Gene/Protein Disease Symptom Drug Enzyme Compound
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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)

This study determined whether a single 60-mg dose of ferrous sulfate interferes with fractional zinc absorption (FZA) at 7-9 wk of lactation. In a crossover design, 5 exclusively breast-feeding women were given either a single 60-mg iron supplement or no supplement. FZA was measured by analyzing zinc stable isotope tracers ((70)Zn and (67)Zn) in urine samples collected for 7 d after isotope dosing. A 0.7-micromol intravenous (IV) infusion of (70)Zn as ZnCl(2) in saline was followed by a 0.03-mmol oral dose of (67)Zn as ZnCl(2) given with a standardized meal. After a 7-d wash-out period, the supplement given was reversed and a second FZA measurement was taken. FZA was calculated from isotopic enrichments in urine measured by inductively coupled plasma mass spectrometry. Hemoglobin, plasma ferritin and transferrin receptor, and plasma 5'-nucleotidase, plasma zinc and erythrocyte zinc did not differ before the two measurements of zinc absorption. When women were given a single iron supplement, FZA was significantly lower, 21.7 +/- 1.7% compared with 26.9 +/- 2.6% when no supplement was given (P = 0.032). A single 60-mg iron dose significantly decreases FZA during early lactation.
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PMID:A single 60-mg iron dose decreases zinc absorption in lactating women. 1209 67

Cupric sulfate is an inorganic salt which is widely used in industry, agriculture, and veterinary medicine. Its applications include use as an algicide in potable waters and as a feed additive and therapeutic agent in swine, sheep, and cattle. Because copper salts are found in human water supplies, toxicity studies of cupric sulfate pentahydrate were conducted in male and female F344/N rats and B6C3F1 mice by the drinking water (2-week studies only) and dosed feed routes (2-week and 13-week studies). Animals were evaluated for hematology, clinical chemistry, urinalysis, reproductive toxicity, tissue metal accumulation, and histopathology. In the 2-week drinking water studies, groups of five rats and five mice per sex received cupric sulfate at concentrations of 300 to 30,000 ppm for 15 days. One female rat, one male mouse, and three female mice in the 3000 ppm groups and all rats and mice in the 10,000 and 30,000 ppm groups died before the end of the studies. The remaining mice and rats in the 3000 ppm groups gained little or lost weight. Water consumption in the three highest dose groups of both species was reduced by more than 65%. Clinical signs observed in these groups were typical of those seen in moribund animals and were attributed to dehydration. The only gross or microscopic change specifically related to cupric sulfate toxicity was an increase in the size and number of cytoplasmic protein droplets in the epithelium of the renal proximal convoluted tubule in male rats from the 300 and 1000-ppm groups. In the 2-week feed studies, groups of five rats and five mice per sex were fed diets containing 1000 to 16,000 ppm cupric sulfate. No chemical-related deaths occurred in any dose group. Compared to the controls, rats and mice in the two highest dose groups had reduced body weight gains which were attributed to decreased feed consumption. Hyperplasia with hyperkeratosis of the squamous epithelium on the limiting ridge of the forestomach was seen in rats and mice of each sex; this lesion was more severe in rats than in mice. Inflammation of the liver, periportal to midzonal in distribution, occurred in rats in the 8000 and 16,000 ppm groups. Depletion of hematopoietic cells was evident in rats of each sex in the bone marrow (8000 and 16,000 ppm) and spleen (16,000 ppm). Kidneys of male and female rats in the 4000, 8000, and 16,000 ppm groups had an increased number and size of protein droplets in the epithelia of the renal cortical tubules. In the 13-week feed studies, groups of 10 rats per sex received diets containing 500 to 8000 ppm cupric sulfate, and groups of 10 mice per sex received diets containing 1000 to 16,000 ppm cupric sulfate for 92 days; estimates of cupric sulfate consumption ranged from 32 to 551 mg/kg per day for rats and 173 to 4157 mg/kg per day for mice. There were no chemical-related deaths in rats or mice, and no clinical signs of cupric sulfate toxicity were recorded. Final mean body weights were lower than those of the controls for animals of both species receiving doses of 4000 ppm cupric sulfate and greater. In mice in the 13-week studies, there was a dose-related decrease in liver weights. Hematologic, clinical chemistry, and urinalysis evaluations of rats in the 13-week study revealed variable chemical-related changes that were, for the most part, restricted to the 4000 and 8000 ppm groups. Increases in serum alanine aminotransferase and sorbitol dehydrogenase activities in both sexes were indicative of hepatocellular damage, as were increases in 5'-nucleotidase and bile salts in males. Decreases in mean cell volume, hematocrit, and hemoglobin indicated the development of a microcytic anemia, while increases in reticulocyte numbers at the same time points suggested a compensatory response to the anemia by the bone marrow. Increases in urinary glucose and N-acetyl-beta-D-glucosaminidase (a lysosomal enzyme) and aspartate aminotransferase (alpha-cytosolic enzyme) were suggestive of renal tubule epithelial damage. Dose-related increases in copper occurred in all male rat tissues examined (lissues examined (liver, kidney, plasma, and testis). These increases were accompanied by increases in zinc in the liver and kidney. Plasma calcium was significantly reduced in the 4000 and 8000 ppm groups, and there was a trend toward reductions in calcium in the kidney and testis as well. In the 8000 ppm group, plasma magnesium was significantly increased relative to the controls. Rats in the three highest dose groups had hyperplasia and hyperkeratosis of the forestomach, inflammation of the liver, and increases in the number and size of protein droplets in the epithelial cytoplasm and the lumina of the proximal convoluted tubules. These effects were similar to those seen in the 2-week feed study, and the incidence and severity of these lesions were dose related. Many of the droplets in male rat kidneys were large and had irregular crystalline shapes. These droplets stained strongly positive for protein but were negative by iron, PAS, and acid-fast (lipofuscin) staining methods. α-2-Microglobulin was present in the droplets of male rats, but there was no dose- related, qualitative difference in the content of this protein. In the 4000 and 8000 ppm groups, copper was distributed in a periportal to midzonal pattern in the liver and was restricted to the cytoplasm of the proximal convoluted tubule epithelium in the kidney. Copper was present in some, but not all, of the protein droplets. Transmission electron microscopy of the livers of rats of each sex revealed increases in the number of secondary lysosomes in hepatocytes in the periportal area. In mice of each sex receiving 4000 ppm cupric sulfate and higher in the 13-week study, there was a dose-related increase in hyperplasia with hyperkeratosis of the squamous mucosa on the limiting ridge of the forestomach. Minimal positive staining for copper was present in the liver and was limited to high-dose (16,000 ppm) male and female mice. Cupric sulfate produced no adverse effects on any of the reproductive parameters measured in rats or mice of either sex. In summary, administration of cupric sulfate to rats in feed or drinking water resulted in significant gastric changes and hepatic and renal damage. The primary lesion in rats was an increase in the size and number of proteinaceous droplets in the epithelial cytoplasm and lumen of the proximal convoluted tubule. For rats in the 13-week study, the no-observed-adverse-effect level (NOAEL) for evidence of histologic injury to the kidney was 1000 ppm for males and 500 ppm for females, while the NOAEL for liver inflammation was 1000 ppm for males and 2000 ppm for females. Hyperplasia with hyperkeratosis of the epithelium on the limiting ridge separating the forestomach from the glandular stomach was also seen in rats of each sex, and the NOAEL for this change was 1000-ppm cupric sulfate in the feed. Additionally, clinical pathology alterations noted in the 13-week study, along with histologic changes in bone marrow noted in the 2-week feed study, were indicative of a microcytic anemia with a compensatory bone marrow response. Mice appeared to be much more resistant to the toxic effects of cupric sulfate than rats. The primary target tissue in mice was the epithelium of the limiting ridge of the forestomach. The NOAEL for the hyperplasia and hyperkeratosis seen at this site in mice was 2000-ppm cupric sulfate in the feed. Synonyms: Chalcanthite; Copper sulfate; cupric sulfate pentahydrate; bluestone; blue vitriol; Roman vitriol; Salzburg vitriol. (NOTE: These studies were supported in part by funds from the Comprehensive Environmental Response, Compensation, and Liability Act trust fund (Superfund) by an interagency agreement with the Agency for Toxic Substances and Disease Registry, U.S. Public Health Service.)
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PMID:NTP technical report on the toxicity studies of Cupric Sulfate (CAS No. 7758-99-8) Administered in Drinking Water and Feed to F344/N Rats and B6C3F1 Mice. 1220 95

A phosphodiesterase was purified from the venom of the snake Bothrops alternatus by a combination of gel filtration and ion exchange chromatographies. In SDS-PAGE, the enzyme gave a single band with a molecular mass of 105 kDa, which was unaltered in the presence of beta-mercaptoethanol, indicating that the protein contained no subunits. A single protein band was also observed in native PAGE. There were no contaminating 5'-nucleotidase, alkaline phosphatase and protease activities. The enzyme was recognized by commercial bothropic antiserum and gave a single band in immunoblotting. The enzyme had a pH optimum in the range of 7.5-9.5 and the optimum temperature was 60 degrees C, with activity being rapidly lost within 1 min at > or = 70 degrees C. The Km of the enzyme was 2.69 mM. PDE activity was potentiated by cobalt and, to a lesser extent, by calcium, whereas copper, manganese, zinc, EDTA, and beta-mercaptoethanol were inhibitory. These properties show that this enzyme is very similar to that isolated from other snake venoms.
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PMID:Purification and characterization of a phosphodiesterase from Bothrops alternatus snake venom. 1263 51

Male weaning rats were divided randomly into five groups. They were fed with diets containing zinc deficient(DZ), high zinc(HZ), normal zinc (NZ) and high zinc pair-fed with zinc deficient group(HZP) respectively. The rats in DZ and HZ groups were exchanged diets after 20 days. A part of rats in each group were killed at days 20, 50 and 70. The activities of alkaline phosphatase(ALP), 5'-nucleotidase(5'-NT) and copper-zinc-superoxidase dismutase(Cu-Zn-SOD), the zinc concentration in plasma and kidney were determined to assess the better indices for zinc nutrition. The results indicted that: The activities of ALP in DZ group at 20 d was significantly lower than that in the same group at the beginning, in the HZ group and in the HZP group, and increased significantly after the diet was changed to HZ diet after 30 days. The activities of 5'-NT in DZ group rats was decreasing with the extension of experimental period. These results indicated that the activities of ALP and 5'-NT were sensitive to zinc supplementation even though they were changed a little during zinc exhausted. The activity of ALP was decreasing with growing, and the activity of 5'-NT was increased with growing. Zinc concentration in plasma of DZ group was significantly lower than that of other groups which include DZ-HZ group at the 50th day, and it was also the lowest among groups at the end of experiment. Zinc concentration in the kidney of HZ-DZ group was significantly lower than that of HZ and DZ-HZ groups by the end of experiment. There were little changes of the activity of Cu-Zn SOD and the zinc content in kidney during the experiment period. These results indicated that the activities of both ALP and 5'-NT and plasma zinc were sensitive to zinc supplementacior and zinc deficiency.
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PMID:[Research on some enzyme activities in the assessment of zinc nutritional status of growing rats]. 1271 98

Bacteriophage lambda protein phosphatase (lambdaPP) is a member of a large superfamily of metallophosphoesterases, including serine/threonine protein phosphatases, purple acid phosphatases, 5'-nucleotidase, and DNA repair enzymes such as Mre11. Members of this family share several common characteristics, including a common phosphoesterase motif, secondary structural fold (betaalphabetaalphabeta), and metal ligand environment, and often accommodate a dinuclear metal center. The identity of the active site metals often differs between family members. Despite the extensive spectroscopic studies of several family members, only the standard redox potential of porcine purple acid phosphate (PAP) has been measured. In this report, we investigate the redox properties of another member of this protein family. The standard redox potentials of the mono-Fe, Fe-Zn, and Fe-Fe metalloisoforms of lambdaPP were determined from anaerobic redox titration experiments. Two different S = 5/2, mono-Fe3+ lambdaPP species were identified: the first with an E/D approximately 0.17, g = 8.9 and 4.8, and an Eo' approximately +130 mV; the second with E/D approximately 0.05, g = 6.7, 5.9, and 4.4, and an Eo' approximately +120 mV. The first and second mono-Fe3+ species are thought to represent Fe present in the M2 and M1 sites, respectively. The addition of Zn2+ to mono-Fe3+ lambdaPP results in a decrease in both mono-Fe3+ species and the appearance of a new S = 5/2, Fe(3+)-Zn2+ species (E/D approximately 0.02, g = 5.9, and an Eo' > +175 mV). The Fe-Fe lambdaPP titration revealed an S = 1/2, Fe(3+)-Fe2+ (g < 2) species with an Eo' > +128 mV. These results suggest that the active site of lambdaPP supports a high oxidation potential for both metal sites and may indicate an equally oxidizing active site for other member metallophosphoesterases.
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PMID:Electrochemical studies of the mono-Fe, Fe-Zn, and Fe-Fe metalloisoforms of bacteriophage lambda protein phosphatase. 1473 Sep 83

The trace element zinc is essential for the survival and function of all cells. Zinc deficiency, whether nutritional or genetic, is fatal if left untreated. The effects of zinc deficiency are particularly obvious in the skin, seen as an erythematous rash, scaly plaques, and ulcers. Electron microscopy reveals degenerative changes within keratinocytes. Despite the well-documented association between zinc deficiency and skin pathology, it is not clear which cellular processes are most sensitive to zinc deficiency and could account for the typical pathological features. We used the cultured HaCaT keratinocyte line to obtain insight into the cellular effects of zinc deficiency, as these cells show many characteristics of normal skin keratinocytes. Zinc deficiency was induced by growing cells in the presence of the zinc chelator, TPEN, or by growth in zinc-deficient medium. Growth of cells in zinc-deficient medium resulted in a 44% reduction of intracellular zinc levels and a 75% reduction in the activity of the zinc-dependent enzyme, 5'-nucleotidase, relative to the control cells. Over a period of 7 days of exposure to zinc-deficient conditions, no changes in cell viability and growth, or in the cytoskeletal and cell adhesion systems, were found in HaCaT cells. At 7 days, however, induction of apoptosis was indicated by the presence of DNA fragmentation and expression of active caspase-3 in cells. These results demonstrate that apoptosis is the earliest detectable cellular change induced by zinc deficiency in HaCaT keratinocytes. Our observations account for many of the features of zinc deficiency, including the presence of degenerate nuclei, chromatin aggregates and abnormal organization of keratin, that may represent the later stages of apoptosis. In summary, a major causal role for apoptosis in the pathology of zinc deficiency in the skin is proposed. This role is consistent with the previously unexplained diverse range of degenerative cellular changes seen at the ultrastructural level in zinc-deficient keratinocytes.
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PMID:Apoptosis may underlie the pathology of zinc-deficient skin. 1640 50

Zinc and cadmium are environmental contaminants that induce a wide range of effects on CNS. Here we tested the in vitro effect of these metals on acetylcholinesterase (AChE) and ectonucleotidase (NTPDase and ecto-5'-nucleotidase) activities in zebrafish brain. Both zinc and cadmium treatments did not alter significantly the zebrafish brain AChE activity. ATP hydrolysis presented a significant increase at 1 mM zinc (17%) and the AMPase activity had a dose-dependent increase at 0.5 and 1 mM zinc exposure (188% and 199%). After cadmium treatment, ATPase activity was significantly increased (53% and 48%) at 0.5 and 1 mM, respectively. Cadmium, in the range 0.25-1 mM, inhibited ADP hydrolysis in a dose-dependent manner (13.4-69%). Ecto-5'-nucleotidase activity was only inhibited (38%) in the presence of 1 mM cadmium. It is possible to suggest that changes on NTPDase and ecto-5'-nucleotidase activities can be an important mechanism involved in neurotoxic effects promoted by zinc and cadmium.
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PMID:In vitro effect of zinc and cadmium on acetylcholinesterase and ectonucleotidase activities in zebrafish (Danio rerio) brain. 1644 75

Zinc, copper and cadmium are important environmental contaminants and differences in purinergic and cholinergic systems of invertebrates have been described when compared to characteristics of these signaling systems in vertebrates. Here we evaluate the effect in vitro of these metals on the ATPase, 5'-nucleotidase and cholinesterase (ChE) activities in the digestive gland of Helix aspersa. Zinc (500 and 1000 microM) promoted a significant decrease in 5'-nucleotidase activity. However, it did not induce changes in ATP hydrolysis. Copper (25 and 50 microM), inhibited significantly ATPase activity, but did not alter 5'-nucleotidase when compared to control (no metal added). In relation to effects of cadmium, an inhibitory effect on ATP hydrolysis has been observed at concentrations of 100, 500 and 1000 microM and a similar decrease of AMP hydrolysis was observed at 500 and 1000 microM. However, there were no significant changes in ChE activity from homogenates of the digestive gland of H. aspersa for all metals tested. This study demonstrated that zinc, cadmium and copper affect ATPase and 5'-nucleotidase in digestive gland, but not ChE, suggesting that the purinergic system may be a target related to toxicity induced by these metals and a possible indicator of biological impact of exposure to these contaminants.
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PMID:In vitro exposure of heavy metals on nucleotidase and cholinesterase activities from the digestive gland of Helix aspersa. 1673 Feb 35

We evaluated whether a daily high-dose calcium supplement perturbs the zinc status in 23 postmenopausal women (mean age: 63 yr) with low bone mineral density. Plasma and erythrocyte zinc concentrations, plasma bone-specific alkaline phosphatase (BSAP) and 5'-nucleotidase activities, and urinary zinc and calcium excretion were determined first at the end of 4 wk of daily oral calcium (1200 mg) and were measured again at the end of the subsequent 4 wk of daily cosupplementation with calcium (1200 mg) and zinc (30 mg). Mean plasma and erythrocyte zinc concentrations after 4 wk of calcium alone were not significantly different from concentrations after cosupplementation of calcium and zinc. Mean plasma BSAP activities before cosupplementation with zinc was significantly higher than that after zinc (p < 0.02), whereas plasma 5'-nucleotidase activities were not affected by zinc supplementation. Urinary zinc excretion slightly, but significantly, increased after the supplementation of zinc (p < 0.05), whereas calcium excretion remained similar. Our data indicate that a 4-wk zinc supplementation did not significantly improve zinc status. Although limited by the small sample size and short study duration, our data suggest that a daily calcium dose of 1200 mg had no effect on the zinc status of our subjects.
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PMID:Zinc status of women with low bone mineral density who receive calcium supplements. 1684 58

An experiment was conducted to estimate the optimal dietary zinc level for broiler chicks fed a corn-soybean meal diet. A total of 384 one-day-old male broiler chicks were assigned randomly to dietary treatments for 21 d. These treatments included a basal corn-soybean meal diet (28.32 mg of Zn/kg) supplemented with 0, 20, 40, 60, 80, 100, 120, or 140 mg of Zn/kg in the form of reagent-grade ZnSO(4).7H(2)O. All treatments were replicated 6 times using 8 chicks per pen. Tissue Zn concentration, Zn metalloenzyme activity, metallothionein (MT) concentration, MT mRNA level, and Zn transporter-2 (ZnT-2) mRNA level were analyzed for choosing suitable criterion to determine the optimal dietary Zn level for broilers. Regression analysis was performed to estimate optimal dietary Zn level in the presence of quadratic or asymptotic responses. Results showed that weight gain and feed intake were increased with dietary Zn level (P < 0.05), and the maximum weight gain and feed intake were observed in the diet supplemented with 20 mg of Zn/kg (48.37 mg/kg, total dietary Zn). Pancreas MT and MT mRNA increased linearly with Zn supplementation. According to the asymptotic model, the optimal Zn requirement of chicks from hatch to 21 d of age was 59.15 mg/kg for pancreas Zn and 61.70 mg/kg for bone Zn respectively. Quadratic responses were exhibited by serum 5'-nucleotidase activity and pancreas Zn transporter-2 mRNA level, resulting in total optimal dietary levels of 80.50 and 84.09 mg/kg, respectively. Based on results from this study, the optimal dietary Zn level of chicks from hatch to 21 d of age is 84 mg/kg.
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PMID:An optimal dietary zinc level of broiler chicks fed a corn-soybean meal diet. 1802 4


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