Glutathione S-transferase P1 (GSTP1) polymorphism in patients with chronic obstructive pulmonary disease

被引:137
作者
Ishii, T
Matsuse, T
Teramoto, S
Matsui, H
Miyao, M
Hosoi, T
Takahashi, H
Fukuchi, Y
Ouchi, Y
机构
[1] Univ Tokyo, Dept Geriatr Med, Bunkyo Ku, Tokyo 1138655, Japan
[2] Juntendo Univ, Sch Med, Dept Resp Med, Tokyo 113, Japan
关键词
glutathione S-transferase P1 (GSTP1); polymorphism; chronic obstructive pulmonary disease; tobacco;
D O I
10.1136/thx.54.8.693
中图分类号
R56 [呼吸系及胸部疾病];
学科分类号
摘要
Background-Enzymes that contribute to the local detoxification in alveoli and bronchioles have an important role in the defence mechanism against tobacco smoke. It has been suggested that genetic susceptibility to smoking injury may confer a risk for the development of chronic obstructive pulmonary disease (COPD). The polymorphisms in glutathione S-transferase P1 (GSTP1), a xenobiotic metabolising enzyme, were investigated in patients with COPD. Methods-Polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) were performed to genotype GSTP1 polymorphisms in exon 5 (Ile105Val) and exon 6 (Ala114Val). Blood samples were taken from 53 patients with COPD and 50 control subjects at the Tokyo University Hospital, the Juntendo University Hospital, and the Tokyo Kenbikyoin Clinic for use in the study. Results-The proportion of GSTP1/Ile105 homozygotes was significantly higher in the patients with COPD than in the control subjects (79% vs 52%). The odds ratio for GSTP1/Ile105 homozygotes versus all other genotypes was 3.5 (95% CI 2.7 to 4.6) for COPD. Polymorphism at residue 114 of GSTP1 was not found in either group. Conclusions-Genetic polymorphism of exon 5 of GSTP1 may be associated with COPD because the GSTP1/Ile105 genotype is predominantly found in COPD. It is suggested that the GSTP1/Ile105 genotype may be less protective against xenobiotics in tobacco smoke.
引用
收藏
页码:693 / 696
页数:4
相关论文
共 25 条
[1]   DIFFERENTIAL SUSCEPTIBILITY TO TOBACCO-SMOKE - POSSIBLE MECHANISMS [J].
BASCOM, R .
PHARMACOGENETICS, 1991, 1 (02) :102-106
[2]   ISOLATION OF A CDNA CLONE AND LOCALIZATION OF THE HUMAN GLUTATHIONE S-TRANSFERASE 3-GENES TO CHROMOSOME BANDS 11Q13 AND 12Q13-14 [J].
BOARD, PG ;
WEBB, GC ;
COGGAN, M .
ANNALS OF HUMAN GENETICS, 1989, 53 :205-213
[3]   HETEROGENEOUS EXPRESSION AND POLYMORPHIC GENOTYPE OF GLUTATHIONE S-TRANSFERASES IN HUMAN LUNG [J].
CANTLAY, AM ;
SMITH, CAD ;
WALLACE, WA ;
YAP, PL ;
LAMB, D ;
HARRISON, DJ .
THORAX, 1994, 49 (10) :1010-1014
[4]  
CANTLAY AM, 1995, J CLIN PATHOL-CL MOL, V48, pM210
[5]   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
[6]   Inhibition of embryonic retinoic acid synthesis by aldehydes of lipid peroxidation and prevention of inhibition by reduced glutathione and glutathione S-transferases [J].
Chen, H ;
Juchau, MR .
FREE RADICAL BIOLOGY AND MEDICINE, 1998, 24 (03) :408-417
[7]   FREE-RADICAL CHEMISTRY OF CIGARETTE-SMOKE AND ITS TOXICOLOGICAL IMPLICATIONS [J].
CHURCH, DF ;
PRYOR, WA .
ENVIRONMENTAL HEALTH PERSPECTIVES, 1985, 64 :111-126
[8]   NATURAL-HISTORY OF CHRONIC AIR-FLOW OBSTRUCTION [J].
FLETCHER, C ;
PETO, R .
BMJ-BRITISH MEDICAL JOURNAL, 1977, 1 (6077) :1645-1648
[9]   DEFINITIONS OF EMPHYSEMA, CHRONIC-BRONCHITIS, ASTHMA, AND AIR-FLOW OBSTRUCTION - 25 YEARS ON FROM THE CIBA SYMPOSIUM [J].
FLETCHER, CM ;
PRIDE, NB .
THORAX, 1984, 39 (02) :81-85
[10]   Frequency of glutathione S-transferase M1 deletion in smokers with emphysema and lung cancer [J].
Harrison, DJ ;
Cantlay, AM ;
Rae, F ;
Lamb, D ;
Smith, CAD .
HUMAN & EXPERIMENTAL TOXICOLOGY, 1997, 16 (07) :356-360