Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.15.1 (ACE)
18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To study the anaerobic degradation of the chimera 3-chloro-4-hydroxybenzoate (3-Cl,4-OHB), anaerobic freshwater sediment samples from the vicinity of Athens, Ga., were adapted for the transformation of 4-hydroxybenzoate (4-OHB), 3-chlorobenzoate (3-CB), 2-chlorophenol (2-CP), and 2,4-dichlorophenol (2,4-DCP). In nonadapted samples, both 4-OHB (product of aryl dechlorination) and 2-CP (product of aryl decarboxylation) were observed as intermediates in the transformation of 3-Cl,4-OHB to phenol. The accumulated phenol was subsequently transformed to benzoate, an intermediate in the conversion to methane and CO2. In 4-OHB-adapted samples (i.e., samples adapted for aryl decarboxylation), 2-CP was the first intermediate which was subsequently dechlorinated to phenol. In 3-CB-adapted samples (i.e., samples adapted for meta-chlorobenzoate dehalogenation), 3-Cl,4-OHB was stoichiometrically dechlorinated to 4-OHB. In 2-CP-adapted samples (i.e., samples adapted for ortho-chlorophenol dehalogenation), 4-OHB was the first major intermediate. Furthermore, 3-CB was not dechlorinated in 2-CP-adapted sediment samples, suggesting the possibility that different 3-Cl,4-OHB dechlorinating systems were induced in the 2-CP- and 3-CB-adapted sediments. Adaptation of sediment samples for dechlorination of 2,4-DCP did not lead to adaptation for dechlorination of 3-Cl,4-OHB. However, 3-Cl,4-OHB was dechlorinated to 4-OHB in our stable, sediment-free 2,4-DCP-dechlorinating enrichment, isolated previously from the same environment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The anaerobic degradation of 3-chloro-4-hydroxybenzoate in freshwater sediment proceeds via either chlorophenol or hydroxybenzoate to phenol and subsequently to benzoate. 148 80

Cor pulmonale is an important consequence of COPD. Although the incidence is not precisely known, it is seen more frequently in patients with hypoxemia, CO2 retention and severely reduced FEV1. When present, it limits peripheral oxygen delivery, increases shortness of breath, and reduces exercise endurance. It is also associated with higher mortality rates independent of other prognostic variables. Numerous factors may contribute to the development of cor pulmonale in patients with COPD, but its primary cause is chronic alveolar hypoxia resulting in pulmonary vasoconstriction, vascular remodeling and pulmonary hypertension. The physical exam, chest radiograph and ECG may be helpful in detecting the presence of cor pulmonale, but because of anatomic changes that occur in the chest, these tests are often insensitive in patients with COPD. Noninvasive diagnostic techniques utilizing Doppler echocardiography and radionuclide angiography allow for detection of RV dysfunction at an earlier stage and in most cases, preclude the need for right heart catheterization. LTO2 is the only therapy shown to improve survival in patients with COPD. However, statistical proof correlating improvements in pulmonary hemodynamics with increased survival is lacking. Bronchodilators, such as the beta 2 agonists and especially theophylline, may have beneficial effects on pulmonary hemodynamics in addition to their effect on respiratory function and are useful in COPD when RV dysfunction is present. Diuretics and phlebotomy are also useful in improving symptoms in appropriate patients. Vasodilators such as calcium channel blockers and ACE-inhibitors may improve pulmonary hemodynamics acutely, but may lower arterial PO2 by worsening ventilation-perfusion matching or blunt the improvement in pulmonary hemodynamics seen with supplemental oxygen. The long-term benefits of these agents have not been proven and their routine use in patients with cor pulmonale due to COPD cannot be recommended.
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PMID:Right ventricular dysfunction in chronic obstructive pulmonary disease. Evaluation and management. 199 28

2,4-Dichlorophenol (2,4-DCP) was anaerobically degraded in freshwater lake sediments. From observed intermediates in incubated sediment samples and from enrichment cultures, the following sequence of transformations was postulated. 2,4-DCP is dechlorinated to 4-chlorophenol (4-CP), 4-CP is dechlorinated to phenol, phenol is carboxylated to benzoate, and benzoate is degraded via acetate to methane and CO2; at least five different organisms are involved sequentially. The rate-limiting step was the transformation of 4-CP to phenol. Sediment-free enrichment cultures were obtained which catalyzed only the dechlorination of 2,4-DCP, the carboxylation of phenol, and the degradation of benzoate, respectively. Whereas the dechlorination of 2,4-DCP was not inhibited by H2, the dechlorination of 4-CP, and the transformation of phenol and benzoate were. Low concentrations of 4-CP inhibited phenol and benzoate degradation. Transformation rates and maximum concentrations allowing degradation were determined in both freshly collected sediments and in adapted samples: at 31 degrees C, which was the optimal temperature for the dechlorination, the average adaptation time for 2,4-DCP, 4-CP, phenol, and benzoate transformations were 7, 37, 11 and 2 days, respectively. The maximal observed transformation rates for these compounds in acclimated sediments were 300, 78, 2, 130, and 2,080 micromol/liter(-1)/day(-1), respectively. The highest concentrations which still allowed the transformation of the compound in acclimated sediments were 3.1 m/M 2,4-DCP, 3.1 mM 4-CP, 13 mM phenol, and greater than 52 mM benzoate. The corresponding values were lower for sediments which had not been adapted for the transformation steps.
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PMID:Sequential anaerobic degradation of 2,4-dichlorophenol in freshwater sediments. 211 Nov 12

The authors evaluated the influence of NAD, NADP, G-6-P and G-6-PDH on the synthesis of steroid hormones in the interstitial gland of the rat. The animals were killed by decapitation, and sections of the nucleus weighing altogether 20 mg were incubated with NAD (0.4 mM), NADP (0.4 mM), G-6-P (3.5 mM) and G-6-PDH (2 j.m./ml) for 4 hours in CO2 incubator. Then the tissue was homogenized, removed by centrifugation and then from the homogenous supernatant the authors extracted steroids which were in the incubating medium and in the tissue. Steroid hormones examined were marked radioimmunologically, they were: pregnenolon as the first and testosterone as the second stage of synthesis of nucleus androgens. The search carried out shows that the strongest stimulator in biosynthesis of pregnenolon was NADP together with the reducing system (G-6-P and G-6-PDH). On the other hand, in case of testosterone the highest effectiveness was achieved by simultaneous use of the cofactors examined. Applying cofactors separately the authors were able to find that both NAD and NADP together with the reducing system were responsible for testosterone synthesis and their simultaneous applying in the incubating medium leads to a synergistic effect.
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PMID:[The role of gonadotropins, cyclic AMP, 22-R-hydroxycholesterol and cofactors in regulating endocrine functions of the Leydig cells in rats. I. Effect of cofactors on the synthesis of steroid hormones in the interstitial gland of rats]. 263 80

We compared exercise responses in two groups of hypertensive patients treated with an angiotensin converting enzyme (ACE) inhibitor (lisinopril, 20-80 mg/day, n = 17) or a cardioselective beta-blocker (atenolol, 50-200 mg/day, n = 9). Measurements were made at rest and during exercise at 25 W (2.7 mets) and at 50 W (3.8 mets) on a bicycle ergometer (where mets is exercising oxygen consumption/resting oxygen consumption) after 4 weeks of placebo, and again after 12 weeks of drug administration. Both drugs reduced (P less than 0.05) mean arterial pressure. Atenolol caused significant decreases in the heart rate (approximately 25%) and cardiac output (approximately 26%; Defares CO2 rebreathing), and significant increases in total peripheral resistance (approximately 30%) and arteriovenous O2 content (approximately 20%). Lisinopril decreased (P less than 0.05) stroke volume. At the same exercise intensity systolic blood pressure, arteriovenous O2 and total peripheral resistance were lower (P less than 0.05) and the heart rate was higher (P less than 0.05) after lisinopril than after atenolol. After the treatment of hypertension with the ACE inhibitor the responses to exercise were less restrictive than those after treatment with the cardioselective beta-blocker.
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PMID:Effects of angiotensin converting enzyme inhibition and beta-blockade on exercise responses in hypertensive patients. 285 65

At the present time, comprehensive metabolism studies of 2,3-dichloro-1-propene (2,3-DCP) have not yet been reported. We have investigated the biotransformation of 2,3-DCP using female Wistar rats in order to elucidate the bioactivation mechanisms. 175 mg/kg, 1,3-14C-2,3-DCP in corn oil was administered to a rat. The animal was killed 20 hr later. Approximately 56.7% of the radioactivity was excreted in the urine, 1.6% in the feces, 5.3% was exhaled as unchanged 2,3-DCP, and 0.3% as CO2. 31.3% remained in the organs and the carcass. Three metabolic pathways were established. 1) Conjugation with GSH leading to S-(2-chloro-2-propenyl)mercapturic acid. 2) The P450 induced epoxidation with subsequent rearrangement to highly mutagenic 1,3-dichloroacetone. 1,3-Dichloroacetone was further converted to the dimercapturic acid, 1,3-(2-propanone)-bis-S-(N-acetylcysteine). 3) The hydrolysis to 2-chloroallyl alcohol followed by alcohol dehydrogenase catalyzed formation of highly mutagenic 2-chloroacrolein. The 2-chloroallyl alcohol is excreted directly in the urine and as the glucuronide. 2-Chloroacrolein is further oxidized to 2-chloroacrylic acid which is also excreted in the urine.
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PMID:Metabolism of 2,3-dichloro-1-propene in the rat. Consideration of bioactivation mechanisms. 289 57

Chronic obstructive pulmonary disease (COPD) is equated with chronic bronchitis and emphysema as one disease entity. In COPD airflow limitation is relatively persistent--unlike asthma. Tests for "small-airways disease" form no part of routine practice, for their accuracy in detecting pathological change is debatable. The proteolytic theory of the pathogenesis of emphysema highlights the role of neutrophil elastase, antielastases, oxidants, antioxidants, and thus of potential new treatments. Clinical features of COPD include breathlessness, cough, and sputum, with airflow obstruction and lung hyperinflation. The differential diagnosis includes bronchiectasis, cystic fibrosis, and pulmonary hypertension, but pulmonary fibrosis, etc., is distinguished by radiological infiltrates. Plain chest radiography cannot reliably diagnose emphysema in life, but a new method measuring lung density from the computed tomographic (CT) scan allows location, quantitation, and diagnosis of emphysema (defined by enlargement of distal air spaces) in humans in life. "Pink puffers" with breathlessness, hyperinflation, mild hypoxemia, and a low PCO2 are contrasted with "blue bloaters" with hypoxemia, secondary polycythemia, CO2 retention, and pulmonary hypertension and cor pulmonale. Antismoking measures are a major aim in management. A bronchodilator regimen combining a slow-release oral theophylline with an inhaled beta 2-agonist, ipratropium, and high-dose inhaled steroids is proposed because even modest improvement in obstruction can help these patients. In acute exacerbations with purulent sputum, antimicrobials against Streptococcus pneumoniae and Hemophilus influenzae are used with controlled oxygen therapy aiming to keep the arterial PO2 over 50 mm Hg without the pH falling below 7.25. Influenza prophylaxis is recommended, but pneumococcal vaccination remains debatable. Chronic under-nutrition in "emphysema" implies controlled trials of feeding regimens--but these remain to be assessed. Long-term oxygen therapy is the only treatment known to prolong life in blue bloaters, and oxygen concentrators and transtracheal oxygen delivery are discussed. Pulmonary vasodilators (e.g., beta 2-agonists, hydralazine, nifedipine, angiotensin-converting enzyme [ACE] inhibitors, etc.) have not yet been proved to provide long-term reduction in pulmonary arterial pressure. Blue bloaters have severe nocturnal hypoxemia in rapid eye movement (REM) sleep that is corrected by oxygen or the investigational drug almitrine.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Chronic obstructive pulmonary disease. 304 40

Isogenic strains of Escherichia coli W3110 containing pyruvate dehydrogenase complexes with three (wild-type), two or one lipoyl domains per lipoate acetyltransferase (E2p) chain, were constructed. The maximum growth rates (mumax) for batch cultures growing in minimal medium containing different carbon sources showed that reducing the number of lipoyl domains adversely mumax value of the mutant containing one lipoyl domain per E2p chain was restored by the presence of compatible multicopy plasmids encoding PDH complexes with either one or three lipoyl domains per E2p chain. In glucose-limited chemostat cultures the protein contents of all strains were similar and substrate carbon was totally accounted for in the biomass and CO2 produced. However, the carbon efficiencies (percentage carbon conversion to biomass) were significantly lower when the lipoyl domain content of the E2p subunit was reduced from three to one. Similarly, the cellular maintenance energy (m(e)) and the maximum growth yield (Ymax) were lower in bacteria containing PDH complexes with fewer than three lipoyl domains per E2p chain. Wild-type values were restored by supplementing the medium with either casamino acids (0.01%) or acetate (up to 0.1 mM). The lower growth efficiencies of the mutants were further confirmed in competition experiments where equal numbers of genetically marked (NalR) mutant and wild-type bacteria were used to inoculate glucose-limited chemostat cultures (dilution rate 0.075 h-1). The mutants with one or two lipoyl domains per E2p chain were washed out, whereas in controls, the initial ratio of wild-type (Nals) to reconstructed wild-type (NalR) bacteria was maintained over 50 generations.
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PMID:Metabolic engineering in Escherichia coli: lowering the lipoyl domain content of the pyruvate dehydrogenase complex adversely affects the growth rate and yield. 755 Oct 48

Resting cells of Desulfitobacterium dehalogenans JW/IU-DC1 growth with pyruvate and 3-chloro-4-hydroxyphenylacetate (3-Cl-4-OHPA) as the electron acceptor and inducer of dehalogenation reductively ortho-dehalogenate pentachlorophenol (PCP); tetrachlorophenols (TeCPs); the trichlorophenols 2,3,4-TCP, 2,3,6-TCP, and 2,4,6-TCP; the dichlorophenols 2,3-DCP, 2,4-DCP, and 2,6-DCP; 2,6-dichloro-4-R-phenols (2,6-DCl-4-RPs, where R is -H, -F, -Cl, -NO2, -CO2, or -COOCH3; 2-chloro-4-R-phenols (2-Cl-4-RPs, where R is -H, -F, -Cl, -Br, -NO2, -CO2-, -CH2CO2, or -COOCH3); and the bromophenols 2-BrP, 2,6-DBrP, and 2-Br-4ClP [corrected]. Monochlorophenols, the dichlorophenols 2,5-DCP, 3,4-DCP, and 3,5-DCP, the trichlorophenols 2,3,5-TCP, 2,4,5-TCP, and 3,4,5-TCP, and the fluorinated analog of 3-Cl-4-OHPA, 3-F-4-OHPA ("2-F-4-CH2CO2- P"), are not dehalogenated. A chlorine substituent in position 3 (meta), 4 (para), or 6 (second ortho) of the phenolic moiety facilitates ortho dehalogenation in position 2. Chlorine in the 5 (second meta) position has a negative effect on the dehalogenation rate or even prevents dechlorination in the 2 position. In general, 2,6-DCl-4-RPs are dechlorinated faster than the corresponding 2-Cl-4-RPs with the same substituent R in the 4 position. The highest dechlorination rate, however, was found for dechlorination of 2,3-DCP, with a maximal observed first-order rate constant of 19.4 h-1 g (dry weight) of biomass-1.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Specificity of reductive dehalogenation of substituted ortho-chlorophenols by Desulfitobacterium dehalogenans JW/IU-DC1. 788 14

The effects of L-carnitine on 14CO2 release from [1-14C]pyruvate oxidation (an index of pyruvate dehydrogenase activity, PDH), [2-14C]pyruvate, and [6-14C]glucose oxidation (indices of the acetyl-CoA flux through citric acid cycle), and [U-14C]glucose (an index of both PDH activity and the flux of acetyl-CoA through the citric acid cycle), were studied using isolated rat cardiac myocytes. L-carnitine increased the release of 14CO2 from [1-14C]pyruvate, and decreased that of [2-14C]pyruvate in a time and concentration-dependent manner. At a concentration of 2.5 mM, L-carnitine produced a 50% increase of CO2 release from [1-14C]pyruvate and a 50% decrease from [2-14C]pyruvate oxidation. L-carnitine also increased CO2 release from [1-14C]pyruvate oxidation by 35%, and decreased that of [2-14C]pyruvate oxidation 30%, in isolated rat heart mitochondria. The fatty acid oxidation inhibitor, etomoxir, stimulated the release of CO2 from both [1-14]pyruvate and [2-14C]pyruvate. These results were supported by the effects of L-carnitine on the CO2 release from [6-14C]- and [U-14C]glucose oxidation. L-carnitine (5 mM) decreased the CO2 release from [6-14C]glucose by 37%, while etomoxir (50 microM) increased its release by 24%. L-carnitine had no effect on the oxidation of [U-14C]glucose. L-carnitine increased palmitate oxidation in a time- and concentration-dependent manner in myocytes. Also, it increased the rate of efflux of acetylcarnitine generated from pyruvate in myocytes. These results suggest that L-carnitine stimulates pyruvate dehydrogenase complex activity and enhances non-oxidative glucose metabolism by increasing the mitochondrial acetylcarnitine efflux in the absence of exogenous fatty acids.
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PMID:Stimulation of non-oxidative glucose utilization by L-carnitine in isolated myocytes. 859 97


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