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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-induced oxidative stress (a) and NF-κB activation (b). Human astrocytes were treated with 1.1 × 109–5.5 × 1011 AuNPs/mL for 96 h. (a) The steady-state level of reactive oxygen species (ROS) was measured using 2′,7′-dichlorodihydrofluorescein diacetate (H2DCF-DA) and imaging cytometry. The level of ROS is presented as relative fluorescence units (RFUs). The bars indicate the SD, n = 3, ∗∗∗P < 0.001 compared with control (ANOVA and Dunnett's a posteriori test). (b) After AuNP treatment, NF-κB p65 was translocated into nucleus (green). Nuclei were visualized with Hoechst 33342 (blue). The bars indicate the SD, n = 3, ∗∗P < 0.01, and ∗P < 0.05 compared with control (ANOVA and Dunnett's a posteriori test).
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fig3: Nanogold-induced oxidative stress (a) and NF-κB activation (b). Human astrocytes were treated with 1.1 × 109–5.5 × 1011 AuNPs/mL for 96 h. (a) The steady-state level of reactive oxygen species (ROS) was measured using 2′,7′-dichlorodihydrofluorescein diacetate (H2DCF-DA) and imaging cytometry. The level of ROS is presented as relative fluorescence units (RFUs). The bars indicate the SD, n = 3, ∗∗∗P < 0.001 compared with control (ANOVA and Dunnett's a posteriori test). (b) After AuNP treatment, NF-κB p65 was translocated into nucleus (green). Nuclei were visualized with Hoechst 33342 (blue). The bars indicate the SD, n = 3, ∗∗P < 0.01, and ∗P < 0.05 compared with control (ANOVA and Dunnett's a posteriori test).

Mentions: Nanogold also induced oxidative stress in human astrocytes (Figure 3(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-induced oxidative stress (a) and NF-κB activation (b). Human astrocytes were treated with 1.1 × 109–5.5 × 1011 AuNPs/mL for 96 h. (a) The steady-state level of reactive oxygen species (ROS) was measured using 2′,7′-dichlorodihydrofluorescein diacetate (H2DCF-DA) and imaging cytometry. The level of ROS is presented as relative fluorescence units (RFUs). The bars indicate the SD, n = 3, ∗∗∗P < 0.001 compared with control (ANOVA and Dunnett's a posteriori test). (b) After AuNP treatment, NF-κB p65 was translocated into nucleus (green). Nuclei were visualized with Hoechst 33342 (blue). The bars indicate the SD, n = 3, ∗∗P < 0.01, and ∗P < 0.05 compared with control (ANOVA and Dunnett's a posteriori test).
© Copyright Policy
Related In: Results  -  Collection

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fig3: Nanogold-induced oxidative stress (a) and NF-κB activation (b). Human astrocytes were treated with 1.1 × 109–5.5 × 1011 AuNPs/mL for 96 h. (a) The steady-state level of reactive oxygen species (ROS) was measured using 2′,7′-dichlorodihydrofluorescein diacetate (H2DCF-DA) and imaging cytometry. The level of ROS is presented as relative fluorescence units (RFUs). The bars indicate the SD, n = 3, ∗∗∗P < 0.001 compared with control (ANOVA and Dunnett's a posteriori test). (b) After AuNP treatment, NF-κB p65 was translocated into nucleus (green). Nuclei were visualized with Hoechst 33342 (blue). The bars indicate the SD, n = 3, ∗∗P < 0.01, and ∗P < 0.05 compared with control (ANOVA and Dunnett's a posteriori test).
Mentions: Nanogold also induced oxidative stress in human astrocytes (Figure 3(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.