Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Starvation for 24 h causes a striking fall in glutathione content from 3.19 +/- 0.27 to 1.88 +/- 0.14 (X +/- SEM) mumol/g tissue and of GGT activity from 31.75 +/- 4.17 to 19.49 +/- 3.13 (X +/- SEM) nmol/min/mg protein in the homogenate from whole mucosa of the upper small intestinal segments. This was associated with a significant increase in GSH-Px activity and the content of lipid peroxides (measured by the thiobarbituric assay). On semi-synthetic iron-supplemented diet the activities of GSH-T and GGT were significantly decreased as compared with crude diet. On semisynthetic iron-depleted diet GSH-T and GGT activities were further depressed, but this was accompanied with an additional depression of GSH, glutathione reductase (GSSG-R), and glutathione peroxidase (GSH-Px) activities and lipid peroxide concentrations. Food deprivation significantly lowers the mucosal GSH-content and could lead to a destabilization of this system presumably by increased oxidative stress. As compared to normal "crude" diet, semisynthetic diets and oral iron depletion have been shown to cause a depression of the intestinal GSH system. As a consequence of these effects, the resistance of the small intestinal mucosa toward exogeneous dietary toxins might be reduced.
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PMID:Glutathione and its related enzymes in the small intestinal mucosa of rats: effects of starvation and diet. 256 68

We compared trace element status in multiple sclerosis (MS) patients (n = 27) with and without treatment with corticosteroids and groups of healthy subjects. Concentrations of plasma ceruloplasmin, selenium, and zinc and erythrocyte (RBC) glutathione peroxidase, Se, and Zn were similar in all groups. RBC copper concentrations were significantly lower in MS patients than in control subjects (mean +/- SEM: 0.048 +/- 0.005 vs 0.060 +/- 0.002 mumol/g Hb) because of decreased RBC Cu with steroid therapy. RBC Zn-Cu ratios were significantly higher (14.9 +/- 1.0 vs 10.1 +/- 0.3) in MS patients than in control subjects, differing in both groups of MS patients. In MS and control subjects, RBC Cu correlated significantly with RBC Zn (r = 0.56, 0.49). Disease acuity and disability had no effect on trace-mineral status. These data suggest that in MS there is altered Cu and Zn homeostasis that may cause or result from the disease and is influenced by corticosteroid therapy. Systemic trace element alterations might provide clinically useful markers of MS.
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PMID:Trace element status in multiple sclerosis. 275 Jun 86

The tolerance against two different levels of enzymatically generated oxygen radicals was studied in isolated Langendorff-perfused hearts from selenium (Se)-deficient and control rats. The glutathione peroxidase activity of the Se-deficient hearts was less than 5% of that of the controls. Examination of the ultrastructure was made after random sampling using morphometric methods. Selenium-deficient hearts demonstrated some areas with myocytes with intracellular oedema. Oxygen radicals (hydrogen peroxide and superoxide) were generated by adding xanthine oxidase for 12 min (high dose: 25 U/l; low dose: 12.5 U/l) and hypoxanthine to the buffer of isolated Langendorff-perfused rat hearts. Left ventricle-developed pressure (LVDP) and high-energy phosphates (ATP and CP) were measured. After the low dose of oxygen radicals, LVDP was reduced to 32.7 +/- 6.5% (mean +/- SEM) of initial values in the Se-deficient group, but only to 58.3 +/- 8.4% in the control group (p less than 0.05). After the high dose, LVDP decreased abruptly to zero in both groups. However, ATP content was significantly (p less than 0.05) lower in Se-deficient than in control hearts. Perfusion with oxygen radicals (low dose) resulted in the appearance of mitochondrial damage in both groups, but intracellular oedema was still present only in the Se-deficient hearts. It is concluded that protection against oxygen radicals was reduced in Se-deficient hearts. This was probably due to loss of myocardial glutathione peroxidase activity.
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PMID:The selenium-deficient rat heart with special reference to tolerance against enzymatically generated oxygen radicals. 283 46

Because both vitamin E and selenium protect against lipid peroxidation, we evaluated the relationship between breath pentane, evolved from the peroxidation of linoleic acid, and plasma levels of alpha-tocopherol (vitamin E), Se, and Se-dependent glutathione peroxidase (Se-GSHPx). Nine home parenteral-nutrition (HPN) patients received added Se in intravenous solutions and were compared with 10 normal control subjects. The excretion of pentane (pmol.kg-1.min-1, means +/- SEM) in control subjects (6.34 +/- 0.96) was significantly lower than in HPN patients (15.02 +/- 1.12, p less than 0.001). alpha-Tocopherol (mumol/L), Se (mumol/L), and Se-GSHPx (U) values were, respectively, 18.13 +/- 1.70, 1.70 +/- 0.05, and 5.34 +/- 0.27 in control subjects and 10.21 +/- 1.66, 1.35 +/- 0.14, and 7.01 +/- 0.31 in HPN patients. All differences were statistically significant. Significant negative correlations were observed between plasma alpha-tocopherol levels and HPN duration and between pentane output and plasma alpha-tocopherol levels (r = -0.58, p less than 0.01). In HPN patients with reduced plasma alpha-tocopherol levels associated with increased pentane output, there is, inferentially, increased lipid peroxidation despite normal plasma Se and Se-GSHPx levels.
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PMID:Plasma vitamin E and selenium and breath pentane in home parenteral nutrition patients. 314 46

Selenium deficiency has been implicated as contributing to hepatic injury in alcoholics. The mechanism by which this occurs is most likely lipoperoxidation secondary to decreased activity of the selenoenzyme glutathione peroxidase. To further assess this relationship, we measured selenium content in autopsy livers in 12 patients with alcoholic cirrhosis compared to 13 patients matched for age and sex dying from other causes, mostly with cardiopulmonary diseases. The mean (+/- SEM) hepatic selenium content in cirrhosis was 0.731 +/- 0.077 microgram/g dry weight versus 1.309 +/- 0.166 microgram/g in controls (P less than 0.005; Student's t test). Clinical and biochemical indices of significant hepatic dysfunction, including encephalopathy, ascites, and elevations of serum bilirubin or prothrombin time, were only present in the cirrhotic group. A significant inverse correlation between hepatic selenium content and the prothrombin time was noted (r = -0.50; P less than 0.02). No significant relationships between hepatic selenium and the abnormalities of bilirubin, albumin, or aspartate aminotransferase were found. We conclude that significantly decreased hepatic selenium stores are present in patients with severe alcoholic cirrhosis compared to controls. The magnitude of that selenium deficit does correlate with some indices of hepatic function, specifically the prothrombin time. These data lend further support to a true selenium deficiency state in alcoholic cirrhosis. It is highly possible that selenium deficiency represents an important link, synergistically joining the nutritional and hepatotoxic backgrounds of alcoholic liver injury and cirrhosis.
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PMID:Decreased hepatic selenium content in alcoholic cirrhosis. 316 92

Foodstuffs produced and/or purchased locally were analyzed for Se. The effect of income and gender on Se intake and status of Utah County residents was evaluated by measurement of the following indicators: erythrocyte (RBC) and plasma Se concentration, and activity of Se-glutathione peroxidase (Se-GSH-Px) (EC 1.11.1.9) in RBCs, platelets, and plasma. A Random Digit Dialing procedure was employed to stratify subjects according to gender and annual family income (less than +10,000, +10,000-20,000, greater than +20,000) in a 2 x 3 factorial design, seven subjects per cell. The weekly consumption of 44 foods shown to contribute over 90% of the Se intake of U.S. subjects was recorded for each study participant. The estimated minimum daily intake for this sample was 76.0 +/- 4.5 micrograms Se/day (mean +/- SEM). Available grain products are not produced locally, and their Se content is lower than average values reported by the U.S.D.A. Locally produced meat and dairy products had higher than average Se contents. In spite of lower grain Se and higher meat Se concentrations, subjects in this study derived more Se from grain and dairy products, and less from meat products than did subjects in a nationwide sample. The Se status of Utah County residents is similar to several other populations in the United States. There were no significant differences in Se status or intake due to gender or income. The results suggest that consumption of other foods produced in a "high Se" area can maintain Se intake and status in spite of reduced consumption of meat products generally viewed as more reliable sources of dietary Se.
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PMID:The effect of income on selenium intake and status in Utah County, Utah. 336 Oct 40

To investigate whether iron is involved in the reperfusion syndrome by aggravating free radical injury, the hearts from iron-loaded and control rats were perfused under normoxic, anoxic, and reperfusion conditions. Normoxic perfusion revealed no change in coronary flow, contractility, or lactate dehydrogenase (LDH) release between these two groups. Under anoxic and reperfusion conditions, however, we found a significant increase of ventricle fibrillation (56% vs. 0%, p less than 0.01, n = 9), a significantly lower recovery of contractility (21 +/- 7.4% vs. 81 +/- 6.6%, mean +/- SEM; p less than 0.001), and a significant increase of LDH release (667 +/- 142 vs. 268 +/- 37 mU LDH/min/g wet wt, mean +/- SEM; p less than 0.05). Administration of either 20 microM of the antioxidant (+)-cyanidanol-3 or 50 microM of the iron-chelator deferoxamine totally prevented the generation of ventricle fibrillation and normalized contractility to control levels in the iron-loaded group. Moreover, 20 microM (+)-cyanidanol-3 significantly lowered LDH release in this period (312 +/- 67 mU), whereas deferoxamine had no protective effect on this LDH release (1,494 +/- 288 mU). Normal hearts appeared to be protected by 20 microM (+)-cyanidanol-3 as well. In this group (n = 6), a significantly higher recovery of contractility (97.1 +/- 3.2% vs. 81 +/- 6.6%, p less than 0.05) and a significantly lower release of LDH (110 +/- 27 vs. 268 +/- 37 mU, p less than 0.05) was found compared with the control group (n = 9). No difference in superoxide dismutase or glutathione peroxidase activity was found between the groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Iron-load increases the susceptibility of rat hearts to oxygen reperfusion damage. Protection by the antioxidant (+)-cyanidanol-3 and deferoxamine. 339 80

The capacity of human blood monocytes to secrete hydrogen peroxide (H2O2) and superoxide (O2-) was measured as the cells differentiated during 4 wk of culture. Morphologic transformation of monocytes into macrophages, epithelioid cells, and multinucleated giant cells accompanied a steady increase in the content of protein per cell, from 0.77 mg/10(7) cells on days 0 to 11.77 mg/10(7) cells on days 20 to 29. In contrast, secretion of H2O2 by adherent monocytes was 859 +/- 73 nmol/60 min per mg protein (mean +/- SEM, n = 18) on day 0, rose 40% on day 3, and then fell rapidly, remaining below 6% of the initial values after day 10. The decline in capacity to secrete reactive oxygen intermediates was observed whether H2O2 or O2- were measured, whether the cells were challenged with phorbol myristate acetate or with opsonized zymosan, and whether the results were expressed per milligram cell protein or per cell. Superoxide dismutase activity tripled in adherent monocytes from day 0 to day 3, and thereafter remained elevated through at least day 16. In contrast, the activity of myeloperoxidase declined rapidly, catalase and glutathione peroxidase declined more gradually, and glutathione reductase and glutathione remained constant through the period of observation. Thus, the decline in capacity to secrete H2O2 could not be attributed to increases in cellular levels of these antioxidants. On the first day of culture, H2O2 release was enhanced up to fourfold by inclusion of sodium azide or potassium cyanide in the assay medium. This enhancement appeared to be due to inhibition of monocyte myeloperoxidase, rather than catalase. This conclusion was based on the kinetics and dose-response relationships for the effects of azide and cyanide on H2O2 release and on the activities of catalase and myeloperoxidase. Thus, the differentiation of human monocytes into macrophages in vitro is accompanied by an apparent reduction in the capacity to produce H2O2 and O2-. In this regard, the human monocyte-derived macrophage comes to resemble the resting tissue macrophage previously characterized in the mouse peritoneal cavity.
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PMID:Hydrogen peroxide metabolism in human monocytes during differentiation in vitro. 627 9

Reduced glutathione (GSH) and activity of GSH related enzymes play a key role in defence against oxygen free radicals, whose production is, as known, raised in patients affected by diabetes mellitus, and at the same time they may contribute to the process of platelet aggregation. The purpose of this study was to evaluate GSH levels and activity of glutathione peroxidase (GSH-Px), glutathione reductase (GSSG-Red), glutathione transferase (GSH-Tr), glucose-6-phosphate-dehydrogenase (G6PDH), and thioltransferase (TT) in platelets of insulin-dependent diabetic patients in fair metabolic control (mean glycated haemoglobin: 6.5%), as related to presence of retinopathy, neuropathy or nephropathy and to platelet aggregation by arachidonic acid (AA) in vitro. Mean effective dose (ED50) of AA was on average significantly lower in the group of insulin-dependent diabetic patients (0.41 +/- 0.02 mM (SEM), n = 46) as compared with that of control subjects strictly matched for age, sex and weight (0.77 +/- 0.02, n = 51; P = 0.0001). Mean platelet GSH as well as the activity of GSH related enzymes expressed as geometric mean (95% confidence intervals) were similar in diabetic patients and in controls, except for GSSG-Red whose activity was significantly higher in diabetic subjects (28.5 (14.4-57.5) mU 10(-9) platelets vs. 20.3 (8.7-56) mU 10(-9) platelets; P = 0.01). In the diabetic group TT was reduced when compared with healthy controls (3.8 (0.9-12.2) mU 10(-9) platelets vs. 6 (1.6-26.1) mU 10(-9) platelets; P = 0.04).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Glutathione, glutathione utilizing enzymes and thioltransferase in platelets of insulin-dependent diabetic patients: relation with platelet aggregation and with microangiopatic complications. 749 40

The effect of an increased intake of wheat selenium (Se) on platelet Se, serum Se, whole-blood Se, and glutathione peroxidase (GSH-Px) levels was investigated in 14 healthy Norwegian females (age 21-53 years). The intake of 60 micrograms Se per day as wheat Se, for six weeks, significantly increased the platelet Se (mean +/- SEM) from 9.1 +/- 1.1 mumol/L to 11.4 +/- 0.9 mumol/L, the serum Se from 1.43 +/- 0.18 mumol/L to 1.63 +/- 0.25 mumol/L, and the whole blood Se from 1.77 +/- 0.18 mumol/L to 2.01 +/- 0.18 mumol/L. The increase in percent of initial Se values was twice as high for platelets as for serum and whole blood. The GSH-Px levels were not altered during the experiment. Platelet Se was not significantly correlated to the Se intake initially. At the end of the experimental period, the Se in platelets reflected the total Se intake, but not with a simple linear correlation. No significant correlation between the total Se intake and the Se concentration in whole blood or serum was found.
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PMID:Platelet selenium as indicator of wheat selenium intake. 815 90


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