- Email: [email protected]
Reductive stress in pathophysiology
D. Rossin et al. / Free Radical Biology and Medicine 108 (2017) S18–S107
disease patients and in normal individuals at high risk of developing Alzheimer's (because they carry the ApoE4 allele), will be discussed to highlight the role of reductive stress in these pathophysiological processes.
S41
P-071
Taking up the cudgels for the traditional reactive oxygen and nitrogen species detection assays and their use in the cardiovascular system
E-mail address: [email protected] (J. Viña) http://dx.doi.org/10.1016/j.freeradbiomed.2017.04.154
Andreas Daiber, Matthias Oelze, Sebastian Steven, Swenja Kröller-Schön, Thomas Münzel Center for Cardiology 1, University Medical Center Mainz, Germany
P-070
Environmental noise and particulate matter exposure, oxidative stress and vascular function - the underestimated cardiovascular risk factors Andreas Daiber University Medical Center Mainz, Germany Keywords: Environmental risk factors; traffic noise exposure; particulate matter exposure; mental stress; stress hormones; endothelial dysfunction; oxidative stress; hypertension
Epidemiological studies have demonstrated that traffic noise and particulate matter exposure is associated with cardiovascular diseases such as arterial hypertension, myocardial infarction and stroke. Persistent chronic noise and particulate matter exposure increases the risk of cardiovascular and metabolic diseases such as arterial hypertension, coronary artery disease, diabetes and stroke. Data of the Heinz Nixdorf Recall Study (Kälsch et al. Eur. Heart J. 2014) but also large epidemiological studies (reviewed in Münzel et al. Eur. Heart J. 2017) point towards a link between the incidence of ischemic heart diseases and exposure to noise and/or particulate matter, supporting their role as independent cardiovascular risk factors, suggesting synergistic effects by both stressors and warranting further detailed studies to understand the mechanistic basis of this association. Recently, the underlying molecular mechanisms leading to noise-dependent adverse effects on the vasculature were characterized in an animal model of aircraft noise exposure identifying oxidative stress as a central player in mediating vascular dysfunction, which shares striking similarities with the pathomechanisms reported for particulate matter exposure. With the present overview the mechanistic parallels in the pathophysiological processes induced by noise and particulate matter exposure will be discussed. E-mail address: [email protected]
Acknowledgements
Funding was provided by Boehringer Ingelheim Foundation "Novel and neglected cardiovascular risk factors: molecular mechanisms and therapeutic implications". http://dx.doi.org/10.1016/j.freeradbiomed.2017.04.155
Keywords: Oxidative stress; redox signaling; fluorescence and chemiluminescence-based assays; dihydroethidium oxidative fluorescence microtopography; lucigenin-enhanced chemiluminescence; L-012-enhanced chemiluminescence
Reactive oxygen and nitrogen species (RONS such as H2O2, nitric oxide) confer redox regulation of essential cellular functions, initiate and catalyze adaptive stress responses. In contrast, excessive formation of RONS may lead to appreciable impairment of cellular function and in the worst case to cell death, organ dysfunction and severe disease phenotypes of the entire organism. Therefore, the knowledge of the severity of oxidative stress and tissue specific localization is of great biological and clinical importance. However, at this level of investigation quantitative information may be enough, whereas for the development of specific drugs, the cellular and subcellular localization of the sources of RONS or even the nature of the reactive species may be of great importance, and accordingly, more qualitative information is required. These two different philosophies currently compete with each other and their different needs (also reflected by different detection assays) often lead to controversial discussions within the redox research community. With the present overview we discuss these different philosophies and needs, but also to defend some of the traditional assays for the detection of RONS that work very well in our hands. We will also provide an overview on the “new assays” with a brief discussion on their strengths but also weaknesses and limitations. E-mail address: [email protected] (A. Daiber) Acknowledgements
Funding was provided by European Cooperation in Science and Technology (COST Action BM1203/EU-ROS) http://dx.doi.org/10.1016/j.freeradbiomed.2017.04.156
P-072
Oxidative modifications of α- and β- caseins induced by AAPH-derived peroxyl radicals: Role of tryptophan and tyrosine residues Eduardo Felipe Fuentes-Lemus 1,2, Camilo López-Alarcón 1, Eduardo Silva 1, Fabian Leinisch 2, Michael J. Davies 2 1
Departamento de Química Física, Facultad de Química, Pontificia Universidad Católica de Chile, Chile 2 Department of Biomedical Sciences, Panum Institute, University of Copenhagen Keywords: Caseins; peroxyl radicals; protein aggregation/fragmentation; tryptophan oxidation; tyrosine oxidation
disease patients and in normal individuals at high risk of developing Alzheimer's (because they carry the ApoE4 allele), will be discussed to highlight the role of reductive stress in these pathophysiological processes.
S41
P-071
Taking up the cudgels for the traditional reactive oxygen and nitrogen species detection assays and their use in the cardiovascular system
E-mail address: [email protected] (J. Viña) http://dx.doi.org/10.1016/j.freeradbiomed.2017.04.154
Andreas Daiber, Matthias Oelze, Sebastian Steven, Swenja Kröller-Schön, Thomas Münzel Center for Cardiology 1, University Medical Center Mainz, Germany
P-070
Environmental noise and particulate matter exposure, oxidative stress and vascular function - the underestimated cardiovascular risk factors Andreas Daiber University Medical Center Mainz, Germany Keywords: Environmental risk factors; traffic noise exposure; particulate matter exposure; mental stress; stress hormones; endothelial dysfunction; oxidative stress; hypertension
Epidemiological studies have demonstrated that traffic noise and particulate matter exposure is associated with cardiovascular diseases such as arterial hypertension, myocardial infarction and stroke. Persistent chronic noise and particulate matter exposure increases the risk of cardiovascular and metabolic diseases such as arterial hypertension, coronary artery disease, diabetes and stroke. Data of the Heinz Nixdorf Recall Study (Kälsch et al. Eur. Heart J. 2014) but also large epidemiological studies (reviewed in Münzel et al. Eur. Heart J. 2017) point towards a link between the incidence of ischemic heart diseases and exposure to noise and/or particulate matter, supporting their role as independent cardiovascular risk factors, suggesting synergistic effects by both stressors and warranting further detailed studies to understand the mechanistic basis of this association. Recently, the underlying molecular mechanisms leading to noise-dependent adverse effects on the vasculature were characterized in an animal model of aircraft noise exposure identifying oxidative stress as a central player in mediating vascular dysfunction, which shares striking similarities with the pathomechanisms reported for particulate matter exposure. With the present overview the mechanistic parallels in the pathophysiological processes induced by noise and particulate matter exposure will be discussed. E-mail address: [email protected]
Acknowledgements
Funding was provided by Boehringer Ingelheim Foundation "Novel and neglected cardiovascular risk factors: molecular mechanisms and therapeutic implications". http://dx.doi.org/10.1016/j.freeradbiomed.2017.04.155
Keywords: Oxidative stress; redox signaling; fluorescence and chemiluminescence-based assays; dihydroethidium oxidative fluorescence microtopography; lucigenin-enhanced chemiluminescence; L-012-enhanced chemiluminescence
Reactive oxygen and nitrogen species (RONS such as H2O2, nitric oxide) confer redox regulation of essential cellular functions, initiate and catalyze adaptive stress responses. In contrast, excessive formation of RONS may lead to appreciable impairment of cellular function and in the worst case to cell death, organ dysfunction and severe disease phenotypes of the entire organism. Therefore, the knowledge of the severity of oxidative stress and tissue specific localization is of great biological and clinical importance. However, at this level of investigation quantitative information may be enough, whereas for the development of specific drugs, the cellular and subcellular localization of the sources of RONS or even the nature of the reactive species may be of great importance, and accordingly, more qualitative information is required. These two different philosophies currently compete with each other and their different needs (also reflected by different detection assays) often lead to controversial discussions within the redox research community. With the present overview we discuss these different philosophies and needs, but also to defend some of the traditional assays for the detection of RONS that work very well in our hands. We will also provide an overview on the “new assays” with a brief discussion on their strengths but also weaknesses and limitations. E-mail address: [email protected] (A. Daiber) Acknowledgements
Funding was provided by European Cooperation in Science and Technology (COST Action BM1203/EU-ROS) http://dx.doi.org/10.1016/j.freeradbiomed.2017.04.156
P-072
Oxidative modifications of α- and β- caseins induced by AAPH-derived peroxyl radicals: Role of tryptophan and tyrosine residues Eduardo Felipe Fuentes-Lemus 1,2, Camilo López-Alarcón 1, Eduardo Silva 1, Fabian Leinisch 2, Michael J. Davies 2 1
Departamento de Química Física, Facultad de Química, Pontificia Universidad Católica de Chile, Chile 2 Department of Biomedical Sciences, Panum Institute, University of Copenhagen Keywords: Caseins; peroxyl radicals; protein aggregation/fragmentation; tryptophan oxidation; tyrosine oxidation