TY  - JOUR
AU  - Jakovljević-Uzelac, Jovana
AU  - Stanić, Marina
AU  - Krstić, Danijela Z.
AU  - Čolović, Mirjana B.
AU  - Đurić, Dragan M.
PY  - 2018
UR  - http://link.springer.com/10.1007/s11010-017-3238-z
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/7788
AB  - The objective of this study was to investigate in vitro effects of 10 A mu M dl-homocysteine (dl-Hcy), dl-homocysteine thiolactone-hydrochloride (dl-Hcy TLHC), and l-homocysteine thiolactone-hydrochloride (l-Hcy TLHC) on the oxygen consumption of rat heart tissue homogenate, as well as the involvement of the gasotransmitters NO, H2S and CO in the effects of the most toxic homocysteine compound, dl-Hcy TLHC. The possible contribution of the gasotransmitters in these effects was estimated by using the appropriate inhibitors of their synthesis (N (omega)-nitro-l-arginine methyl ester (l-NAME), dl-propargylglycine (dl-PAG), and zinc protoporphyrin IX (ZnPPR IX), respectively). The oxygen consumption of rat heart tissue homogenate was measured by Clark/type oxygen electrode in the absence and presence of the investigated compounds. All three homocysteine-based compounds caused a similar decrease in the oxygen consumption rate compared to control: 15.19 +/- 4.01%, 12.42 +/- 1.01%, and 16.43 +/- 4.52% for dl-Hcy, dl-Hcy TLHC, or l-Hcy TLHC, respectively. All applied inhibitors of gasotransmitter synthesis also decreased the oxygen consumption rate of tissue homogenate related to control: 13.53 +/- 1.35% for l-NAME (30 A mu M), 5.32 +/- 1.23% for dl-PAG (10 A mu M), and 5.56 +/- 1.39% for ZnPPR IX (10 A mu M). Simultaneous effect of l-NAME (30 A mu M) or ZnPPR IX (10 A mu M) with dl-Hcy TLHC (10 A mu M) caused a larger decrease of oxygen consumption compared to each of the substances individually. However, when dl-PAG (10 A mu M) was applied together with dl-Hcy TLHC (10 A mu M), it attenuated the effect of dl-Hcy TLHC from 12.42 +/- 1.01 to 9.22 +/- 1.58%. In conclusion, cardiotoxicity induced by Hcy-related compounds, which was shown in our previous research, could result from the inhibition of the oxygen consumption, and might be mediated by the certain gasotransmitters.
T2  - Molecular and Cellular Biochemistry
T1  - Effects of homocysteine and its related compounds on oxygen consumption of the rat heart tissue homogenate: the role of different gasotransmitters
VL  - 444
IS  - 1-2
SP  - 143
EP  - 148
DO  - 10.1007/s11010-017-3238-z
ER  - 

@article{
author = "Jakovljević-Uzelac, Jovana and Stanić, Marina and Krstić, Danijela Z. and Čolović, Mirjana B. and Đurić, Dragan M.",
year = "2018",
abstract = "The objective of this study was to investigate in vitro effects of 10 A mu M dl-homocysteine (dl-Hcy), dl-homocysteine thiolactone-hydrochloride (dl-Hcy TLHC), and l-homocysteine thiolactone-hydrochloride (l-Hcy TLHC) on the oxygen consumption of rat heart tissue homogenate, as well as the involvement of the gasotransmitters NO, H2S and CO in the effects of the most toxic homocysteine compound, dl-Hcy TLHC. The possible contribution of the gasotransmitters in these effects was estimated by using the appropriate inhibitors of their synthesis (N (omega)-nitro-l-arginine methyl ester (l-NAME), dl-propargylglycine (dl-PAG), and zinc protoporphyrin IX (ZnPPR IX), respectively). The oxygen consumption of rat heart tissue homogenate was measured by Clark/type oxygen electrode in the absence and presence of the investigated compounds. All three homocysteine-based compounds caused a similar decrease in the oxygen consumption rate compared to control: 15.19 +/- 4.01%, 12.42 +/- 1.01%, and 16.43 +/- 4.52% for dl-Hcy, dl-Hcy TLHC, or l-Hcy TLHC, respectively. All applied inhibitors of gasotransmitter synthesis also decreased the oxygen consumption rate of tissue homogenate related to control: 13.53 +/- 1.35% for l-NAME (30 A mu M), 5.32 +/- 1.23% for dl-PAG (10 A mu M), and 5.56 +/- 1.39% for ZnPPR IX (10 A mu M). Simultaneous effect of l-NAME (30 A mu M) or ZnPPR IX (10 A mu M) with dl-Hcy TLHC (10 A mu M) caused a larger decrease of oxygen consumption compared to each of the substances individually. However, when dl-PAG (10 A mu M) was applied together with dl-Hcy TLHC (10 A mu M), it attenuated the effect of dl-Hcy TLHC from 12.42 +/- 1.01 to 9.22 +/- 1.58%. In conclusion, cardiotoxicity induced by Hcy-related compounds, which was shown in our previous research, could result from the inhibition of the oxygen consumption, and might be mediated by the certain gasotransmitters.",
journal = "Molecular and Cellular Biochemistry",
title = "Effects of homocysteine and its related compounds on oxygen consumption of the rat heart tissue homogenate: the role of different gasotransmitters",
volume = "444",
number = "1-2",
pages = "143-148",
doi = "10.1007/s11010-017-3238-z"
}

Jakovljević-Uzelac, J., Stanić, M., Krstić, D. Z., Čolović, M. B.,& Đurić, D. M.. (2018). Effects of homocysteine and its related compounds on oxygen consumption of the rat heart tissue homogenate: the role of different gasotransmitters. in Molecular and Cellular Biochemistry, 444(1-2), 143-148.
https://doi.org/10.1007/s11010-017-3238-z

Jakovljević-Uzelac J, Stanić M, Krstić DZ, Čolović MB, Đurić DM. Effects of homocysteine and its related compounds on oxygen consumption of the rat heart tissue homogenate: the role of different gasotransmitters. in Molecular and Cellular Biochemistry. 2018;444(1-2):143-148.
doi:10.1007/s11010-017-3238-z .

Jakovljević-Uzelac, Jovana, Stanić, Marina, Krstić, Danijela Z., Čolović, Mirjana B., Đurić, Dragan M., "Effects of homocysteine and its related compounds on oxygen consumption of the rat heart tissue homogenate: the role of different gasotransmitters" in Molecular and Cellular Biochemistry, 444, no. 1-2 (2018):143-148,
https://doi.org/10.1007/s11010-017-3238-z . .

TY  - CONF
AU  - Jakovljević-Uzelac, Jovana
AU  - Čolović, Mirjana B.
AU  - Krstić, Danijela Z.
AU  - Đurić, Marko
AU  - Đurić, Dragan M.
PY  - 2017
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/7175
C3  - Atherosclerosis
T1  - The Effects of Nitric Oxide Synthase Inhibition Following Acute Administration of Homocysteine on Oxidative Stress Markers in Rat Plasma
VL  - 263
SP  - E137
EP  - E138
DO  - 10.1016/j.atherosclerosis.2017.06.440
ER  - 

@conference{
author = "Jakovljević-Uzelac, Jovana and Čolović, Mirjana B. and Krstić, Danijela Z. and Đurić, Marko and Đurić, Dragan M.",
year = "2017",
journal = "Atherosclerosis",
title = "The Effects of Nitric Oxide Synthase Inhibition Following Acute Administration of Homocysteine on Oxidative Stress Markers in Rat Plasma",
volume = "263",
pages = "E137-E138",
doi = "10.1016/j.atherosclerosis.2017.06.440"
}

Jakovljević-Uzelac, J., Čolović, M. B., Krstić, D. Z., Đurić, M.,& Đurić, D. M.. (2017). The Effects of Nitric Oxide Synthase Inhibition Following Acute Administration of Homocysteine on Oxidative Stress Markers in Rat Plasma. in Atherosclerosis, 263, E137-E138.
https://doi.org/10.1016/j.atherosclerosis.2017.06.440

Jakovljević-Uzelac J, Čolović MB, Krstić DZ, Đurić M, Đurić DM. The Effects of Nitric Oxide Synthase Inhibition Following Acute Administration of Homocysteine on Oxidative Stress Markers in Rat Plasma. in Atherosclerosis. 2017;263:E137-E138.
doi:10.1016/j.atherosclerosis.2017.06.440 .

Jakovljević-Uzelac, Jovana, Čolović, Mirjana B., Krstić, Danijela Z., Đurić, Marko, Đurić, Dragan M., "The Effects of Nitric Oxide Synthase Inhibition Following Acute Administration of Homocysteine on Oxidative Stress Markers in Rat Plasma" in Atherosclerosis, 263 (2017):E137-E138,
https://doi.org/10.1016/j.atherosclerosis.2017.06.440 . .