Original contributionExhalation of H2O2 and thiobarbituric acid reactive substances (TBARs) by healthy subjects
Introduction
Measurement of hydrogen peroxide (H2O2) and thiobarbituric acid reactive substances (TBARs) in EBC is suggested to reflect free radical generation and peroxidative damage in the airways [1], [2], [3], [4]. Increased H2O2 and/or TBARs exhalation has been reported in numerous inflammatory lung disorders including bronchial asthma [1], [3], [5], [6], chronic obstructive pulmonary disease [2], [7], adult respiratory distress syndrome [8], [9], [10], pneumonia [10], and also in asymptomatic cigarette smokers [11]. Pulmonary phagocytes, type II pneumocytes, and other cells of the respiratory tract are potential sources of exhaled H2O2 [12], [13], [14], [15]. TBARs (mainly malondialdehyde) are recognized as end products of polyunsaturated fatty acid peroxidation, however, they are also formed during oxidative injury of DNA, proteins, or carbohydrates [16]. The activity of H2O2 producing cells and pathways leading to TBARs formation may change in response to many endogenic and exogenic physicochemical factors. Moreover, generation/exhalation of these compounds depends on antioxidant defense in the airways. This may explain why some healthy subjects and patients with lung inflammatory disorders did not exhale detectable amounts of H2O2 and TBARs [1], [2], [7]. Most studies on H2O2 and TBARs exhalation in patients with lung inflammatory disorders involved only single determination of these compounds [1], [2], [3], [5], [7], [11]. Little is known about variability of H2O2 and TBARs in EBC of healthy subjects.
Therefore, we investigated the circadian rhythm of H2O2 and TBARs exhalation in healthy subjects, its variability during 2 week observation and the effect of moderate exercise, acute exposure to cigarette smoke, and single dose of inhaled bronchodilators. The correlations between subjects’ age, spirometric parameters, and cigarette smoking habits were also analyzed.
Section snippets
Study populations
Fifty-eight healthy volunteers (University Hospital staff) were enrolled (18 current cigarette smokers and 40 never smoking persons) who had not suffered from any infectious diseases for at least 3 months prior to the study (Table 1). They were free of any medication and routine physical examination showed nothing abnormal.
Study design
Subjects were asked to attend the laboratory three times every 7 d during 2 consecutive weeks (visit I at 1st day, visit II at 7th day and visit III at 14th day) for EBC
Factors influencing H2O2 and TBARs levels in EBC
Neglecting of mouth washing with distilled water just before and at 7th and 14th min of EBC collection resulted in significant rise of H2O2 levels and tended to increase TBARs readings (Table 2). Wearing the nose clip while collecting EBC had no effect on both H2O2 and TBARs levels. However, the nasal airflow blockade made the whole exhaled air pass through the collecting part of the tube and undergo condensation. The yield of 20 min condensate collection was slightly higher (but not
Discussion
We found that one third of never smoked subjects and all current cigarette smokers continuously exhale detectable amounts of H2O2. Moreover, almost all never smoked healthy volunteers (35 of 40; 87.5%) had positive EBC H2O2 readings on at least one of three measurements during 2 week observation. It differs from our previous studies showing only 22% and 49% of H2O2 positive readings in healthy never smoked subjects and asymptomatic cigarette smokers, respectively [11]. In our present study we
References (37)
- et al.
Increased content of thiobarbituric acid reactive substances and hydrogen peroxide in the expired breath condensate of patients with stable chronic obstructive pulmonary disease. No significant effect of cigarette smoking
Respir. Med
(1999) - et al.
Increased hydrogen peroxide in the expired breath of patients with acute hypoxemic respiratory failure
Chest
(1989) - et al.
Oxidant activity in expired breath of patients with adult respiratory distress syndrome
Lancet
(1986) - et al.
Spontaneous chemiluminescence of human breath
J. Biol. Chem
(1983) - et al.
Release of hydrogen peroxide by rat type II pneumocytes in the prolonged culture
Toxicol. In Vitro
(2000) Malondialdehyde and thiobarbituric acid-reactivity as diagnostic indices of lipid peroxidation and peroxidative tissue injury
Free. Radic. Biol. Med
(1990)- et al.
Assay of H2O2 production by macrophages and neutrophils with homovanillic acid and horseradish peroxidase
J. Immunol. Methods
(1983) - et al.
Xanthine oxidase activity in bronchoalveolar lavage fluid from patients with chronic obstructive lung disease
Free Radic. Biol. Med.
(1996) - et al.
Quantitative analysis of the hydrogen peroxide formed in aqueous cigarette tar extracts
Free Radic. Biol. Med
(1989) - et al.
The fifth component of complement (C5) is necessary for maximal pulmonary leukocytosis in mice chronically exposed to cigarette smoke
Clin. Immunol. Immunopathol
(1987)
Influence of age on the release of reactive oxygen species by phagocytes as measured by a whole blood chemiluminescence assay
Free Radic. Biol. Med
Evaluation of the iron status of a population
Blood
Increased hydrogen peroxide and TBA-reactive products in expired breath condensate of asthmatic patients
Eur. Respir. J
Expired breath hydrogen peroxide is a marker of acute airway inflammation in pediatric patients with asthma
Am. Rev. Respir. Dis
Oxidative stress in chronic obstructive pulmonary disease
Am. J. Respir. Crit. Care Med
Hydrogen peroxide in exhaled air is increased in stable asthmatic children
Eur. Respir. J
Hydrogen peroxide in expired air condensate correlates positively with early steps of peripheral neutrophil activation in asthmatic patients
Arch. Immunol. Ther. Exp. (Warsz.)
Increased exhalation of hydrogen peroxide in patients with stable and unstable chronic obstructive pulmonary disease
Am. J. Respir. Crit. Care Med
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