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)

A vitamin and trace element supplement containing recommended dietary amounts or "safe and adequate" levels was given to ten healthy subjects for 12 to 35 weeks. Plasma levels of selenium and zinc, activity of glutathione peroxidase in plasma and platelets, whole blood manganese, activity of superoxide dismutase in hemolysate, activity of alkaline phosphatase in serum, iron status indices and urinary excretion of zinc and selenium were measured. A small but significant change in plasma selenium from 1.01 +/- 0.14 mumol/L to 1.08 +/- 0.10 mumol/L was observed after two weeks. However, at the end of the supplementation plasma selenium levels did not differ from the initial levels. Plasma glutathione peroxidase levels showed a similar trend and changes in glutathione peroxidase activity in platelets were also transient. A small increase in serum zinc values was observed after 30 weeks of supplementation. No significant changes were observed in the other blood and urine parameters studied. In seven of the subjects absorption of zinc, manganese and selenium was measured after 30-31 weeks of supplementation by a radionuclide technique. The absorption of selenium and manganese after long term supplementation was 30-50% lower than observed previously in non-supplemented subjects. In conclusion, present available indices of trace element status are only to a limited extent affected by 30 weeks of a doubling of the normal dietary intake.
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PMID:Effect of long-term trace element supplementation on blood trace element levels and absorption of (75Se), (54Mn) and (65Zn). 213 27

1. The sequence of renal cellular membrane damage induced by gentamicin was studied in the rat by using the release of alkaline phosphatase, acid phosphatase, muramidase and protein from renal cells as indices of renal damage. 2. The protective effect of a combination of vitamin E and selenium against renal damage was also investigated. 3. Gentamicin (60 mg kg-1 body weight) was nephrotoxic within 12 h of the first dose. 4. The plasma membrane of the renal tubules is damaged before the lysosomal membrane is affected. 5. A combination of vitamin E (1 mg g-1 body weight) and selenium (4 x 10(-3) mg g-1 body weight) attenuates the renal damage induced by gentamicin. Results suggest synergism between vitamin E and selenium in attenuating the renal damage. The possible mechanism of attenuation is discussed. 6. Vitamin E and selenium may have anti-diuretic potential.
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PMID:Vitamin E and selenium in gentamicin nephrotoxicity. 226 Dec 41

Sodium selenite was administered to the rats bearing subcutaneously transplanted adenocarcinoma. The following determinations were carried out in serum: gamma-glutamyl transferase, aminotransferases, alkaline phosphatase and its placental isoform, haptoglobin, protein- and lipid-bound sialic acid. Changes observed in catalytic activities and concentrations of the examined parameters could be ascribed rather to the presence of the tumor than to the effect of the selenium treatment.
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PMID:Enzymes and acute phase reactants in serum of selenium treated rats bearing adenocarcinoma. 245 7

A feed loading experiment was applied in 2 phases to 45 young cocks over 12 weeks, using 1.2 (N, N-bis/methylmercury/-p-toluolsulphamide)-dressed wheat (50% of base ration). The experimental animals were White-Leghorn laying hybrids. Investigations were conducted to study the effects of exclusive exposure to mercury and those of mercury with addition of 0.2 mg of sodium selenite/l drinking water on biochemical parameters (calcium, phosphorus, total protein, albumin, creatinine, urea, activity of alkaline phosphatase, hematocrit, hemoglobin, and leucocyte count) as well as on parameters relating to toxicological residues (selenium and mercury levels in liver, musculature, and kidneys). Statistically secured differences were found to exist between the experimental groups with regard to selenium and mercury in the liver and mercury concentrations in kidneys. These data have shown that the problem of residualisation cannot be solved by selenium supplementation in parallel to methylmercury loading. The results recorded are likely to confirm the need for a general ban on feeding mercury-dressed seed.
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PMID:[Experimental laboratory diagnostic and residual toxicological studies in young cocks after feeding mercury-disinfected seed with and without selenium supplementation]. 261 87

Three groups of 5 pigs each were fed a high selenium (Se) diet by mixing either Astragalus praelongus (31.6 ppm Se in feed), A bisulcatus (31.7 ppm Se in feed), or sodium selenate (26.6 ppm Se in feed) with commercial hog feed. Ten control pigs were fed only commercial hog chow containing trace selenium (0.44 ppm Se). Pigs were fed for 9 weeks and necropsied when they had ataxia or paralysis. Blood was collected for hematologic and serum biochemical determinations, and samples of various tissues were collected and fixed in neutral-buffered 10% formalin for histologic evaluation or frozen for determination of selenium concentration. All forms of selenium induced clinical signs of weight and hair loss, with cracked hooves and inflamed coronary bands developing in all Na2SeO4-fed pigs and 1 A praelongus-fed pig, but not in A bisulcatus-fed pigs. Serum calcium, phosphorus, and albumin concentrations were unchanged or significantly decreased from prefeeding values in groups fed selenium. Serum aspartate transaminase (AST) activities in Astragalus species-fed groups, and amylase activities and PCV in all groups of pigs fed selenium, were increased. Serum alkaline phosphatase and creatine kinase activities were significantly increased in the A praelongus-fed pigs and significantly decreased in Na2SeO4-fed pigs. Terminal tissue and body fluid selenium concentrations were determined in all groups of pigs fed selenium and compared with values in control pigs. Urine and bile concentrations were increased by the greatest factor (40 to 100x), with tissue concentrations of selenium increased by a lesser factor (6 to 17x).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Toxicosis in pigs fed selenium-accumulating Astragalus plant species or sodium selenate. 278 23

Although WR-2721, S-2-(3-aminopropylamino)ethylphosphorothioic acid, is an effective radioprotector, its use is limited by its toxicity. Combining WR-2721 with other agents might decrease its toxicity and/or increase its effectiveness. The effect of selenium (Se) pretreatment on the acute toxicity and radioprotective effect of WR-2721 was studied in male CD2F1 mice. Injection of 1.6 mg/kg Se 24 hr before WR-2721 (800-1200 mg/kg, IP) decreased the lethality of WR-2721 significantly. Lower doses of Se were also effective, but simultaneous administration was not effective. Se injection alone (1.6 mg/kg) 24 hr before cobalt-60 irradiation increased the survival (dose reduction factor, DRF = 1.1) significantly. A synergistic effect on post-irradiation survival was observed when Se was injected 24 hr before WR-2721 (200-600 mg/kg IP 1/2 before irradiation). For example, after exposure to 22 Gy (1 Gy/min), 30-day survival was 100% when mice were treated with both Se and 600 mg/kg WR-2721, and was 13% with WR-2721 alone. The DRF after 400 mg/kg WR-2721 was 2.6 with Se compared to 2.2 without Se pretreatment. Alkaline phosphatase activity in bone marrow cells and serum was significantly depressed after treatment with 1.6 mg/kg Se, suggesting that a retardation of conversion of WR-2721 to its active free sulfhydryl form through the action of alkaline phosphatase might be partly responsible for the effects of Se. Other possible mechanisms related to the antioxidant properties of Se are under investigation.
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PMID:Selenium pretreatment enhances the radioprotective effect and reduces the lethal toxicity of WR-2721. 285 28

Selenium deficient calves when compared to selenium supplemented calves had increased plasma thyroxine concentrations and decreased plasma tri-iodothyronine concentrations. These changes in the selenium deficient calves were accompanied by significant increases in plasma urea and creatinine concentrations and decreased plasma alkaline phosphatase activity. The demonstration that low selenium status can cause imbalances in thyroid hormone metabolism may provide an explanation for some of the effects of the deficiency.
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PMID:Thyroid hormone concentrations in selenium deficient and selenium sufficient cattle. 322 43

The preventive effect of zinc for the toxic actions of germanium and selenium on bone metabolism was investigated in the femoral diaphysis of weanling rats. Germanium tetrachloride (1.53-30.60 mumol Ge/100 g b.w.) and selenium tetrachloride (1.53-7.65 mumol Se/100 g) was administered orally for 3 days. The doses of 1.53 and 7.65 mumol Ge/100 g caused a significant increase in DNA content although alkaline phosphatase activity was not altered significantly. By the dose of 30.60 mumol Ge/100 g, both alkaline phosphatase activity and DNA content were decreased significantly. Administration of selenium (1.53 and 7.65 mumol/100 g) produced significantly decreases in alkaline phosphatase activity and DNA content. The decreases of the enzyme activity and DNA content caused by administration of germanium (30.60 mumol/100 g) and selenium (7.65 mumol/100 g) were prevented completely by simultaneous injection of zinc sulfate (7.65 mumol Zn/100 g) for 3 days. Administration of zinc also produced appreciable increase in alkaline phosphatase activity and DNA content. The present study indicates that germanium and selenium disturbs bone metabolism in weanling rats, and that this disturbance is reversed by zinc.
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PMID:Preventive effect of zinc for toxic actions of germanium and selenium on bone metabolism in weanling rats. 343 41

The protective effect of selenite, seleno-dl-methionine and biological selenium against the renotoxicity of mercury was tested in rats. As the source of biological selenium, the liver soluble fraction of rats given 60 mumoles/kg selenite 3 days before sacrifice was used. The aim of the experiments was to test whether protective efficiency follows the reported order of ability to form HgSe. Mercury was given subcutaneously in doses of 2.5, 5.0 and 7.5 mumoles/kg HgCl2 and selenium was given in equimolar doses at the same time as Hg2+. Liver soluble fraction, biological selenium or liver soluble fraction supplemented with selenite or seleno-dl-methionine were given orally, while in experiments without liver soluble fraction the two selenium compounds were given subcutaneously. Biological selenium was tested only at the two lower dose levels. Both biological selenium and seleno-dl-methionine decreased the urinary excretion of mercury in the first 48 h, but less so than selenite and only selenite decreased the renal content of mercury at the end of this period. Urinary alkaline phosphatase activity and plasma urea nitrogen at the 2.5 and 5.0 mumoles/kg dose levels decreased in the order of no selenium greater than biological selenium greater than seleno-dl-methionine greater than selenite. As the reported HgSe formation increases in the same order, the experiments support the role of HgSe formation in the protective effect. The degree of necrotic damage in the P2 and P3 regions of the proximal tubular cells increased in the same order as the biochemical indicators at the 5.0 and 7.5 mumoles/kg dose levels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of the protection given by selenite, selenomethionine and biological selenium against the renotoxicity of mercury. 366 17

Experiments were conducted to examine the interrelationships between methionine, choline and inorganic sulfate in the diet of weanling pigs, and to evaluate the selenium (Se) status of pigs fed diets with or without supplemental sulfate. Two trials utilized 288 weanling (3-wk-old) pigs allotted to dietary treatment based on weight, sex and litter origin. There were six pigs/pen and three replicate pens/treatment in each trial. The basal corn-soybean meal diet was formulated to supply .55% sulfur amino acids and contained a choline and sulfur-free vitamin and mineral premix. Lysine was added to provide a total of 1.13% lysine. Seven additional treatments were formulated by substituting for corn .17% DL-methionine, .29% choline dihydrogen citrate or .25% Na2SO4 to create a 2(3) factorial arrangement of treatments. There were methionine X choline X sulfate interactions for average daily gain (P less than .001) and feed-to-gain ratio (F:G; P less than .05). Adding choline, methionine, Na2SO4 or choline plus methionine to the basal diet did not improve gains. However, when Na2SO4 plus methionine or Na2SO4 plus choline were added, daily gains were increased (P less than .05) and F:G was improved (P less than .1). Addition of all three supplements did not result in a further increase in gain. Pigs fed choline-supplemented diets had higher (P less than .01) hematocrit and tended (P = .07) to have increased hemoglobin concentration. There was no effect on serum triglycerides or alkaline phosphatase activity due to dietary treatment. The concentration of Se in muscle, liver, kidney and blood was not influenced by sulfate content of the diet.
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PMID:Methionine, choline and sulfate interrelationships in the diet of weanling swine. 375 83


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