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:3.2.1.20 (alpha-glucosidase)
4,237 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Multidimensional scaling (MDS) was applied to the numerical taxonomy of Candida species based on isoenzyme profiles. Multidimensional scaling uses proximity measures to generate a spatial configuration of points in multidimensional space where distances between points reflect similarity among types. The biochemical profiles of 35 types of Candida species based on 26 tests consisting of isoenzymes of alpha-glucosidase, alkaline phosphatase, glucose-6-phosphate dehydrogenase, malate dehydrogenase, isocitrate dehydrogenase, and superoxide dismutase were analyzed. Cluster analysis of MDS, using the Euclidean distance as a proximity measure, separated C. tropicalis and C. paratropicalis from C. albicans and C. stellatoidea. Stepwise multiple linear regression revealed the isoenzyme tests which influenced each of the MDS dimensions. MDS was able to reduce the dimensionality of the test profile.
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PMID:Application of multidimensional scaling in numerical taxonomy: analysis of isoenzyme types of Candida species. 202 78

The dose dependent effect of superoxide dismutase in providing protection against oxygen free radicals mediated tissue damage was investigated. Xanthine-xanthine oxidase system was used to generate oxygen free radicals in vitro and damage renal brush border membrane of mice. At lower concentrations, superoxide dismutase was found to rather aggravate renal brush border membrane damage as shown by significant increase (p less than 0.05) in the malondialdehyde levels and corresponding decrease (p less than .05) in the activities of marker enzymes of renal tissue injury i.e. alkaline phosphatase, gamma-glutamyl transpeptidase and leucine aminopeptidase except maltase whose activity increased correspondingly. At higher doses of superoxide dismutase, significant protection (p less than .05) was observed against tissue damage in a dose dependent manner. On the other hand, catalase and mannitol provided dose dependent protection and their combinations with superoxide dismutase could alleviate the enhanced tissue damage produced by lower doses of superoxide dismutase. The implications of these findings have been discussed.
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PMID:Concentration dependent function of superoxide dismutase in oxygen free radicals mediated tissue injury in renal brush border membrane. 281 3

Reactive oxygen species have been found to be responsible for the tissue injury caused in experimental pyelonephritis in mice. The extent of lipid peroxidation (as assayed by malondialdehyde formation) was found to be increased significantly (p less than .001) in the infected group as compared to the normal mice. Superoxide dismutase and catalase (oxygen free radical scavengers) showed a significant decrease (p less than .001) in the extent of lipid peroxidation even in the presence of infection. Dimethyl sulfoxide, a hydroxyl ion scavenger, was however found to be effective only at 4 and 7 days postinfection (p less than .001). Allopurinol, an inhibitor of xanthine oxidase, did not significantly (p greater than .05) inhibit the formation of lipid peroxides, even upto 7 days postinfection. There was a significant decrease (p less than .05) in the activities of renal brush border membrane enzymes used as markers of renal tissue damage (i.e. alkaline phosphatase, leucine amino-peptidase and gamma-glutamyl transpeptidase) in the infected group as compared to the normal group. In the presence of superoxide dismutase, dimethylsulfoxide and catalase except allopurinol, the activities of all the enzymes but maltase were found to be increased significantly (p less than .05) as compared to the infected group. There was a significant increase (p less than .01) in the bacterial count in the presence of superoxide dismutase and DMSO in infected mice as compared to the infected control mice. However, no significant difference was observed in the catalase and allopurinol treated groups.
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PMID:Effect of various oxygen free radical scavengers in preventing tissue injury caused by Escherichia coli in pyelonephritic mice. 305 56

Activities of the enzymes lactase, sucrase, maltase, alkaline phosphatase, and superoxide dismutase (SOD) were measured in mucosa of duodenum and ileum of the rat after 70% resection of mid-small intestine or sham operation (transection). We also measured the concentrations of zinc, copper, and manganese in several tissues to assess trace metal homeostasis postresection. Resection resulted in decreased specific activities of disaccharidases and alkaline phosphatase in duodenum, while specific activities remained unchanged in ileum. Specific activity of total SOD (the sum of Cu-Zn and Mn SOD) and Mn SOD was the same in duodenum after resection but was markedly increased in ileum. Tissue trace metal concentrations changed minimally. Because of postresection mucosal growth, total segmental activity of disaccharidases and alkaline phosphatase was the same in duodenum and increased in ileum of resected compared to transected rats. Segmental activity of total SOD and Mn SOD doubled in duodenum and trebled in ileum of resected as compared to transected rats. Thus, total segmental enzyme activity is maintained or increased postresection by increased enterocyte proliferation rate and mucosal growth.
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PMID:Adaptation of the duodenum and ileum of the rat to mid-gut resection: enzyme activity and trace metal status. 308 Aug 64

We report in detail the ontogeny and the response of antioxidant enzymes to glucocorticoids in the rat small intestine. Pregnant rats in the treatment group received four injections of dexamethasone starting on days 18, 19, or 20 of gestation; fetuses were killed 2 days later. Control rats were injected with 0.9% saline solution. Postnatal rats reaching 14, 19, and 104 days of age received four injections of hydrocortisone and were killed 2 days later. Age-matched controls were injected with 0.9% saline solution. The activities of xanthine oxidase, superoxide dismutase, and catalase were measured in small intestines from fetal (20 and 21 days gestation), newborn, and older (aged 16, 21, and 106 days) rats. Xanthine oxidase rose with maturation; the major increase occurred on postnatal day 21. Catalase and superoxide dismutase rose minimally during intrauterine life. On day 16 postpartum, catalase and superoxide dismutase values were 160% and 60%, respectively, higher than at birth. Glucocorticoid administration stimulated maltase and sucrase activities, but had no effect on the antioxidant enzymes or xanthine oxidase.
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PMID:Maturation of antioxidant enzymes in rat small intestine: lack of glucocorticoid stimulation. 362 18

After twenty weeks of continuous dosing with Trichostrongylus colubriformis larvae substantial, but declining, numbers of worms had persisted in most of the lambs examined, although there were wide inter-individual variations. Mucosal lesions were found in the proximal small intestines of all the infected animals, their severity being directly related to worm burden. Representative brush border enzyme activities analysed in intestinal mucosal extracts from the same lambs showed differing responses. Alkaline phosphatase and glycyl-L-leucine dipeptidase were significantly depleted, whereas maltase activity was only marginally reduced, and leucine aminopeptidase activity was normal. Mucosal acetylcholinesterase activity was significantly elevated in the parasitised animals and, interestingly in view of the postulated role of this enzyme in nematode pathogenicity, the level of activity was directly correlated with individual worm burdens. Intestinal trypsin and chymotrypsin activities were unaffected and the level of superoxide dismutase, an enzyme associated with the inflammatory response, was normal. There were also no consistent changes in the mucosal activities of several enzymes including lactic dehydrogenase, creatine phosphokinase, aldolase, and glutamic oxaloacetate transaminase, whose leakage from damaged or necrotic tissues has been well defined in terms of the concomitant increase in their activity in the circulation. Lambs treated orally with fenbendazole five and/or ten weeks before slaughter either in the presence or absence of continued larval intake, had negligible worm burdens, and showed little evidence of intestinal damage at post mortem. Brush border enzyme levels, with the exception of alkaline phosphatase and, in two cases dipeptidase, were normal in these animals. The activity of alkaline phosphatase was approximately double that in the continuously infected, untreated lambs, but remained markedly lower than in the uninfected controls. The activities of the other enzymes studied, including acetylcholinesterase, were within the control range. In summary, in chronic trichostrongylosis even relatively low nematode burdens were associated with marked pathological and biochemical damage in the intestine with both lesion severity and mucosal acetylcholinesterase activity being directly related to worm numbers. Although morphological integrity was completely restored after anthelmintic treatment, the persistent low activity of brush border alkaline phosphatase coupled with the enzymological findings in untreated, infected animals suggests that recovery of the full functional capability of the intestinal mucosa may take longer.
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PMID:Intestinal enzyme activity in lambs chronically infected with Trichostrongylus colubriformis: effect of anthelmintic treatment. 634 11

The pathology and enzymology of the intestinal mucosae of lambs dosed daily with 2500 Trichostrongylus vitrinus larvae and killed at five, nine or 14 weeks were compared with worm-free animals. The proximal small intestines of the infected lambs exhibited extensive mucosal damage at five and nine weeks, but only isolated lesions were found at 14 weeks. Activities of the brush border enzymes alkaline phosphatase, leucine amino-peptidase, maltase and glycyl-L-leucine dipeptidase were all significantly depleted during infection, although the magnitude, time of onset and duration of the individual enzyme responses varied. Mucosal activities of the pancreatic enzymes, trypsin and to a lesser extent chymotrypsin were also markedly decreased particularly during the first nine weeks of infection. Specific acetylcholinesterase activity was significantly increased throughout the study, maximal levels being observed at five weeks. In contrast 'pseudo'-cholinesterase levels were consistently within the control range. During the early stages of infection (five weeks) glutamine-oxaloacetate transaminase activity was significantly decreased, while aldolase and creatine phosphokinase levels were significantly elevated. At nine weeks low glutamine-oxaloacetate transaminase activities were again detected and lactate dehydrogenase activity was also markedly reduced. At 14 weeks the mean activities of all four enzymes were within the normal range as were superoxide dismutase levels throughout. Significant correlations were found between alkaline phosphatase, trypsin, chymotrypsin, aldolase and glutamine-oxaloacetate transaminase activities and the degree of mucosal damage within the individual lambs.
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PMID:Changes in the intestinal enzyme activity of lambs during chronic infection with Trichostrongylus vitrinus. 710 Jun 47

Among progeny of a hybrid (Rana shqiperica x R. lessonae) x R. lessonae, 14 of 22 loci form four linkage groups (LGs): (1) mitochondrial aspartate aminotransferase, carbonate dehydratase-2, esterase 4, peptidase D; (2) mannosephosphate isomerase, lactate dehydrogenase-B, sex, hexokinase-1, peptidase B; (3) albumin, fructose-biphosphatase-1, guanine deaminase; (4) mitochondrial superoxide dismutase, cytosolic malic enzyme, xanthine oxidase. Fructose-biphosphate aldolase-2 and cytosolic aspartate aminotransferase possibly form a fifth LG. Mitochondrial aconitate hydratase, alpha-glucosidase, glyceraldehyde-3-phosphate dehydrogenase, phosphogluconate dehydrogenase, and phosphoglucomutase-2 are unlinked to other loci. All testable linkages (among eight loci of LGs 1, 2, 3, and 4) are shared with eastern palearctic water frogs. Including published data, 44 protein loci can be assigned to 10 of the 13 chromosomes in Holarctic Rana. Of testable pairs among 18 protein loci, agreement between Palearctic and Nearctic Rana is complete (125 unlinked, 14 linked pairs among 14 loci of five syntenies), and Holarctic Rana and Xenopus laevis are highly concordant (125 shared nonlinkages, 13 shared linkages, three differences). Several Rana syntenies occur in mammals and fish. Many syntenies apparently have persisted for 60-140 x 10(6) years (frogs), some even for 350-400 x 10(6) years (mammals and teleosts).
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PMID:Linkage groups of protein-coding genes in western palearctic water frogs reveal extensive evolutionary conservation. 928 85

Excessive chronic ethanol administration to animals has been shown to cause oxidative insults to many body organs, including the liver and brain. In many instances, iron supplementation to the diet may further aggravate ethanol-induced liver damage. However, whether increased dietary iron can enhance the damage in the brain is unknown. In this study, four groups of Sprague-Dawley rats were fed a Lieber-DeCarli liquid diet containing 5% (w/v) ethanol or isocaloric amount of maltase and/or 0.25% (w/v) carbonyl iron for 2 months. At the end of the feeding regimen, iron contents were determined in the plasma, liver, cerebral cortex, and cerebellum. Cerebellar superoxide dismutase (SOD) and nitric oxide synthase (NOS) activities were measured and mRNA levels of MnSOD, CuZnSOD, and nNOS in the cerebellar granule cell layer were quantitated by in situ hybridization. Ethanol treatment alone caused an increase in iron levels in plasma, no change in the liver and cerebral cortex, but a decrease in the cerebellum. Iron supplementation increased liver iron >4-fold but did not alter iron contents in the cerebellum and cortex. All of the mRNA species examined and SOD activity were not affected by either iron or ethanol administration. However, NOS activity in the cerebellum was significantly enhanced by ethanol, whereas iron supplementation had an opposite effect. Our results indicate that iron supplementation to animals consuming ethanol may have tissue-specific effects. Furthermore, ethanol-induced increase in NOS activity in the cerebellum may explain the sensitivity of cerebellar neurons to oxidative insult.
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PMID:Chronic ethanol and iron administration on iron content, neuronal nitric oxide synthase, and superoxide dismutase in rat cerebellum. 1023 6

We sought to determine whether a single reduction of hyperglycemia and those derivatives from nonenzymatic protein glycosylation may be effective in reducing the development of diabetic endothelial dysfunction. Therefore, we investigated how acarbose, an inhibitor of intestinal alpha-glucosidase that reduce hyperglycemia by lowering glucose absorption, may prevent the impairment of acetylcholine (ACh)-induced endothelium-dependent relaxations observed in isolated vascular segments from untreated streptozotocin-induced diabetic rats. When administered after diabetes induction, 10 mg/kg acarbose decreased modestly the enhancement of blood glucose and glycosylated hemoglobin (HbA1c) levels, but not those of advanced glycosylation end products (AGEs). This effect was linked to a partial improvement of ACh-induced responses both in conductance vessels, such as aortic segments, and resistance vasculature, like mesenteric microvessels. When acarbose was introduced after 6 weeks of untreated diabetes, blood glucose, HbA1c, and AGE levels were not affected and endothelial dysfunction remained unchanged in mesenteric microvessels, whereas a small improvement was observed in aortic segments. The addition of 100 U/ml superoxide dismutase enhanced the impaired relaxations to values similar to vessels from nondiabetic rats, indicating a main role for superoxide anions in diabetes-induced endothelial dysfunction. We conclude that hyperglycemia itself or elevated HbA1c, but not plasma AGEs, are related to enhanced oxidative stress and to the impairment of endothelium function associated to diabetes. This process can be partially prevented by reducing glucose absorption with acarbose.
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PMID:Treatment with acarbose may improve endothelial dysfunction in streptozotocin-induced diabetic rats. 1094 69


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