TY  - JOUR
AU  - Vujačić-Mirski, Ksenija
AU  - Bruns, Kai
AU  - Kalinović, Sanela
AU  - Oelze, Matthias
AU  - Kröller-Schön, Swenja
AU  - Steven, Sebastian
AU  - Mojović, Miloš
AU  - Korać, Bato
AU  - Münzel, Thomas
AU  - Daiber, Andreas
PY  - 2020
UR  - https://www.mdpi.com/2076-3921/9/5/388
UR  - http://www.ncbi.nlm.nih.gov/pubmed/32384768
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3672
AB  - Reactive oxygen and nitrogen species (RONS) cause oxidative damage, which is associated with endothelial dysfunction and cardiovascular disease, but may also contribute to redox signaling. Therefore, their precise detection is important for the evaluation of disease mechanisms. Here, we compared three different methods for the detection of 3-nitrotyrosine (3-NT), a marker of nitro-oxidative stress, in biological samples. Nitrated proteins were generated by incubation with peroxynitrite or 3-morpholino sydnonimine (Sin-1) and subjected to total hydrolysis using pronase, a mixture of different proteases. The 3-NT was then separated by high performance liquid chromatography (HPLC) and quantified by electrochemical detection (ECD, CoulArray) and compared to classical methods, namely enzyme-linked immunosorbent assay (ELISA) and dot blot analysis using specific 3-NT antibodies. Calibration curves for authentic 3-NT (detection limit 10 nM) and a concentration-response pattern for 3-NT obtained from digested nitrated bovine serum albumin (BSA) were highly linear over a wide 3-NT concentration range. Also, ex vivo nitration of protein from heart, isolated mitochondria, and serum/plasma could be quantified using the HPLC/ECD method and was confirmed by LC-MS/MS. Of note, nitro-oxidative damage of mitochondria results in increased superoxide (O2•-) formation rates (measured by dihydroethidium-based HPLC assay), pointing to a self-amplification mechanism of oxidative stress. Based on our ex vivo data, the CoulArray quantification method for 3-NT seems to have some advantages regarding sensitivity and selectivity. Establishing a reliable automated HPLC assay for the routine quantification of 3-NT in biological samples of cell culture, of animal and human origin seems to be more sophisticated than expected.
T2  - Antioxidants (Basel, Switzerland)
T2  - Antioxidants (Basel, Switzerland)
T1  - Development of an Analytical Assay for Electrochemical Detection and Quantification of Protein-Bound 3-Nitrotyrosine in Biological Samples and Comparison with Classical, Antibody-Based Methods.
IS  - 5
VL  - 9
DO  - 10.3390/antiox9050388
SP  - 388
ER  - 

@article{
author = "Vujačić-Mirski, Ksenija and Bruns, Kai and Kalinović, Sanela and Oelze, Matthias and Kröller-Schön, Swenja and Steven, Sebastian and Mojović, Miloš and Korać, Bato and Münzel, Thomas and Daiber, Andreas",
year = "2020",
abstract = "Reactive oxygen and nitrogen species (RONS) cause oxidative damage, which is associated with endothelial dysfunction and cardiovascular disease, but may also contribute to redox signaling. Therefore, their precise detection is important for the evaluation of disease mechanisms. Here, we compared three different methods for the detection of 3-nitrotyrosine (3-NT), a marker of nitro-oxidative stress, in biological samples. Nitrated proteins were generated by incubation with peroxynitrite or 3-morpholino sydnonimine (Sin-1) and subjected to total hydrolysis using pronase, a mixture of different proteases. The 3-NT was then separated by high performance liquid chromatography (HPLC) and quantified by electrochemical detection (ECD, CoulArray) and compared to classical methods, namely enzyme-linked immunosorbent assay (ELISA) and dot blot analysis using specific 3-NT antibodies. Calibration curves for authentic 3-NT (detection limit 10 nM) and a concentration-response pattern for 3-NT obtained from digested nitrated bovine serum albumin (BSA) were highly linear over a wide 3-NT concentration range. Also, ex vivo nitration of protein from heart, isolated mitochondria, and serum/plasma could be quantified using the HPLC/ECD method and was confirmed by LC-MS/MS. Of note, nitro-oxidative damage of mitochondria results in increased superoxide (O2•-) formation rates (measured by dihydroethidium-based HPLC assay), pointing to a self-amplification mechanism of oxidative stress. Based on our ex vivo data, the CoulArray quantification method for 3-NT seems to have some advantages regarding sensitivity and selectivity. Establishing a reliable automated HPLC assay for the routine quantification of 3-NT in biological samples of cell culture, of animal and human origin seems to be more sophisticated than expected.",
journal = "Antioxidants (Basel, Switzerland), Antioxidants (Basel, Switzerland)",
title = "Development of an Analytical Assay for Electrochemical Detection and Quantification of Protein-Bound 3-Nitrotyrosine in Biological Samples and Comparison with Classical, Antibody-Based Methods.",
number = "5",
volume = "9",
doi = "10.3390/antiox9050388",
pages = "388"
}

Vujačić-Mirski, K., Bruns, K., Kalinović, S., Oelze, M., Kröller-Schön, S., Steven, S., Mojović, M., Korać, B., Münzel, T.,& Daiber, A.. (2020). Development of an Analytical Assay for Electrochemical Detection and Quantification of Protein-Bound 3-Nitrotyrosine in Biological Samples and Comparison with Classical, Antibody-Based Methods.. in Antioxidants (Basel, Switzerland), 9(5), 388.
https://doi.org/10.3390/antiox9050388

Vujačić-Mirski K, Bruns K, Kalinović S, Oelze M, Kröller-Schön S, Steven S, Mojović M, Korać B, Münzel T, Daiber A. Development of an Analytical Assay for Electrochemical Detection and Quantification of Protein-Bound 3-Nitrotyrosine in Biological Samples and Comparison with Classical, Antibody-Based Methods.. in Antioxidants (Basel, Switzerland). 2020;9(5):388.
doi:10.3390/antiox9050388 .

Vujačić-Mirski, Ksenija, Bruns, Kai, Kalinović, Sanela, Oelze, Matthias, Kröller-Schön, Swenja, Steven, Sebastian, Mojović, Miloš, Korać, Bato, Münzel, Thomas, Daiber, Andreas, "Development of an Analytical Assay for Electrochemical Detection and Quantification of Protein-Bound 3-Nitrotyrosine in Biological Samples and Comparison with Classical, Antibody-Based Methods." in Antioxidants (Basel, Switzerland), 9, no. 5 (2020):388,
https://doi.org/10.3390/antiox9050388 . .

TY  - JOUR
AU  - Daiber, Andreas
AU  - Kröller-Schön, Swenja
AU  - Frenis, Katie
AU  - Oelze, Matthias
AU  - Kalinović, Sanela
AU  - Vujačić-Mirski, Ksenija
AU  - Kuntić, Marin
AU  - Bayo Jimenez, Maria Teresa
AU  - Helmstädter, Johanna
AU  - Steven, Sebastian
AU  - Korać, Bato
AU  - Münzel, Thomas
PY  - 2019
UR  - https://onlinelibrary.wiley.com/doi/abs/10.1002/biof.1506
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3329
AB  - Environmental noise is a well-recognized health risk and part of the external exposome-the World Health Organization estimates that 1 million healthy life years are lost annually in Western Europe alone due to noise-related complications, including increased incidence of hypertension, heart failure, myocardial infarction, and stroke. Previous data suggest that noise works through two paired pathways in a proposed reaction model for noise exposure. As a nonspecific stressor, chronic low-level noise exposure can cause a disruption of sleep and communication leading to annoyance and subsequent sympathetic and endocrine stress responses leading to increased blood pressure, heart rate, stress hormone levels, and in particular more oxidative stress, being responsible for vascular dysfunction and representing changes of the internal exposome. Chronic stress generates cardiovascular risk factors on its own such as increased blood pressure, blood viscosity, blood glucose, and activation of blood coagulation. To this end, persistent chronic noise exposure increases cardiometabolic diseases, including arterial hypertension, coronary artery disease, arrhythmia, heart failure, diabetes mellitus type 2, and stroke. The present review discusses the mechanisms of the nonauditory noise-induced cardiovascular and metabolic consequences, focusing on mental stress signaling pathways, activation of the hypothalamic-pituitary-adrenocortical axis and sympathetic nervous system, the association of these activations with inflammation, and the subsequent onset of oxidative stress and vascular dysfunction. © 2019 BioFactors, 2019.
T2  - BioFactors (Oxford, England)
T1  - Environmental noise induces the release of stress hormones and inflammatory signaling molecules leading to oxidative stress and vascular dysfunction-Signatures of the internal exposome.
DO  - 10.1002/biof.1506
ER  - 

@article{
author = "Daiber, Andreas and Kröller-Schön, Swenja and Frenis, Katie and Oelze, Matthias and Kalinović, Sanela and Vujačić-Mirski, Ksenija and Kuntić, Marin and Bayo Jimenez, Maria Teresa and Helmstädter, Johanna and Steven, Sebastian and Korać, Bato and Münzel, Thomas",
year = "2019",
abstract = "Environmental noise is a well-recognized health risk and part of the external exposome-the World Health Organization estimates that 1 million healthy life years are lost annually in Western Europe alone due to noise-related complications, including increased incidence of hypertension, heart failure, myocardial infarction, and stroke. Previous data suggest that noise works through two paired pathways in a proposed reaction model for noise exposure. As a nonspecific stressor, chronic low-level noise exposure can cause a disruption of sleep and communication leading to annoyance and subsequent sympathetic and endocrine stress responses leading to increased blood pressure, heart rate, stress hormone levels, and in particular more oxidative stress, being responsible for vascular dysfunction and representing changes of the internal exposome. Chronic stress generates cardiovascular risk factors on its own such as increased blood pressure, blood viscosity, blood glucose, and activation of blood coagulation. To this end, persistent chronic noise exposure increases cardiometabolic diseases, including arterial hypertension, coronary artery disease, arrhythmia, heart failure, diabetes mellitus type 2, and stroke. The present review discusses the mechanisms of the nonauditory noise-induced cardiovascular and metabolic consequences, focusing on mental stress signaling pathways, activation of the hypothalamic-pituitary-adrenocortical axis and sympathetic nervous system, the association of these activations with inflammation, and the subsequent onset of oxidative stress and vascular dysfunction. © 2019 BioFactors, 2019.",
journal = "BioFactors (Oxford, England)",
title = "Environmental noise induces the release of stress hormones and inflammatory signaling molecules leading to oxidative stress and vascular dysfunction-Signatures of the internal exposome.",
doi = "10.1002/biof.1506"
}

Daiber, A., Kröller-Schön, S., Frenis, K., Oelze, M., Kalinović, S., Vujačić-Mirski, K., Kuntić, M., Bayo Jimenez, M. T., Helmstädter, J., Steven, S., Korać, B.,& Münzel, T.. (2019). Environmental noise induces the release of stress hormones and inflammatory signaling molecules leading to oxidative stress and vascular dysfunction-Signatures of the internal exposome.. in BioFactors (Oxford, England).
https://doi.org/10.1002/biof.1506

Daiber A, Kröller-Schön S, Frenis K, Oelze M, Kalinović S, Vujačić-Mirski K, Kuntić M, Bayo Jimenez MT, Helmstädter J, Steven S, Korać B, Münzel T. Environmental noise induces the release of stress hormones and inflammatory signaling molecules leading to oxidative stress and vascular dysfunction-Signatures of the internal exposome.. in BioFactors (Oxford, England). 2019;.
doi:10.1002/biof.1506 .

Daiber, Andreas, Kröller-Schön, Swenja, Frenis, Katie, Oelze, Matthias, Kalinović, Sanela, Vujačić-Mirski, Ksenija, Kuntić, Marin, Bayo Jimenez, Maria Teresa, Helmstädter, Johanna, Steven, Sebastian, Korać, Bato, Münzel, Thomas, "Environmental noise induces the release of stress hormones and inflammatory signaling molecules leading to oxidative stress and vascular dysfunction-Signatures of the internal exposome." in BioFactors (Oxford, England) (2019),
https://doi.org/10.1002/biof.1506 . .