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Inducible Nitric Oxide Synthase mRNA Expression and Nitric Oxide Production in Silica-Induced Acute Inflammatory Lung Injury

Lee, Ji-Hee   (Department of Physiology, College of Medicine, Ewha Womans University and Division of Cell Biology, Ewha Medical Research CenterUU0001056  );
  • 초록

    Stimulated alveolar macrophages and neutrophils produce nitric oxide, a free radical by an inducible nitric oxide synthase(iNOS), which reacts with superoxide anion to form peroxynitrite, a more highly reactive toxic species. The objectives of the present study were to evaluate acute inflammatory lung injury and to determine iNOS mRNA induction and nitric oxide production by rat broncho-alveolar lavage cells following intratracheal treatment of silica. After 4 h exposure to silica, differential counts of broncho-alveolar lavage cells and lactate dehydrogenase(LDH) activity as well as total protein in the broncho-alveolar lavage fluid were determined. Broncho-alveolar lavage cells were also assayed for iNOS mRNA and the productions of nitrite and nitrate measured in the cells cultured. Differential analysis of broncho-alveolar lavage cells showed that the number of alveolar macrophages slightly decreased following silica treatment; however, red blood cells, lymphocytes, and neutrophils significantly were increased by 9-, 14-, and 119-fold following silica treatment, respectively, compared with the saline control. It was also found significant increases in the LDH activity and total protein in the lavage fluid obtained from silica-treated rats, indicating silica-induced acute lung injury. Northern blot analysis demonstrated that the steady state levels of iNOS mRNA in broncho-alveolar lavage cells were increased following silica treatment. The productions of nitrite and nitrate in the cultured cells were significantly increased by 2-fold following silica treatment, respectively, which were attenuated by the NOS inhibitor $N{\omega}-nitro-L-arginine-methyl$ ester(L-NAME) and partially reversed by L-arginine. These findings suggest that nitric oxide production in alveolar macrophages and recruited neutrophils is increased in response to silica. Nitric oxide may contribute in part to acute inflammatory lung injury.


  • 주제어

    iNOS mRNA .   Nitric oxide .   Silica .   Acute inflammatory lung injury.  

 저자의 다른 논문

  • Lee, Ji-Hee (6)

    1. 1995 "Effects of In Vitro Exposure to Silica on Bioactive Mediator Release by Alveolar Macrophages" 대한생리학회지 = Korean journal of physiology 29 (1): 1~11    
    2. 1995 "Platelet-Activating Factor Potentiates the Activity of Respiratory Burst and Interleukin-1 in Rat Alveolar Macrophages" 대한생리학회지 = Korean journal of physiology 29 (2): 251~257    
    3. 1996 "Effects of Platelet-Activating Factor on Tumor Necrosis $Factor-_{\alpha}$ Production by Muramyl Dipeptide- or Silica-Stimulated Alveolar Macrophages" 대한생리학회지 = Korean journal of physiology 30 (1): 77~83    
    4. 1997 "Platelet-Activating Factor Enhances Interleukin-1 Activity by Alveolar Macrophages : Inhibition by PAF Specific Receptor Antagonists" The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology 1 (2): 201~208    
    5. 1998 "Study on the Action by PAF on IL-1 Modulation in Alveolar Macrophages: Involvement of Endogenous Arachidonate Metabolites and Intracellular $Ca^{++}$ Mobilization" The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology 2 (2): 241~249    
    6. 1999 "Acute Pulmonary Responses in Vivo to Silica Complexed with $H^+$, $Zn^{2+}$, or $Fe^{3+}$" The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology 3 (2): 183~189    

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