Increased content of hydrogen peroxide in the expired breath of cigarette smokers

被引:120
作者
Nowak, D
Antczak, A
Krol, M
Pietras, T
Shariati, B
Bialasiewicz, P
Jeczkowski, K
Kula, P
机构
[1] Dept. of Pneumology and Allergology, Medical University of Lodz, Lodz
[2] Dept. of Pneumology and Allergology, Medical University of Lodz, 90-153 Lodz
关键词
breath condensate; cigarette smoking; cotinine; expired breath; hydrogen peroxide;
D O I
10.1183/09031936.96.09040652
中图分类号
R56 [呼吸系及胸部疾病];
学科分类号
摘要
Cigarette smoking causes an influx of mononuclear phagocytes and polymorphonuclear leucocytes into the lower airways. These cells have altered oxygen metabolism and release more H2O2 than phagocytes from nonsmokers. In this study, we intended to determine whether asymptomatic cigarette smokers exhale more H2O2 than healthy nonsmokers. The content of H2O2 in the expired condensate of 27 nonsmokers and 33 cigarette smokers was measured spectrofluorimetrically (homovanillic acid method). The mean H2O2 level in the expired breath condensate of all cigarette smokers was about fivefold higher than that found in the whole nonsmoker group (0.24+/-0.32 versus 0.05+/-0.11 nM). However, only 16 smokers (49%) and 6 nonsmokers (22%) had detectable levels of H2O2 in expired breath that reached values 0.49+/-0.28 and 0.23+/-0.10 nM, respectively. Although the cigarette smoking status was similar for both male and female smokers, females expired 2.5 fold less H2O2 than males (0.15+/-0.24 (n=21) versus 0.38+/-0.39 (n=12) nM. No correlation was found between expired H2O2 levels and cigarette smoking status expressed as the daily cigarette consumption, cumulative cigarette consumption and urinary cotinine concentration. It is suggested that in some smokers, expressed H2O2 can be a noninvasive marker of oxidant overload in the lower airways related to cigarette smoking.
引用
收藏
页码:652 / 657
页数:6
相关论文
共 38 条
[1]  
BALDWIN SR, 1986, LANCET, V1, P11
[2]   THE DIRECT BARBITURIC-ACID ASSAY FOR NICOTINE METABOLITES IN URINE - A SIMPLE COLORIMETRIC TEST FOR THE ROUTINE ASSESSMENT OF SMOKING STATUS AND CIGARETTE-SMOKE INTAKE [J].
BARLOW, RD ;
STONE, RB ;
WALD, NJ ;
PUHAKAINEN, EVJ .
CLINICA CHIMICA ACTA, 1987, 165 (01) :45-52
[3]  
BAUGHMAN RP, 1986, J LAB CLIN MED, V107, P233
[4]  
BEATTY K, 1982, J LAB CLIN MED, V100, P186
[5]  
BENOWITZ NL, 1983, CLIN PHARMACOL THER, V30, P139
[6]  
BLUE ML, 1978, AM REV RESPIR DIS, V117, P317
[7]   ANTIOXIDANT MACROMOLECULES IN THE EPITHELIAL LINING FLUID OF THE NORMAL HUMAN LOWER RESPIRATORY-TRACT [J].
CANTIN, AM ;
FELLS, GA ;
HUBBARD, RC ;
CRYSTAL, RG .
JOURNAL OF CLINICAL INVESTIGATION, 1990, 86 (03) :962-971
[8]   POTENTIAL MECHANISM OF EMPHYSEMA - ALPHA-1-PROTEINASE INHIBITOR RECOVERED FROM LUNGS OF CIGARETTE SMOKERS CONTAINS OXIDIZED METHIONINE AND HAS DECREASED ELASTASE INHIBITORY CAPACITY [J].
CARP, H ;
MILLER, F ;
HOIDAL, JR ;
JANOFF, A .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA-BIOLOGICAL SCIENCES, 1982, 79 (06) :2041-2045
[9]   CATHEPSIN-D ACTIVITY IS INCREASED IN ALVEOLAR MACROPHAGES AND BRONCHOALVEOLAR LAVAGE FLUID OF SMOKERS [J].
CHANG, JC ;
YOO, OH ;
LESSER, M .
AMERICAN REVIEW OF RESPIRATORY DISEASE, 1989, 140 (04) :958-960
[10]   EXPIRED BREATH HYDROGEN-PEROXIDE IS A MARKER OF ACUTE AIRWAY INFLAMMATION IN PEDIATRIC-PATIENTS WITH ASTHMA [J].
DOHLMAN, AW ;
BLACK, HR ;
ROYALL, JA .
AMERICAN REVIEW OF RESPIRATORY DISEASE, 1993, 148 (04) :955-960