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Gold Nanoparticles Promote Oxidant-Mediated Activation of NF-κB and 53BP1 Recruitment-Based Adaptive Response in Human Astrocytes.

Mytych J, Lewinska A, Zebrowski J, Wnuk M - Biomed Res Int (2015)

Bottom Line: In contrast, nanogold provoked changes in the astrocyte cell cycle and induced senescence-associated β-galactosidase activity.The robust 53BP1 recruitment resulted in reduced micronuclei production.Thus, nanogold treatment stimulated an adaptive response in a human astrocyte cell.

View Article: PubMed Central - PubMed

Affiliation: Department of Genetics, University of Rzeszow, Rejtana 16C, 35-959 Rzeszow, Poland.

ABSTRACT
Nanogold-based materials are promising candidate tools for nanobased medicine. Nevertheless, no conclusive information on their cytotoxicity is available. In the present study, we investigated the effects of gold nanoparticles (AuNPs) on human astrocytes in vitro. Nanogold treatment in a wide range of concentrations did not result in cytotoxicity. In contrast, nanogold provoked changes in the astrocyte cell cycle and induced senescence-associated β-galactosidase activity. AuNPs promoted oxidative stress and caused activation of NF-κB pathway. After nanogold treatment, an inverse correlation between the formation of 53BP1 foci and micronuclei generation was observed. The robust 53BP1 recruitment resulted in reduced micronuclei production. Thus, nanogold treatment stimulated an adaptive response in a human astrocyte cell.

No MeSH data available.


Nanogold-mediated cytotoxicity (a), changes in the cell cycle (b), and ability to induce stress-induced premature senescence (SIPS) (c). Human astrocytes were treated with 1.1 × 109–5.5 × 1011 AuNPs/mL for 96 h. (a) Cell viability was assessed using acridine orange-ethidium bromide staining. Arrows indicate live cells (green) and a dead cell (red). (b) Cell cycle analysis using an In Cell Analyzer 2000 (GE Healthcare, UK). (c) SIPS was assessed as SA-β-gal activity. The bars indicate the SD, n = 3, ∗∗∗P < 0.001, and ∗∗P < 0.01 compared with control (ANOVA and Dunnett's a posteriori test). Typical micrographs showing a SA-β-gal-positive cell and a SA-β-gal-negative cell are also presented.
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fig2: Nanogold-mediated cytotoxicity (a), changes in the cell cycle (b), and ability to induce stress-induced premature senescence (SIPS) (c). Human astrocytes were treated with 1.1 × 109–5.5 × 1011 AuNPs/mL for 96 h. (a) Cell viability was assessed using acridine orange-ethidium bromide staining. Arrows indicate live cells (green) and a dead cell (red). (b) Cell cycle analysis using an In Cell Analyzer 2000 (GE Healthcare, UK). (c) SIPS was assessed as SA-β-gal activity. The bars indicate the SD, n = 3, ∗∗∗P < 0.001, and ∗∗P < 0.01 compared with control (ANOVA and Dunnett's a posteriori test). Typical micrographs showing a SA-β-gal-positive cell and a SA-β-gal-negative cell are also presented.

Mentions: As nanogold in a range of concentrations from 36 to 1000 ng/mL was screened for cytotoxic effects in different mammalian cell lines [14], we used AuNP concentrations ranging from 1.4 to 700 ng/mL that corresponds to 1.1 × 109–5.5 × 1011 AuNPs/mL [17]. As a negative control, supernatant of AuNP after centrifugation was used. We were not able to observe any differences compared to control conditions (data not shown). Cytotoxic potential of AuNPs was minimal as estimated using acridine orange-ethidium bromide staining (Figure 2(a)).


Gold Nanoparticles Promote Oxidant-Mediated Activation of NF-κB and 53BP1 Recruitment-Based Adaptive Response in Human Astrocytes.

Mytych J, Lewinska A, Zebrowski J, Wnuk M - Biomed Res Int (2015)

Nanogold-mediated cytotoxicity (a), changes in the cell cycle (b), and ability to induce stress-induced premature senescence (SIPS) (c). Human astrocytes were treated with 1.1 × 109–5.5 × 1011 AuNPs/mL for 96 h. (a) Cell viability was assessed using acridine orange-ethidium bromide staining. Arrows indicate live cells (green) and a dead cell (red). (b) Cell cycle analysis using an In Cell Analyzer 2000 (GE Healthcare, UK). (c) SIPS was assessed as SA-β-gal activity. The bars indicate the SD, n = 3, ∗∗∗P < 0.001, and ∗∗P < 0.01 compared with control (ANOVA and Dunnett's a posteriori test). Typical micrographs showing a SA-β-gal-positive cell and a SA-β-gal-negative cell are also presented.
© Copyright Policy
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4493286&req=5

fig2: Nanogold-mediated cytotoxicity (a), changes in the cell cycle (b), and ability to induce stress-induced premature senescence (SIPS) (c). Human astrocytes were treated with 1.1 × 109–5.5 × 1011 AuNPs/mL for 96 h. (a) Cell viability was assessed using acridine orange-ethidium bromide staining. Arrows indicate live cells (green) and a dead cell (red). (b) Cell cycle analysis using an In Cell Analyzer 2000 (GE Healthcare, UK). (c) SIPS was assessed as SA-β-gal activity. The bars indicate the SD, n = 3, ∗∗∗P < 0.001, and ∗∗P < 0.01 compared with control (ANOVA and Dunnett's a posteriori test). Typical micrographs showing a SA-β-gal-positive cell and a SA-β-gal-negative cell are also presented.
Mentions: As nanogold in a range of concentrations from 36 to 1000 ng/mL was screened for cytotoxic effects in different mammalian cell lines [14], we used AuNP concentrations ranging from 1.4 to 700 ng/mL that corresponds to 1.1 × 109–5.5 × 1011 AuNPs/mL [17]. As a negative control, supernatant of AuNP after centrifugation was used. We were not able to observe any differences compared to control conditions (data not shown). Cytotoxic potential of AuNPs was minimal as estimated using acridine orange-ethidium bromide staining (Figure 2(a)).

Bottom Line: In contrast, nanogold provoked changes in the astrocyte cell cycle and induced senescence-associated β-galactosidase activity.The robust 53BP1 recruitment resulted in reduced micronuclei production.Thus, nanogold treatment stimulated an adaptive response in a human astrocyte cell.

View Article: PubMed Central - PubMed

Affiliation: Department of Genetics, University of Rzeszow, Rejtana 16C, 35-959 Rzeszow, Poland.

ABSTRACT
Nanogold-based materials are promising candidate tools for nanobased medicine. Nevertheless, no conclusive information on their cytotoxicity is available. In the present study, we investigated the effects of gold nanoparticles (AuNPs) on human astrocytes in vitro. Nanogold treatment in a wide range of concentrations did not result in cytotoxicity. In contrast, nanogold provoked changes in the astrocyte cell cycle and induced senescence-associated β-galactosidase activity. AuNPs promoted oxidative stress and caused activation of NF-κB pathway. After nanogold treatment, an inverse correlation between the formation of 53BP1 foci and micronuclei generation was observed. The robust 53BP1 recruitment resulted in reduced micronuclei production. Thus, nanogold treatment stimulated an adaptive response in a human astrocyte cell.

No MeSH data available.