TY  - JOUR
AU  - Krunić, Matija
AU  - Ristić, Biljana
AU  - Bošnjak, Mihajlo
AU  - Paunović, Verica
AU  - Tovilović-Kovačević, Gordana
AU  - Zogović, Nevena
AU  - Mirčić, Aleksandar
AU  - Marković, Zoran
AU  - Todorović-Marković, Biljana
AU  - Jovanović, Svetlana
AU  - Kleut, Duška
AU  - Mojović, Miloš
AU  - Nakarada, Đura
AU  - Marković, Olivera
AU  - Vuković, Irena
AU  - Harhaji-Trajković, Ljubica
AU  - Trajković, Vladimir
PY  - 2021
UR  - https://cer.ihtm.bg.ac.rs/handle/123456789/4812
AB  - We investigated the ability of graphene quantum dot (GQD) nanoparticles to protect SH-SY5Y human neuroblastoma 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 autophagylimiting Akt/PRAS40/mTOR signaling and increase in autophagy gene transcription, protein levels of proautophagic 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.
PB  - Elsevier
T2  - Free Radical Biology and Medicine
T1  - Graphene quantum dot antioxidant and proautophagic actions protect SH-SY5Y neuroblastoma cells from oxidative stress-mediated apoptotic death
VL  - 177
SP  - 167
EP  - 180
DO  - 10.1016/j.freeradbiomed.2021.10.025
ER  - 

@article{
author = "Krunić, Matija and Ristić, Biljana and Bošnjak, Mihajlo and Paunović, Verica and Tovilović-Kovačević, Gordana and Zogović, Nevena and Mirčić, Aleksandar and Marković, Zoran and Todorović-Marković, Biljana and Jovanović, Svetlana and Kleut, Duška and Mojović, Miloš and Nakarada, Đura and Marković, Olivera and Vuković, Irena and Harhaji-Trajković, Ljubica and Trajković, Vladimir",
year = "2021",
abstract = "We investigated the ability of graphene quantum dot (GQD) nanoparticles to protect SH-SY5Y human neuroblastoma 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 autophagylimiting Akt/PRAS40/mTOR signaling and increase in autophagy gene transcription, protein levels of proautophagic 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.",
publisher = "Elsevier",
journal = "Free Radical Biology and Medicine",
title = "Graphene quantum dot antioxidant and proautophagic actions protect SH-SY5Y neuroblastoma cells from oxidative stress-mediated apoptotic death",
volume = "177",
pages = "167-180",
doi = "10.1016/j.freeradbiomed.2021.10.025"
}

Krunić, M., Ristić, B., Bošnjak, M., Paunović, V., Tovilović-Kovačević, G., Zogović, N., Mirčić, A., Marković, Z., Todorović-Marković, B., Jovanović, S., Kleut, D., Mojović, M., Nakarada, Đ., Marković, O., Vuković, I., Harhaji-Trajković, L.,& Trajković, V.. (2021). Graphene quantum dot antioxidant and proautophagic actions protect SH-SY5Y neuroblastoma cells from oxidative stress-mediated apoptotic death. in Free Radical Biology and Medicine
Elsevier., 177, 167-180.
https://doi.org/10.1016/j.freeradbiomed.2021.10.025

Krunić M, Ristić B, Bošnjak M, Paunović V, Tovilović-Kovačević G, Zogović N, Mirčić A, Marković Z, Todorović-Marković B, Jovanović S, Kleut D, Mojović M, Nakarada Đ, Marković O, Vuković I, Harhaji-Trajković L, Trajković V. Graphene quantum dot antioxidant and proautophagic actions protect SH-SY5Y neuroblastoma cells from oxidative stress-mediated apoptotic death. in Free Radical Biology and Medicine. 2021;177:167-180.
doi:10.1016/j.freeradbiomed.2021.10.025 .

Krunić, Matija, Ristić, Biljana, Bošnjak, Mihajlo, Paunović, Verica, Tovilović-Kovačević, Gordana, Zogović, Nevena, Mirčić, Aleksandar, Marković, Zoran, Todorović-Marković, Biljana, Jovanović, Svetlana, Kleut, Duška, Mojović, Miloš, Nakarada, Đura, Marković, Olivera, Vuković, Irena, Harhaji-Trajković, Ljubica, Trajković, Vladimir, "Graphene quantum dot antioxidant and proautophagic actions protect SH-SY5Y neuroblastoma cells from oxidative stress-mediated apoptotic death" in Free Radical Biology and Medicine, 177 (2021):167-180,
https://doi.org/10.1016/j.freeradbiomed.2021.10.025 . .

TY  - JOUR
AU  - Krunić, Matija
AU  - Ristić, Biljana
AU  - Bošnjak, Mihajlo
AU  - Paunović, Verica
AU  - Tovilović-Kovačević, Gordana
AU  - Zogović, Nevena
AU  - Mirčić, Aleksandar
AU  - Marković, Zoran
AU  - Todorović-Marković, Biljana
AU  - Jovanović, Svetlana
AU  - Kleut, Duška
AU  - Mojović, Miloš
AU  - Nakarada, Đura
AU  - Marković, Olivera
AU  - Vuković, Irena
AU  - Harhaji-Trajković, Ljubica
AU  - Trajković, Vladimir
PY  - 2021
UR  - https://cer.ihtm.bg.ac.rs/handle/123456789/4818
AB  - We investigated the ability of graphene quantum dot (GQD) nanoparticles to protect SH-SY5Y human neuroblastoma 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 autophagylimiting Akt/PRAS40/mTOR signaling and increase in autophagy gene transcription, protein levels of proautophagic 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.
PB  - Elsevier
T2  - Free Radical Biology and Medicine
T1  - Graphene quantum dot antioxidant and proautophagic actions protect SH-SY5Y neuroblastoma cells from oxidative stress-mediated apoptotic death
VL  - 177
SP  - 167
EP  - 180
DO  - 10.1016/j.freeradbiomed.2021.10.025
ER  - 

@article{
author = "Krunić, Matija and Ristić, Biljana and Bošnjak, Mihajlo and Paunović, Verica and Tovilović-Kovačević, Gordana and Zogović, Nevena and Mirčić, Aleksandar and Marković, Zoran and Todorović-Marković, Biljana and Jovanović, Svetlana and Kleut, Duška and Mojović, Miloš and Nakarada, Đura and Marković, Olivera and Vuković, Irena and Harhaji-Trajković, Ljubica and Trajković, Vladimir",
year = "2021",
abstract = "We investigated the ability of graphene quantum dot (GQD) nanoparticles to protect SH-SY5Y human neuroblastoma 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 autophagylimiting Akt/PRAS40/mTOR signaling and increase in autophagy gene transcription, protein levels of proautophagic 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.",
publisher = "Elsevier",
journal = "Free Radical Biology and Medicine",
title = "Graphene quantum dot antioxidant and proautophagic actions protect SH-SY5Y neuroblastoma cells from oxidative stress-mediated apoptotic death",
volume = "177",
pages = "167-180",
doi = "10.1016/j.freeradbiomed.2021.10.025"
}

Krunić, M., Ristić, B., Bošnjak, M., Paunović, V., Tovilović-Kovačević, G., Zogović, N., Mirčić, A., Marković, Z., Todorović-Marković, B., Jovanović, S., Kleut, D., Mojović, M., Nakarada, Đ., Marković, O., Vuković, I., Harhaji-Trajković, L.,& Trajković, V.. (2021). Graphene quantum dot antioxidant and proautophagic actions protect SH-SY5Y neuroblastoma cells from oxidative stress-mediated apoptotic death. in Free Radical Biology and Medicine
Elsevier., 177, 167-180.
https://doi.org/10.1016/j.freeradbiomed.2021.10.025

Krunić M, Ristić B, Bošnjak M, Paunović V, Tovilović-Kovačević G, Zogović N, Mirčić A, Marković Z, Todorović-Marković B, Jovanović S, Kleut D, Mojović M, Nakarada Đ, Marković O, Vuković I, Harhaji-Trajković L, Trajković V. Graphene quantum dot antioxidant and proautophagic actions protect SH-SY5Y neuroblastoma cells from oxidative stress-mediated apoptotic death. in Free Radical Biology and Medicine. 2021;177:167-180.
doi:10.1016/j.freeradbiomed.2021.10.025 .

Krunić, Matija, Ristić, Biljana, Bošnjak, Mihajlo, Paunović, Verica, Tovilović-Kovačević, Gordana, Zogović, Nevena, Mirčić, Aleksandar, Marković, Zoran, Todorović-Marković, Biljana, Jovanović, Svetlana, Kleut, Duška, Mojović, Miloš, Nakarada, Đura, Marković, Olivera, Vuković, Irena, Harhaji-Trajković, Ljubica, Trajković, Vladimir, "Graphene quantum dot antioxidant and proautophagic actions protect SH-SY5Y neuroblastoma cells from oxidative stress-mediated apoptotic death" in Free Radical Biology and Medicine, 177 (2021):167-180,
https://doi.org/10.1016/j.freeradbiomed.2021.10.025 . .

TY  - JOUR
AU  - Popović, Marjan
AU  - Stanojević, Željka
AU  - Tosic, Jelena
AU  - Isaković, Aleksandra
AU  - Paunović, Verica
AU  - Petricevic, Sasa
AU  - Martinović, Tamara
AU  - Ciric, Darko
AU  - Kravić-Stevović, Tamara
AU  - Šoškić, Vukić
AU  - Kostić Rajačić, Slađana
AU  - Shakib, Kaveh
AU  - Bumbasirevic, Vladimir
AU  - Trajković, Vladimir
PY  - 2015
UR  - https://cer.ihtm.bg.ac.rs/handle/123456789/1812
AB  - Arylpiperazine-based dopaminergic/serotonergic ligands exert neuroprotective activity. We examined the effect of arylpiperazine D-2/5-HT1A ligands, N-{4-[2-(4-phenyl-piperazin-1-yl)-ethyl}-phenyl]- picolinamide (6a) and N-{3-[2-(4-phenyl-piperazin-1-yl)ethyl]- phenyl}-picolinamide (6b), in experimental autoimmune encephalomyelitis (EAE), a model of neuroinflammation. Both compounds (10 mg/kg i.p.) reduced EAE clinical signs in spinal cord homogenate-immunized Dark Agouti rats. Compound 6b was more efficient in delaying the disease onset and reducing the maximal clinical score, which correlated with its higher affinity for D-2 and 5-HT1A receptors. The protectionwas retainedif treatment was limited to the effector (from day 8 onwards), but not the induction phase (day 0-7) of EAE. Compound 6b reduced CNS immune infiltration and expression of mRNA encoding the proinflammatory cytokines tumor necrosis factor, IL-6, IL-1, and GM-CSF, T(H)1 cytokine IFN-gamma, T(H)17 cytokine IL-17, as well as the signature transcription factors of T(H)1 (T-bet) and T(H)17 (ROR gamma t) cells. Arylpiperazine treatment reduced apoptosis and increased the activation of anti-apoptotic mediators Akt and p70S6 kinase in the CNS of EAE animals. The in vitro treatment with 6b protected oligodendrocyte cell line OLN-93 and neuronal cell line PC12 from mitogen-activated normal T cells or myelin basic proteinactivated encephalitogenic T cells. In conclusion, arylpiperazine dopaminergic/serotonergic ligands suppress EAE through a direct neuroprotective action and decrease inCNS inflammation.
PB  - Wiley, Hoboken
T2  - Journal of Neurochemistry
T1  - Neuroprotective arylpiperazine dopaminergic/serotonergic ligands suppress experimental autoimmune encephalomyelitis in rats
VL  - 135
IS  - 1
SP  - 125
EP  - 138
DO  - 10.1111/jnc.13198
ER  - 

@article{
author = "Popović, Marjan and Stanojević, Željka and Tosic, Jelena and Isaković, Aleksandra and Paunović, Verica and Petricevic, Sasa and Martinović, Tamara and Ciric, Darko and Kravić-Stevović, Tamara and Šoškić, Vukić and Kostić Rajačić, Slađana and Shakib, Kaveh and Bumbasirevic, Vladimir and Trajković, Vladimir",
year = "2015",
abstract = "Arylpiperazine-based dopaminergic/serotonergic ligands exert neuroprotective activity. We examined the effect of arylpiperazine D-2/5-HT1A ligands, N-{4-[2-(4-phenyl-piperazin-1-yl)-ethyl}-phenyl]- picolinamide (6a) and N-{3-[2-(4-phenyl-piperazin-1-yl)ethyl]- phenyl}-picolinamide (6b), in experimental autoimmune encephalomyelitis (EAE), a model of neuroinflammation. Both compounds (10 mg/kg i.p.) reduced EAE clinical signs in spinal cord homogenate-immunized Dark Agouti rats. Compound 6b was more efficient in delaying the disease onset and reducing the maximal clinical score, which correlated with its higher affinity for D-2 and 5-HT1A receptors. The protectionwas retainedif treatment was limited to the effector (from day 8 onwards), but not the induction phase (day 0-7) of EAE. Compound 6b reduced CNS immune infiltration and expression of mRNA encoding the proinflammatory cytokines tumor necrosis factor, IL-6, IL-1, and GM-CSF, T(H)1 cytokine IFN-gamma, T(H)17 cytokine IL-17, as well as the signature transcription factors of T(H)1 (T-bet) and T(H)17 (ROR gamma t) cells. Arylpiperazine treatment reduced apoptosis and increased the activation of anti-apoptotic mediators Akt and p70S6 kinase in the CNS of EAE animals. The in vitro treatment with 6b protected oligodendrocyte cell line OLN-93 and neuronal cell line PC12 from mitogen-activated normal T cells or myelin basic proteinactivated encephalitogenic T cells. In conclusion, arylpiperazine dopaminergic/serotonergic ligands suppress EAE through a direct neuroprotective action and decrease inCNS inflammation.",
publisher = "Wiley, Hoboken",
journal = "Journal of Neurochemistry",
title = "Neuroprotective arylpiperazine dopaminergic/serotonergic ligands suppress experimental autoimmune encephalomyelitis in rats",
volume = "135",
number = "1",
pages = "125-138",
doi = "10.1111/jnc.13198"
}

Popović, M., Stanojević, Ž., Tosic, J., Isaković, A., Paunović, V., Petricevic, S., Martinović, T., Ciric, D., Kravić-Stevović, T., Šoškić, V., Kostić Rajačić, S., Shakib, K., Bumbasirevic, V.,& Trajković, V.. (2015). Neuroprotective arylpiperazine dopaminergic/serotonergic ligands suppress experimental autoimmune encephalomyelitis in rats. in Journal of Neurochemistry
Wiley, Hoboken., 135(1), 125-138.
https://doi.org/10.1111/jnc.13198

Popović M, Stanojević Ž, Tosic J, Isaković A, Paunović V, Petricevic S, Martinović T, Ciric D, Kravić-Stevović T, Šoškić V, Kostić Rajačić S, Shakib K, Bumbasirevic V, Trajković V. Neuroprotective arylpiperazine dopaminergic/serotonergic ligands suppress experimental autoimmune encephalomyelitis in rats. in Journal of Neurochemistry. 2015;135(1):125-138.
doi:10.1111/jnc.13198 .

Popović, Marjan, Stanojević, Željka, Tosic, Jelena, Isaković, Aleksandra, Paunović, Verica, Petricevic, Sasa, Martinović, Tamara, Ciric, Darko, Kravić-Stevović, Tamara, Šoškić, Vukić, Kostić Rajačić, Slađana, Shakib, Kaveh, Bumbasirevic, Vladimir, Trajković, Vladimir, "Neuroprotective arylpiperazine dopaminergic/serotonergic ligands suppress experimental autoimmune encephalomyelitis in rats" in Journal of Neurochemistry, 135, no. 1 (2015):125-138,
https://doi.org/10.1111/jnc.13198 . .

TY  - JOUR
AU  - Trifunović, Snežana
AU  - Isaković, Anđelka M.
AU  - Isaković, Aleksandra
AU  - Vučković, Ivan
AU  - Mandić, Boris
AU  - Novaković, Miroslav
AU  - Vajs, Vlatka
AU  - Milosavljević, Slobodan
AU  - Trajković, Vladimir
PY  - 2014
UR  - https://cer.ihtm.bg.ac.rs/handle/123456789/3120
AB  - Further phytochemical investigation into the aerial parts of Achillea clavennae has resulted in the 3 isolation of three new sesquiterpene lactones: two highly oxygenated germacranolides (1, 2) and 4 the iso-seco-guaianolide, 9(R)-acetoxy-3-O-methyl-iso-seco-tanapartholide (3). Eight known 5 compounds were also found in this plant species, of which 9 α -acetoxycanin (5), sintenin (6) and 6 oleanolic acid (7) were detected for the first time. The structures of the isolated compounds were 7 elucidated by combined spectroscopic methods (1D and 2D NMR, HRESIMS, CIMS, FTIR). 8 While the predominant metabolite germacranolide sintenin (6) was not cytotoxic, the new iso-9 seco-guaianolide (3) displayed cytotoxicity comparable to that of cisplatin and the lactone 10 apressin (4), inducing partly apoptotic death in human U251 and rat C6 glioma cell lines.
PB  - Georg Thieme Verlag
T2  - Planta medica
T1  - Isolation, characterization and in vitro cytotoxicity of new sesquiterpenoids from Achillea clavennae
VL  - 80
IS  - 4
SP  - 275
EP  - 305
DO  - 10.1055/s-0033-1360312
ER  - 

@article{
author = "Trifunović, Snežana and Isaković, Anđelka M. and Isaković, Aleksandra and Vučković, Ivan and Mandić, Boris and Novaković, Miroslav and Vajs, Vlatka and Milosavljević, Slobodan and Trajković, Vladimir",
year = "2014",
abstract = "Further phytochemical investigation into the aerial parts of Achillea clavennae has resulted in the 3 isolation of three new sesquiterpene lactones: two highly oxygenated germacranolides (1, 2) and 4 the iso-seco-guaianolide, 9(R)-acetoxy-3-O-methyl-iso-seco-tanapartholide (3). Eight known 5 compounds were also found in this plant species, of which 9 α -acetoxycanin (5), sintenin (6) and 6 oleanolic acid (7) were detected for the first time. The structures of the isolated compounds were 7 elucidated by combined spectroscopic methods (1D and 2D NMR, HRESIMS, CIMS, FTIR). 8 While the predominant metabolite germacranolide sintenin (6) was not cytotoxic, the new iso-9 seco-guaianolide (3) displayed cytotoxicity comparable to that of cisplatin and the lactone 10 apressin (4), inducing partly apoptotic death in human U251 and rat C6 glioma cell lines.",
publisher = "Georg Thieme Verlag",
journal = "Planta medica",
title = "Isolation, characterization and in vitro cytotoxicity of new sesquiterpenoids from Achillea clavennae",
volume = "80",
number = "4",
pages = "275-305",
doi = "10.1055/s-0033-1360312"
}

Trifunović, S., Isaković, A. M., Isaković, A., Vučković, I., Mandić, B., Novaković, M., Vajs, V., Milosavljević, S.,& Trajković, V.. (2014). Isolation, characterization and in vitro cytotoxicity of new sesquiterpenoids from Achillea clavennae. in Planta medica
Georg Thieme Verlag., 80(4), 275-305.
https://doi.org/10.1055/s-0033-1360312

Trifunović S, Isaković AM, Isaković A, Vučković I, Mandić B, Novaković M, Vajs V, Milosavljević S, Trajković V. Isolation, characterization and in vitro cytotoxicity of new sesquiterpenoids from Achillea clavennae. in Planta medica. 2014;80(4):275-305.
doi:10.1055/s-0033-1360312 .

Trifunović, Snežana, Isaković, Anđelka M., Isaković, Aleksandra, Vučković, Ivan, Mandić, Boris, Novaković, Miroslav, Vajs, Vlatka, Milosavljević, Slobodan, Trajković, Vladimir, "Isolation, characterization and in vitro cytotoxicity of new sesquiterpenoids from Achillea clavennae" in Planta medica, 80, no. 4 (2014):275-305,
https://doi.org/10.1055/s-0033-1360312 . .

TY  - JOUR
AU  - Trifunović, Snežana
AU  - Isaković, Anđelka M.
AU  - Isaković, Aleksandra
AU  - Vučković, Ivan
AU  - Mandić, Boris
AU  - Novaković, Miroslav
AU  - Vajs, Vlatka
AU  - Milosavljević, Slobodan
AU  - Trajković, Vladimir
PY  - 2014
UR  - https://cer.ihtm.bg.ac.rs/handle/123456789/1534
AB  - Further phytochemical investigation of the aerial parts of Achillea clavennae has resulted in the isolation of three new sesquiterpene lactones: two highly oxygenated germacranolides (1, 2) and the iso-seco-guaianolide 9(R)-acetoxy-3-O-methyl-iso-seco-tanapartholide (3). Eight known compounds were also found, of which 9-acetoxycanin (5), sintenin (6), and oleanolic acid (7) were detected for the first time. The structures of the isolated compounds were elucidated by combined spectroscopic methods (1D and 2DNMR, HRESIMS, CIMS, and FTIR). While the predominant metabolite germacranolide sintenin (6) was not cytotoxic, the new iso-seco-guaianolide (3) displayed cytotoxicity comparable to that of cisplatin and the lactone apressin (4), inducing partly apoptotic death in human U251 and rat C6 glioma cell lines.
PB  - Georg Thieme Verlag Kg, Stuttgart
T2  - Planta Medica
T1  - Isolation, Characterization, and In Vitro Cytotoxicity of New Sesquiterpenoids from Achillea clavennae
VL  - 80
IS  - 4
SP  - 297
EP  - 305
DO  - 10.1055/s-0033-1360312
ER  - 

@article{
author = "Trifunović, Snežana and Isaković, Anđelka M. and Isaković, Aleksandra and Vučković, Ivan and Mandić, Boris and Novaković, Miroslav and Vajs, Vlatka and Milosavljević, Slobodan and Trajković, Vladimir",
year = "2014",
abstract = "Further phytochemical investigation of the aerial parts of Achillea clavennae has resulted in the isolation of three new sesquiterpene lactones: two highly oxygenated germacranolides (1, 2) and the iso-seco-guaianolide 9(R)-acetoxy-3-O-methyl-iso-seco-tanapartholide (3). Eight known compounds were also found, of which 9-acetoxycanin (5), sintenin (6), and oleanolic acid (7) were detected for the first time. The structures of the isolated compounds were elucidated by combined spectroscopic methods (1D and 2DNMR, HRESIMS, CIMS, and FTIR). While the predominant metabolite germacranolide sintenin (6) was not cytotoxic, the new iso-seco-guaianolide (3) displayed cytotoxicity comparable to that of cisplatin and the lactone apressin (4), inducing partly apoptotic death in human U251 and rat C6 glioma cell lines.",
publisher = "Georg Thieme Verlag Kg, Stuttgart",
journal = "Planta Medica",
title = "Isolation, Characterization, and In Vitro Cytotoxicity of New Sesquiterpenoids from Achillea clavennae",
volume = "80",
number = "4",
pages = "297-305",
doi = "10.1055/s-0033-1360312"
}

Trifunović, S., Isaković, A. M., Isaković, A., Vučković, I., Mandić, B., Novaković, M., Vajs, V., Milosavljević, S.,& Trajković, V.. (2014). Isolation, Characterization, and In Vitro Cytotoxicity of New Sesquiterpenoids from Achillea clavennae. in Planta Medica
Georg Thieme Verlag Kg, Stuttgart., 80(4), 297-305.
https://doi.org/10.1055/s-0033-1360312

Trifunović S, Isaković AM, Isaković A, Vučković I, Mandić B, Novaković M, Vajs V, Milosavljević S, Trajković V. Isolation, Characterization, and In Vitro Cytotoxicity of New Sesquiterpenoids from Achillea clavennae. in Planta Medica. 2014;80(4):297-305.
doi:10.1055/s-0033-1360312 .

Trifunović, Snežana, Isaković, Anđelka M., Isaković, Aleksandra, Vučković, Ivan, Mandić, Boris, Novaković, Miroslav, Vajs, Vlatka, Milosavljević, Slobodan, Trajković, Vladimir, "Isolation, Characterization, and In Vitro Cytotoxicity of New Sesquiterpenoids from Achillea clavennae" in Planta Medica, 80, no. 4 (2014):297-305,
https://doi.org/10.1055/s-0033-1360312 . .

TY  - JOUR
AU  - Tovilović, Gordana
AU  - Zogovic, Nevena
AU  - Šoškić, Vukić
AU  - Schrattenholz, Andre
AU  - Kostić Rajačić, Slađana
AU  - Misirkić-Marjanović, Maja
AU  - Janjetovic, Kristina
AU  - Vucicevic, Ljubica
AU  - Arsikin, Katarina
AU  - Harhaji-Trajković, Ljubica
AU  - Trajković, Vladimir
PY  - 2013
UR  - https://cer.ihtm.bg.ac.rs/handle/123456789/1201
AB  - We investigated the ability of 19 recently synthesized arylpiperazine compounds to protect human SH-SY5Y neuroblastoma cells from the neurotoxin 6-hydroxydopamine (6-OHDA). The compound with the most potent neuroprotective action was N-{3-[2-(4-phenyl-piperazin-1-yl)-ethyl]-phenyl}-picolinamide (6b), which reduced 6-OHDA-induced apoptotic death through stabilization of mitochondrial membrane and subsequent prevention of superoxide production, caspase activation and DNA fragmentation. 6-OHDA-triggered autophagic response was also reduced by 6b, which prevented inactivation of the main autophagy repressor mTOR, upregulation of proautophagic beclin-1, conversion of microtubule-associated protein 1 light chain 3 (LC3)-I to autophagosome-associAed LC3-II, as well as intracytoplasmic acidification induced by 6-OHDA. The inhibition of autophagy using LC3 beta gene silencing or pharmacological autophagy blockers 3-methyladenine or bafilomycin A1, mimicked the cytoprotective effect of 6b. While the treatment with 6b had no effect on the phosphorylation of proapoptotic MAP kinases ERR and JNK, it markedly increased the phosphorylation of the prosurvival kinase Akt in 6-OHDA-treated cells. Akt inhibitor DEBC or RNA interference-mediated Akt silencing reduced the ability of 6b to block 6-0HDA-triggered apoptotic and autophagic responses, thus confirming their dependency on Akt activation. The cytoprotective effect of 6b was also observed in 6-OHDA-treated neuronal PC12 cells, but not in SH-SY5Y or PC12 cells exposed to 1-methyl-4-phenylpyridinium, indicating that the observed neuroprotection was dependent on the cytotoxic stimulus. Because of the ability to prevent 6-OHDA induced apoptotic/autophagic cell death through activation of Akt, the investigated arylpiperazines could be potential candidates for treatment of neurodegenerative diseases.
PB  - Oxford : Pergamon-Elsevier Science Ltd
T2  - Neuropharmacology
T1  - Arylpiperazine-mediated activation of Akt protects SH-SY5Y neuroblastoma cells from 6-hydroxydopamine-induced apoptotic and autophagic death
VL  - 72
SP  - 224
EP  - 235
DO  - 10.1016/j.neuropharm.2013.04.037
ER  - 

@article{
author = "Tovilović, Gordana and Zogovic, Nevena and Šoškić, Vukić and Schrattenholz, Andre and Kostić Rajačić, Slađana and Misirkić-Marjanović, Maja and Janjetovic, Kristina and Vucicevic, Ljubica and Arsikin, Katarina and Harhaji-Trajković, Ljubica and Trajković, Vladimir",
year = "2013",
abstract = "We investigated the ability of 19 recently synthesized arylpiperazine compounds to protect human SH-SY5Y neuroblastoma cells from the neurotoxin 6-hydroxydopamine (6-OHDA). The compound with the most potent neuroprotective action was N-{3-[2-(4-phenyl-piperazin-1-yl)-ethyl]-phenyl}-picolinamide (6b), which reduced 6-OHDA-induced apoptotic death through stabilization of mitochondrial membrane and subsequent prevention of superoxide production, caspase activation and DNA fragmentation. 6-OHDA-triggered autophagic response was also reduced by 6b, which prevented inactivation of the main autophagy repressor mTOR, upregulation of proautophagic beclin-1, conversion of microtubule-associated protein 1 light chain 3 (LC3)-I to autophagosome-associAed LC3-II, as well as intracytoplasmic acidification induced by 6-OHDA. The inhibition of autophagy using LC3 beta gene silencing or pharmacological autophagy blockers 3-methyladenine or bafilomycin A1, mimicked the cytoprotective effect of 6b. While the treatment with 6b had no effect on the phosphorylation of proapoptotic MAP kinases ERR and JNK, it markedly increased the phosphorylation of the prosurvival kinase Akt in 6-OHDA-treated cells. Akt inhibitor DEBC or RNA interference-mediated Akt silencing reduced the ability of 6b to block 6-0HDA-triggered apoptotic and autophagic responses, thus confirming their dependency on Akt activation. The cytoprotective effect of 6b was also observed in 6-OHDA-treated neuronal PC12 cells, but not in SH-SY5Y or PC12 cells exposed to 1-methyl-4-phenylpyridinium, indicating that the observed neuroprotection was dependent on the cytotoxic stimulus. Because of the ability to prevent 6-OHDA induced apoptotic/autophagic cell death through activation of Akt, the investigated arylpiperazines could be potential candidates for treatment of neurodegenerative diseases.",
publisher = "Oxford : Pergamon-Elsevier Science Ltd",
journal = "Neuropharmacology",
title = "Arylpiperazine-mediated activation of Akt protects SH-SY5Y neuroblastoma cells from 6-hydroxydopamine-induced apoptotic and autophagic death",
volume = "72",
pages = "224-235",
doi = "10.1016/j.neuropharm.2013.04.037"
}

Tovilović, G., Zogovic, N., Šoškić, V., Schrattenholz, A., Kostić Rajačić, S., Misirkić-Marjanović, M., Janjetovic, K., Vucicevic, L., Arsikin, K., Harhaji-Trajković, L.,& Trajković, V.. (2013). Arylpiperazine-mediated activation of Akt protects SH-SY5Y neuroblastoma cells from 6-hydroxydopamine-induced apoptotic and autophagic death. in Neuropharmacology
Oxford : Pergamon-Elsevier Science Ltd., 72, 224-235.
https://doi.org/10.1016/j.neuropharm.2013.04.037

Tovilović G, Zogovic N, Šoškić V, Schrattenholz A, Kostić Rajačić S, Misirkić-Marjanović M, Janjetovic K, Vucicevic L, Arsikin K, Harhaji-Trajković L, Trajković V. Arylpiperazine-mediated activation of Akt protects SH-SY5Y neuroblastoma cells from 6-hydroxydopamine-induced apoptotic and autophagic death. in Neuropharmacology. 2013;72:224-235.
doi:10.1016/j.neuropharm.2013.04.037 .

Tovilović, Gordana, Zogovic, Nevena, Šoškić, Vukić, Schrattenholz, Andre, Kostić Rajačić, Slađana, Misirkić-Marjanović, Maja, Janjetovic, Kristina, Vucicevic, Ljubica, Arsikin, Katarina, Harhaji-Trajković, Ljubica, Trajković, Vladimir, "Arylpiperazine-mediated activation of Akt protects SH-SY5Y neuroblastoma cells from 6-hydroxydopamine-induced apoptotic and autophagic death" in Neuropharmacology, 72 (2013):224-235,
https://doi.org/10.1016/j.neuropharm.2013.04.037 . .

TY  - JOUR
AU  - Tovilović, Gordana
AU  - Zogovic, Nevena
AU  - Harhaji-Trajković, Ljubica
AU  - Misirkić-Marjanović, Maja
AU  - Janjetovic, Kristina
AU  - Vucicevic, Ljubica
AU  - Kostić Rajačić, Slađana
AU  - Schrattenholz, Andre
AU  - Isaković, Aleksandra
AU  - Šoškić, Vukić
AU  - Trajković, Vladimir
PY  - 2012
UR  - https://cer.ihtm.bg.ac.rs/handle/123456789/1037
AB  - The protective ability of novel arylpiperazine-based dopaminergic ligands against nitric oxide (NO)-mediated neurotoxicity is investigated. The most potent neuroprotective arylpiperazine identified during the study was N-{4-[2-(4-phenyl-piperazin-1-yl)ethyl]-phenyl}picolinamide, which protected SH-SY5Y human neuron-like cells from the proapoptotic effect of NO donor sodium nitroprusside (SNP) by decreasing oxidative stress, mitochondrial membrane depolarization, caspase activation and subsequent phosphatydilserine externalization/DNA fragmentation. The protective effect was associated with the inhibition of proapoptotic (JNK, ERK, AMPK) and activation of antiapoptotic (Akt) signaling pathways, in the absence of interference with intracellular NO accumulation. The neuroprotective action of arylpiperazines was shown to be independent of dopamine receptor binding, as it was not affected by the high-affinity D1/D2 receptor blocker butaclamol. These results reported support the further study of arylpiperazines as potential neuroprotective agents.
PB  - Wiley-V C H Verlag Gmbh, Weinheim
T2  - Chemmedchem
T1  - Arylpiperazine Dopamineric Ligands Protect Neuroblastoma Cells from Nitric Oxide (NO)-Induced Mitochondrial Damage and Apoptosis
VL  - 7
IS  - 3
SP  - 495
EP  - 508
DO  - 10.1002/cmdc.201100537
ER  - 

@article{
author = "Tovilović, Gordana and Zogovic, Nevena and Harhaji-Trajković, Ljubica and Misirkić-Marjanović, Maja and Janjetovic, Kristina and Vucicevic, Ljubica and Kostić Rajačić, Slađana and Schrattenholz, Andre and Isaković, Aleksandra and Šoškić, Vukić and Trajković, Vladimir",
year = "2012",
abstract = "The protective ability of novel arylpiperazine-based dopaminergic ligands against nitric oxide (NO)-mediated neurotoxicity is investigated. The most potent neuroprotective arylpiperazine identified during the study was N-{4-[2-(4-phenyl-piperazin-1-yl)ethyl]-phenyl}picolinamide, which protected SH-SY5Y human neuron-like cells from the proapoptotic effect of NO donor sodium nitroprusside (SNP) by decreasing oxidative stress, mitochondrial membrane depolarization, caspase activation and subsequent phosphatydilserine externalization/DNA fragmentation. The protective effect was associated with the inhibition of proapoptotic (JNK, ERK, AMPK) and activation of antiapoptotic (Akt) signaling pathways, in the absence of interference with intracellular NO accumulation. The neuroprotective action of arylpiperazines was shown to be independent of dopamine receptor binding, as it was not affected by the high-affinity D1/D2 receptor blocker butaclamol. These results reported support the further study of arylpiperazines as potential neuroprotective agents.",
publisher = "Wiley-V C H Verlag Gmbh, Weinheim",
journal = "Chemmedchem",
title = "Arylpiperazine Dopamineric Ligands Protect Neuroblastoma Cells from Nitric Oxide (NO)-Induced Mitochondrial Damage and Apoptosis",
volume = "7",
number = "3",
pages = "495-508",
doi = "10.1002/cmdc.201100537"
}

Tovilović, G., Zogovic, N., Harhaji-Trajković, L., Misirkić-Marjanović, M., Janjetovic, K., Vucicevic, L., Kostić Rajačić, S., Schrattenholz, A., Isaković, A., Šoškić, V.,& Trajković, V.. (2012). Arylpiperazine Dopamineric Ligands Protect Neuroblastoma Cells from Nitric Oxide (NO)-Induced Mitochondrial Damage and Apoptosis. in Chemmedchem
Wiley-V C H Verlag Gmbh, Weinheim., 7(3), 495-508.
https://doi.org/10.1002/cmdc.201100537

Tovilović G, Zogovic N, Harhaji-Trajković L, Misirkić-Marjanović M, Janjetovic K, Vucicevic L, Kostić Rajačić S, Schrattenholz A, Isaković A, Šoškić V, Trajković V. Arylpiperazine Dopamineric Ligands Protect Neuroblastoma Cells from Nitric Oxide (NO)-Induced Mitochondrial Damage and Apoptosis. in Chemmedchem. 2012;7(3):495-508.
doi:10.1002/cmdc.201100537 .

Tovilović, Gordana, Zogovic, Nevena, Harhaji-Trajković, Ljubica, Misirkić-Marjanović, Maja, Janjetovic, Kristina, Vucicevic, Ljubica, Kostić Rajačić, Slađana, Schrattenholz, Andre, Isaković, Aleksandra, Šoškić, Vukić, Trajković, Vladimir, "Arylpiperazine Dopamineric Ligands Protect Neuroblastoma Cells from Nitric Oxide (NO)-Induced Mitochondrial Damage and Apoptosis" in Chemmedchem, 7, no. 3 (2012):495-508,
https://doi.org/10.1002/cmdc.201100537 . .

TY  - JOUR
AU  - Trmcic, Milena V.
AU  - Matović, Radomir
AU  - Tovilović, Gordana
AU  - Ristic, Biljana Z.
AU  - Trajković, Vladimir
AU  - Ferjančić, Zorana
AU  - Saičić, Radomir N.
PY  - 2012
UR  - https://cer.ihtm.bg.ac.rs/handle/123456789/981
AB  - The design, synthesis and biological evaluation of a novel C, D-spirolactone analogue of paclitaxel is described. This is the first paclitaxel analogue without an oxetane D-ring that shows a significant cytotoxic effect (activity one order of magnitude lower than paclitaxel). More importantly, its cytotoxicity is a result of a different mechanism of action, involving mTOR inhibition-dependent autophagy instead of G(2)/M cell cycle arrest-dependent apoptosis.
PB  - Royal Soc Chemistry, Cambridge
T2  - Organic & Biomolecular Chemistry
T1  - A novel C,D-spirolactone analogue of paclitaxel: autophagy instead of apoptosis as a previously unknown mechanism of cytotoxic action for taxoids
VL  - 10
IS  - 25
SP  - 4933
EP  - 4942
DO  - 10.1039/c2ob25514f
ER  - 

@article{
author = "Trmcic, Milena V. and Matović, Radomir and Tovilović, Gordana and Ristic, Biljana Z. and Trajković, Vladimir and Ferjančić, Zorana and Saičić, Radomir N.",
year = "2012",
abstract = "The design, synthesis and biological evaluation of a novel C, D-spirolactone analogue of paclitaxel is described. This is the first paclitaxel analogue without an oxetane D-ring that shows a significant cytotoxic effect (activity one order of magnitude lower than paclitaxel). More importantly, its cytotoxicity is a result of a different mechanism of action, involving mTOR inhibition-dependent autophagy instead of G(2)/M cell cycle arrest-dependent apoptosis.",
publisher = "Royal Soc Chemistry, Cambridge",
journal = "Organic & Biomolecular Chemistry",
title = "A novel C,D-spirolactone analogue of paclitaxel: autophagy instead of apoptosis as a previously unknown mechanism of cytotoxic action for taxoids",
volume = "10",
number = "25",
pages = "4933-4942",
doi = "10.1039/c2ob25514f"
}

Trmcic, M. V., Matović, R., Tovilović, G., Ristic, B. Z., Trajković, V., Ferjančić, Z.,& Saičić, R. N.. (2012). A novel C,D-spirolactone analogue of paclitaxel: autophagy instead of apoptosis as a previously unknown mechanism of cytotoxic action for taxoids. in Organic & Biomolecular Chemistry
Royal Soc Chemistry, Cambridge., 10(25), 4933-4942.
https://doi.org/10.1039/c2ob25514f

Trmcic MV, Matović R, Tovilović G, Ristic BZ, Trajković V, Ferjančić Z, Saičić RN. A novel C,D-spirolactone analogue of paclitaxel: autophagy instead of apoptosis as a previously unknown mechanism of cytotoxic action for taxoids. in Organic & Biomolecular Chemistry. 2012;10(25):4933-4942.
doi:10.1039/c2ob25514f .

Trmcic, Milena V., Matović, Radomir, Tovilović, Gordana, Ristic, Biljana Z., Trajković, Vladimir, Ferjančić, Zorana, Saičić, Radomir N., "A novel C,D-spirolactone analogue of paclitaxel: autophagy instead of apoptosis as a previously unknown mechanism of cytotoxic action for taxoids" in Organic & Biomolecular Chemistry, 10, no. 25 (2012):4933-4942,
https://doi.org/10.1039/c2ob25514f . .

TY  - JOUR
AU  - Isaković, Aleksandra
AU  - Janković, Teodora
AU  - Harhaji, Ljubica
AU  - Kostić Rajačić, Slađana
AU  - Nikolić, Zoran
AU  - Vajs, Vlatka
AU  - Trajković, Vladimir
PY  - 2008
UR  - https://cer.ihtm.bg.ac.rs/handle/123456789/478
AB  - The present study identifies xanthones gentiakochianin and gentiacaulein as the active principles responsible for the in vitro antiglioma action of ether and methanolic extracts of the plant Gentiana kochiana. Gentiakochianin and gentiacaulein induced cell cycle arrest in G2/M and G0/G1 phases, respectively, in both C6 rat glioma and U251 human glioma cell lines. The more efficient antiproliferative action of gentiakochianin was associated with its ability to induce microtubule stabilization in a cell-free assay. Both the xanthones reduced mitochondrial membrane potential and increased the production of reactive oxygen species in glioma cells, but only the effects of gentiakochianin were pronounced enough to cause caspase activation and subsequent apoptotic cell death. The assessment of structure-activity relationship in a series of structurally related xanthones from G. kochiana and Gentianella austriaca revealed dihydroxylation at positions 7, 8 of the xanthonic nucleus as the key structural feature responsible for the ability of gentiakochianin to induce microtubule-associated G2/M cell block and apoptotic cell death in glioma cells.
PB  - Oxford : Pergamon-Elsevier Science Ltd
T2  - Bioorganic and Medicinal Chemistry
T1  - Antiglioma action of xanthones from Gentiana kochiana: Mechanistic and structure-activity requirements
VL  - 16
IS  - 10
SP  - 5683
EP  - 5694
DO  - 10.1016/j.bmc.2008.03.069
ER  - 

@article{
author = "Isaković, Aleksandra and Janković, Teodora and Harhaji, Ljubica and Kostić Rajačić, Slađana and Nikolić, Zoran and Vajs, Vlatka and Trajković, Vladimir",
year = "2008",
abstract = "The present study identifies xanthones gentiakochianin and gentiacaulein as the active principles responsible for the in vitro antiglioma action of ether and methanolic extracts of the plant Gentiana kochiana. Gentiakochianin and gentiacaulein induced cell cycle arrest in G2/M and G0/G1 phases, respectively, in both C6 rat glioma and U251 human glioma cell lines. The more efficient antiproliferative action of gentiakochianin was associated with its ability to induce microtubule stabilization in a cell-free assay. Both the xanthones reduced mitochondrial membrane potential and increased the production of reactive oxygen species in glioma cells, but only the effects of gentiakochianin were pronounced enough to cause caspase activation and subsequent apoptotic cell death. The assessment of structure-activity relationship in a series of structurally related xanthones from G. kochiana and Gentianella austriaca revealed dihydroxylation at positions 7, 8 of the xanthonic nucleus as the key structural feature responsible for the ability of gentiakochianin to induce microtubule-associated G2/M cell block and apoptotic cell death in glioma cells.",
publisher = "Oxford : Pergamon-Elsevier Science Ltd",
journal = "Bioorganic and Medicinal Chemistry",
title = "Antiglioma action of xanthones from Gentiana kochiana: Mechanistic and structure-activity requirements",
volume = "16",
number = "10",
pages = "5683-5694",
doi = "10.1016/j.bmc.2008.03.069"
}

Isaković, A., Janković, T., Harhaji, L., Kostić Rajačić, S., Nikolić, Z., Vajs, V.,& Trajković, V.. (2008). Antiglioma action of xanthones from Gentiana kochiana: Mechanistic and structure-activity requirements. in Bioorganic and Medicinal Chemistry
Oxford : Pergamon-Elsevier Science Ltd., 16(10), 5683-5694.
https://doi.org/10.1016/j.bmc.2008.03.069

Isaković A, Janković T, Harhaji L, Kostić Rajačić S, Nikolić Z, Vajs V, Trajković V. Antiglioma action of xanthones from Gentiana kochiana: Mechanistic and structure-activity requirements. in Bioorganic and Medicinal Chemistry. 2008;16(10):5683-5694.
doi:10.1016/j.bmc.2008.03.069 .

Isaković, Aleksandra, Janković, Teodora, Harhaji, Ljubica, Kostić Rajačić, Slađana, Nikolić, Zoran, Vajs, Vlatka, Trajković, Vladimir, "Antiglioma action of xanthones from Gentiana kochiana: Mechanistic and structure-activity requirements" in Bioorganic and Medicinal Chemistry, 16, no. 10 (2008):5683-5694,
https://doi.org/10.1016/j.bmc.2008.03.069 . .

TY  - JOUR
AU  - Isaković, Aleksandra
AU  - Marković, Zoran M.
AU  - Nikolić, Nadežda
AU  - Todorović-Marković, Biljana
AU  - Vranješ-Đurić, Sanja
AU  - Harhaji, Ljubica
AU  - Raičević, Nevena
AU  - Romčević, Nebojša
AU  - Vasiljević-Radović, Dana
AU  - Dramićanin, Miroslav
AU  - Trajković, Vladimir
PY  - 2006
UR  - https://cer.ihtm.bg.ac.rs/handle/123456789/4120
AB  - We investigated the effect of γ-irradiation on the cytotoxicity of pure C 60 solubilized in water by using tetrahydrofuran (THF/n-C 60 or THF/n-C 60 ). In contrast to THF/n-C 60 , its γ-irradiated counterpart failed to generate oxygen radicals and cause extracellular signal-regulated kinase (ERK)-dependent necrotic cell death in various types of mammalian cells. Moreover, γ-irradiated THF/n-C 60 protected cells from the oxidative stress induced by native THF/n-C 60 or hydrogen peroxide. The observed biological effects were associated with γ-irradiation-mediated decomposition of THF and subsequent derivatization of the n-C 60 surface. These results for the first time demonstrate γ-irradiation-mediated changes in the physico-chemical properties of THF-prepared nanocrystalline C 60 , resulting in a complete loss of its cytotoxic effect and its conversion to a cytoprotective agent.
PB  - Elsevier
T2  - Biomaterials
T1  - Inactivation of nanocrystalline C60 cytotoxicity by γ-irradiation
VL  - 27
IS  - 29
SP  - 5049
EP  - 5058
DO  - 10.1016/j.biomaterials.2006.05.047
ER  - 

@article{
author = "Isaković, Aleksandra and Marković, Zoran M. and Nikolić, Nadežda and Todorović-Marković, Biljana and Vranješ-Đurić, Sanja and Harhaji, Ljubica and Raičević, Nevena and Romčević, Nebojša and Vasiljević-Radović, Dana and Dramićanin, Miroslav and Trajković, Vladimir",
year = "2006",
abstract = "We investigated the effect of γ-irradiation on the cytotoxicity of pure C 60 solubilized in water by using tetrahydrofuran (THF/n-C 60 or THF/n-C 60 ). In contrast to THF/n-C 60 , its γ-irradiated counterpart failed to generate oxygen radicals and cause extracellular signal-regulated kinase (ERK)-dependent necrotic cell death in various types of mammalian cells. Moreover, γ-irradiated THF/n-C 60 protected cells from the oxidative stress induced by native THF/n-C 60 or hydrogen peroxide. The observed biological effects were associated with γ-irradiation-mediated decomposition of THF and subsequent derivatization of the n-C 60 surface. These results for the first time demonstrate γ-irradiation-mediated changes in the physico-chemical properties of THF-prepared nanocrystalline C 60 , resulting in a complete loss of its cytotoxic effect and its conversion to a cytoprotective agent.",
publisher = "Elsevier",
journal = "Biomaterials",
title = "Inactivation of nanocrystalline C60 cytotoxicity by γ-irradiation",
volume = "27",
number = "29",
pages = "5049-5058",
doi = "10.1016/j.biomaterials.2006.05.047"
}

Isaković, A., Marković, Z. M., Nikolić, N., Todorović-Marković, B., Vranješ-Đurić, S., Harhaji, L., Raičević, N., Romčević, N., Vasiljević-Radović, D., Dramićanin, M.,& Trajković, V.. (2006). Inactivation of nanocrystalline C60 cytotoxicity by γ-irradiation. in Biomaterials
Elsevier., 27(29), 5049-5058.
https://doi.org/10.1016/j.biomaterials.2006.05.047

Isaković A, Marković ZM, Nikolić N, Todorović-Marković B, Vranješ-Đurić S, Harhaji L, Raičević N, Romčević N, Vasiljević-Radović D, Dramićanin M, Trajković V. Inactivation of nanocrystalline C60 cytotoxicity by γ-irradiation. in Biomaterials. 2006;27(29):5049-5058.
doi:10.1016/j.biomaterials.2006.05.047 .

Isaković, Aleksandra, Marković, Zoran M., Nikolić, Nadežda, Todorović-Marković, Biljana, Vranješ-Đurić, Sanja, Harhaji, Ljubica, Raičević, Nevena, Romčević, Nebojša, Vasiljević-Radović, Dana, Dramićanin, Miroslav, Trajković, Vladimir, "Inactivation of nanocrystalline C60 cytotoxicity by γ-irradiation" in Biomaterials, 27, no. 29 (2006):5049-5058,
https://doi.org/10.1016/j.biomaterials.2006.05.047 . .

TY  - JOUR
AU  - Ferjančić, Zorana
AU  - Matović, Radomir
AU  - Čeković, Živorad
AU  - Jiang, Yi
AU  - Snyder, James P.
AU  - Trajković, Vladimir
AU  - Saičić, Radomir N.
PY  - 2006
UR  - https://cer.ihtm.bg.ac.rs/handle/123456789/2772
AB  - A C,D-seco-paclitaxel derivative 26 was prepared from taxine and tested for biological activity. Chemical reactivity of the seco-compounds proved to be substantially modified, with respects to taxoids. The corresponding C,D-seco-taxoid does not show tubulin stabilizing activity or cytotoxicity. Explanation of these observations based on molecular modeling is provided. (c) 2006 Elsevier Ltd. All rights reserved.
PB  - Oxford : Pergamon-Elsevier Science Ltd
T2  - Tetrahedron
T1  - Synthesis, biology, and modeling of a C-4 carbonyl C,D-seco-taxoid
VL  - 62
IS  - 36
SP  - 8503
EP  - 8514
DO  - 10.1016/j.tet.2006.06.080
ER  - 

@article{
author = "Ferjančić, Zorana and Matović, Radomir and Čeković, Živorad and Jiang, Yi and Snyder, James P. and Trajković, Vladimir and Saičić, Radomir N.",
year = "2006",
abstract = "A C,D-seco-paclitaxel derivative 26 was prepared from taxine and tested for biological activity. Chemical reactivity of the seco-compounds proved to be substantially modified, with respects to taxoids. The corresponding C,D-seco-taxoid does not show tubulin stabilizing activity or cytotoxicity. Explanation of these observations based on molecular modeling is provided. (c) 2006 Elsevier Ltd. All rights reserved.",
publisher = "Oxford : Pergamon-Elsevier Science Ltd",
journal = "Tetrahedron",
title = "Synthesis, biology, and modeling of a C-4 carbonyl C,D-seco-taxoid",
volume = "62",
number = "36",
pages = "8503-8514",
doi = "10.1016/j.tet.2006.06.080"
}

Ferjančić, Z., Matović, R., Čeković, Ž., Jiang, Y., Snyder, J. P., Trajković, V.,& Saičić, R. N.. (2006). Synthesis, biology, and modeling of a C-4 carbonyl C,D-seco-taxoid. in Tetrahedron
Oxford : Pergamon-Elsevier Science Ltd., 62(36), 8503-8514.
https://doi.org/10.1016/j.tet.2006.06.080

Ferjančić Z, Matović R, Čeković Ž, Jiang Y, Snyder JP, Trajković V, Saičić RN. Synthesis, biology, and modeling of a C-4 carbonyl C,D-seco-taxoid. in Tetrahedron. 2006;62(36):8503-8514.
doi:10.1016/j.tet.2006.06.080 .

Ferjančić, Zorana, Matović, Radomir, Čeković, Živorad, Jiang, Yi, Snyder, James P., Trajković, Vladimir, Saičić, Radomir N., "Synthesis, biology, and modeling of a C-4 carbonyl C,D-seco-taxoid" in Tetrahedron, 62, no. 36 (2006):8503-8514,
https://doi.org/10.1016/j.tet.2006.06.080 . .