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)

Selenium-ACE, a formulation containing the trace element selenium with three vitamins, is widely promoted for the treatment of arthritis. A controlled double-blind trial of Selenium-ACE in osteoarthritis failed to demonstrate any significant efficacy for the compound over placebo at 3 or 6 months though there was a non-significant trend to improvement in some clinical parameters in both groups. Side-effects were more frequently seen in the placebo group.
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PMID:Failure of selenium-ace to improve osteoarthritis. 219 71

The authors performed a controlled trial in 18 top athletes (9 weight lifters and 9 rowers, girls) in order to make evident some chronic and acute effects (antioxidant) of selenium. Nonprotein--SH (essential glutathione), lipid peroxides (MDA-malondialdehyde), glucose-6-phosphate dehydrogenases (G-6-PDH) and fructose-1,6-diphosphate aldolase in serum, have been recorded initially on basal conditions, after 3 weeks of treatment (100 micrograms/day selenium or placebo) and again after 3 weeks of treatment, also on basal conditions, when crossing over the groups (between a free interval of 10 days). In another trial we registered these parameters on basal conditions and after two hours of hard training accompanied by a per oral administration of 150 micrograms selenium (respectively placebo). The results show significant changes under selenium treatment of the peroxides, G-6-PDH and light changes, not significant of the nonprotein--SH, changes which could suggest an antioxidant effect of this element.
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PMID:Studies on selenium in top athletes. 314 41

We have characterized the effect of angiotensin converting enzyme (ACE) inhibitors on the activity of CuZn-superoxide dismutase (CuZn-SOD), Mn-superoxide dismutase (Mn-SOD), catalase, and selenium-dependent glutathione peroxidase (Se-GPx). CF1 mice (4-month-old females) were administered water containing enalapril (20 mg/l) or captopril (50 mg/l), during 4 to 11 weeks. After 11 weeks, enalapril treatment caused an increase in the activity of CuZn-SOD, Mn-SOD and Se-GPx, from 19 +/- 4 to 46 +/- 7, 2.1 +/- 0.2 to 3.8 +/- 0.2 units/mg protein and 27 +/- 3 to 54 +/- 3 milliunits/mg protein, respectively. After 11 weeks, captopril treatment increased the activities (P < 0.05) of CuZn-SOD, MnSOD and Se-GPx to 35 +/- 4, 2.9 +/- 0.2 units/mg protein, and 38 +/- 2 milliunits/mg protein, respectively. Catalase activity was not affected by the treatments. These results suggest that ACE inhibitors may protect cell components from oxidative damage by increasing the enzymatic antioxidant defenses.
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PMID:Superoxide dismutase and glutathione peroxidase activities are increased by enalapril and captopril in mouse liver. 789 34

Of the nine biological trace elements, zinc, copper and selenium are important in reproduction in males and females. Zinc content is high in the adult testis, and the prostate has a higher concentration of zinc than any other organ of the body. Zinc deficiency first impairs angiotensin converting enzyme (ACE) activity, and this in turn leads to depletion of testosterone and inhibition of spermatogenesis. Defects in spermatozoa are frequently observed in the zinc-deficient rat. Zinc is thought to help to extend the functional life span of the ejaculated spermatozoa. Zinc deficiency in the female can lead to such problems as impaired synthesis/secretion of (FSH) and (LH), abnormal ovarian development, disruption of the estrous cycle, frequent abortion, a prolonged gestation period, teratogenicity, stillbirths, difficulty in parturition, pre-eclampsia, toxemia and low birth weights of infants. The level of testosterone in the male has been suggested to play a role in the severity of copper deficiency. Copper-deficient female rats are protected against mortality due to copper deficiency, and the protection has been suggested to be provided by estrogens, since estrogens alter the subcellular distribution of copper in the liver and increase plasma copper levels by inducing ceruloplasmin synthesis. The selenium content of male gonads increases during pubertal maturation. Selenium is localized in the mitochondrial capsule protein (MCP) of the midpiece. Maximal incorporation in MCP occurs at steps 7 and 12 of spermatogenesis and uptake decreases by step 15. Selenium deficiency in females results in infertility, abortions and retention of the placenta. The newborns from a selenium-deficient mother suffer from muscular weakness, but the concentration of selenium during pregnancy does not have any effect on the weight of the baby or length of pregnancy. The selenium requirements of a pregnant and lactating mother are increased as a result of selenium transport to the fetus via the placenta and to the infant via breast milk.
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PMID:Zinc, copper and selenium in reproduction. 803 70

This study is aimed at examining whether essential arterial hypertension (HTN) or ACE inhibitors have any effect on erythrocyte selenium (Se)-dependent and Se-non-dependent glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) activity. Eleven patients with HTN (2 men and 9 women) and 9 healthy volunteers were included in this study after clinical examination and laboratory investigation. The activities of all three enzymes were determined and then the patients were assigned to receive ACE inhibitor therapy consisting of captopril, 25 to 50 mg daily, or enalapril, 10 to 40 mg daily. After 1 year, the determination of antioxidant enzymes was repeated. Our results showed that the initial values of Se-dependent GSH-Px in patients treated with ACE inhibitors were significantly lower (19.60 +/- 3.50 microM NADPH/min(-1)/mgHb(-1)) compared with the controls (28.64 +/- 4.93 microM NADPH/min(-1)/mgHb(-1); p < 0.001), whereas the activity of Se-non-dependent GSH-Px was significantly enhanced (13.55 +/- 1.46 microM NADPH/min(-1)/mgHb(-1); p < 0.001) compared with the control group (9.44 +/- 0.81 microM NADPH/min(-1)/mgHb(-1); p < 0.001). ACE inhibitors did not significantly change the activity of Se-dependent GSH-Px or Se-non-dependent GSH-Px. No significant alteration was observed in SOD activity.
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PMID:Selenium-dependent GSH-Px in erythrocytes of patients with hypertension treated with ACE inhibitors. 972 2

The capabilities of ICP-MS far exceed the slow, single-element analysis of GFAAS for determination of multiple trace elements. Additionally, its sensitivity is superior to that of DCP, ICP, and FAAS. The analytic procedure for ICP-MS is relatively straightforward and bypasses the need for digestion in many cases. It enables the physician to identify the target trace element(s) in intoxication cases, nutritional deficiency, or disease, thus eliminating the treatment delays experienced with sequential testing methods. This technology has its limitations as well. The ICP-MS cannot be used in the positive ion mode to analyze with sufficient sensitivity highly electronegative elements such as fluorine, because F+ is unstable and forms only by very high ionization energy. The ICP mass spectrometers used in most commercial laboratories utilize the quadrupole mass selector, which is limited by low resolution and, thus, by the various interferences previously discussed. For example, when an argon plasma is used, selenium (m/e 80) and chromium (m/e 52) in serum, plasma, and blood specimens are subject to polyatomic and molecular ion interferences. Low-resolution ICP mass spectrometers can therefore be used to analyze many trace elements, but they are not universal analyzers. High-resolution ICP-MS can resolve these interferences, but with greater expense. With the advent of more research and development of new techniques, some of these difficulties may be overcome, making this technique even more versatile. Contamination during sample collection and analysis causes falsely elevated results. Attention and care must be given to avoid contamination. Proper collection devices containing negligible amounts of trace elements should be used. Labware, preferably plastic and not glass, must be decontaminated prior to use by acid-washing and rinsed with [table: see text] de-ionized water. A complete description of sample collection and contamination has been written by Aitio and Jarvisalo as well as by Chan and Gerson. Lutz et al observed the ranges in blood shown in Table 4. We have adopted the ranges listed in Table 5 in urines of healthy, ambulatory, and community-dwelling individuals through a limited in-house study and review of literature. In conclusion, differentiation of trace element abnormalities (primary intoxication or disease versus secondary underlying disease) can be made only by utilizing results from trace element analyses in clinical specimens, medical history, and careful observation of symptoms. Repeat analysis on a second specimen collection is recommended when contamination is suspected.
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PMID:Technical and clinical aspects of spectrometric analysis of trace elements in clinical samples. 989 2

The effect of enalapril and captopril on total glutathione content (GSSG + GSH) and selenium-dependent glutathione peroxidase (Se-GPx) and glutathione reductase (GSSG-Rd) activities was investigated in mouse tissues. CF-1 mice (4-mo-old females) received water containing enalapril (20 mg/l) or captopril (50 mg/l) for 11 wk. Enalapril increased GSSG + GSH content (P < 0.05) in erythrocytes (147%), brain (112%), and lung (67%), and captopril increased GSSG + GSH content in erythrocytes (190%) and brain (132%). Enalapril enhanced Se-GPx activity in kidney cortex (42%) and kidney medulla (23%) and captopril in kidney cortex (30%). GSSG-Rd activity was enhanced by enalapril in erythrocytes (21%), brain (21%), liver (18%), and kidney cortex (53%) and by captopril in erythrocytes (25%), brain (19%), and liver (34%). In vitro erythrocyte oxidant stress was evaluated by thiobarbituric acid-reactive substances (TBARS) production (control 365 +/- 11, enalapril 221 +/- 26, captopril 206 +/- 17 nmol TBARS x g Hb(-1) x h(-1); both P < 0.05 vs. control) and phenylhydrazine-induced methemoglobin (MetHb) formation (control 66.5 +/- 3.5, enalapril 52.9 +/- 0.4, captopril: 56.4 +/- 2.9 micromol MetHb/g Hb; both P < 0.05 vs. control). Both angiotensin-converting enzyme inhibitor treatments were associated with increased nitric oxide production, as assessed by plasma NO-(3) + NO-(2) level determination (control 9.22 +/- 0.64, enalapril 13.7 +/- 1.9, captopril 17.3 +/- 3.0 micromol NO-(3) + NO-(2)/l plasma; both P < 0.05 vs. control). These findings support our previous reports on the enalapril- and captopril-induced enhancement of endogenous antioxidant defenses and include new data on glutathione-dependent defenses, thus furthering current knowledge on the association of ACE inhibition and antioxidants.
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PMID:Enalapril and captopril enhance glutathione-dependent antioxidant defenses in mouse tissues. 1071 74

Numerous recent investigations on the development and morphology of atherosclerotic lesions have shown programmed cell death or apoptosis to be an important factor in atherogenesis. Enzymes known as caspases are essential for completion of the apoptotic program. With regard to the origin of signals inducing apoptosis, there are two ways of initiating caspase activation: (a) cellular death receptor-mediated activation; and (b) activation mediated by mitochondrial permeability and expression of the p53 oncogene. Both of these pathways are involved in atherogenesis. Oxidative stress, angiotensin II and cholesterol overload are the primary factors that induce apoptosis in vascular cells. Considering apoptosis in endothelial cells, exposed phosphatidylserine on the cell membrane activates thrombin increasing the probability of arterial thromboses. Further progression of atherosclerosis is promoted by the formation of apoptotic bodies with oxidized phospholipids exposed on the membrane; these also activate adhesion of monocytes. Apoptosis of smooth muscle cells is usually observed in the fibrous portion of an atherosclerotic plaque in which the cells produce collagen important for plaque stability. As apoptosis occurs in smooth muscle cells, the fibrous cap grows thinner. This can result in both plaque rupture, formation of thrombi as well as calcification of the plaque from apoptotic smooth muscle cells remnants. Smooth muscle cells apoptosis is beneficial in that it offers protection to the walls of arteries against proliferative restenosis induced by invasive procedures. Apoptosis of macrophages contributes to the formation and progression of the lipidic core and promotes thrombosis of atherosclerosis in damaged arteries. By contrast, apoptosis of macrophages diminishes the production of matrix methaloproteinases that decompose collagen fibers. New facts concerning the effects of antioxidants (selenium, vitamin C and vitamin E), inhibitors of angiotensin converting enzyme, beta-blockers, calcium chanel blockers, and statins are also considered in this review.
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PMID:[Programmed cellular death and atherogenesis: from molecular mechanisms to clinical aspects]. 1282 74

There were few reports on the antioxidant response of aquatic organisms exposed to 2,4-dichlorophenol (2,4-DCP). This research explored the hepatic antioxidant responses of fish to long-term exposure of 2,4-DCP for the first time. Freshwater fish Carassius auratus were chosen as experimental animals. The fish were exposed to six different concentrations of 2,4-DCP (0.005-1.0 mg/l) for 40 days and then liver tissues were separated for determination. As shown from the results, 40 days afterwards, the activities of catalase (CAT) and selenium-dependent glutathione peroxidase (Se-GPx) and the content of oxidized glutathione (GSSG) were induced significantly on the whole compared to control group; superoxide dismutase (SOD) responded to 2,4-DCP exposure at only 0.005 mg/l; the content of reduced glutathione (GSH) was suppressed continuously except Group 7; the activity of glutathione reductase was inhibited initially and then restored to control level from Group 4 on; glutathione S-transferase had only slight responses in Groups 3 and 4. Total glutathione (tGSH) and GSH/GSSG ratio were also calculated to analyze the occurrence of oxidative stress. Besides, good dose-effect relations, which cover most of the exposure concentration range, were found between 2,4-DCP level and CAT activity, GSSG content, Se-GPx activity, respectively. In conclusion, SOD and Se-GPx may be potential early biomarkers of 2,4-DCP contamination in aquatic ecosystems, and further studies will be necessary.
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PMID:Effects of chronic exposure of 2,4-dichlorophenol on the antioxidant system in liver of freshwater fish Carassius auratus. 1476 89

Forty five smokers were classified into schistosomal cases with type-2 diabetis mellitus (GI) and with associated history of bronchial asthma (GII) and without T-2 DM (GIII). A control group (GIV) of non-diabetic non schistosomal age matched subjects who quitted smoking for >6 months were included. Assessed parameters included indices of glycemic status (glycated hemoglobin), angiogenesis (vascular endothelial growth factor) hepatic and bronchoalveolar disposition (Liver function test, metallothionein, serum levels of cotinine, cadmium selenium, copper & zinc) and bronchoalveolar lavage) (BAL) levels of surfactant proteins A & D, zinc and copper oxidative stress and fibrogenesis (total antioxidant capacity thiobarbituric acid reactive substance) and vasculopathy (angiotensin converting enzyme, P-selectin, nitrate) and periodontitis (collagenase and elastase in GCF) impact of cigarette smoking associated with trace element disbalance and enzymatic changes in crevicular fluid on altered parameters collaborative out-come. The study reflected the collaborative outcome of immune mediated mechanisms initiated by liver affection, glycemic status and history of predisposed bronchial integrity induced by oxidative stress.
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PMID:Cigarette smoking induced liver insult concomitant with inflammatory mediators in serum crevicular fluid and bronchio alveolar lavage of schistosomal diabetic subjects with history of bronchial asthma. 1792 10


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