Long-Term Effects of Aircraft Noise Exposure on Vascular Oxidative Stress, Endothelial Function and Blood Pressure: No Evidence for Adaptation or Tolerance Development

被引:19
作者
Frenis, Katie [1 ,2 ,3 ]
Kalinovic, Sanela [1 ]
Ernst, Benjamin P. [4 ]
Kvandova, Miroslava [1 ]
Al Zuabi, Ahmad [1 ]
Kuntic, Marin [1 ]
Oelze, Matthias [1 ]
Stamm, Paul [1 ]
Bayo Jimenez, Maria Teresa [1 ]
Kij, Agnieszka [5 ]
Keppeler, Karin [1 ]
Klein, Veronique [1 ]
Strohm, Lea [1 ]
Ubbens, Henning [1 ]
Daub, Steffen [1 ]
Hahad, Omar [1 ,6 ]
Kroeller-Schoen, Swenja [1 ]
Schmeisser, Michael J. [8 ]
Chlopicki, Stefan [7 ,9 ]
Eckrich, Jonas [4 ]
Strieth, Sebastian
Daiber, Andreas [1 ,6 ,10 ]
Steven, Sebastian [1 ,10 ]
Muenzel, Thomas [1 ,6 ,10 ]
机构
[1] Johannes Gutenberg Univ Mainz, Univ Med Ctr, Lab Mol Cardiol, Dept Cardiol,Cardiol 1, Mainz, Germany
[2] Boston Childrens Hosp, Boston, MA USA
[3] Harvard Med Sch, Dept Hematol Oncol, Boston, MA 02115 USA
[4] Univ Med Ctr Bonn UKB, Dept Otorhinolaryngol, Bonn, Germany
[5] Jagiellonian Univ, Jagiellonian Ctr Expt Therapeut JCET, Krakow, Poland
[6] German Ctr Cardiovasc Res DZHK, Partner Site Rhine Main, Mainz, Germany
[7] Johannes Gutenberg Univ Mainz, Univ Med Ctr, Inst Microscop Anat & Neurobiol, Mainz, Germany
[8] Johannes Gutenberg Univ Mainz, Univ Med Ctr, Focus Program Translat Neurosci FTN, Mainz, Germany
[9] Jagiellonian Univ, Dept Pharmacol, Med Coll, Krakow, Poland
[10] Johannes Gutenberg Univ Mainz, Univ Med Ctr, Ctr Thrombosis & Hemostasis, Mainz, Germany
关键词
acute and chronic aircraft noise exposure; hypertension; endothelial dysfunction; oxidative stress; hearing threshold by audiometry; stress adaptation; ROAD TRAFFIC NOISE; CROSS-SECTIONAL ANALYSIS; AMBIENT AIR-POLLUTION; NITRIC-OXIDE; COGNITIVE IMPAIRMENT; SUPEROXIDE-DISMUTASE; RATS; DYSFUNCTION; MEMORY; HYPERTENSION;
D O I
10.3389/fmolb.2021.814921
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Transportation noise is recognized as an important cardiovascular risk factor. Key mechanisms are noise-triggered vascular inflammation and oxidative stress with subsequent endothelial dysfunction. Here, we test for adaptation or tolerance mechanisms in mice in response to chronic noise exposure. C57BL/6J mice were exposed to aircraft noise for 0, 4, 7, 14 and 28d at a mean sound pressure level of 72 dB(A) and peak levels of 85 dB(A). Chronic aircraft noise exposure up to 28d caused persistent endothelial dysfunction and elevation of blood pressure. Likewise, reactive oxygen species (ROS) formation as determined by dihydroethidium (DHE) staining and HPLC-based measurement of superoxide formation in the aorta/heart/brain was time-dependently increased by noise. Oxidative burst in the whole blood showed a maximum at 4d or 7d of noise exposure. Increased superoxide formation in the brain was mirrored by a downregulation of neuronal nitric oxide synthase (Nos3) and transcription factor Foxo3 genes, whereas Vcam1 mRNA, a marker for inflammation was upregulated in all noise exposure groups. Induction of a pronounced hearing loss in the mice was excluded by auditory brainstem response audiometry. Endothelial dysfunction and inflammation were present during the entire 28d of aircraft noise exposure. ROS formation gradually increases with ongoing exposure without significant adaptation or tolerance in mice in response to chronic noise stress at moderate levels. These data further illustrate health side effects of long-term noise exposure and further strengthen a consequent implementation of the WHO noise guidelines in order to prevent the development of noise-related future cardiovascular disease.
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页数:15
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