EFFECTS OF CIGARETTE-SMOKE ON THE GLUTATHIONE STATUS OF THE UPPER AND LOWER RESPIRATORY-TRACT OF RATS

被引:12
作者
MAPLES, KR [1 ]
NIKULA, KJ [1 ]
CHEN, BT [1 ]
FINCH, GL [1 ]
GRIFFITH, WC [1 ]
HARKEMA, JR [1 ]
机构
[1] LOVELACE BIOMED & ENVIRONM RES INST, INHALAT TOXICOL RES INST, ALBUQUERQUE, NM 87185 USA
关键词
D O I
10.3109/08958379308998394
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 ;
摘要
Endogenous antioxidants, like the tripeptide glutathione (GSH), protect the respiratory airways from potentially injurious agents within inhaled pollutants like cigarette smoke. The purpose of this study was to determine the effects of cigarette smoke exposure on respiratory tract tissue. Twenty-four F344/N male rats were exposed to cigarette smoke (249 mg total particulate matter/m(3)) or filtered air for 6 h/day for 9 days. Rats were sacrificed 1 day or 14 days after the last exposure. The most dramatic changes in GSH concentrations occurred in the tissues of the nasal cavity 1 day following exposure, with tissues from the proximal nasal airways showing the greatest response. These same proximal nasal airway tissues also had the greatest histopathological changes. Within 2 wk after exposure, the GSH concentrations in the nasal tissues from smoke-exposed rats were similar to air-exposed controls, and there was only minimal histopathological evidence of tissue alteration. GSH concentrations were not significantly elevated in the left extrapulmonary bronchi or main axial airway, nor were there any histologic alterations evident in these tissues at any time point. Thus, the extent of the cellular GSH response paralleled the extent of respiratory tract tissue injury and recovery. Our results suggest that the reactive agent(s) in cigarette smoke cause increased GSH in nasal tissue and that squamous metaplasia occurs in nasal surface epithelium. Both changes, however, are resolved by 14 days after a short-term cigarette smoke exposure.
引用
收藏
页码:389 / 401
页数:13
相关论文
共 22 条
[1]  
Basrur P K, 1979, Prog Exp Tumor Res, V24, P283
[2]  
Chen B.T., 1989, INHAL TOXICOL, V1, P331, DOI [10.3109/08958378909145237, DOI 10.3109/08958378909145237]
[3]   DESCRIPTION AND EVALUATION OF A CIGARETTE-SMOKE GENERATION SYSTEM FOR INHALATION STUDIES [J].
CHEN, BT ;
BECHTOLD, WE ;
MAUDERLY, JL .
JOURNAL OF AEROSOL MEDICINE-DEPOSITION CLEARANCE AND EFFECTS IN THE LUNG, 1992, 5 (01) :19-30
[4]   DIETARY VITAMIN-E AND PULMONARY BIOCHEMICAL RESPONSES OF RATS TO CIGARETTE-SMOKING [J].
CHOW, CK ;
CHEN, LH ;
THACKER, RR ;
GRIFFITH, RB .
ENVIRONMENTAL RESEARCH, 1984, 34 (01) :8-17
[5]   THE EFFECT OF ACUTE CIGARETTE-SMOKE INHALATION ON PULMONARY AND SYSTEMIC CYSTEINE AND GLUTATHIONE REDOX STATES IN THE RAT [J].
COTGREAVE, IA ;
JOHANSSON, U ;
MOLDEUS, P ;
BRATTSAND, R .
TOXICOLOGY, 1987, 45 (02) :203-212
[6]  
DAVIS L, 1984, 1984 COR M LEX
[7]   EFFECT OF CIGARETTE-SMOKE INHALATION ON ANTIOXIDANT ENZYMES AND LIPID-PEROXIDATION IN THE RAT [J].
GUPTA, MP ;
KHANDUJA, KL ;
SHARMA, RR .
TOXICOLOGY LETTERS, 1988, 41 (02) :107-114
[8]  
HAAGEN-SMIT A J, 1959, AMA Arch Ind Health, V20, P399
[9]   PROLIFERATIVE CAPACITY OF HUMAN PERIPHERAL-BLOOD LYMPHOCYTES SORTED ON THE BASIS OF GLUTATHIONE CONTENT [J].
KAVANAGH, TJ ;
GROSSMANN, A ;
JAECKS, EP ;
JINNEMAN, JC ;
EATON, DL ;
MARTIN, GM ;
RABINOVITCH, PS .
JOURNAL OF CELLULAR PHYSIOLOGY, 1990, 145 (03) :472-480
[10]  
LEUCHTENBERGER C, 1958, CANCER, V11, P490, DOI 10.1002/1097-0142(195805/06)11:3<490::AID-CNCR2820110309>3.0.CO