Abstract
Vascular oxidative stress, inflammation, and subsequent endothelial dysfunction are consequences of traditional cardiovascular risk factors, all of which contribute to cardiovascular disease. Environmental stressors, such as traffic noise and air pollution, may also facilitate the development and progression of cardiovascular and metabolic diseases. In our previous studies, we investigated the influence of aircraft noise exposure on molecular mechanisms, identifying oxidative stress and inflammation as central players in mediating vascular function. The present study investigates the role of heme oxygenase-1 (HO-1) as an antioxidant response preventing vascular consequences following exposure to aircraft noise. C57BL/6J mice were treated with the HO-1 inducer hemin (25 mg/kg i.p.) or the NRF2 activator dimethyl fumarate (DMF, 20 mg/kg p.o.). During therapy, the animals were exposed to noise at a maximum sound pressure level of 85 dB(A) and a mean sound pressure level of 72 dB(A). Our data showed a marked protective effect of both treatments on animals exposed to noise for 4 days by normalization of arterial hypertension and vascular dysfunction in the noise-exposed groups. We observed a partial normalization of noise-triggered oxidative stress and inflammation by hemin and DMF therapy, which was associated with HO-1 induction. The present study identifies possible new targets for the mitigation of the adverse health effects caused by environmental noise exposure. Since natural dietary constituents can achieve HO-1 and NRF2 induction, these pathways represent promising targets for preventive measures.
Highlights
The mRNA expression of heme oxygenase-1 (HO-1) in cardiac tissue was increased in all treatment groups by trend, whereas the most significantly upregulated HO-1 mRNA levels were observed in the HEMIN + NOISE and dimethyl fumarate (DMF) + NOISE as compared with control mice (Figure 2A)
Noise exposure in mice [4,5,28] and men [33,34,35] was demonstrated to induce a prooxidative and proinflammatory phenotype associated with cardiovascular damage, endothelial function, and increased blood pressure (Figure 8)
As the HO-1 inducer hemin and the nuclear-factor erythroid 2-related factor 2 (NRF2) activator DMF possess potent antioxidant and anti-inflammatory properties and display beneficial cardiovascular effects (Figure 8), these compounds were expected to ameliorate the cardiovascular damage and dysfunction induced by noise exposure
Summary
Most traditional cardiovascular risk factors such as diabetes, smoking, and hyperlipidemia are associated with vascular complications such as endothelial dysfunction [1]. It has been shown that environmental stressors such as air pollution and excess of noise may facilitate the development of cardiovascular diseases (CVD) [2,3]. We previously identified oxidative stress and inflammation as central molecular mechanisms incurring vascular dysfunction following noise exposure [4,5]. A peak sound level of 85 db (A) and a mean sound level of 72 db (A) applied for 1, 2, and 4 days caused an increase in systolic blood pressure and circulating stress hormones, as well as oxidative stress and inflammation, resulting in endothelial dysfunction
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