Oxidative stress and inflammation contribute to traffic noise-induced vascular and cerebral dysfunction via uncoupling of nitric oxide synthases
Environmental pollution and non-chemical stressors such as mental stress or traffic noise exposure are increasingly accepted as health risk factors with substantial contribution to chronic noncommunicable diseases (e.g. cardiovascular, metabolic and mental). Whereas the mechanisms of air pollution-m...
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| Format: | Article |
| Language: | English |
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Elsevier
2020-07-01
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| Series: | Redox Biology |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S2213231720302603 |
| _version_ | 1818498676951089152 |
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| author | Andreas Daiber Swenja Kröller-Schön Matthias Oelze Omar Hahad Huige Li Rainer Schulz Sebastian Steven Thomas Münzel |
| author_facet | Andreas Daiber Swenja Kröller-Schön Matthias Oelze Omar Hahad Huige Li Rainer Schulz Sebastian Steven Thomas Münzel |
| author_sort | Andreas Daiber |
| collection | DOAJ |
| description | Environmental pollution and non-chemical stressors such as mental stress or traffic noise exposure are increasingly accepted as health risk factors with substantial contribution to chronic noncommunicable diseases (e.g. cardiovascular, metabolic and mental). Whereas the mechanisms of air pollution-mediated adverse health effects are well characterized, the mechanisms of traffic noise exposure are not completely understood, despite convincing clinical and epidemiological evidence for a significant contribution of environmental noise to overall mortality and disability. The initial mechanism of noise-induced cardiovascular, metabolic and mental disease is well defined by the „noise reaction model“ and consists of neuronal activation involving the hypothalamic-pituitary-adrenal (HPA) axis as well as the sympathetic nervous system, followed by a classical stress response via cortisol and catecholamines. Stress pathways are initiated by noise-induced annoyance and sleep deprivation/fragmentation. This review highlights the down-stream pathophysiology of noise-induced mental stress, which is based on an induction of inflammation and oxidative stress. We highlight the sources of reactive oxygen species (ROS) involved and the known targets for noise-induced oxidative damage. Part of the review emphasizes noise-triggered uncoupling/dysregulation of endothelial and neuronal nitric oxide synthase (eNOS and nNOS) and its central role for vascular dysfunction. |
| first_indexed | 2024-12-10T20:18:49Z |
| format | Article |
| id | doaj.art-d4ce92c1b4a3497f87acf0fa35b10d93 |
| institution | Directory Open Access Journal |
| issn | 2213-2317 |
| language | English |
| last_indexed | 2024-12-10T20:18:49Z |
| publishDate | 2020-07-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Redox Biology |
| spelling | doaj.art-d4ce92c1b4a3497f87acf0fa35b10d932022-12-22T01:35:07ZengElsevierRedox Biology2213-23172020-07-0134101506Oxidative stress and inflammation contribute to traffic noise-induced vascular and cerebral dysfunction via uncoupling of nitric oxide synthasesAndreas Daiber0Swenja Kröller-Schön1Matthias Oelze2Omar Hahad3Huige Li4Rainer Schulz5Sebastian Steven6Thomas Münzel7Center for Cardiology, Molecular Cardiology, University Medical Center, Mainz, Germany; Partner Site Rhine-Main, German Center for Cardiovascular Research (DZHK), Langenbeckstr. 1, 55131, Mainz, Germany; Corresponding author. Universitätsmedizin der Johannes Gutenberg-Universität Zentrum für Kardiologie 1 – Labor für Molekulare Kardiologie, Geb. 605 – Raum 3.262, Langenbeckstr. 1, 55131, Mainz, Germany.Center for Cardiology, Molecular Cardiology, University Medical Center, Mainz, GermanyCenter for Cardiology, Molecular Cardiology, University Medical Center, Mainz, GermanyCenter for Cardiology, Molecular Cardiology, University Medical Center, Mainz, Germany; Partner Site Rhine-Main, German Center for Cardiovascular Research (DZHK), Langenbeckstr. 1, 55131, Mainz, GermanyDepartment of Pharmacology, University Medical Center, Mainz, GermanyInstitute of Physiology, Justus-Liebig University, Giessen, GermanyCenter for Cardiology, Molecular Cardiology, University Medical Center, Mainz, GermanyCenter for Cardiology, Molecular Cardiology, University Medical Center, Mainz, Germany; Partner Site Rhine-Main, German Center for Cardiovascular Research (DZHK), Langenbeckstr. 1, 55131, Mainz, Germany; Corresponding author. Universitätsmedizin der Johannes Gutenberg-Universität Zentrum für Kardiologie 1 – Labor für Molekulare Kardiologie, Geb. 605 – Raum 3.262, Langenbeckstr. 1, 55131, Mainz, Germany.Environmental pollution and non-chemical stressors such as mental stress or traffic noise exposure are increasingly accepted as health risk factors with substantial contribution to chronic noncommunicable diseases (e.g. cardiovascular, metabolic and mental). Whereas the mechanisms of air pollution-mediated adverse health effects are well characterized, the mechanisms of traffic noise exposure are not completely understood, despite convincing clinical and epidemiological evidence for a significant contribution of environmental noise to overall mortality and disability. The initial mechanism of noise-induced cardiovascular, metabolic and mental disease is well defined by the „noise reaction model“ and consists of neuronal activation involving the hypothalamic-pituitary-adrenal (HPA) axis as well as the sympathetic nervous system, followed by a classical stress response via cortisol and catecholamines. Stress pathways are initiated by noise-induced annoyance and sleep deprivation/fragmentation. This review highlights the down-stream pathophysiology of noise-induced mental stress, which is based on an induction of inflammation and oxidative stress. We highlight the sources of reactive oxygen species (ROS) involved and the known targets for noise-induced oxidative damage. Part of the review emphasizes noise-triggered uncoupling/dysregulation of endothelial and neuronal nitric oxide synthase (eNOS and nNOS) and its central role for vascular dysfunction.http://www.sciencedirect.com/science/article/pii/S2213231720302603Environmental risk factorsTraffic noise exposureOxidative stressNOS uncouplingCardiovascular disease |
| spellingShingle | Andreas Daiber Swenja Kröller-Schön Matthias Oelze Omar Hahad Huige Li Rainer Schulz Sebastian Steven Thomas Münzel Oxidative stress and inflammation contribute to traffic noise-induced vascular and cerebral dysfunction via uncoupling of nitric oxide synthases Redox Biology Environmental risk factors Traffic noise exposure Oxidative stress NOS uncoupling Cardiovascular disease |
| title | Oxidative stress and inflammation contribute to traffic noise-induced vascular and cerebral dysfunction via uncoupling of nitric oxide synthases |
| title_full | Oxidative stress and inflammation contribute to traffic noise-induced vascular and cerebral dysfunction via uncoupling of nitric oxide synthases |
| title_fullStr | Oxidative stress and inflammation contribute to traffic noise-induced vascular and cerebral dysfunction via uncoupling of nitric oxide synthases |
| title_full_unstemmed | Oxidative stress and inflammation contribute to traffic noise-induced vascular and cerebral dysfunction via uncoupling of nitric oxide synthases |
| title_short | Oxidative stress and inflammation contribute to traffic noise-induced vascular and cerebral dysfunction via uncoupling of nitric oxide synthases |
| title_sort | oxidative stress and inflammation contribute to traffic noise induced vascular and cerebral dysfunction via uncoupling of nitric oxide synthases |
| topic | Environmental risk factors Traffic noise exposure Oxidative stress NOS uncoupling Cardiovascular disease |
| url | http://www.sciencedirect.com/science/article/pii/S2213231720302603 |
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