Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P04040 (Catalase)
 3,577 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Free radicals have been suggested to play an important role in the pathogenesis of interstitial lung diseases, the most important of which are chronic interstitial pneumonias such as usual interstitial pneumonia (UIP) and desquamative interstitial pneumonia (DIP) and granulomatous lung diseases such as sarcoidosis. Because manganese superoxide dismutase (MnSOD) and catalase are two important intracellular antioxidant enzymes that probably play a central role in lung defense, the localization and intensity of these two enzymes were assessed by immunohistochemistry in biopsies of UIP (n = 9), DIP (n = 11), pulmonary sarcoidosis (n = 14), and extrinsic allergic alveolitis (n = 6). The mRNA of these enzymes in selected samples of bronchoalveolar lavage was assessed by Northern blotting. Catalase, but not MnSOD, was constitutively expressed, especially in type II pneumocytes of the healthy lung of nonsmoking individuals. In contrast, manganese SOD immunoreactivity was markedly upregulated in all of the interstitial lung diseases investigated, whereas no increased expression of catalase could be detected in any case. Both enzymes were expressed, especially in type II pneumocytes and alveolar macrophages of DIP and UIP, in the well-preserved areas of the lung, in the acute fibromyxoid lesions of UIP, and in the granulomas of sarcoidosis and extrinsic allergic alveolitis. The simultaneous expression of MnSOD and catalase in the alveolar region suggests their protective role against the progression of lung disease.
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PMID:Manganese superoxide dismutase and catalase are coordinately expressed in the alveolar region in chronic interstitial pneumonias and granulomatous diseases of the lung. 1067 8

Chronic Obstructive Pulmonary Disorder (COPD) is projected to rank third leading cause of deaths by 2030 as per WHO. COPD is a multi-etiological disease. The airflow dysfunction is usually progressive, associated with an abnormal inflammatory response of the lungs to noxious particles or gasses. As the lung is exposed to high levels of oxygen, it is more susceptible to oxidants mediated injury. Gender based differences are identifiable risk factors. Smoking is found to be a major risk factor in the causation of COPD resulting in oxidative stress . The aim of the present study is to evaluate the oxidant antioxidant imbalance in healthy non smoker controls and smokers with COPD. A total of 60 control (healthy non smokers) and 121 smokers having COPD were studied. The mean age is more in smoker group as compared to healthy controls, which identifies advancing age as a risk factor for COPD. The mean BMI and weight of smoker group is reduced as compared to control group. GOLD 2008 criteria was used to assess lung functions. Lung functions namely FEV1, FVC, FEV1/FVC% and FEV1% Predicted showed significant reduction in smoker group as compared to healthy non smoker controls. MDA in control and smoker group (1.09 +/- 0.09 and 1.41 +/- 0.23 nmol/ml respectively) showed significant changes (P < 0.001). Our results also demonstrate significant reduction in anti oxidant enzymes namely SOD (units/mg of serum protein), Catalase (units/mg of serum protein) and GPX (nmol of NADPH oxidized/ min/mg of serum protein) in smoker group as compared to healthy controls. On the basis of study it is concluded that smoking, gender and oxidant antioxidant imbalance are identifiable risk factors in COPD.
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PMID:Comparative study of pulmonary functions and oxidative stress in smokers and non-smokers. 2378 54