Приказ основних података о документу
Graphene quantum dot antioxidant and proautophagic actions protect SH-SY5Y neuroblastoma cells from oxidative stress-mediated apoptotic death
dc.creator | Krunić, Matija | |
dc.creator | Ristić, Biljana | |
dc.creator | Bošnjak, Mihajlo | |
dc.creator | Paunović, Verica | |
dc.creator | Tovilović-Kovačević, Gordana | |
dc.creator | Zagović, Nevena | |
dc.creator | Mirčić, Aleksandar | |
dc.creator | Marković, Zoran | |
dc.creator | Todorović Marković, Biljana | |
dc.creator | Jovanović, Svetlana | |
dc.creator | Kleut, Duška | |
dc.creator | Mojović, Miloš | |
dc.creator | Nakarada, Đura | |
dc.creator | Marković, Olivera S. | |
dc.creator | Vuković, Irena | |
dc.creator | Harhaji-Trajković, Ljubica | |
dc.creator | Trajković, Vladimir | |
dc.date.accessioned | 2022-08-24T10:33:57Z | |
dc.date.available | 2022-08-24T10:33:57Z | |
dc.date.issued | 2021 | |
dc.identifier.issn | 0891-5849 | |
dc.identifier.uri | http://cherry.chem.bg.ac.rs/handle/123456789/5467 | |
dc.description.abstract | We investigated the ability of graphene quantum dot (GQD) nanoparticles to protect SH-SY5Y human neuro blastoma cells from oxidative/nitrosative stress induced by iron-nitrosyl complex sodium nitroprusside (SNP). GQD reduced SNP cytotoxicity by preventing mitochondrial depolarization, caspase-2 activation, and subsequent apoptotic death. Although GQD diminished the levels of nitric oxide (NO) in SNP-exposed cells, NO scavengers displayed only a slight protective effect, suggesting that NO quenching was not the main protective mechanism of GQD. GQD also reduced SNP-triggered increase in the intracellular levels of hydroxyl radical ( • OH), superoxide anion (O2 •− ), and lipid peroxidation. Nonselective antioxidants, • OH scavenging, and iron chelators, but not superoxide dismutase, mimicked GQD cytoprotective activity, indicating that GQD protect cells by neutralizing • OH generated in the presence of SNP-released iron. Cellular internalization of GQD was required for optimal protection, since a removal of extracellular GQD by extensive washing only partly diminished their protective effect. Moreover, GQD cooperated with SNP to induce autophagy, as confirmed by the inhibition of autophagy limiting Akt/PRAS40/mTOR signaling and increase in autophagy gene transcription, protein levels of proauto phagic beclin-1 and LC3-II, formation of autophagic vesicles, and degradation of autophagic target p62. The antioxidant activity of GQD was not involved in autophagy induction, as antioxidants N-acetylcysteine and dimethyl sulfoxide failed to stimulate autophagy in SNP-exposed cells. Pharmacological inhibitors of early (wortmannin, 3-methyladenine) or late stages of autophagy (NH4Cl) efficiently reduced the protective effect of GQD. Therefore, the ability of GQD to prevent the in vitro neurotoxicity of SNP depends on both • OH/NO scavenging and induction of cytoprotective autophagy. | sr |
dc.language.iso | en | sr |
dc.publisher | Elsevier | sr |
dc.relation | info:eu-repo/grantAgreement/MESTD/inst-2020/200007/RS// | sr |
dc.relation | info:eu-repo/grantAgreement/MESTD/inst-2020/200110/RS// | sr |
dc.relation | info:eu-repo/grantAgreement/MESTD/inst-2020/200017/RS// | sr |
dc.relation | info:eu-repo/grantAgreement/MESTD/inst-2020/200026/RS// | sr |
dc.relation | info:eu-repo/grantAgreement/MESTD/inst-2020/200146/RS// | sr |
dc.rights | restrictedAccess | sr |
dc.source | Free Radical Biology and Medicine | sr |
dc.subject | Graphene quantum dots | sr |
dc.subject | Sodium nitroprusside | sr |
dc.subject | Neurotoxicity | sr |
dc.subject | Oxidative stress | sr |
dc.subject | Hydroxyl radical | sr |
dc.subject | Nitric oxide | sr |
dc.subject | Autophagy | sr |
dc.title | Graphene quantum dot antioxidant and proautophagic actions protect SH-SY5Y neuroblastoma cells from oxidative stress-mediated apoptotic death | sr |
dc.type | article | sr |
dc.rights.license | ARR | sr |
dc.citation.volume | 177 | |
dc.citation.spage | 167 | |
dc.citation.epage | 180 | |
dc.identifier.wos | 000717740300004 | |
dc.identifier.doi | 10.1016/j.freeradbiomed.2021.10.025 | |
dc.citation.rank | M21 | |
dc.type.version | publishedVersion | sr |
dc.identifier.scopus | 2-s2.0-85117824181 |