Altered expression of Peroxiredoxin and Thioredoxin in septic animal model.
10.4046/trd.1999.47.4.451
- Author:
Hyung Jung KIM
1
;
Ho Zoon CHAE
;
Chul Min AHN
;
Sung Kyu KIM
;
Won Young LEE
Author Information
1. Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Peroxiredoxin;
Thioredoxin;
Sepsis;
Bronchoalveolar Lavage;
Peritoneal Lavage
- MeSH:
Acute Lung Injury;
Animals*;
Antibodies;
Antioxidants;
Bronchoalveolar Lavage;
Bronchoalveolar Lavage Fluid;
Catalase;
Erythrocytes;
Humans;
Lung;
Macrophages, Alveolar;
Mice;
Models, Animal*;
Neutrophils;
Oxidative Stress;
Peritoneal Lavage;
Peroxiredoxins*;
Pneumonia;
Reactive Oxygen Species;
Sepsis;
Thioredoxins*;
Vitamin K 3
- From:Tuberculosis and Respiratory Diseases
1999;47(4):451-459
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: In sepsis, excessive generation of reactive oxygen species plays key roles in the pathogenesis of acute lung injury. The serum antioxidants such as catalase and MnSOD are elevated in sepsis and considered as predictors of acute respiratory distress syndrome(ARDS) and prognostic factors of sepsis. Peroxiredoxin(Prx) has recently been known as an unique and major intracellular antioxidant. In this study, we evaluated the expression of Prx I and Prx II in mouse monocyte-macrophage cells(RAW267.7) after treatment of oxidative stress and endotoxin and measured the amount of Prx I, Prx II and thioredoxin(Trx) in peritoneal and bronchoalveolar lavage fluid of septic animal model. METHODS: Using immunoblot analysis with specific antibodies against Prx I, Prx II and Trx, we evaluated the distribution of Prx I and Prx II in human neutrophil, alveolar macrophage and red blood cell. We evaluated the expression of Prx I and Prx II in mouse monocyte-macrophage cells after treatment of 5 micro M menadione and 1 micro gram/ml lipopolysaccharide(LPS) and measured the amount of Prx I, Prx II and Trx in peritoneal lavage fluid of intraperitoneal septic animals(septic animal model induced with intraperitoneal 6 micro gram/kg LPS injection) and those in bronchoalveolar lavage fluid of intraperitoneal septic animals and intravenous septic animals(septic animal model induced with intravenous 5 micro gram/kg LPS injection) and compared with the severity of lung inflammation. RESULTS: The distribution of Prx I and Prx II were so different among human neutrophil, alveolar macrophage and red blood cell. The expression of Prx I in mouse monocyte-macrophage cells was increased after treatment of 5 micro M menadione and 1 micro gram/ml lipopolysaccharide but that of Prx II was not increased. The amount of Prx I, Prx II and Trx are increased in peritoneal lavage fluid of intraperitoneal septic animals but were not increased in bronchoalveolar lavage fluid of intraperitoneal and intravenous septic animals regardless of the severity of lung inflammation. CONCLUSION: As intracellular antioxidant, the expression of Prx I is increased in mouse monocyte-macrophage cells after treatment of oxidative stress and endotoxin. The amount of Prx I, Prx II and Trx are increased in local inflammatory site but not increased in injured lung of septic animal model.
