Oxidative stress and inflammation contribute to traffic noise-induced vascular and cerebral dysfunction via uncoupling of nitric oxide synthases

Redox Biology

Matthias Oelze¹  Sebastian Steven²  Swenja Kröller-Schön²  Omar Hahad³  Huige Li³  Andreas Daiber³  Rainer Schulz³  Thomas Münzel⁴ 

[1] 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.;Partner Site Rhine-Main, German Center for Cardiovascular Research (DZHK), Langenbeckstr. 1, 55131, Mainz, Germany;Center for Cardiology, Molecular Cardiology, University Medical Center, Mainz, Germany;Department of Pharmacology, University Medical Center, Mainz, Germany;

关键词: Environmental risk factors;    Traffic noise exposure;    Oxidative stress;    NOS uncoupling;    Cardiovascular disease;   

DOI  :  

来源: DOAJ

【 摘 要 】

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.

【 授权许可】

Unknown