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:3.1.3.1 (alkaline phosphatase)
47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acid and alkaline phosphatase changes in various parts of the central nervous system (olfactory bulbs, cerebral hemispheres, cerebellum, medulla oblongata, and spinal cord) were analyzed during methylmercury chloride (MMC) treatment with a dose of 5 mg/kg/day body weight. The drug was subcutaneously introduced into the animals and the enzymes were analyzed after 2, 7, and 15 days' treatment. One group of animals was treated for seven days and kept without drug for another seven days (withdrawal group). The antagonizing capacities of four chelators, namely, N-acetyl-DL-homocysteine thiolactone (NAHT), D-penicillamine (DPA), glutathione (GSH), and sodium selenite (SEL), were also analyzed in relation to the restoration of enzymes. Study results show a linear inhibition of acid and alkaline phosphatases with increasing duration of MMC treatment. However, the magnitude of enzymatic inhibition is different in different brain areas. After 15 days' treatment, maximum inhibition of acid and alkaline phosphatases was recorded in the spinal cord and cerebellum, respectively. Chelators also exhibited differential recovery of the enzymes in various animal groups, as well as in discrete brain areas. No uniformity in the recovery of the enzymes with chelators was observed. However, study results show that biochemical parameters are good indicators of early recognition of neurotoxicity.
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PMID:A therapeutic profile of metal chelators in the detoxication of methylmercury chloride inhibited acid and alkaline phosphatases in different areas of the central nervous system of rats. 256 Nov 58

The stability and storage characteristics were studied of 11 bovine enzymes of potential clinical significance, namely, aldolase, alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, acetylcholinesterase, creatine kinase, gamma glutamyltransferase, glutathione peroxidase (GSH-Px), alpha-hydroxybutyrate dehydrogenase, lactate dehydrogenase and superoxide dismutase (SOD). Enzyme activities in fresh serum were compared with those in plasma containing various anticoagulants including lithium heparin, EDTA and oxalate/fluoride. The same preservatives were assessed for their effects on the whole blood activities of GSH-Px and SOD. Stabilities of enzymes in plasma and serum stored at room (+20 degrees C), refrigerator (4 degrees C) or deep freeze (-20 degrees C) temperatures were also compared. In addition, SOD and GSH-Px activities in samples stored, at the same temperatures, as whole blood or aqueous lysates were monitored.
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PMID:Stability and storage characteristics of enzymes in cattle blood. 286 28

The stability and storage characteristics were studied of 11 ovine enzymes of potential clinical significance, namely, aldolase, alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, acetylcholinesterase, creatine kinase, gamma glutamyltransferase, glutathione peroxidase (GSH-Px), alpha-hydroxybutyrate dehydrogenase, lactate dehydrogenase and superoxide dismutase (SOD). Enzyme activities in fresh serum were compared with those in plasma containing various anticoagulants including lithium heparin, EDTA and oxalate/fluoride. The same preservatives were assessed for their effects on the whole blood activities of GSH-Px and SOD. Stabilities of enzymes in plasma and serum stored at room (+20 degrees C), refrigerator (4 degrees C) or deep freeze (-20 degrees C) temperatures were also compared. In addition, SOD and GSH-Px activities in samples stored, at the same temperatures, as whole blood or aqueous lysates were monitored. The results are discussed with particular reference to the differences between sheep and cattle.
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PMID:Stability and storage characteristics of enzymes in sheep blood. 286 29

Previous methods to deplete in vivo concentrations of reduced glutathione (GSH) have not been able to lower tissue GSH levels for extended periods, have been toxic, and can alter the metabolism of xenobiotics. A possible alternative to lower in vivo concentrations of GSH may be the use of buthionine-S,R-sulfoximine (BSO) in the drinking water of laboratory animals to inhibit the biosynthesis of GSH. It has been previously reported that 20 mM BSO in the drinking water given to mice was able to lower GSH levels in a variety of tissues after 15 days. In order to more fully characterize the in vivo depletion of GSH in tissues by ingestion of BSO and determine if this method would be suitable in studies requiring depressed levels of GSH for extended periods, we added different amounts of this agent to the drinking water given to mice for various times up to 28 days. We found that ingested BSO at the highest concentration used in drinking water (30 mM) was able to maximally lower GSH concentrations in mouse lungs, lung lavage fluid, liver, kidneys, and blood to 59.0 +/- 3.6%, 35.0 +/- 5.1%, 44.3 +/- 1.5%, 69.5 +/- 3.9%, and 70.0 +/- 6.0% of control mice, respectively, for up to 28 days. These lowered concentrations of tissue GSH returned to control levels after mice were returned to untreated drinking water for 7 days. The potential toxicity of such treatments was also evaluated. Levels of alkaline phosphatase, lactate dehydrogenase, glucose-6-phosphate dehydrogenase, glutathione peroxidase, and glutathione reductase in lungs and lung lavage fluid, and total and differential cell counts from lung lavage fluid were not different between control and BSO-treated mice. This showed that BSO treatment did not produce indications of lung injury as measured by these biochemical parameters. Serum aspartyl transferase and gamma-glutamyl transpeptidase activities were unaffected by the BSO treatments, indicating normal liver functions. Lung and liver cytochrome P-450 concentrations were also not different between controls and BSO-treated animals. Thus, BSO in the drinking water of mice was able to effectively lower in vivo levels of GSH without eliciting acute toxic responses.
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PMID:Effects of the long-term depletion of reduced glutathione in mice administered L-buthionine-S,R-sulfoximine. 286 40

The effect on liver tissue of glutathione administration to rats treated for 7-14 days with 2-acetylaminofluorene was investigated. The DNA damage induced by the hepatotoxic agent and evaluated by the alkaline elution technique was significantly reduced by glutathione. Furthermore, GSH administration maintained liver GSH level, prevented the increase in alkaline phosphatase and reduced the decrease in glucose-6-phosphatase activity. GSH did not significantly influence the increase in gamma-glutamyl-transpeptidase and glutathione-S-transferase activities.
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PMID:Effect of glutathione on alterations of liver DNA structure and metabolic activities induced in vivo by 2-acetylaminofluorene. 288 May 50

Substitution reactions with biologic nucleophiles appear to govern the antitumor and toxic properties of platinum complexes. In this paper we have characterized the reactions of several platinum antitumor agents with sulfur-containing amino acids, peptides, proteins, and nonbiologic nucleophiles. The rate constants for the reactions of trans-diamminedichloroplatinum(II) (trans-DDP), cis-diamminedichloroplatinum(II) (DDP), diammine (1,1-cyclobutanedicarboxylato)platinum(II) (CBDCA) and cis-diisopropylamine-cis-dichloro-trans-dihydroxy platinum(IV) (CHIP) with cysteine (Cys), methionine (Met), and glutathione (GSH) were determined at 37 degrees. A reactivity ratio of 1:1.5:22:6500 was determined for the reaction of GSH with CHIP, CBDCA, DDP, and trans-DDP respectively. The rate constant for the binding of DDP to DNA, 7.4 X 10(-5) sec-1, decreased to 5.9 X 10(-5) sec-1 and 1.7 X 10(-5) sec-1 in the presence of 0.5 and 5 mM GSH respectively. The products formed in the reaction of GSH with trans-DDP, DDP, and CBDCA were also examined. Under conditions of high platinum concentration (2-3 mM), CBDCA and DDP form large molecular weight species with GSH as indicated by 1H-NMR and ultrafiltration experiments. The complex [Pt(GSH)2 X 3H2O]n was isolated from the reaction of 3 mM DDP with 6 mM GSH. The product formed in the reaction of 3 mM trans-DDP with 6 mM GSH was not macromolecular in nature, and 1H-NMR spectra revealed that platinum was bound to the Cys sulfhydryl group. Rate constants were determined for the reactions of these platinum complexes with diethyldithiocarbamate (DDTC) and thiosulfate, two agents known to reduce platinum-mediated nephrotoxicity. DDTC, but not thiosulfate, was shown to rapidly chelate platinum from [Pt(GSH)2 X 3H2O]n. The effects of DDP, CBDCA, and CHIP on the sulfhydryl-dependent rat renal proximal tubule membrane enzymes alkaline phosphatase (AP), gamma-glutamyltranspeptidase (GGTP), leucine aminopeptidase (LAP), and the Na+/K+- and Mg2+-adenosine-5'-triphosphatases (ATPases) were also investigated in vitro. The ability of platinum complexes to inhibit these enzymes parallels their reactivity with other nucleophiles. DDTC and thiourea were shown to restore activity to platinum-inhibited enzymes. Chloride ion was found to reduce platinum-mediated enzyme inhibition in an unpredictable manner, the greatest effect being observed with LAP and GGTP and the least with the ATPases. None of these renal enzymes was directly inhibited by DDP in vivo.
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PMID:Characterization of the reactions of platinum antitumor agents with biologic and nonbiologic sulfur-containing nucleophiles. 295 56

The synergistic hepatotoxicity of dietary disulfiram (DSF) with 1,2-dichloroethane (DCE) subchronically administered by inhalation at three concentration levels (150, 300, and 450 ppm) was studied. The criteria for hepatotoxicity were treatment-related increases in serum activities of sorbitol dehydrogenase, 5'-nucleotidase, and alkaline phosphatase, and in liver-to-body weight ratios. DSF alone did not elicit these responses while DCE at the highest concentration level increased liver-to-body weight ratios and the activity of 5'-nucleotidase. Exposure to DSF alone decreased cytochrome P450 levels, but in combination with DCE, the decrement of cytochrome P450 was additive in a DCE concentration-dependent manner. However, depression of cytochrome P450 by DCE alone was not concentration dependent. Although DSF and DSF/DCE combination increased the activity of glutathione S-transferases (GSTs), both DSF and DCE singly and in combination increased the tissue levels of reduced glutathione (GSH). Evidence is presented showing that the potentiation of the hepatotoxicity of DCE observed in the presence of DSF may be due to an inhibition of microsomal mixed-function oxidase-mediated metabolism of DCE and to a compensatory increase in DCE metabolism to reactive metabolites generated by GST-mediated conjugation of DCE with GSH.
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PMID:Interaction between 1,2-dichloroethane and tetraethylthiuram disulfide (disulfiram). II. Hepatotoxic manifestations with possible mechanism of action. 378 26

Male BALB/c mice were treated with intraperitoneal injections of carbon tetrachloride (CCl4) (0.2 g/kg body weight) and/or 50 R of whole-body gamma irradiation, three times per week, for 4 weeks. The effects of the treatments on superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in liver extracts and homogenates, and on alkaline phosphatase (ALP) in serum were investigated. A significant decrease in the SOD and GSH-Px activities in liver extracts and an increase of serum ALP of hepatic origin were found in CCl4-treated animals. In contrast, only an increase in SOD activity was observed in liver homogenates after the combined treatment.
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PMID:Interaction of low doses of ionizing radiation and carbon tetrachloride on liver superoxide dismutase and glutathione peroxidase in mice. 408 56

In two separate experiments, 72 crossbred ewes were fed hay, haylage (50% dry matter) and corn diets with ad libitum salt-mineral mixtures (SMM; Exp. 1) or salt (Exp. 2). Calcium phosphates (Ca X P) and(or) zinc (Zn) were added in a 2 X 2 factorial arrangement to salt + trace minerals for ewes 7 mo prepartum through lactation in Exp. 1 and to salt only for ewes 3 mo prepartum through lactation in Exp. 2. The diets fed were estimated to contain 23 and 28 mg Zn/kg dry diet (ppm), respectively, and .08 and .05 ppm Se. Large variations (up to fivefold) were found in SMM intake per month between replicates and from month-to-month within treatment; thus, monthly variations of up to sevenfold occurred in Zn and Se intakes of supplemented groups. There were no significant treatment effects on SMM intake. Small but significant Zn treatment effects were detected for plasma and wool Zn of ewes and lambs, but all values were in the normal range. There was no significant treatment effect on plasma alkaline phosphatase activity. In Exp. 2, erythrocyte glutathione peroxidase (GSH-Px) activity was significantly lower in all treatment groups compared with a Se-supplemented control group but only rare occurrences of subclinical muscular dystrophy were found. There was no significant treatment effect on GSH-Px activity, whole blood Se in ewes and lambs or plasma creatine phosphokinase activity in lambs. These results indicate large animal and seasonal variability in SMM intake and no significant treatment effects of Ca X P on SMM intake or on Zn and Se status. Zinc addition to SMM had no effect on Se status.
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PMID:Effect of calcium phosphates and zinc in salt-mineral mixtures on ad libitum salt-mix intake and on zinc and selenium status of sheep. 652 62

The present study was undertaken to compare the effects of 10-50 mg/kg b.wt. of Pb acetate after chronic treatment through oral gavage on: (a) the distribution of trace elements such as Fe, Cu, Zn, and Mn, (b) enzyme activity of delta-amino levulinic acid dehydratase (delta-ALAD) and alkaline phosphatase, and (c) glutathione (GSH) in kidney and (d) delta-ALAD in blood of pregnant and non-pregnant mice. Treatment with Pb acetate was given on every alternate day for 4 weeks prior to mating and for 3-4 weeks until pregnancy became apparent and confirmed by laporatomy. Lead administration reduced the rate of reproduction as assessed by number of living viable embryos. During normal pregnancy renal Cu, Fe and GSH tended to decline although non-significantly and continued to do so after lead administration. Mn was considerably and significantly elevated, whereas activity of delta-ALAD (non-activated) was quite low in pregnant mice. Following administration of Pb acetate, kidneys of pregnant and non-pregnant dams accumulated Pb in a dose-dependent manner, but as compared to non-pregnant mice, Pb increase in pregnant dams was significantly lower. Pb toxicity was associated with the loss of delta-ALAD in blood and kidney, but unlike the non-activated form of delta-ALAD, the dithiothreitol-activated form of delta-ALAD declined in a significant amount. The residual activity showed a high degree of negative correlation with endogenous Pb as well as with Zn/Pb ratio. Pb toxicity did not modify renal Fe, Cu, and Zn in the pregnant state, but reduced renal Fe during pregnancy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal toxicity after oral administration of lead acetate during pre- and post-implantation periods: effects on trace metal composition, metallo-enzymes and glutathione. 761 47


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