Silver nanoparticles induce apoptotic cell death in cultured cerebral cortical neurons

Kim, Sunghwan; Ko, Je‐Won; Koh, Suk-Kyu; Lee, In-Chul; Son, Jung-Mo; Moon, Changjong; Kim, Sung Hoon; Shin, Dong–Ho; Kim, Jong-Choon

doi:10.1007/s13273-014-0019-6

Cited by 30 publications

(20 citation statements)

References 37 publications

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“…Our western blot results showed that high concentrations of AgSCs upregulated the expression of cleaved caspase-3 compared to the control group. Similarly, in a study by Kim et al (Kim et al, 2014), the apoptosis of cortical neuronal cells was detected as increased levels of cleaved caspase-3 after 12 and 24 h of exposure to AgNPs (10 µg/mL).…”

Section: Discussionsupporting

confidence: 53%

Silver nanoparticles induce neurotoxicity in a human embryonic stem cell-derived neuron and astrocyte network

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Aguilar

et al. 2018

Nanotoxicology

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Silver nanoparticles (AgNPs) are among the most extensively used nanoparticles and are found in a variety of products. This ubiquity leads to inevitable exposure to these particles in everyday life. However, the effects of AgNPs on neuron and astrocyte networks are still largely unknown. In this study, we used neurons and astrocytes derived from human embryonic stem cells as a cellular model to study the neurotoxicity that is induced by citrate-coated AgNPs (AgSCs). Immunostaining with the astrocyte and neuron markers, glial fibrillary acidic protein and microtubule-associated protein 2 (MAP2), respectively, showed that exposure to AgSCs at the concentration of 0.1 µg/mL increased the astrocyte/neuron ratio. In contrast, a higher concentration of AgSCs (5.0 µg/ml) significantly changed the morphology of astrocytes. These results suggest that astrocytes are sensitive to AgSC exposure and that low concentrations of AgSCs promote astrogenesis. Furthermore, our results showed that AgSCs reduced neurite outgrowth, decreased the expression of postsynaptic density protein 95 and synaptophysin, and induced neurodegeneration in a concentration-dependent manner. Our findings additionally suggest that the expression and phosphorylation status of MAP2 isoforms, as modulated by the activation of the Akt/glycogen synthase kinase-3/caspase-3 signaling pathway, may play an important role in AgSC-mediated neurotoxicity. We also found that AgNO3 exposure only slightly reduced neurite outgrowth and had little effect on MAP2 expression, suggesting that AgSCs and AgNO3 have different neuronal toxicity mechanisms. In addition, most of these effects were reduced when the cell culture was co-treated with AgSCs and the antioxidant ascorbic acid, which implies that oxidative stress is the major cause of AgSC-mediated astrocytic/neuronal toxicity and that antioxidants may have a neuroprotective effect.

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Section: Discussionsupporting

confidence: 53%

Silver nanoparticles induce neurotoxicity in a human embryonic stem cell-derived neuron and astrocyte network

Repar

Aguilar

et al. 2018

Nanotoxicology

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“…The radical scavenging properties of hyaluronan have been demonstrated previously in various experimental models [22,23] . An excess of ROS may lead to DNA damage, and these damaged cells subsequently undergo either cell cycle arrest to facilitate DNA repair or apoptosis to eliminate the excessively damaged cells [24] . The results of this study indicate that lidocaine induced an overall delay in cell cycle progression by affecting the G 2 /M phase of the cell cycle, and this effect could be a result of ROS production.…”

Section: Wwwchinapharcom Lee Yj Et Almentioning

confidence: 99%

Hyaluronan suppresses lidocaine-induced apoptosis of human chondrocytes in vitro by inhibiting the p53-dependent mitochondrial apoptotic pathway

2016

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Aim: Intra-articular injection of local anesthetics (LAs) is a common procedure for therapeutic purposes. However, LAs have been found toxic to articular cartilage, and hyaluronan may attenuate this toxicity. In this study we investigated whether hyaluronan attenuated lidocaine-induced chondrotoxicity, and if so, to elucidate the underlying mechanisms. Methods: Human chondrocyte cell line SW1353 and newly isolated murine chondrocytes were incubated in culture medium containing hyaluronan and/or lidocaine for 72 h. Cell viability was evaluated using MTT assay. Cell apoptosis was detected with DAPI staining, caspase 3/7 activity assay and flow cytometry. Cell cycle distributions, ROS levels and mitochondrial membrane potential (ΔΨm) were determined using flow cytometry. The expression of p53 and p53-regulated gene products was measured with Western blotting. Results: Lidocaine (0.005%−0.03%) dose-dependently decreased the viability of SW1353 cells. This local anesthetic (0.015%, 0.025%) induced apoptosis, G 2 /M phase arrest and loss of ΔΨm, and markedly increased ROS production in SW1353 cells. Hyaluronan (50−800 µg/mL) alone did not affect the cell viability, but co-treatment with hyaluronan (200 µg/mL) significantly attenuated lidocaine-induced apoptosis and other abnormalities in SW1353 cells. Furthermore, co-treatment with lidocaine and hyaluronan significantly decreased the levels of p53 and its transcription targets Bax and p21 in SW1353 cells, although treatment with lidocaine alone did not significantly change these proteins. Similar results were obtained in ex vivo cultured murine chondrocytes. Conclusion: Hyaluronan suppresses lidocaine-induced apoptosis of human chondrocytes in vitro through inhibiting the p53-dependent mitochondrial apoptotic pathway.

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“…Oxidative stress and inflammation which occur following the passage of nanoparticles from circulation to placenta, endometrium, yolk sac, or fetus, lead to placental dysfunction, retarded neonatal growth, fetal malformations, and neurotoxicity in offspring; furthermore inflammatory cytokines that are induced by nanoparticles in the dam, following their entrance, will affect the brain development of fetuses (Li et al, 2014). It is believed that Ag-NPs mediate their detrimental effects primarily through producing oxidative stress (Rahman et al, 2009;Park et al, 2010;Kim et al, 2014). Collectively, Ag-NPs may produce neurotoxicity by inducing oxidative stress, altering gene expression and producing apoptosis (Rahman et al, 2009;Yin et al, 2013;Xu et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

Induced adverse effects of prenatal exposure to silver nanoparticles on neurobehavioral development of offspring of mice

et al. 2015

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Steadily increased use of silver nanoparticles (Ag-NPs), has increased the amount of its exposure to humans and animals. Current scarce knowledge about the influences of prenatal exposure to Ag-NPs on postnatal outcomes, motivated us to investigate whether being exposed to it during pregnancy has any effects on neurobehavioral development of the adult offspring. Thirty virgin female NMRI mice were mated and treated subcutaneously once every three days from gestation day 3 until delivery, by 0, 0.2 and 2 mg/kg of bodyweight (BW) of Ag-NPs. Behavioral functions of adult offspring including spatial memory, passive avoidance learning, stress, anxiety-like behaviors and locomotor activities were assessed by commonly used neurobehavioral paradigms and the results were compared according to treatment and sex. Prenatal exposure to Ag-NPs significantly impaired their cognitive behavior in the Morris water maze. Although no evidence was observed indicating more anxiety-like behaviors in the treated offspring in the elevated plus maze, the number of defecations and leanings in the open field assay and number of passages in the light-dark box were greater in groups prenatally treated by Ag-NPs. Most of the impairments were more apparent in the offspring which had been prenatally exposed to high doses of Ag-NPs, particularly female ones. The present study indicated that the exposure of pregnant animals to Ag-NPs may lead to various neurobehavioral disorders in their offspring. Thus, more attention should be paid to avoid exposure to Ag-NPs, especially from pregnant females.

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Silver nanoparticles induce apoptotic cell death in cultured cerebral cortical neurons

Cited by 30 publications

References 37 publications

Silver nanoparticles induce neurotoxicity in a human embryonic stem cell-derived neuron and astrocyte network

Silver nanoparticles induce neurotoxicity in a human embryonic stem cell-derived neuron and astrocyte network

Hyaluronan suppresses lidocaine-induced apoptosis of human chondrocytes in vitro by inhibiting the p53-dependent mitochondrial apoptotic pathway

Induced adverse effects of prenatal exposure to silver nanoparticles on neurobehavioral development of offspring of mice

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