Grujić-Milanović, Jelica

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  • Grujić-Milanović, Jelica (4)

Author's Bibliography

Oxidative stress status assessment of rats' brains injury following subacute exposure to K-oximes

Jaćević, Vesna; Dumanović, Jelena; Grujić-Milanović, Jelica; Milovanović, Zoran; Amidžić, Ljiljana; Vojinović, Nataša; Nežić, Lana; Marković, Bojan; Dobričić, Vladimir; Milosavljević, Petar; Nepovimova, Eugenie; Kuča, Kamil

(Elsevier B.V., 2023)


                                            

                                            
Jaćević, V., Dumanović, J., Grujić-Milanović, J., Milovanović, Z., Amidžić, L., Vojinović, N., Nežić, L., Marković, B., Dobričić, V., Milosavljević, P., Nepovimova, E.,& Kuča, K.. (2023). Oxidative stress status assessment of rats' brains injury following subacute exposure to K-oximes. in Chemico-biological interactions
Elsevier B.V.., 383, 110658.
https://doi.org/10.1016/j.cbi.2023.110658
Jaćević V, Dumanović J, Grujić-Milanović J, Milovanović Z, Amidžić L, Vojinović N, Nežić L, Marković B, Dobričić V, Milosavljević P, Nepovimova E, Kuča K. Oxidative stress status assessment of rats' brains injury following subacute exposure to K-oximes. in Chemico-biological interactions. 2023;383:110658.
doi:10.1016/j.cbi.2023.110658 .
Jaćević, Vesna, Dumanović, Jelena, Grujić-Milanović, Jelica, Milovanović, Zoran, Amidžić, Ljiljana, Vojinović, Nataša, Nežić, Lana, Marković, Bojan, Dobričić, Vladimir, Milosavljević, Petar, Nepovimova, Eugenie, Kuča, Kamil, "Oxidative stress status assessment of rats' brains injury following subacute exposure to K-oximes" in Chemico-biological interactions, 383 (2023):110658,
https://doi.org/10.1016/j.cbi.2023.110658 . .

Age-dependent role of NMDA receptors in experimental autoimmune encephalomyelitis

Ćuruvija, Ivana; Bufan, Biljana; Đorović, Emilija; Blagojević, Veljko; Grujić-Milanović, Jelica; Marković, Milica; Đuretić, Jasmina

(Federation of European Neuroscience Societies (FENS), 2022)

TY  - CONF
AU  - Ćuruvija, Ivana
AU  - Bufan, Biljana
AU  - Đorović, Emilija
AU  - Blagojević, Veljko
AU  - Grujić-Milanović, Jelica
AU  - Marković, Milica
AU  - Đuretić, Jasmina
PY  - 2022
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/5132
AB  - Aims Ageing affects N-methyl-D-aspartate receptors (NMDARs), their expression and function in neuronal and non-neuronal 
cells. Contribution of NMDARs to pathogenesis of experimental autoimmune encephalomyelitis (EAE) has been investigated 
but further study is still needed. The aim of this study was to determine whether ageing affects the role of NMDARs in EAE. 
Methods Memantine, a non-competitive NMDAR antagonist which limits pathological activity of NMDARs while sparing 
normal synaptic activity, was administered orally from day 7 after immunization to 3- and 24-month-old female Dark Agouti 
rats. The animals were sacrificed at the peak of the disease. Spinal cord mononuclear cells were analyzed by flow cytometry. 
Brain tissue was collected for biochemical analysis of redox status and RT-qPCR. Results Semiprophylactic administration of 
memantine ameliorated clinical disease course, with greater effect in aged rats. Memantine reduced the number, frequency, 
and reactivation of CD4+ T lymphocytes and increased the relative percentage of CX3CR1-expressing microglia in spinal 
cord, but to a greater extent in aged rats. Additionally, analysis of brain redox status parameters showed that memantine was 
more effective in reducing superoxide anion radical, malondialdehyde and advanced oxidation protein products in aged rats 
than in young ones. In accordance with previous findings, NMDAR inhibition by memantine decreased NADPH oxidase and 
IL-1β expression and increased the nuclear factor erythroid 2-related factor 2 and heme oxygenase-1 expression, to a greater 
extent in aged rats. Conclusions The involvement of NMDARs in the pathogenesis of EAE was age-dependent, being more 
pronounced in aged than in young rats.
PB  - Federation of European Neuroscience Societies (FENS)
C3  - FENS Forum 2022, 9 - 13 July, Paris, France, Book of Abstracts
T1  - Age-dependent role of NMDA receptors in experimental autoimmune encephalomyelitis
SP  - S05-250
UR  - https://hdl.handle.net/21.15107/rcub_farfar_5132
ER  - 
@conference{
author = "Ćuruvija, Ivana and Bufan, Biljana and Đorović, Emilija and Blagojević, Veljko and Grujić-Milanović, Jelica and Marković, Milica and Đuretić, Jasmina",
year = "2022",
abstract = "Aims Ageing affects N-methyl-D-aspartate receptors (NMDARs), their expression and function in neuronal and non-neuronal 
cells. Contribution of NMDARs to pathogenesis of experimental autoimmune encephalomyelitis (EAE) has been investigated 
but further study is still needed. The aim of this study was to determine whether ageing affects the role of NMDARs in EAE. 
Methods Memantine, a non-competitive NMDAR antagonist which limits pathological activity of NMDARs while sparing 
normal synaptic activity, was administered orally from day 7 after immunization to 3- and 24-month-old female Dark Agouti 
rats. The animals were sacrificed at the peak of the disease. Spinal cord mononuclear cells were analyzed by flow cytometry. 
Brain tissue was collected for biochemical analysis of redox status and RT-qPCR. Results Semiprophylactic administration of 
memantine ameliorated clinical disease course, with greater effect in aged rats. Memantine reduced the number, frequency, 
and reactivation of CD4+ T lymphocytes and increased the relative percentage of CX3CR1-expressing microglia in spinal 
cord, but to a greater extent in aged rats. Additionally, analysis of brain redox status parameters showed that memantine was 
more effective in reducing superoxide anion radical, malondialdehyde and advanced oxidation protein products in aged rats 
than in young ones. In accordance with previous findings, NMDAR inhibition by memantine decreased NADPH oxidase and 
IL-1β expression and increased the nuclear factor erythroid 2-related factor 2 and heme oxygenase-1 expression, to a greater 
extent in aged rats. Conclusions The involvement of NMDARs in the pathogenesis of EAE was age-dependent, being more 
pronounced in aged than in young rats.",
publisher = "Federation of European Neuroscience Societies (FENS)",
journal = "FENS Forum 2022, 9 - 13 July, Paris, France, Book of Abstracts",
title = "Age-dependent role of NMDA receptors in experimental autoimmune encephalomyelitis",
pages = "S05-250",
url = "https://hdl.handle.net/21.15107/rcub_farfar_5132"
}
Ćuruvija, I., Bufan, B., Đorović, E., Blagojević, V., Grujić-Milanović, J., Marković, M.,& Đuretić, J.. (2022). Age-dependent role of NMDA receptors in experimental autoimmune encephalomyelitis. in FENS Forum 2022, 9 - 13 July, Paris, France, Book of Abstracts
Federation of European Neuroscience Societies (FENS)., S05-250.
https://hdl.handle.net/21.15107/rcub_farfar_5132
Ćuruvija I, Bufan B, Đorović E, Blagojević V, Grujić-Milanović J, Marković M, Đuretić J. Age-dependent role of NMDA receptors in experimental autoimmune encephalomyelitis. in FENS Forum 2022, 9 - 13 July, Paris, France, Book of Abstracts. 2022;:S05-250.
https://hdl.handle.net/21.15107/rcub_farfar_5132 .
Ćuruvija, Ivana, Bufan, Biljana, Đorović, Emilija, Blagojević, Veljko, Grujić-Milanović, Jelica, Marković, Milica, Đuretić, Jasmina, "Age-dependent role of NMDA receptors in experimental autoimmune encephalomyelitis" in FENS Forum 2022, 9 - 13 July, Paris, France, Book of Abstracts (2022):S05-250,
https://hdl.handle.net/21.15107/rcub_farfar_5132 .

DNA, protein and lipid oxidative damage in tissues of spontaneously hypertensive versus normotensive rats

Bruić, Marija; Grujić-Milanović, Jelica; Miloradović, Zoran; Jovović, Đurđica; Živković, Lada; Mihailović-Stanojević, Nevena; Karanović, Danijela; Spremo-Potparević, Biljana

(Elsevier Ltd, 2021)

TY  - JOUR
AU  - Bruić, Marija
AU  - Grujić-Milanović, Jelica
AU  - Miloradović, Zoran
AU  - Jovović, Đurđica
AU  - Živković, Lada
AU  - Mihailović-Stanojević, Nevena
AU  - Karanović, Danijela
AU  - Spremo-Potparević, Biljana
PY  - 2021
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/3981
AB  - Oxidative damage to protein and lipid macromolecules in target organs in hypertension has been recognized as a major factor contributing to cardiovascular, cerebrovascular, and renal diseases. Data on protein and lipid oxidative damage in spontaneously hypertensive rats are numerous, but there is no information on DNA damage in tissues measured by comet assay. The aim of this study was to determine the baseline damage to DNA, protein, and lipid macromolecules in different organs of spontaneously hypertensive rats. Markers of lipid peroxidation, protein oxidation, and DNA damage were measured in blood, heart, kidney, and liver of 24-week-old spontaneously hypertensive rats. Plasma prooxidant and antioxidant status were determined as well. Age-matched normotensive Wistar rats were used as control. A rise in markers of lipid peroxidation and protein oxidation, malondialdehyde, and advanced oxidation protein products, was detected in all tissues of spontaneously hypertensive rats, with particularly high values in the liver. DNA damage, measured by the comet assay, was significantly higher in all the studied tissues of spontaneously hypertensive rats compared to normotensive control, with more severe damage in the cardiac and renal cells. Significant depletion of the plasma antioxidant barrier in spontaneously hypertensive rats was also observed. This study showed increased damage to all macromolecules in all studied samples of spontaneously hypertensive rats in comparison with control Wistar rats.
PB  - Elsevier Ltd
T2  - International Journal of Biochemistry and Cell Biology
T1  - DNA, protein and lipid oxidative damage in tissues of spontaneously hypertensive versus normotensive rats
VL  - 141
DO  - 10.1016/j.biocel.2021.106088
ER  - 
@article{
author = "Bruić, Marija and Grujić-Milanović, Jelica and Miloradović, Zoran and Jovović, Đurđica and Živković, Lada and Mihailović-Stanojević, Nevena and Karanović, Danijela and Spremo-Potparević, Biljana",
year = "2021",
abstract = "Oxidative damage to protein and lipid macromolecules in target organs in hypertension has been recognized as a major factor contributing to cardiovascular, cerebrovascular, and renal diseases. Data on protein and lipid oxidative damage in spontaneously hypertensive rats are numerous, but there is no information on DNA damage in tissues measured by comet assay. The aim of this study was to determine the baseline damage to DNA, protein, and lipid macromolecules in different organs of spontaneously hypertensive rats. Markers of lipid peroxidation, protein oxidation, and DNA damage were measured in blood, heart, kidney, and liver of 24-week-old spontaneously hypertensive rats. Plasma prooxidant and antioxidant status were determined as well. Age-matched normotensive Wistar rats were used as control. A rise in markers of lipid peroxidation and protein oxidation, malondialdehyde, and advanced oxidation protein products, was detected in all tissues of spontaneously hypertensive rats, with particularly high values in the liver. DNA damage, measured by the comet assay, was significantly higher in all the studied tissues of spontaneously hypertensive rats compared to normotensive control, with more severe damage in the cardiac and renal cells. Significant depletion of the plasma antioxidant barrier in spontaneously hypertensive rats was also observed. This study showed increased damage to all macromolecules in all studied samples of spontaneously hypertensive rats in comparison with control Wistar rats.",
publisher = "Elsevier Ltd",
journal = "International Journal of Biochemistry and Cell Biology",
title = "DNA, protein and lipid oxidative damage in tissues of spontaneously hypertensive versus normotensive rats",
volume = "141",
doi = "10.1016/j.biocel.2021.106088"
}
Bruić, M., Grujić-Milanović, J., Miloradović, Z., Jovović, Đ., Živković, L., Mihailović-Stanojević, N., Karanović, D.,& Spremo-Potparević, B.. (2021). DNA, protein and lipid oxidative damage in tissues of spontaneously hypertensive versus normotensive rats. in International Journal of Biochemistry and Cell Biology
Elsevier Ltd., 141.
https://doi.org/10.1016/j.biocel.2021.106088
Bruić M, Grujić-Milanović J, Miloradović Z, Jovović Đ, Živković L, Mihailović-Stanojević N, Karanović D, Spremo-Potparević B. DNA, protein and lipid oxidative damage in tissues of spontaneously hypertensive versus normotensive rats. in International Journal of Biochemistry and Cell Biology. 2021;141.
doi:10.1016/j.biocel.2021.106088 .
Bruić, Marija, Grujić-Milanović, Jelica, Miloradović, Zoran, Jovović, Đurđica, Živković, Lada, Mihailović-Stanojević, Nevena, Karanović, Danijela, Spremo-Potparević, Biljana, "DNA, protein and lipid oxidative damage in tissues of spontaneously hypertensive versus normotensive rats" in International Journal of Biochemistry and Cell Biology, 141 (2021),
https://doi.org/10.1016/j.biocel.2021.106088 . .
9
6

Assessment of DNA damage in blood, liver and kidney cells in a hypertensive rat model using comet assay

Bruić, Marija; Grujić-Milanović, Jelica; Živković, Lada; Topalović, Dijana; Spremo-Potparević, Biljana

(Institute for Genetic Engineering and Biotechnology, University of Sarajevo, 2019)

TY  - CONF
AU  - Bruić, Marija
AU  - Grujić-Milanović, Jelica
AU  - Živković, Lada
AU  - Topalović, Dijana
AU  - Spremo-Potparević, Biljana
PY  - 2019
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/5194
AB  - Hypertension is one of the primary risk factors for heart disease and stroke, the leading causes of death worldwide. Numerous factors have been implicated in the pathophysiology of hypertension: endothelial dysfunction, arterial remodeling and vascular inflammation. Common to all these processes is increased bioavailability of reactive oxygen species in the vessels, heart, brain and kidneys. Oxidative stress and increased reactive oxygen species levels damage all macromolecules, with DNA being particularly susceptible to oxidative damage. The aim of this study was to determine whether there is a difference in the level of DNA damage between normotensive and hypertensive rats using the alkaline comet assay. Blood samples and cells suspension from liver and kidney from three male spontaneously hypertensive rats were obtained. Three normotensive male Wistar rats were used as a control. Increased level of DNA damage was detected in blood and both of the studied tissues of hypertensive rats compared to the control, where significant difference was present in the liver and kidney cell suspensions. These results indicate that untreated hypertension in rats leads to an increased DNA damage in all of the studied samples, detected by comet assay.
PB  - Institute for Genetic Engineering and Biotechnology, University of Sarajevo
C3  - Genetics & Applications
T1  - Assessment of DNA damage in blood, liver and kidney cells in a hypertensive rat model using comet assay
VL  - 3
IS  - 2
SP  - 89
EP  - 89
UR  - https://hdl.handle.net/21.15107/rcub_farfar_5194
ER  - 
@conference{
author = "Bruić, Marija and Grujić-Milanović, Jelica and Živković, Lada and Topalović, Dijana and Spremo-Potparević, Biljana",
year = "2019",
abstract = "Hypertension is one of the primary risk factors for heart disease and stroke, the leading causes of death worldwide. Numerous factors have been implicated in the pathophysiology of hypertension: endothelial dysfunction, arterial remodeling and vascular inflammation. Common to all these processes is increased bioavailability of reactive oxygen species in the vessels, heart, brain and kidneys. Oxidative stress and increased reactive oxygen species levels damage all macromolecules, with DNA being particularly susceptible to oxidative damage. The aim of this study was to determine whether there is a difference in the level of DNA damage between normotensive and hypertensive rats using the alkaline comet assay. Blood samples and cells suspension from liver and kidney from three male spontaneously hypertensive rats were obtained. Three normotensive male Wistar rats were used as a control. Increased level of DNA damage was detected in blood and both of the studied tissues of hypertensive rats compared to the control, where significant difference was present in the liver and kidney cell suspensions. These results indicate that untreated hypertension in rats leads to an increased DNA damage in all of the studied samples, detected by comet assay.",
publisher = "Institute for Genetic Engineering and Biotechnology, University of Sarajevo",
journal = "Genetics & Applications",
title = "Assessment of DNA damage in blood, liver and kidney cells in a hypertensive rat model using comet assay",
volume = "3",
number = "2",
pages = "89-89",
url = "https://hdl.handle.net/21.15107/rcub_farfar_5194"
}
Bruić, M., Grujić-Milanović, J., Živković, L., Topalović, D.,& Spremo-Potparević, B.. (2019). Assessment of DNA damage in blood, liver and kidney cells in a hypertensive rat model using comet assay. in Genetics & Applications
Institute for Genetic Engineering and Biotechnology, University of Sarajevo., 3(2), 89-89.
https://hdl.handle.net/21.15107/rcub_farfar_5194
Bruić M, Grujić-Milanović J, Živković L, Topalović D, Spremo-Potparević B. Assessment of DNA damage in blood, liver and kidney cells in a hypertensive rat model using comet assay. in Genetics & Applications. 2019;3(2):89-89.
https://hdl.handle.net/21.15107/rcub_farfar_5194 .
Bruić, Marija, Grujić-Milanović, Jelica, Živković, Lada, Topalović, Dijana, Spremo-Potparević, Biljana, "Assessment of DNA damage in blood, liver and kidney cells in a hypertensive rat model using comet assay" in Genetics & Applications, 3, no. 2 (2019):89-89,
https://hdl.handle.net/21.15107/rcub_farfar_5194 .