Journalartikel
Autorenliste: Daiber, Andreas; Kroeller-Schoen, Swenja; Oelze, Matthias; Hahad, Omar; Li, Huige; Schulz, Rainer; Steven, Sebastian; Muenzel, Thomas
Jahr der Veröffentlichung: 2020
Zeitschrift: Redox Biology
Bandnummer: 34
ISSN: 2213-2317
Open Access Status: Gold
DOI Link: https://doi.org/10.1016/j.redox.2020.101506
Verlag: Elsevier
Abstract:
Environmental pollution and non-chemical stressors such as mental stress or traffic noise exposure are in- creasingly 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 depriva- tion/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 empha- sizes noise-triggered uncoupling/dysregulation of endothelial and neuronal nitric oxide synthase (eNOS and nNOS) and its central role for vascular dysfunction.
Zitierstile
Harvard-Zitierstil: Daiber, A., Kroeller-Schoen, S., Oelze, M., Hahad, O., Li, H., Schulz, R., et al. (2020) Oxidative stress and inflammation contribute to traffic noise-induced vascular and cerebral dysfunction via uncoupling of nitric oxide synthases, Redox Biology, 34, Article 101506. https://doi.org/10.1016/j.redox.2020.101506
APA-Zitierstil: Daiber, A., Kroeller-Schoen, S., Oelze, M., Hahad, O., Li, H., Schulz, R., Steven, S., & Muenzel, T. (2020). Oxidative stress and inflammation contribute to traffic noise-induced vascular and cerebral dysfunction via uncoupling of nitric oxide synthases. Redox Biology. 34, Article 101506. https://doi.org/10.1016/j.redox.2020.101506
Schlagwörter
AIR-POLLUTION; ANGIOTENSIN-II; BLOOD-PRESSURE; DIHYDROFOLATE-REDUCTASE; ENDOTHELIAL NO SYNTHASE; Environmental risk factors; NAD(P)H OXIDASE; NOS uncoupling; S-GLUTATHIONYLATION; SUPEROXIDE-PRODUCTION; Traffic noise exposure