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)

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

Studies of V79-171 cells were undertaken to determine what extracellular or intracellular derivative of the drug WR-2721 is associated with radioprotection. The effect of preincubation at 23 +/- 1 degree C with WR-2721, and with derivatives of WR-2721 produced in medium containing alkaline phosphatase, upon survival of cells following subsequent gamma-irradiation was examined. It was established that WR-2721, WR-1065, WR-33278, WRSSCys, and other disulfide forms produced by reactions of WR-1065 with the medium do not provide significant protection when present only extracellularly. Protection was found to correlate with cellular levels of the thiol form of the drug (WR-1065) but not with the cellular level of the disulfide forms of WR-1065. Similar results were obtained with HeLa, Me-180, Ovary 2008, HT-29/SP-1d, and Colo 395 cell lines showing that human tumor cell lines behave in the same fashion as the V79-171 nontumorigenic hamster diploid cell line. None of the drug forms produced significant cytotoxicity under the conditions used. It was concluded that it is the cellular level of WR-1065 at the time of irradiation which determines protection. The results are consistent with protection mechanisms involving scavenging of hydroxyl radicals, hydrogen atom transfer to DNA radicals, depletion of oxygen near DNA, enhancement of rapid biochemical repair processes, or some combination of these mechanisms.
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PMID:Radioprotection of cells in culture by WR-2721 and derivatives: form of the drug responsible for protection. 283 20

New light microscopic visualization methods were developed for the histochemical detection of non-specific alkaline and acid phosphatase, Mg-, Ca- and Na, K-dependent adenosine triphosphatase, myosin adenosine triphosphatase, glucose-6-phosphatase, 5'-nucleotidase and thiamine pyrophosphatase with cerium ions as trapping agents in cryostat and plastic sections. The techniques are based on the conversion of cerium phosphate into cerium perhydroxide by H2O2 which decomposes at 55 degrees-60 degrees C into cerium hydroxide and oxygen radicals. These radicals are able to oxidize diaminobenzidine (DAB) to DAB brown. Addition of nickel ions to the DAB-H2O2 mixture generates bluish-black stained nickel-DAB complexes. Compared with the classical metal precipitation, azo, azoindoxyl and tetrazolium procedures the H2O2-DAB and especially the H2O2-DAB-nickel methods provided identical or superior results in catalytic phosphatase histochemistry and immunohistochemistry when using non-specific alkaline phosphatase as the enzyme label.
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PMID:The cerium perhydroxide-diaminobenzidine (Ce-H2O2-DAB) procedure. New methods for light microscopic phosphatase histochemistry and immunohistochemistry. 285 63

Parathyroid hormone (PTH) and cAMP inhibit sodium, water, and bicarbonate reabsorption in the proximal tubule. We wished to determine whether these agents directly inhibit proximal tubular Na+/H+ exchange. A suspension of rabbit proximal tubules was prepared by enzymatic digestion and Ficoll gradient centrifugation. Oxygen consumption at 37 degrees C was stable over 60 min, averaged 20 nmol X mg protein-1 X min-1, and was inhibited 60% by ouabain. Over 96% of cells excluded trypan blue. From this suspension, brush border membrane vesicles were isolated. The vesicles were enriched 12.7 times in alkaline phosphatase relative to a cortical homogenate and demonstrated pH gradient-stimulated, amiloride-sensitive Na+/H+ countertransport and sodium-phosphate and sodium-D-glucose cotransport. When the tubule suspension was exposed to PTH or dibutyryl cAMP, the activity of Na+/H+ countertransport in the resultant brush border vesicles was inhibited. Neither PTH nor dibutyryl cAMP affected the amiloride-insensitive component of sodium transport or sodium-phosphate or sodium-D-glucose cotransport. The effect of PTH on Na+/H+ counter-transport could not be explained by an alteration in fluidity of the brush border membrane. These experiments demonstrate that PTH and dibutyryl cAMP directly inhibit Na+/H+ countertransport in the brush border membrane of the rabbit proximal tubule.
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PMID:Parathyroid hormone and dibutyryl cAMP inhibit Na+/H+ exchange in renal brush border vesicles. 298 85

Asbestos-associated damage to cells of the respiratory tract in vitro can be prevented by the simultaneous addition of scavengers of active oxygen species to cultures. To determine if administration of scavenger enzymes to animals and humans is a plausible approach to the prevention of asbestos-induced lung disease, osmotic pumps were filled with various concentrations of PEG-coupled catalase and implanted subcutaneously into Fischer 344 rats over a 28-day period. At 3, 14, and 28 days after implantation of the pumps, the animals were evaluated for levels of catalase in serum and lung. In addition, lung tissue and lavage fluids were examined at 28 days for biochemical and morphologic indications of cell injury, inflammation, and fibrotic lung disease. At all time points examined, the administration of PEG-catalase caused a dosage-dependent increase in serum levels of catalase. The levels of lung catalase were evaluated at 28 days but not at earlier time periods. In comparison to control rats, the amounts of enzymes (lactic dehydrogenase, alkaline phosphatase), protein, and cells in lavage fluids from treated animals were unaltered. Moreover, the lungs showed no evidence of inflammation or fibrotic disease as determined by differential cell counts in lavage and measurement of hydroxyproline. These studies suggest that administration of PEG-catalase does not cause injury or other alterations in lung tissue and can be pursued as a feasible approach to prevention of asbestosis.
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PMID:Approaches to prevention of asbestos-induced lung disease using polyethylene glycol (PEG)-conjugated catalase. 303 29

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

Liver cirrhosis was induced in rats by the combined action of oral phenobarbitone and inhalations of carbon tetrachloride vapors. These rats manifested hepatosplenomegaly, hypoalbuminemia, and 2- to 17-fold elevations in serum transaminases and alkaline phosphatase levels. The hepatic antioxidant enzymes, superoxide dismutase and catalase, showed 28 and 60% decreases, respectively. There was, however, no increase in the hepatic lipid peroxidation. These studies suggest that in cirrhosis liver cell damage may result due to the direct attack of the oxygen free radicals. Lipid peroxidation in the liver may not be a prerequisite for the development of cirrhosis, as is generally believed.
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PMID:Hepatic antioxidant enzymes and lipid peroxidation in carbon tetrachloride-induced liver cirrhosis in rats. 321 29

The polynucleotides poly(U), poly(C), poly(A) and poly(G) have been gamma-irradiated in N2O- and N2O/O2 (4:1)-saturated aqueous solutions. Hydroxyl radicals from the radiolysis of water react with the polynucleotides thereby producing among other lesions strand breaks. Strand breakage is connected with the formation of phosphomonoester end groups. Such end groups have been determined by measuring inorganic phosphate after a three hour incubation at 37 degrees C with acid or alkaline phosphatase. In the absence of oxygen G(phosphomonoester end groups) (in units of mumol J-1) are 0.47 (poly(U)), 0.17 (poly(C)) and less than or equal to 0.04 (poly(A) and poly(G)). In the case of poly(U) and poly(C) on heating the sample for one hour at 95 degrees C prior to incubation with phosphatases the above values increased by 0.14 and 0.07 mumol J-1, resp., whereas such treatment of the purine polynucleotides still did not produce a measurable yield of phosphomonoester end groups. Comparing these values with G values for strand breakage taken from the literature, about two phosphomonoester end groups are formed per strand break in poly(U) while for poly(C) this ratio is about unity. The purine polynucleotides show very low yields of strand breakage in agreement with the negligible phosphomonoester yields. In the presence of oxygen G(phosphomonoester end groups) are 0.46 (poly(U)), 0.21 (poly(C)), and less than or equal to 0.04 (poly(A) and poly(G)). On heating, these values increase, most markedly for poly(U) and poly(C). This is possibly linked to the decomposition of unstable hydroperoxides which are formed in high yields in poly(U) and poly(C) (G = 0.7 and 0.19 mumol J-1, resp.).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The formation of phosphate end groups in the radiolysis of polynucleotides in aqueous solution. 322 34

The effect of silymarin (100 mg/kg i.p.) on the biochemical indicators of liver damage induced by thallium (10 mg/kg p.o.) was studied in rats. The production of malondialdehyde and the content of reduced glutathione in the liver were measured as indicators of lipid peroxidation. Thallium intoxication increased the serum activities of glutamic pyruvic transaminase, gamma-glutamyl transpeptidase, alkaline phosphatase and the liver concentration of triglycerides. Thallium decreased the activity of alkaline phosphatase and increased that of gamma-glutamyl transpeptidase in the liver cell membrane. It also abolished the membrane activity of Na+/K+ ATPase. Lipid peroxidation was enhanced by thallium as malondialdehyde production was increased and the content of reduced glutathione was decreased in the liver. Silymarin completely prevented all these changes. It is suggested that thallium toxicity is due, at least in part, to the promotion of lipid peroxidation. The membrane stabilizing effect of silymarin observed in this and in other models of liver toxicity is due to some antioxidant property, possibly related to its ability to scavenge free oxygen radicals.
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PMID:Protection against thallium hepatotoxicity by silymarin. 323 Feb 45

To examine the effects on protein and electrolyte reabsorption of reducing the energy supply to the proximal tubules, an inhibitor of the citric acid cycle, maleate (600 mg.kg-1), was administered to anesthetized dogs during continuous ethacrynic acid infusion. One hour after infusion, maleate reduced renal oxygen consumption from 128 +/- 3 to 48 +/- 6 mumol.min-1. Comparisons at similar GFR showed that maleate reduced bicarbonate reabsorption by 65%, chloride reabsorption by 60% and phosphate reabsorption by 90%. Tubular reabsorption of lysozyme, determined by the 'trapped-label' method, was reduced by 97%. Total protein excretion in urine increased from 0.12 to 1.0 mg.min-1 and was not associated with a significant increase in brush border and lysosome marker enzymes. However, by superimposing a carbonic anhydrase inhibitor, acetazolamide (100 mg.kg-1), electrolyte reabsorption was slightly further reduced but protein excretion increased to 2.7 mg.min-1, coincidentally with a dramatic increase in enzyme excretion: approximately 20-fold in the brush border enzymes, alanine aminopeptidase and alkaline phosphatase, and 10-fold in the lysosomal enzymes, acid phosphatase and N-acetyl-beta-glucosaminidase. Our data indicate that maleate stops protein reabsorption without signs of acute tubular damage, whereas subsequent administration of acetazolamide results in tubular desquamation and albumin leakage.
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PMID:Effect of maleate on tubular protein reabsorption in dog kidneys. 323 92


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