Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.9.3.1 (cytochrome oxidase)
 8,822 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have previously shown that the activity of cytochrome oxidase (CytOx) in skeletal muscle of patients with chronic obstructive pulmonary disease (COPD) was higher than in healthy control subjects. The mechanisms and implications of this observation were unclear. In particular, it was not known if this abnormality can occur also in: (1) cell types other than muscle cells, and (2) other chronic inflammatory diseases. To obtain further insight into these questions, we measured the activity of CytOx in circulating lymphocytes in patients with stable COPD (n = 17), bronchial asthma (n = 6), or chronic arthritis (n = 5), and in healthy control subjects (n = 8). We found that, compared with healthy subjects (280 +/- 117 nKat/microg protein), patients with COPD showed increased CytOx activity (430 +/- 150 nKat/microg protein, p = 0.01) in lymphocytes. Further, this activity was negatively related to the degree of airflow obstruction present in these patients (r = -0.53, p < 0.05). We also found that the activity of CytOx in circulating lymphocytes was higher than normal in patients with chronic arthritis (411 +/- 130 nKat/microg protein, p < 0.05) and, particularly, in patients with bronchial asthma (1,667 +/- 1,027 nKat/microg protein, p < 0.001). These results show that the increased CytOx activity previously reported in skeletal muscle of patients with COPD is also detected in other cell types (such as circulating lymphocytes) and in other chronic inflammatory diseases (such as bronchial asthma and chronic arthritis). The mechanisms and implications of these findings deserve further investigation.
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PMID:The activity of cytochrome oxidase is increased in circulating lymphocytes of patients with chronic obstructive pulmonary disease, asthma, and chronic arthritis. 1061 94

Beta-agonists and glucocorticoids are frequently coprescribed for chronic asthma treatment. In this study the effects of 4 week treatment with beta-agonist clenbuterol (CL) and glucocorticoid dexamethasone (DEX) on respiratory (diaphragm and parasternal) and limb (soleus and tibialis) muscles of the mouse were studied. Myosin heavy chain (MHC) distribution, fibres cross sectional area (CSA), glycolytic (phosphofructokinase, PFK; lactate dehydrogenase, LDH) and oxidative enzyme (citrate synthase, CS; cytochrome oxidase, COX) activities were determined. Muscle samples were obtained from four groups of adult C57/B16 mice: (1) Control (2) Mice receiving CL (CL, 1.5 mg kg(-1) day(-1) in drinking water) (3) Mice receiving DEX (DEX, 5.7 mg kg(-1) day(-1) s.c.) (4) Mice receiving both treatments (DEX + CL). As a general rule, CL and DEX showed opposite effects on CSA, MHC distribution, glycolytic and mitochondrial enzyme activities: CL alone stimulated a slow-to-fast transition of MHCs, an increase of PFK and LDH and an increase of muscle weight and fibre CSA; DEX produced an opposite (fast-to-slow transition) change of MHC distribution, a decrease of muscle weight and fibre CSA and in some case an increase of CS. The response varied from muscle to muscle with mixed muscles, as soleus and diaphragm, being more responsive than fast muscles, as tibialis and parasternal. In combined treatments (DEX + CL), the changes induced by DEX or CL alone were generally minimized: in soleus, however, the effects of CL predominated over those of DEX, whereas in diaphragm DEX prevailed over CL. Taken together the results suggest that CL might counteract the unwanted effects on skeletal muscles of chronic treatment with glucocorticoids.
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PMID:Clenbuterol antagonizes glucocorticoid-induced atrophy and fibre type transformation in mice. 1510 14

We showed recently that IL-4 causes mitochondrial dysfunction in allergic asthma. IL-4 is also known to induce 12/15-lipoxygenase (12/15-LOX), a potent candidate molecule in asthma. Because vitamin E (Vit-E) reduces IL-4 and inhibits 12/15-LOX in vitro, here we tested the hypothesis that Vit-E may be effective in restoring key mitochondrial dysfunctions, thus alleviating asthma features in an experimental allergic murine model. Ovalbumin (OVA)-sensitized and challenged male BALB/c mice showed the characteristic features of asthma such as airway hyperresponsiveness (AHR), airway inflammation, and airway remodeling. In addition, these mice showed increase in the expression and metabolites of 12/15-LOX, reduction in the activity and expression of the third subunit of mitochondrial cytochrome-c oxidase, and increased cytochrome c in lung cytosol, which indicate that OVA sensitization and challenge causes mitochondrial dysfunction. Vit-E was administered orally to these mice, and 12/15-LOX expression, key mitochondrial functions, ultrastructural changes of mitochondria in bronchial epithelia, and asthmatic parameters were determined. Vit-E treatment reduced AHR, Th2 response including IL-4, IL-5, IL-13, and OVA-specific IgE, eotaxin, transforming growth factor-beta1, airway inflammation, expression and metabolites of 12/15-LOX in lung cytosol, lipid peroxidation, and nitric oxide metabolites in the lung, restored the activity and expression of the third subunit of cytochrome-c oxidase in lung mitochondria and bronchial epithelia, respectively, reduced the appearance of cytochrome c in lung cytosol, and also restored mitochondrial ultrastructural changes of bronchial epithelia. In summary, these findings show that Vit-E reduces key mitochondrial dysfunctions and alleviates asthmatic features.
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PMID:Effects of vitamin E on mitochondrial dysfunction and asthma features in an experimental allergic murine model. 1962 25