TY  - JOUR
AU  - Topalović Žukovec, Dijana
AU  - Živković, Lada
AU  - Čabarkapa, Andrea
AU  - Đelić, Ninoslav
AU  - Bajić, Vladan P.
AU  - Dekanski, Dragana
AU  - Spremo-Potparević, Biljana
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/432
AB  - The thyroid hormones change the rate of basal metabolism, modulating the consumption of oxygen and causing production of reactive oxygen species, which leads to the development of oxidative stress and DNA strand breaks. Olive (Olea europaea L.) leaf contains many potentially bioactive compounds, making it one of the most potent natural antioxidants. The objective of this study was to evaluate the genotoxicity of L-thyroxine and to investigate antioxidative and antigenotoxic potential of the standardized oleuropein-rich dry olive leaf extract (DOLE) against hydrogen peroxide and L-thyroxine-induced DNA damage in human peripheral blood leukocytes by using the comet assay. Various concentrations of the extract were tested with both DNA damage inducers, under two different experimental conditions, pretreatment and posttreatment. Results indicate that L-thyroxine exhibited genotoxic effect and that DOLE displayed protective effect against thyroxine-induced genotoxicity. The number of cells with DNA damage, was significantly reduced, in both pretreated and posttreated samples (P LT 0.05). Comparing the beneficial effect of all tested concentrations of DOLE, in both experimental protocols, it appears that extract was more effective in reducing DNA damage in the pretreatment, exhibiting protective role against L-thyroxine effect. This feature of DOLE can be explained by its capacity to act as potent free radical scavenger.
T2  - Oxidative Medicine and Cellular Longevity
T1  - Dry Olive Leaf Extract Counteracts L-Thyroxine-Induced Genotoxicity in Human Peripheral Blood Leukocytes In Vitro
DO  - 10.1155/2015/762192
ER  - 

@article{
author = "Topalović Žukovec, Dijana and Živković, Lada and Čabarkapa, Andrea and Đelić, Ninoslav and Bajić, Vladan P. and Dekanski, Dragana and Spremo-Potparević, Biljana",
year = "2015",
abstract = "The thyroid hormones change the rate of basal metabolism, modulating the consumption of oxygen and causing production of reactive oxygen species, which leads to the development of oxidative stress and DNA strand breaks. Olive (Olea europaea L.) leaf contains many potentially bioactive compounds, making it one of the most potent natural antioxidants. The objective of this study was to evaluate the genotoxicity of L-thyroxine and to investigate antioxidative and antigenotoxic potential of the standardized oleuropein-rich dry olive leaf extract (DOLE) against hydrogen peroxide and L-thyroxine-induced DNA damage in human peripheral blood leukocytes by using the comet assay. Various concentrations of the extract were tested with both DNA damage inducers, under two different experimental conditions, pretreatment and posttreatment. Results indicate that L-thyroxine exhibited genotoxic effect and that DOLE displayed protective effect against thyroxine-induced genotoxicity. The number of cells with DNA damage, was significantly reduced, in both pretreated and posttreated samples (P LT 0.05). Comparing the beneficial effect of all tested concentrations of DOLE, in both experimental protocols, it appears that extract was more effective in reducing DNA damage in the pretreatment, exhibiting protective role against L-thyroxine effect. This feature of DOLE can be explained by its capacity to act as potent free radical scavenger.",
journal = "Oxidative Medicine and Cellular Longevity",
title = "Dry Olive Leaf Extract Counteracts L-Thyroxine-Induced Genotoxicity in Human Peripheral Blood Leukocytes In Vitro",
doi = "10.1155/2015/762192"
}

Topalović Žukovec, D., Živković, L., Čabarkapa, A., Đelić, N., Bajić, V. P., Dekanski, D.,& Spremo-Potparević, B.. (2015). Dry Olive Leaf Extract Counteracts L-Thyroxine-Induced Genotoxicity in Human Peripheral Blood Leukocytes In Vitro. in Oxidative Medicine and Cellular Longevity.
https://doi.org/10.1155/2015/762192

Topalović Žukovec D, Živković L, Čabarkapa A, Đelić N, Bajić VP, Dekanski D, Spremo-Potparević B. Dry Olive Leaf Extract Counteracts L-Thyroxine-Induced Genotoxicity in Human Peripheral Blood Leukocytes In Vitro. in Oxidative Medicine and Cellular Longevity. 2015;.
doi:10.1155/2015/762192 .

Topalović Žukovec, Dijana, Živković, Lada, Čabarkapa, Andrea, Đelić, Ninoslav, Bajić, Vladan P., Dekanski, Dragana, Spremo-Potparević, Biljana, "Dry Olive Leaf Extract Counteracts L-Thyroxine-Induced Genotoxicity in Human Peripheral Blood Leukocytes In Vitro" in Oxidative Medicine and Cellular Longevity (2015),
https://doi.org/10.1155/2015/762192 . .

TY  - JOUR
AU  - Popovic Bubujuk, Slavica
AU  - Bojat, Nenad C.
AU  - Đelić, Ninoslav
AU  - Dronjak, Slađana
AU  - Kostadinovic, Ljiljana
AU  - Coghill Galonja, Tamara
AU  - Anđelković, Marko
PY  - 2013
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/5852
AB  - Cadmium (Cd) is highly toxic heavy metal which may cause severe biological effects in vivo and in vitro. In this study, an evaluation of the acute Cd ability to trigger micronuclei (MNi) formation was carried out on 3-month-old male and female Albino Oxford (AO) rats using micronucleus (MN) test. Experimental animals were treated intraperitoneally with three different concentrations of cadmium chloride (CdCl2): 0.5, 1, and 2 mg CdCl2 per kg of body weight. Control animals received equal volume of sterile phosphate buffered saline. The results showed that 2 mg CdCl2 per kg b.w. concentration caused a highly statistically significant (P LT 0.001) increase in MNi formation in the bone marrow polychromatic erythrocytes (PCEs), exerting a clear-cut concentration-dependent effect. Lower concentrations of CdCl2 used (0.5 and 1 mg/kg b.w.) also caused MNi formation, but with lower statistical significance. Sex differences in MNi production in bone marrow PCEs after acute exposure to different experimental concentrations of CdCl2 were not observed in our study. Our results indicate the ability of CdCl2 to exerts genotoxic effects in bone marrow of AO rats, and complement previous data on the genotoxicity of this important environmental contaminant, burdening the body from different sources-major being industrial exposure, food and cigarette smoking.
T2  - Genetika
T1  - The Effect of Different Acute Concentrations of Cadmium Chloride on the Frequency of Micronuclei in Ao Rats
VL  - 45
IS  - 3
SP  - 727
EP  - 736
DO  - 10.2298/GENSR1303727B
ER  - 

@article{
author = "Popovic Bubujuk, Slavica and Bojat, Nenad C. and Đelić, Ninoslav and Dronjak, Slađana and Kostadinovic, Ljiljana and Coghill Galonja, Tamara and Anđelković, Marko",
year = "2013",
abstract = "Cadmium (Cd) is highly toxic heavy metal which may cause severe biological effects in vivo and in vitro. In this study, an evaluation of the acute Cd ability to trigger micronuclei (MNi) formation was carried out on 3-month-old male and female Albino Oxford (AO) rats using micronucleus (MN) test. Experimental animals were treated intraperitoneally with three different concentrations of cadmium chloride (CdCl2): 0.5, 1, and 2 mg CdCl2 per kg of body weight. Control animals received equal volume of sterile phosphate buffered saline. The results showed that 2 mg CdCl2 per kg b.w. concentration caused a highly statistically significant (P LT 0.001) increase in MNi formation in the bone marrow polychromatic erythrocytes (PCEs), exerting a clear-cut concentration-dependent effect. Lower concentrations of CdCl2 used (0.5 and 1 mg/kg b.w.) also caused MNi formation, but with lower statistical significance. Sex differences in MNi production in bone marrow PCEs after acute exposure to different experimental concentrations of CdCl2 were not observed in our study. Our results indicate the ability of CdCl2 to exerts genotoxic effects in bone marrow of AO rats, and complement previous data on the genotoxicity of this important environmental contaminant, burdening the body from different sources-major being industrial exposure, food and cigarette smoking.",
journal = "Genetika",
title = "The Effect of Different Acute Concentrations of Cadmium Chloride on the Frequency of Micronuclei in Ao Rats",
volume = "45",
number = "3",
pages = "727-736",
doi = "10.2298/GENSR1303727B"
}

Popovic Bubujuk, S., Bojat, N. C., Đelić, N., Dronjak, S., Kostadinovic, L., Coghill Galonja, T.,& Anđelković, M.. (2013). The Effect of Different Acute Concentrations of Cadmium Chloride on the Frequency of Micronuclei in Ao Rats. in Genetika, 45(3), 727-736.
https://doi.org/10.2298/GENSR1303727B

Popovic Bubujuk S, Bojat NC, Đelić N, Dronjak S, Kostadinovic L, Coghill Galonja T, Anđelković M. The Effect of Different Acute Concentrations of Cadmium Chloride on the Frequency of Micronuclei in Ao Rats. in Genetika. 2013;45(3):727-736.
doi:10.2298/GENSR1303727B .

Popovic Bubujuk, Slavica, Bojat, Nenad C., Đelić, Ninoslav, Dronjak, Slađana, Kostadinovic, Ljiljana, Coghill Galonja, Tamara, Anđelković, Marko, "The Effect of Different Acute Concentrations of Cadmium Chloride on the Frequency of Micronuclei in Ao Rats" in Genetika, 45, no. 3 (2013):727-736,
https://doi.org/10.2298/GENSR1303727B . .

TY  - JOUR
AU  - Bajić, Vladan P.
AU  - Su, Bo
AU  - Lee, Hyoung-Gon
AU  - Kudo, Wataru
AU  - Siedlak, Sandra L.
AU  - Živković, Lada
AU  - Spremo-Potparević, Biljana
AU  - Đelić, Ninoslav
AU  - Milicević, Zorana
AU  - Singh, Avneet K.
AU  - Fahmy, Lara M.
AU  - Wang, Xinglong
AU  - Smith, Mark A.
AU  - Zhu, Xiongwei
PY  - 2011
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4429
AB  - Post-mitotic neurons are typically terminally differentiated and in a quiescent status. However, in Alzheimer disease (AD), many neurons display ectopic re-expression of cell cycle-related proteins. Cyclin-dependent kinase 11 (CDK11) mRNA produces a 110-kDa protein (CDK11(p110)) throughout the cell cycle, a 58-kDa protein (CDK11(p58)) that is specifically translated from an internal ribosome entry site and expressed only in the G(2)/M phase of the cell cycle, and a 46-kDa protein (CDK11(p46)) that is considered to be apoptosis specific. CDK11 is required for sister chromatid cohesion and the completion of mitosis. In this study, we found that the expression patterns of CDK11 vary such that cytoplasmic CDK11 is increased in AD cellular processes, compared to a pronounced nuclear expression pattern in most controls. We also investigated the effect of amyloid precursor protein (APP) on CDK11 expression in vitro by using M17 cells overexpressing wild-type APP and APP Swedish mutant phenotype and found increased CDK11 expression compared to empty vector. In addition, amyloid-beta(25-35) resulted in increased CDK11 in M17 cells. These data suggest that CDK11 may play a vital role in cell cycle re-entry in AD neurons in an APP-dependent manner, thus presenting an intriguing novel function of the APP signaling pathway in AD.
T2  - Cellular and Molecular Biology Letters
T1  - Mislocalization of CDK11/PITSLRE, a regulator of the G2/M phase of the cell cycle, in Alzheimer disease
VL  - 16
IS  - 3
SP  - 359
EP  - 372
DO  - 10.2478/s11658-011-0011-2
ER  - 

@article{
author = "Bajić, Vladan P. and Su, Bo and Lee, Hyoung-Gon and Kudo, Wataru and Siedlak, Sandra L. and Živković, Lada and Spremo-Potparević, Biljana and Đelić, Ninoslav and Milicević, Zorana and Singh, Avneet K. and Fahmy, Lara M. and Wang, Xinglong and Smith, Mark A. and Zhu, Xiongwei",
year = "2011",
abstract = "Post-mitotic neurons are typically terminally differentiated and in a quiescent status. However, in Alzheimer disease (AD), many neurons display ectopic re-expression of cell cycle-related proteins. Cyclin-dependent kinase 11 (CDK11) mRNA produces a 110-kDa protein (CDK11(p110)) throughout the cell cycle, a 58-kDa protein (CDK11(p58)) that is specifically translated from an internal ribosome entry site and expressed only in the G(2)/M phase of the cell cycle, and a 46-kDa protein (CDK11(p46)) that is considered to be apoptosis specific. CDK11 is required for sister chromatid cohesion and the completion of mitosis. In this study, we found that the expression patterns of CDK11 vary such that cytoplasmic CDK11 is increased in AD cellular processes, compared to a pronounced nuclear expression pattern in most controls. We also investigated the effect of amyloid precursor protein (APP) on CDK11 expression in vitro by using M17 cells overexpressing wild-type APP and APP Swedish mutant phenotype and found increased CDK11 expression compared to empty vector. In addition, amyloid-beta(25-35) resulted in increased CDK11 in M17 cells. These data suggest that CDK11 may play a vital role in cell cycle re-entry in AD neurons in an APP-dependent manner, thus presenting an intriguing novel function of the APP signaling pathway in AD.",
journal = "Cellular and Molecular Biology Letters",
title = "Mislocalization of CDK11/PITSLRE, a regulator of the G2/M phase of the cell cycle, in Alzheimer disease",
volume = "16",
number = "3",
pages = "359-372",
doi = "10.2478/s11658-011-0011-2"
}

Bajić, V. P., Su, B., Lee, H., Kudo, W., Siedlak, S. L., Živković, L., Spremo-Potparević, B., Đelić, N., Milicević, Z., Singh, A. K., Fahmy, L. M., Wang, X., Smith, M. A.,& Zhu, X.. (2011). Mislocalization of CDK11/PITSLRE, a regulator of the G2/M phase of the cell cycle, in Alzheimer disease. in Cellular and Molecular Biology Letters, 16(3), 359-372.
https://doi.org/10.2478/s11658-011-0011-2

Bajić VP, Su B, Lee H, Kudo W, Siedlak SL, Živković L, Spremo-Potparević B, Đelić N, Milicević Z, Singh AK, Fahmy LM, Wang X, Smith MA, Zhu X. Mislocalization of CDK11/PITSLRE, a regulator of the G2/M phase of the cell cycle, in Alzheimer disease. in Cellular and Molecular Biology Letters. 2011;16(3):359-372.
doi:10.2478/s11658-011-0011-2 .

Bajić, Vladan P., Su, Bo, Lee, Hyoung-Gon, Kudo, Wataru, Siedlak, Sandra L., Živković, Lada, Spremo-Potparević, Biljana, Đelić, Ninoslav, Milicević, Zorana, Singh, Avneet K., Fahmy, Lara M., Wang, Xinglong, Smith, Mark A., Zhu, Xiongwei, "Mislocalization of CDK11/PITSLRE, a regulator of the G2/M phase of the cell cycle, in Alzheimer disease" in Cellular and Molecular Biology Letters, 16, no. 3 (2011):359-372,
https://doi.org/10.2478/s11658-011-0011-2 . .