4.7 Article

Role of endogenous melatonin in pathophysiologic and oxidative stress responses to personal air pollutant exposures in asthmatic children

期刊

SCIENCE OF THE TOTAL ENVIRONMENT
卷 773, 期 -, 页码 -

出版社

ELSEVIER
DOI: 10.1016/j.scitotenv.2021.145709

关键词

Air pollution; Melatonin; Pulmonary physiology; Oxidative stress; Airway mechanics; Lung function

资金

  1. Underwriters Laboratories Inc.
  2. National Natural Science Foundation of China [51420105010, 51521005]
  3. Duke Global Health Institute

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The study found that oxidative stress and inflammation are important pathophysiological mechanisms underlying the effects of air pollution in children with asthma. Melatonin can suppress oxidative stress and inflammation, leading to improved airway inflammation and lung elasticity.
Background: Heightening oxidative stress and inflammation is an important pathophysiological mechanism underlying air pollution health effects in people with asthma. Melatonin can suppress oxidative stress and inflammation in pulmonary and circulatory systems. However, the role of melatonin in the oxidative stress and physiological responses to air pollution exposure has not been examined in children with asthma. Methods: In this panel study of 43 asthmatic children (513 years old), each child had 4 clinic visits with a 2-week interval between two consecutive visits. At each visit, urine samples were collected and subsequently analyzed for 6-sulfatoxymelatonin (aMT6s) as a surrogate of circulating melatonin and for malondialdehyde (MDA) and 8-hydroxy-2'-deoxyguanosine (8-OHdG) as two biomarkers of systemic oxidative stress. At each clinic visit, children were measured for pulmonary function and fractional exhaled nitric oxide (FeNO, a marker of pulmonary inflammation). None of the children reported to have taking melatonin supplementation. Concentrations of indoor and ambient PM2.5 and ozone (O-3) were combined with individual time-activity data to calculate personal air pollutant exposures. Results: We found that interquartile range increases in urinary MDA and 8-OHdG concentrations were associated with significantly increased urinary aMT6s concentrations by 73.4% (95% CI: 52.6% to 97.0%) and 41.7% (22.8% to 63.4%), respectively. Increases in daily personal exposure to O-3 and to PM2.5 were each associated with increased urinary aMT6s concentrations. Increasing urinary aMT6s concentrations were associated with decreased FeNO and resonant frequency, indicating improved airway inflammation and lung elasticity, respectively. Conclusion: The results suggest that systemic oxidative stress heightened by air pollution exposure may stimulate melatonin excretion as a defense mechanism to alleviate the adverse effects. (C) 2021 Elsevier B.V. All rights reserved.

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