Fig. 17.

Linkage between exposure to noise and inflammation and oxidative stress. First-line neuronal events in response to noise exposure are sleep disturbance (when exposed during the sleep phase) and stress response reactions via activation of the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic nervous system. This leads to the release of stress hormones (glucocorticoids and catecholamines) and secondary activation of the cerebral (and systemic) renin-angiotensin-aldosterone system (RAAS) as well as endothelin-1 expression. These potent triggers of inflammation and oxidative stress activate NOX-2 via protein kinase C (PKC) and p47^phox phosphorylation in the brain, increase expression of markers of inflammation, lipid peroxidation, and cause downregulation of neuronal nitric oxide synthase (nNOS) and loss of antioxidant genes, such as catalase (Cat) and forkhead box O3 (Foxo3) transcription factor. These changes induce a neuroinflammatory phenotype with cerebral oxidative stress. These stress hormones and vasoconstrictors lead to similar adverse changes in the cardiovascular (and pulmonary) system and increase the risk of cardiometabolic and potentially other non-communicable diseases, such as diabetes or cancer. The HPA axis, sympathetic nervous system, RAAS, endothelin-1 expression, and neuroinflammation are redox-regulated, and vice versa, can induce oxidative stress via NOX-2 activation and other sources. AT-II, angiotensin-II; CRH, corticotrophin-releasing hormone; ACTH, adrenocorticotrophic hormone. Reused from Ref. [45] with permission.