Increased glutathione and glutathione peroxidase in lungs of individuals with chronic beryllium disease

被引:55
作者
Comhair, SAA
Lewis, MJ
Bhathena, PR
Hammel, JP
Erzurum, SC
机构
[1] Cleveland Clin Fdn, Dept Pulm & Crit Care Med, Lerner Res Inst, Cleveland, OH 44195 USA
[2] Cleveland Clin Fdn, Dept Canc Biol, Lerner Res Inst, Cleveland, OH 44195 USA
[3] Cleveland Clin Fdn, Dept Biostat & Epidemiol, Lerner Res Inst, Cleveland, OH 44195 USA
关键词
D O I
10.1164/ajrccm.159.6.9810044
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
Reactive oxygen species (ROS) are mediators of chronic tissue damage and fibrosis. Endogenous antioxidants may increase in response to oxidants and reduce tissue injury. We investigated the antioxidant response of the lungs to the chronic release of ROS, as occurs in the immune-specific granulomatous inflammation of chronic beryllium disease (CBD), and compared it with that in healthy controls and individuals exposed to cigarette smoke. The antioxidants superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), and glutathione (CSH) were quantitated in lung epithelial lining fluid (ELF) and serum from control subjects (n = 10), cigarette smokers (n = 8), and individuals with CBD (n = 9). GPx activity and extracellular GPx (eGPx) protein were increased in the ELF of subjects with CBD in comparison with that of control subjects and smokers (eGPx in ELF: controls, 1.3 +/- 0.2 mu g/ml, smokers, 1.9 +/- 0.3 mu g/ml, CBD, 3.8 +/- 0.8 mu g/ml; p = 0.002; GPx U/ml ELF, controls 1.4 +/- 0.3, smokers 1.8 +/- 0.4, CBD, 4.5 +/- 1, p = 0.02). Smokers' ELF had higher levels of CSH than that of controls, but CBD patients' ELF contained much more CSH than that of either controls or smokers (p < 0.001). Increases in GSH were correlated with eGPx, indicating similar inducing mechanisms for these antioxidants. Thus, coordinate augmentation of the glutathione antioxidant system occurs in granulomatous lung inflammation.
引用
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页码:1824 / 1829
页数:6
相关论文
共 37 条
[1]  
AEBI H, 1984, METHOD ENZYMOL, V105, P121
[2]   Extracellular glutathione peroxidase in human lung epithelial lining fluid and in lung cells [J].
Avissar, N ;
Finkelstein, JN ;
Horowitz, S ;
Willey, JC ;
Coy, E ;
Frampton, MW ;
Watkins, RH ;
Khullar, P ;
Xu, YL ;
Cohen, HJ .
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, 1996, 270 (02) :L173-L182
[3]   ALVEOLAR MACROPHAGES FROM PATIENTS WITH BERYLLIUM DISEASE AND SARCOIDOSIS EXPRESS INCREASED LEVELS OF MESSENGER-RNA FOR TUMOR-NECROSIS-FACTOR-ALPHA AND INTERLEUKIN-6 BUT NOT INTERLEUKIN-1-BETA [J].
BOST, TW ;
RICHES, DWH ;
SCHUMACHER, B ;
CARRE, PC ;
KHAN, TZ ;
MARTINEZ, JAB ;
NEWMAN, LS .
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 1994, 10 (05) :506-513
[4]  
CALHOUN WJ, 1989, J LAB CLIN MED, V114, P682
[5]   NORMAL ALVEOLAR EPITHELIAL LINING FLUID CONTAINS HIGH-LEVELS OF GLUTATHIONE [J].
CANTIN, AM ;
NORTH, SL ;
HUBBARD, RC ;
CRYSTAL, RG .
JOURNAL OF APPLIED PHYSIOLOGY, 1987, 63 (01) :152-157
[6]   Decreased Cu,Zn-SOD activity in asthmatic airway epithelium: Correction by inhaled corticosteroid in vivo [J].
DeRaeve, HR ;
Thunnissen, FBJM ;
Kaneko, FT ;
Guo, FH ;
Lewis, M ;
Kavuru, MS ;
Secic, M ;
Thomassen, MJ ;
Erzurum, SC .
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, 1997, 272 (01) :L148-L154
[7]  
Erzurum S.C., 1993, J APPL PHYSIOL, V75, P1256
[8]   HYDROGEN-PEROXIDE RELEASE BY ALVEOLAR MACROPHAGES FROM SARCOID PATIENTS AND BY ALVEOLAR MACROPHAGES FROM NORMALS AFTER EXPOSURE TO RECOMBINANT INTERFERONS ALPHA-A, BETA, AND GAMMA AND 1,25-DIHYDROXYVITAMIN-D3 [J].
FELS, AOS ;
NATHAN, CF ;
COHN, ZA .
JOURNAL OF CLINICAL INVESTIGATION, 1987, 80 (02) :381-386
[9]   RAT LUNG CU,ZN SUPEROXIDE-DISMUTASE - ISOLATION AND SEQUENCE OF A FULL-LENGTH CDNA AND STUDIES OF ENZYME-INDUCTION [J].
HASS, MA ;
IQBAL, J ;
CLERCH, LB ;
FRANK, L ;
MASSARO, D .
JOURNAL OF CLINICAL INVESTIGATION, 1989, 83 (04) :1241-1246
[10]   Adaptation of lung antioxidants to cigarette smoking in humans [J].
Hilbert, J ;
Mohsenin, V .
CHEST, 1996, 110 (04) :916-920