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Query: EC:3.1.3.5 (5'-nucleotidase)
 3,167 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To test the hypothesis that 5'-nucleotidase activity during ischemia is attenuated by oxygen-derived free radicals, we measured ischemia-induced reactive hyperemic flow, adenosine release, and 5'-nucleotidase activity in dogs (n = 62). A 1-minute occlusion of the coronary artery caused reactive hyperemic flow (307 +/- 5 versus 92 +/- 1 ml.100 g-1.min-1 at baseline) with increased release of adenosine (14.4 +/- 1.4 versus 0.4 +/- 0.1 nmol.100 g-1.min-1 at baseline). Superoxide dismutase augmented (p less than 0.001) both peak coronary blood flow (333 +/- 6 ml.100 g-1.min-1) and repayment (436 +/- 12 versus 320 +/- 7 ml/100 g in the untreated group). Adenosine release during reperfusion was augmented (22.7 +/- 1.9 nmol.100 g-1.min-1, p less than 0.001), and 8-phenyltheophylline completely abolished the enhanced reactive hyperemia. Enzymatic assay of 5'-nucleotidase activity revealed that the administration of superoxide dismutase increases ecto-5'-nucleotidase activity in ischemic myocardium. When an inhibitor of ecto-5'-nucleotidase, alpha, beta-methyleneadenosine 5'-diphosphate, was administered, the effects of superoxide dismutase were completely abolished. Thus, we conclude that 1) the augmentation of reactive hyperemic flow caused by superoxide dismutase is attributed to the enhanced release of adenosine and 2) the enhanced release of adenosine over the untreated controls is attributed to the protection of ecto-5'-nucleotidase activity during ischemia.
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PMID:Superoxide dismutase enhances ischemia-induced reactive hyperemic flow and adenosine release in dogs. A role of 5'-nucleotidase activity. 149 5

Alveolar macrophages (AM) are highly suppressive of the in vitro plaque-forming cell (PFC) response of spleen cells obtained from mice primed with sheep erythrocytes. Comparison of macrophage populations obtained from disparate anatomical sites revealed that although in both cases there was a cell-concentration-dependent suppression of the PFC response, resident AM or AM activated as a result of intravenous injection of Mycobacterium bovis BCG were equally suppressive at the doses examined. Although there was a similar dose-dependent suppression with peritoneal macrophages, BCG-activated cells were more suppressive of the PFC response than were resident cells. In contrast, splenic macrophages at comparable concentrations were not at all suppressive. Resident AM exhibited significantly lower levels of 5'-nucleotidase activity than did resident peritoneal macrophages. Macrophage-mediated suppression of the in vitro PFC response could not be attributed to the release of toxic oxygen metabolites (H2O2, O2- ,and .OH) or prostaglandins, since the addition of catalase, superoxide dismutase, 2-mercaptoethanol, or indomethacin did not completely reverse suppression. These results suggest that the lung microenvironment may maintain AM in an activated state which contributes to their potential immunoregulatory functions.
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PMID:Role of activation in alveolar macrophage-mediated suppression of the plaque-forming cell response. 283 Jan 91

The effect of ethanol on membrane enzymes (Na+, K+ and Mg2+ ATPases, 5'-nucleotidase, adenylate cyclase) alcohol dehydrogenase, aldehyde dehydrogenase and superoxide dismutase were studied in nerve cells (established cell lines, primary cultures of chick and rat brain) cultured in the presence of 100 mM ethanol, and in total rat brain, following various ethanol treatments of the rats (20% ethanol as the sole liquid source, intraperitoneal injection). The results show a difference between neuronal and glial cells. Most of the observed changes in enzymatic activities returned rapidly to control values when ethanol was withdrawn from the culture medium or from the diet. Alcohol dehydrogenase was more stimulated by ethanol than aldehyde dehydrogenase; therefore acetaldehyde may be accumulated. The inhibition of superoxide dismutase activity may allow an accumulation of cytotoxic O2- radicals in nervous tissue and may explain the polymorphism of lesions brought about by alcohol intoxication.
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PMID:Ethanol and neuronal metabolism. 626 95

On exposing promastigotes of L. donovani (Dd-8) to 34 degrees C for 30 hr, the flagella were shed, and size was decreased with 10% viability loss. The in vitro and in vivo infectivity of two forms was more or less similar. The 45Ca2+ uptake by the transformed cells was increased as compared to normal cells. Activity of 5'-nucleotidase was increased while activity of Mg(2+)-ATPase remained same. Parasite antioxidant enzymes were also significantly altered by heat shock. There was significant increase in superoxide dismutase, glutathione reductase and glutathione peroxidase. It was accompanied by decrease in ratio of reduced glutathione to oxidized glutathione.
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PMID:Biochemical changes in heat stressed promastigotes of Leishmania donovani. 760 93

To examine whether activation of polymorphonuclear leukocytes attenuates release of adenosine through attenuation of their own ecto-5'-nucleotidase activity, human polymorphonuclear leukocytes were incubated with and without exposure to either N-formyl-methionyl-leucyl-phenylalanine (FMLP) or complement C5a. Ecto-5'-nucleotidase activity of polymorphonuclear leukocytes was attenuated by both FMLP and complement C5a (22.7 +/- 3.6 vs 9.7 +/- 2.6 nmol/min per 10(7) cells at 10(-6) M FMLP, P < .05; 21.5 +/- 2.2 vs 10.2 +/- 1.2 nmol/min per 10(7) cells at 5 x 10(-7) g/mL complement C5a, P < .001), whereas cytosolic 5'-nucleotidase activity was not affected by either FMLP or complement C5a. These reductions of ecto-5'-nucleotidase activity that were caused by both FMLP and complement C5a were dose and time dependent and were inhibited by superoxide dismutase. Desferrioxamine did not inhibit the decreases in ecto-5'-nucleotidase. In accordance with the decreases in ecto-5'-nucleotidase activity, release of adenosine was attenuated in the FMLP-pretreated and complement C5a-pretreated polymorphonuclear leukocytes, which were restored by concomitant administration of superoxide dismutase. The viability of FMLP-pretreated and complement C5a-pretreated polymorphonuclear leukocytes was markedly decreased compared with the untreated group after 60 minutes of hypoxia followed by 60 minutes of reoxygenation. Thus, we conclude that: (1) activation of polymorphonuclear leukocytes attenuates their own ecto-5'-nucleotidase activity and thereby reduces adenosine release, (2) reduction of ecto-5'-nucleotidase activity is attributable to generated superoxide anion in polymorphonuclear leukocytes, and (3) viability of polymorphonuclear leukocytes after hypoxia and reoxygenation largely depends on the extents of decreases in ecto-5'-nucleotidase activity.
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PMID:Attenuation of ecto-5'-nucleotidase activity and adenosine release in activated human polymorphonuclear leukocytes. 834 95

To evaluate the specificity of some functional indices in assessment of body zinc nutrition status, we used experimental rat model to observe the effects of some factors, such as forced swimming, starvation, trauma and alcohol intoxication on zinc the status. Plasma zinc levels of rats significantly decreased after trauma increased after starvation. Liver zinc content showed a rising tendency in trauma and starvation rats. Activities of superoxide dismutase in red blood cells and alkaline phosphatase, mannosidase, 5'-nucleotidase in plasma of rats with alcohol intoxication declined significantly. Starvation led to decreased activities of alkaline phosphatase and angiotensin-converting enzyme, but increased activities of mannosidase. Trauma and forced swimming could cause increase of angiotensin-converting enzyme activity and decrease of 5'-nucleotidase activity, respectively. These results indicate that physiological and pathological effects should be excluded from of the above indices as plasma zinc index, in the assessment of body zinc nutrition status.
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PMID:[Effects of stress on indices for assessing zinc nutrition status]. 875 64

Cellular redox status and membrane protein activities were analyzed in kidneys from rats with ischemic acute renal failure (ARF). ARF was induced by clamping the left renal artery for 50 min. A parallel group of control animals was processed. In the ischemic group urea plasma levels were statistically increased as compared with the control group. Studies employing whole kidney homogenates revealed that ischemia produces an increment in lipid peroxidation levels and a reduction in glutathione concentration and in superoxide dismutase and glutathione peroxidase activities. Since lipid peroxidation may alter the function of membrane proteins we determined succinate cytochrome c reductase (SuccR), sodium-potassium ATPase (Na-K-ATPase), glucose-6-phosphatase (G-6-Pase) and alkaline phosphatase (ALP) activities in whole renal homogenates. Only G-6-Pase and ALP activities were modified by ischemia. Since ALP is a brush border membrane (BBM) enzyme and BBM is one of the main target structures in ARF, we assessed some parameters of BBM functionality. ALP, gamma-glutamyl transferase (gamma-GT) and 5'-nucleotidase (5'-NT) showed diminished activities in BBM from ischemic kidneys. Ischemia also modified the Vmax of paraaminohippuric acid (PAH) uptake without altering Km. An increment of lipid peroxidation and membrane fluidity in BBM was observed after the treatment. Total membrane proteins and protein recoveries in BBM were similar in both experimental groups. Sialic acid and sulfhydryl levels were similar in BBM from ischemic kidney and control ones. In summary, ARF induced by renal artery clamping for 50 min takes place with a significant increase in urea plasma levels. A decrease in the antioxidant defense system is detected. This induces lipid peroxidation in whole renal tissue, which may justify the diminished activities of some membrane enzymes such as G-6-Pase and ALP. A specific analysis of BBM function reveals a significant increment of lipid peroxidation which may be the cause of an increased membrane fluidity. This latter parameter might be, at least in part, responsible for the damaged function of apical ALP, 5'-NT, gamma-GT and PAH carrier.
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PMID:Impairment of cellular redox status and membrane protein activities in kidneys from rats with ischemic acute renal failure. 968 97

Activities of adenosine deaminase, 5'-nucleotidase, xanthine oxidase, superoxide dismutase, glutathione peroxidase and catalase enzymes were measured in cancerous and non-cancerous adjacent colorectal tissues from 10 patients. Activities of DNA turn-over enzymes (ADA, 5'NT and XO) were found increased and those of free-radical metabolizing enzymes (SOD, GSH-Px and CAT) decreased in cancerous tissues compared with those of non-cancerous adjacent ones. Malondialdehyde (MDA) concentrations in cancerous tissues were also found higher than those of non-cancerous tissues, which indicated accelerated lipid peroxidation in the cancerous tissues. In the correlation analysis, disordered enzymatical relations were observed between the enzymes of both metabolic pathways. Results suggest that activities of purine metabolizing enzymes increase to cope with accelerated purine metabolism in cancerous tissues and, enzymatic antioxidant defense potential of cancerous tissues decreases due to carcinogenic processes in the tissues. Reduced antioxidant defense system makes the cancerous tissue more vulnerable to toxic effects of some free-radical species.
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PMID:Activities of the enzymes participating in purine and free-radical metabolism in cancerous human colorectal tissues. 992 74

5'-Nucleotidase, responsible for the conversion of adenosine-5'-monophosphate into adenosine, was purified from bovine brain membranes, and subjected to oxidative inactivation. The 5'-nucleotidase activity decreased slightly after the exposure to either glutathione or Fe2+. The glutathione-mediated inactivation of 5'-nucleotidase was potentiated remarkably by Fe2+, but not Cu2+, in a concentration-dependent manner. Similarly, glutathione exhibited a concentration-dependent enhancement of the Fe2+-mediated inactivation. In comparison, the glutathione/Fe2+ system was much more effective than the ascorbate/Fe2+ system in inactivating the enzyme. In support of an intermediary role of superoxide ions or H2O2 in the action of glutathione/Fe2+ system, superoxide dismutase and catalase expressed a substantial protection against the inactivation by the glutathione/Fe2+ system. Meanwhile, hydroxyl radical scavengers such as mannitol, benzoate or ethanol were incapable of preventing the inactivation, excluding the participation of extraneous hydroxyl radicals. Whereas adenosine 5'-monophosphate as substrate exhibited a modest protection against the glutathione/Fe2+ action, a remarkable protection was expressed by divalent metal ions such as Zn2+ or Mn2+. Structure-activity study with a variety of thiols indicates that the inactivating action of thiols in combination with Fe2+ resides in the free sulfhydryl group and amino group of thiols. Overall, thiols, expressing more inhibitory effect on the activity of 5'-nucleotidase, were found to be more effective in potentiating the Fe2+-mediated inactivation. Further, kinetic analyses indicate that Fe2+ and thiols inhibit the 5'-nucleotidase in a competitive or uncompetitive manner, respectively. These results suggest that ecto-5'-nucleotidase from brain membrane is one of proteins susceptible to thiols/Fe2+-catalyzed oxidation, and the oxidative inactivation may be related to the selective association of Fe2+ and thiols to the enzyme molecule.
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PMID:Oxidative inactivation of brain ecto-5'-nucleotidase by thiols/Fe2+ system. 1107 66

Administration of aflatoxin B1 to rats (2 mg/kg intraperitoneally) caused significant increase in the activities of gamma-glutamyl transpeptidase, 5'-nucleotidase, acid phosphatase, acid ribonuclease as well as content of lipid peroxides in liver after six weeks. However, the activities of succinate dehydrogenase, glucose-6-phosphatase, catalase, superoxide dismutase, glutathione-S-transferase, glutathione peroxidase and glutathione reductase in liver were decreased. The levels of glycogen and reduced glutathione were also decreased. There were significant elevations in the levels of serum transaminases, phosphatases (acid and alkaline), dehydrogenases (sorbitol, lactate and glutamate) and bilirubin following aflatoxin B1 administration. Picroliv (25 mg/kg/day orally for six weeks), an iridoid glycoside isolated from the roots and rhizomes of Picrorhiza kurroa, significantly prevented the biochemical changes induced by aflatoxin B1.
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PMID:Biochemical changes induced in liver and serum of aflatoxin B1-treated male wistar rats: preventive effect of picroliv. 1116 62


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