nanomaterials: potential toxicity to the central nervous system

Feng¹,

Chen²,

Wang³

et al. 2015

IJN

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Nanomaterials are defined as materials with one or more external dimensions with a size of 1–100 nm. Such materials possess typical nanostructure-dependent properties (eg, chemical, biological, optical, mechanical, and magnetic), which may differ greatly from the properties of their bulk counterparts. In recent years, nanomaterials have been widely used in the production of dental materials, particularly in light polymerization composite resins and bonding systems, coating materials for dental implants, bioceramics, endodontic sealers, and mouthwashes. However, the dental applications of nanomaterials yield not only a significant improvement in clinical treatments but also growing concerns regarding their biosecurity. The brain is well protected by the blood–brain barrier (BBB), which separates the blood from the cerebral parenchyma. However, in recent years, many studies have found that nanoparticles (NPs), including nanocarriers, can transport through the BBB and locate in the central nervous system (CNS). Because the CNS may be a potential target organ of the nanomaterials, it is essential to determine the neurotoxic effects of NPs. In this review, possible dental nanomaterials and their pathways into the CNS are discussed, as well as related neurotoxicity effects underlying the in vitro and in vivo studies. Finally, we analyze the limitations of the current testing methods on the toxicological effects of nanomaterials. This review contributes to a better understanding of the nano-related risks to the CNS as well as the further development of safety assessment systems.

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Section: In Vivo Studies On the Potential Toxicity Of Nanomaterials Osupporting

confidence: 77%

Application of dental nanomaterials: potential toxicity to the central nervous system

Feng¹,

Chen²,

Wang³

et al. 2015

IJN

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“…Male Wistar rats were treated with a single intravenous injection of a suspension of ZnO-NPs in Amara et al's study. 8 The results indicated that plasma and brain zinc concentrations increased after the administration of ZnO-NPs. Han et al 9 used…”

Section: Introductionmentioning

confidence: 74%

“…Briefly, wild-type BV-2 cells, BV-2 cell clones transfected with an empty vector, and PC12 cell clones transfected with PINK1 siRNA were seeded in a 96-well culture plate at a density of 5×10 3 cells/well and incubated overnight for cell attachment. Next, the cells were rinsed with PBS and treated with 10 μg/mL ZnO NPs for 4,8,12, and 24 h. Then, the cells were washed with PBS twice and incubated with 10 μM of DCFH-DA for 1 h. Subsequently, DCF fluorescence intensity was measured using a Synergy-4 microplate reader (Biotek Instruments Inc., Winooski, VT, USA) at an excitation wavelength of 485 nm and an emission wavelength of 535 nm.…”

Section: Rosmentioning

confidence: 99%

“…Briefly, BV-2 cells were seeded at a density of 2×10 4 cells/well in a 6-well culture plate and incubated overnight for cell attachment. The cells were then treated with 10 μg/mL ZnO NPs for 4,8,12, and 24 h. The untreated cells served as the control. After the cells were treated with ZnO NPs, they were collected and stained with MDC following the manufacturer's instructions.…”

Section: Stainingmentioning

confidence: 99%

“…The PINK1 -/-BV-2 cells were treated with 10 μg/mL ZnO NPs for 4,8,12, and 24 h. The JC-1 assay and Western blot results revealed that the total parkin level was maintained; however, the expression of parkin in the mitochondria was lower than that in the mitochondria of wild-type cells, indicating that almost no parkin was translocated to the mitochondria after treatment with ZnO NPs. Compared with the wild-type cells, PINK1…”

mentioning

confidence: 99%

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Involvement of PINK1/parkin-mediated mitophagy in ZnO nanoparticle-induced toxicity in BV-2 cells

Wei

Wang

Chen

et al. 2017

IJN

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With the increasing application of zinc oxide nanoparticles (ZnO NPs) in biological materials, the neurotoxicity caused by these particles has raised serious concerns. However, the underlying molecular mechanisms of the toxic effect of ZnO NPs on brain cells remain unclear. Mitochondrial damage has been reported to be a factor in the toxicity of ZnO NPs. PINK1/parkin-mediated mitophagy is a newly emerging additional function of autophagy that selectively degrades impaired mitochondria. Here, a PINK1 gene knockdown BV-2 cell model was established to determine whether PINK1/parkin-mediated mitophagy was involved in ZnO NP-induced toxicity in BV-2 cells. The expression of total parkin, mito-parkin, cyto-parkin, and PINK1 both in wild type and PINK1 −/− BV-2 cells was evaluated using Western blot analysis after the cells were exposed to 10 μg/mL of 50 nm ZnO NPs for 2, 4, 8, 12, and 24 h. The findings suggested that the downregulation of PINK1 resulted in a significant reduction in the survival rate after ZnO NP exposure compared with that of control cells. ZnO NPs were found to induce the transportation of parkin from the cytoplasm to the mitochondria, implying the involvement of mitophagy in ZnO NP-induced toxicity. The deletion of the PINK1 gene inhibited the recruitment of parkin to the mitochondria, causing failure of the cell to trigger mitophagy. The present study demonstrated that apart from autophagy, PINK1/parkin-mediated mitophagy plays a protective role in ZnO NP-induced cytotoxicity.

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Biodistribution, cardiac and neurobehavioral assessments, and neurotransmitter quantification in juvenile rats following oral administration of aluminum oxide nanoparticles

Mortensen

Caffaro

Patel

et al. 2020

J of Applied Toxicology

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Little is known about the uptake, biodistribution, and biological responses of nanoparticles (NPs) and their toxicity in developing animals. Here, male and female juvenile Sprague–Dawley rats received four consecutive daily doses of 10 mg/kg Al2O3 NP (diameter: 24 nm [transmission electron microscope], hydrodynamic diameter: 148 nm) or vehicle control (water) by gavage between postnatal days (PNDs) 17–20. Basic neurobehavioral and cardiac assessments were performed on PND 20. Animals were sacrificed on PND 21, and selected tissues were collected, weighed, and processed for histopathology or neurotransmitter analysis. The biodistribution of Al2O3 NP in tissue sections of the intestine, liver, spleen, kidney, and lymph nodes were evaluated using enhanced dark‐field microscopy (EDM) and hyperspectral imaging (HSI). Liver‐to‐body weight ratio was significantly increased for male pups administered Al2O3 NP compared with control. HSI suggested that Al2O3 NP was more abundant in the duodenum and ileum tissue of the female pups compared with the male pups, whereas the abundance of NP was similar for males and females in the other tissues. The abundance of NP was higher in the liver compared with spleen, lymph nodes, and kidney. Homovanillic acid and norepinephrine concentrations in brain were significantly decreased following Al2O3 NP administration in female and male pups, whereas 5‐hydroxyindoleacetic acid was significantly increased in male pups. EDM/HSI indicates intestinal uptake of Al2O3 NP following oral administration. Al2O3 NP altered neurotransmitter/metabolite concentrations in juvenile rats' brain tissues. Together, these data suggest that orally administered Al2O3 NP interferes with the brain biochemistry in both female and male pups.

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Acute exposure to zinc oxide nanoparticles does not affect the cognitive capacity and neurotransmitters levels in adult rats

Cited by 52 publications

References 41 publications

Application of dental nanomaterials: potential toxicity to the central nervous system

Application of dental nanomaterials: potential toxicity to the central nervous system

Involvement of PINK1/parkin-mediated mitophagy in ZnO nanoparticle-induced toxicity in BV-2 cells

Biodistribution, cardiac and neurobehavioral assessments, and neurotransmitter quantification in juvenile rats following oral administration of aluminum oxide nanoparticles

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