Graphene quantum dots protect SH-SY5Y neuronal cells from SNP-induced apoptotic death
Autori
Ristić, BiljanaKrunić, Matija
Paunović, Verica
Bošnjak, Mihajlo
Tovilović-Kovačević, Gordana
Zogović, Nevena
Mirčić, Aleksandar
Vuković, Irena
Harhaji-Trajković, Ljubica
Trajković, Vladimir
Konferencijski prilog (Objavljena verzija)
,
Institute of Molecular Genetics and Genetic Engineering (IMGGE), University of Belgrade
Metapodaci
Prikaz svih podataka o dokumentuApstrakt
Introduction: We examined the molecular mechanisms of graphene quantum dot (GQD)- mediated
protection of SH-SY5Y human neuroblastoma cells from oxidative/nitrosative stress induced by iron-nitrosyl complex sodium nitroprusside (SNP).
Methods: GQD was produced by electrochemical oxidation of graphite and characterized by AFM, UVVIS
and FTIR spectroscopy. The antioxidant activity of GQD in cell-free conditions was assessed by DPPH, NBT and EPR analysis. The neuroprotective potential of GQD was determined by cell viability assays MTT, CV. Flow cytometry was used to assess markers of apoptosis and GQD scavenging of intracellular ROS/RNS as well. Cellular internalization of GQD was determined using TEM.
Results: GQD prevented SNP-induced apoptosis, caspase activation and mitochondrial depolarization in neuroblastoma cells. Although GQD diminished the NO levels in SNP-treated cells, NO scavengers displayed only a slight protection. GQD significantly protected SH-SY5Y cells from neurotoxi...city of lightexhausted SNP, incapable of producing NO, implying that protective mechanism is independent of NO-scavenging. GQD reduced SNP-triggered increase in intracellular levels of ROS, particularly •OH, O2•− in cells and cell-free condition. Nonselective antioxidants, •OH scavengers and iron chelators, mimicked GQD cytoprotection, indicating that GQD protect cells by neutralizing •OH generated in the Fenton reaction.
Cellular GQD internalization was required for optimal protection since the removal of extracellular
GQD by extensive washing partly diminished their protective effect, suggesting that GQD exerted
neuroprotective effect intra- and extracellularly.
Conclusion: By demonstrating that GQD protect neuroblastoma cells from SNP-induced apoptosis by •OH/NO scavenging, our results suggest that GQD could be valuable candidates for treatment of neurodegenerative diseases associated with oxidative/nitrosative stress.
Ključne reči:
graphene quantum dots / sodium nitroprusside / neuroprotection / antioxidants / neuronsIzvor:
CoMBoS2 – the Second Congress of Molecular Biologists of Serbia, Abstract Book – Trends in Molecular Biology, Special issue 06-08 October 2023, Belgrade, Serbia, 2023, 27-27Izdavač:
- Belgrade: Institute of Molecular Genetics and Genetic Engineering (IMGGE), University of Belgrade
Finansiranje / projekti:
- Ministarstvo nauke, tehnološkog razvoja i inovacija Republike Srbije, institucionalno finansiranje - 200110 (Univerzitet u Beogradu, Medicinski fakultet) (RS-MESTD-inst-2020-200110)
Institucija/grupa
Institut za medicinska istraživanjaTY - CONF AU - Ristić, Biljana AU - Krunić, Matija AU - Paunović, Verica AU - Bošnjak, Mihajlo AU - Tovilović-Kovačević, Gordana AU - Zogović, Nevena AU - Mirčić, Aleksandar AU - Vuković, Irena AU - Harhaji-Trajković, Ljubica AU - Trajković, Vladimir PY - 2023 UR - http://rimi.imi.bg.ac.rs/handle/123456789/1418 AB - Introduction: We examined the molecular mechanisms of graphene quantum dot (GQD)- mediated protection of SH-SY5Y human neuroblastoma cells from oxidative/nitrosative stress induced by iron-nitrosyl complex sodium nitroprusside (SNP). Methods: GQD was produced by electrochemical oxidation of graphite and characterized by AFM, UVVIS and FTIR spectroscopy. The antioxidant activity of GQD in cell-free conditions was assessed by DPPH, NBT and EPR analysis. The neuroprotective potential of GQD was determined by cell viability assays MTT, CV. Flow cytometry was used to assess markers of apoptosis and GQD scavenging of intracellular ROS/RNS as well. Cellular internalization of GQD was determined using TEM. Results: GQD prevented SNP-induced apoptosis, caspase activation and mitochondrial depolarization in neuroblastoma cells. Although GQD diminished the NO levels in SNP-treated cells, NO scavengers displayed only a slight protection. GQD significantly protected SH-SY5Y cells from neurotoxicity of lightexhausted SNP, incapable of producing NO, implying that protective mechanism is independent of NO-scavenging. GQD reduced SNP-triggered increase in intracellular levels of ROS, particularly •OH, O2•− in cells and cell-free condition. Nonselective antioxidants, •OH scavengers and iron chelators, mimicked GQD cytoprotection, indicating that GQD protect cells by neutralizing •OH generated in the Fenton reaction. Cellular GQD internalization was required for optimal protection since the removal of extracellular GQD by extensive washing partly diminished their protective effect, suggesting that GQD exerted neuroprotective effect intra- and extracellularly. Conclusion: By demonstrating that GQD protect neuroblastoma cells from SNP-induced apoptosis by •OH/NO scavenging, our results suggest that GQD could be valuable candidates for treatment of neurodegenerative diseases associated with oxidative/nitrosative stress. PB - Belgrade: Institute of Molecular Genetics and Genetic Engineering (IMGGE), University of Belgrade C3 - CoMBoS2 – the Second Congress of Molecular Biologists of Serbia, Abstract Book – Trends in Molecular Biology, Special issue 06-08 October 2023, Belgrade, Serbia T1 - Graphene quantum dots protect SH-SY5Y neuronal cells from SNP-induced apoptotic death EP - 27 SP - 27 UR - https://hdl.handle.net/21.15107/rcub_rimi_1418 ER -
@conference{ author = "Ristić, Biljana and Krunić, Matija and Paunović, Verica and Bošnjak, Mihajlo and Tovilović-Kovačević, Gordana and Zogović, Nevena and Mirčić, Aleksandar and Vuković, Irena and Harhaji-Trajković, Ljubica and Trajković, Vladimir", year = "2023", abstract = "Introduction: We examined the molecular mechanisms of graphene quantum dot (GQD)- mediated protection of SH-SY5Y human neuroblastoma cells from oxidative/nitrosative stress induced by iron-nitrosyl complex sodium nitroprusside (SNP). Methods: GQD was produced by electrochemical oxidation of graphite and characterized by AFM, UVVIS and FTIR spectroscopy. The antioxidant activity of GQD in cell-free conditions was assessed by DPPH, NBT and EPR analysis. The neuroprotective potential of GQD was determined by cell viability assays MTT, CV. Flow cytometry was used to assess markers of apoptosis and GQD scavenging of intracellular ROS/RNS as well. Cellular internalization of GQD was determined using TEM. Results: GQD prevented SNP-induced apoptosis, caspase activation and mitochondrial depolarization in neuroblastoma cells. Although GQD diminished the NO levels in SNP-treated cells, NO scavengers displayed only a slight protection. GQD significantly protected SH-SY5Y cells from neurotoxicity of lightexhausted SNP, incapable of producing NO, implying that protective mechanism is independent of NO-scavenging. GQD reduced SNP-triggered increase in intracellular levels of ROS, particularly •OH, O2•− in cells and cell-free condition. Nonselective antioxidants, •OH scavengers and iron chelators, mimicked GQD cytoprotection, indicating that GQD protect cells by neutralizing •OH generated in the Fenton reaction. Cellular GQD internalization was required for optimal protection since the removal of extracellular GQD by extensive washing partly diminished their protective effect, suggesting that GQD exerted neuroprotective effect intra- and extracellularly. Conclusion: By demonstrating that GQD protect neuroblastoma cells from SNP-induced apoptosis by •OH/NO scavenging, our results suggest that GQD could be valuable candidates for treatment of neurodegenerative diseases associated with oxidative/nitrosative stress.", publisher = "Belgrade: Institute of Molecular Genetics and Genetic Engineering (IMGGE), University of Belgrade", journal = "CoMBoS2 – the Second Congress of Molecular Biologists of Serbia, Abstract Book – Trends in Molecular Biology, Special issue 06-08 October 2023, Belgrade, Serbia", title = "Graphene quantum dots protect SH-SY5Y neuronal cells from SNP-induced apoptotic death", pages = "27-27", url = "https://hdl.handle.net/21.15107/rcub_rimi_1418" }
Ristić, B., Krunić, M., Paunović, V., Bošnjak, M., Tovilović-Kovačević, G., Zogović, N., Mirčić, A., Vuković, I., Harhaji-Trajković, L.,& Trajković, V.. (2023). Graphene quantum dots protect SH-SY5Y neuronal cells from SNP-induced apoptotic death. in CoMBoS2 – the Second Congress of Molecular Biologists of Serbia, Abstract Book – Trends in Molecular Biology, Special issue 06-08 October 2023, Belgrade, Serbia Belgrade: Institute of Molecular Genetics and Genetic Engineering (IMGGE), University of Belgrade., 27-27. https://hdl.handle.net/21.15107/rcub_rimi_1418
Ristić B, Krunić M, Paunović V, Bošnjak M, Tovilović-Kovačević G, Zogović N, Mirčić A, Vuković I, Harhaji-Trajković L, Trajković V. Graphene quantum dots protect SH-SY5Y neuronal cells from SNP-induced apoptotic death. in CoMBoS2 – the Second Congress of Molecular Biologists of Serbia, Abstract Book – Trends in Molecular Biology, Special issue 06-08 October 2023, Belgrade, Serbia. 2023;:27-27. https://hdl.handle.net/21.15107/rcub_rimi_1418 .
Ristić, Biljana, Krunić, Matija, Paunović, Verica, Bošnjak, Mihajlo, Tovilović-Kovačević, Gordana, Zogović, Nevena, Mirčić, Aleksandar, Vuković, Irena, Harhaji-Trajković, Ljubica, Trajković, Vladimir, "Graphene quantum dots protect SH-SY5Y neuronal cells from SNP-induced apoptotic death" in CoMBoS2 – the Second Congress of Molecular Biologists of Serbia, Abstract Book – Trends in Molecular Biology, Special issue 06-08 October 2023, Belgrade, Serbia (2023):27-27, https://hdl.handle.net/21.15107/rcub_rimi_1418 .