Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: HUMANGGP:021525 (albumin)
 60,984 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. In previous studies a rat inhalation model was developed to investigate the treatment of acute nitrogen dioxide (NO2) intoxication. 2. Biochemical parameters, which may be important for the evaluation of lung injury and repair, were reviewed and compared with the histology. 3. After exposure to high NO2 concentrations (75 ppm, 125 ppm or 175 for 10 min) the lung injury observed by light microscope was most pronounced after 24 h and became worse with increasing concentration. 4. The most sensitive indicators for lung injury in the broncho-alveolar lavage fluid (BAL) were protein and albumin concentrations, angiotensin converting enzyme activity, beta-glucuronidase activity and the presence of neutrophil leucocytes. The changes observed in these variables were dose-dependent. Following exposure to 175 ppm the protein and albumin concentrations and the angiotensin converting enzyme activity showed a 100-fold increase, while the beta-glucuronidase activity showed a 10-fold increase. 5. Glucose-6-phosphate dehydrogenase and glutathione peroxidase in the supernatant of lung homogenate and gamma-glutamyl transferase activity in BAL are likely to be the most practical parameters for monitoring the phase of repair because their activities were maximal at the moment histological changes were reduced in intensity. 6. Repair was almost complete 7 d following exposure.
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PMID:Biochemical and histological alterations in rats after acute nitrogen dioxide intoxication. 135 14

We investigated the utilization of exogenous 14C-labelled arachidonic acid by the cyclooxygenase system of the gastric mucosa and its alteration by cytosolic factors, protein binding, glutathione peroxidase (GSH-Px), and hydrogen peroxides. Total prostaglandin (PG) synthesis from gastric microsomes was reduced in a dose- dependent manner to 12% and 68% of controls by increasing amounts of the 105,000g supernatant or albumin (8mg protein/ml), respectively (p less than 0.01). The inhibitory cytosolic factor was heat labile, protease sensitive, and was retained by a 300,000 Dalton ultrafiltration membrane. Thus, it was likely a protein. Other possible inhibitory mechanisms like protease- or heme-induced destabilization of the cyclooxygenase, haptoglobin-mediated inhibition, or self-inactivation by endogenous substrate were excluded. N-ethylmaleimide (NEM), an agent that alkylates sulfhydryl-groups thereby inhibiting GSH-Px, abolished the inhibitory effect of cytosol in a dose-dependent fashion. In contrast to their inhibition of prostaglandin synthesis, the binding of arachidonic acid by albumin or cytosolic proteins accounted to 75% and 19% under comparable conditions, respectively, however, cytosolic fatty acid binding was unaffected by NEM. Thus, it was concluded that the inhibitory effect of cytosol, in contrast to albumin, was mediated by a sulfhydryl-depending process, probably a GSH-Px. This conclusion was supported by a qualitatively comparable inhibition by a purified GSH-Px from bovine erythrocytes. The inhibitory action of cytosolic proteins was reduced significantly by increasing concentrations or repeated application of arachidonic acid; therefore, cytosolic GSH-Px was likely to affect substrate utilization by the microsomal PGH synthase through reduction of activating substrate peroxides. Similarly, the in vitro formation of cyclooxygenase products by mucosal homogenate or gastric microsomes in the absence of cytosol was limited at substrate concentrations below 80 microM, despite sufficient nonesterified arachidonic acid remaining in the incubate. This limitation was mediated only partially by self-inactivation of the prostaglandin cyclooxygenase. Neither N-ethylmaleimide nor repeated application of hydrogen peroxides increased substrate utilization by isolated microsomes, excluding contamination by GSH-Px or simply a lack of hydrogen peroxides as possible mechanisms for the limited utilization. From these results, a special role of substrate-linked lipid peroxides in the activation of mucosal prostaglandin synthesis is proposed. The reduction of these peroxides by glutathione dependent or independent peroxidases, e.g. the PGH synthase-linked hydroperoxidase activity itself, could explain the reduced utilization of nonesterified arachidonic acid by the gastric mucosa.
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PMID:Limited utilization of exogenous arachidonic acid by the prostaglandin cyclooxygenase in gastric mucosa: the role of protein binding, glutathione peroxidase, and hydrogen peroxides. 141 May 25

Twenty-seven of 66 patients with Crohn's disease had reduced concentrations of selenium and glutathione peroxidase in plasma and erythrocytes. When the patients were subgrouped according to the length of resected small bowel, a significant reduction of selenium and glutathione peroxidase in both plasma and erythrocytes was only found in patients with a resection > 200 cm. A highly significant correlation between selenium and glutathione peroxidase was found in plasma (r = 0.81) as well as in erythrocytes (r = 0.62), but no correlation was observed in the control group. A statistically significant correlation was also found between plasma selenium and the Harvey-Bradshaw score (r = -0.44), body mass index (wt/ht2) (r = 0.47), and plasma albumin (r = 0.29). Patients with a small-bowel resection > 200 cm appear to be at risk of developing severe selenium deficiency. These patients should have their selenium status monitored and probably receive selenium supplementation.
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PMID:Selenium status in patients with Crohn's disease. 141 13

The male rats were injected i.p. with a trace or a sublethal dose of [75Se]selenite (0.01 mg or 1.58 mg/kg Se of body weight, respectively). During seven days following the injection, the whole-body retention, organ distribution and excretion of 75Se were studied, along with 75Se distribution in blood and in blood fractions. Substantial dose-dependent differences in selenite metabolism were found: (i) The rate of 75Se excretion after the injection of the sublethal dose was observed to be substantially higher than with the trace dose - 86% of injected dose (% inj. d.) vs. 41% inj. d. during seven days. In addition to urinary excretion, the exhalation of 75Se took a considerable part in the former case. (ii) The sharp decrease of 75Se levels was a prevalent feature of the 75Se kinetics in most of the studied tissues after the injection of the sublethal dose. On the other hand, after the trace dose injection a considerable decrease of 75Se level was observed only in the liver. In the brain and particularly in the testis the 75Se level increased during seven days after this dose injection. The highest levels of radionuclide were found in liver after both doses. (iii) Over 80% of blood 75Se was contained in blood cells (RBC) at all time intervals studied following the sublethal dose injection. With the trace dose the blood 75Se was present predominantly in plasma. (iv) The distribution of 75Se in protein fractions of blood plasma and RBC-lysate was studied using gel filtration. The albumin fraction was found to be the main acceptor of 75Se in plasma 15 min after both trace and sublethal dose injection. However, in longer time intervals the 75Se distribution pattern in plasma proteins was affected by the dose applied. Most of 75Se present in RBC-lysate (68.5-91.2%) was detected in the haemoglobine fraction at all time intervals after the injection of the sublethal dose. On the other hand, with the trace dose this fraction contained only 7.5-28.5% of 75Se. Incorporation of a significant amount of 75Se to the GSH-Px (glutathione peroxidase) fraction of plasma and RBC-lysate was observed on day seven after the trace dose injection. GSH-Px represented 19% of plasma 75Se and 80% of 75Se present in RBC-lysate. Data on the molecular weight (M(r)) values of plasma and erythrocyte 75Se-GSH-Px were determined on the basis of elution volumes in the course of gel infiltration - 695,000 and 110,000, respectively. The noticeable difference in these values is discussed.
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PMID:Comparison of the kinetics of a trace and a sublethal dose of selenite in rats, with particular attention being given to blood selenium distribution. 182 17

The chemical forms of selenium (Se) were determined in human plasma fractions. Human plasma was subjected to gel filtration using Sephadex G-150, and the first Se peak from this column was subsequently chromatographed on DEAE-Sephacel. The form of Se in the Se peak which eluted from this column was shown to be selenocysteine (SeCys). In a second approach human plasma was again subjected to gel filtration and the first Se peak was chromatographed on Affigel blue. SeCys was shown to be the form of Se in both the retained and unretained Se on this column. The second gel filtration Se peak was also chromatographed on Reactive Blue 2-Sepharose CL-6B and the form of Se which was not retained was also shown to be SeCys. However, the form which was retained was shown to be selenomethionine. Evidence is presented that there are three Se containing proteins in human plasma, which are selenoprotein P, glutathione peroxidase, and albumin.
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PMID:Chemical forms of selenium in selenium containing proteins from human plasma. 205 9

The contribution of lung glucose-6-phosphate dehydrogenase (G-6-PD) activity to pulmonary antioxidant defenses was investigated in the isolated perfused rabbit lung using dehydroepiandrosterone (DHEA), a specific steroidal inhibitor of G-6-PD. Infusion of xanthine oxidase (0.002 U/ml) generated moderate lung edema as measured by increased lung weight and lung lavage albumin content. Infusion of DHEA caused an augmentation of xanthine oxidase-induced lung edema. Hydrostatic factors did not participate in the worsened lung edema because mean pulmonary artery pressures were similar in both experimental groups. Incubation of lung tissue in vitro with DHEA demonstrated ablation of tissue G-6-PD activity without decreasing catalase, glutathione peroxidase, or superoxide dismutase activity. It was concluded that DHEA is a specific inhibitor of lung G-6-PD, and that G-6-PD provides an important antioxidant defense mechanism in preventing oxidant-induced lung injury.
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PMID:Inhibition of rabbit lung glucose-6-phosphate dehydrogenase by dehydroepiandrosterone augments oxidant injury. 213 22

The specific cause of short stature in juvenile rheumatoid arthritis (JRA) is unknown. One hypothesis links altered growth to inadequate dietary intake. In this study, nutritional status was assessed in 34 children with JRA (8 with systemic JRA, 14 with polyarticular JRA, and 12 with pauciarticular JRA) and 9 healthy controls using 3-day diet records, anthropometrics, and biochemical analyses. Differences in growth were found among the three types of JRA. One third of all subjects were at or below the 10th percentile in height for age (these being predominantly among the systemic and polyarticular groups). With few exceptions, the mean dietary intake for calories and essential nutrients was found to be adequate for each of the three groups. However, more than half of those with systemic JRA reportedly consumed less than the recommended caloric intake for their age and weight. No significant correlations were found linking dietary intake to growth percentiles in any of the groups studied. Biochemical abnormalities were found among the systemic and polyarticular groups. These abnormalities included low plasma levels of vitamins A and C, proteins (albumin, prealbumin, and retinol binding protein) and zinc; and increased levels of copper and glutathione peroxidase activity. Plasma selenium and vitamin E levels were unchanged. The discrepancy between intake and certain circulating nutrient levels may reflect alterations in the requirements, absorption, or use of these nutrients in the presence of chronic inflammation.
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PMID:Nutritional status and growth in juvenile rheumatoid arthritis. 225 10

Lipid peroxidation products and defenses against free radical damage were determined in serum of 55 patients with senile dementia of the Alzheimer type (SDAT) and compared with values in 24 age-matched healthy control subjects. The following parameters were evaluated: lipid-conjugated dienes and trienes, malondialdehyde, superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activity in erythrocytes, vitamins E, C and A, zinc, selenium and copper, ceruloplasmin, transferrin and albumin. The results showed a statistically significant decrease in the levels of GSH-Px, vitamins E, C and A, zinc, transferrin and albumin in the SDAT group. On the other hand, most of the deficiencies concern the malnourished subgroup of the SDAT population (SOD, GSH-Px, vitamins E and C, selenium, zinc, transferrin and albumin). Such an alteration of free radical scavengers in the malnourished subgroup of the SDAT population could combine the radical and nutritional hypothesis advanced by some authors.
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PMID:Lipid peroxidation and free radical scavengers in Alzheimer's disease. 263 Mar 82

Selenium (Se) status was studied in a patient with classical maple syrup urine disease (MSUD) receiving Se supplement. The basal plasma Se concentration was 0.06 mumol/l increasing to 2.1 mumol/l after 40 days of supplementation. When the plasma Se distribution was analysed by gel filtration, a major peak was seen close to the high molecular weight proteins with a second peak in the albumin region. When the Se dose was decreased in a stepwise manner from 50 micrograms/day to 25 micrograms/day and then to 17 micrograms/day plasma Se decreased, but the proportion of plasma Se in the two protein peaks did not change. In a healthy girl not supplemented with Se, the proportion of plasma Se in the albumin region was somewhat lower. In the MSUD patient glutathione peroxidase activity was initially low, and increased ten-fold during Se supplementation. The study indicates that the Se requirement for plasma glutathione peroxidase activity was fulfilled at the lowest dose of Se used and that Se is incorporated into several plasma proteins after supplementation.
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PMID:Effect of selenium supplementation on the distribution of selenium among plasma proteins of a patient with maple syrup urine disease. 279 31

A nonradioisotopic method for measuring red cell volume that involves the use of 52Cr-sodium chromate as the red cell label and of graphite furnace atomic absorption analysis of chromium is described. The technique allows the labelling of 20 mL of packed red cells with 40 to 50 micrograms of sodium chromate (Na2CrO4) in 30 minutes at 22 degrees C with 94 +/- 6 percent uptake. Approximately 40 micrograms of Na2CrO4 was injected for in vivo studies. This results in posttransfusion in vivo red cell chromium levels after sample processing in the range of 1 to 7 micrograms per L, which could be quantitated accurately (coefficient of variation = 4.7%) by Zeeman electrothermal atomic absorption spectrophotometry. The labeling concentration of chromium did not cause increased hemolysis, and the labeled cells exhibited an osmotic fragility curve similar to that of unlabeled, fresh ACD red cells. Red cell glutathione peroxidase was unaffected by labeling, although glutathione reductase was reduced by approximately 13 percent (p less than 0.05). The 52Cr red cell volume-measuring method was evaluated by concurrent in vivo studies with the standard 51Cr and 125I-albumin methods for that procedure. Simultaneous measurement of red cell volumes in seven volunteers by the 51Cr, 52Cr, and 125I-albumin techniques correlated highly with each other (r greater than 0.76), with mean values of 2294 +/- 199, 2191 +/- 180, and 2243 +/- 291 mL, respectively. The standard deviations of the differences were small: 134 mL for 52Cr versus 51Cr and 183 mL for 52Cr versus 125I.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Studies with nonradioisotopic sodium chromate. I. Development of a technique for measuring red cell volume. 279 95


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