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)

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

Alkaline phosphatase is inactivated by mixed function oxidation systems. OH. radicals, generated via an ascorbate-modified Haber-Weiss cycle or a Fenton-type reaction, seem to be responsible for the protein oxidative damage. Experiments with hydroxyl radical scavengers, enzyme substrates, products, and metal cofactors suggest that a "site-specific" radical attack takes place at or near the active center. Vitamin E fails to protect alkaline phosphatase; uric acid, instead, is particularly effective in shielding the protein against covalent modifications.
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PMID:Alkaline phosphatase inactivation by mixed function oxidation systems. 282 17

We studied intestinal absorption of vitamin E in 26 adults with primary biliary cirrhosis (PBC) and 6 control subjects. Seven (27%) PBC patients were vitamin E-deficient based on the ratio of serum vitamin E to serum total lipid concentrations. An oral vitamin E tolerance test was performed in all patients and control subjects using a loading dose of 2000 IU alpha-tocopheryl acetate with measurement of serial serum vitamin E concentrations over 24 h. Vitamin E absorption was expressed as the maximal rise in serum vitamin E above baseline, the area under the oral tolerance test curve, and these two values divided by the fasting total serum lipid concentration. Absorption of vitamin E was significantly impaired in all PBC patients vs. control subjects (p less than 0.01), in vitamin E-deficient vs. vitamin E-sufficient PBC patients (p less than 0.05 to p less than 0.01), and in PBC patients with serum vitamin E levels below 10 micrograms/ml vs. those with serum vitamin E levels above 10 micrograms/ml (p less than 0.01). Vitamin E absorption was inversely related to stage of PBC, serum cholylglycine, total bilirubin, cholesterol, alkaline phosphatase, aspartate aminotransferase, and prothrombin time. Patients with serum vitamin E below 10 micrograms/ml, serum total bilirubin above 3 mg/dl, serum cholylglycine above 600 micrograms/dl, or serum alkaline phosphatase above 1000 IU/L had severe malabsorption of vitamin E and would be at high risk for the development of vitamin E deficiency. Therefore, vitamin E supplementation should be considered not only in patients in whom overt vitamin E deficiency is present, but also in PBC patients meeting these criteria.
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PMID:Intestinal malabsorption of vitamin E in primary biliary cirrhosis. 291 Jul 63

Vitamin E therapy was compared with no treatment in a randomized, prospective trial for treatment of viral hepatitis in children. Patients received either vitamin E. (n:21), 300 mg./day intramuscularly every 24 hours, for seven days, or no treatment (n:20). The mean age (6.6 and 6.2), sex ratio, and the mean duration of illness before administration to study of two groups were similar. No difference was noted in the mean serum transaminases and alkaline phosphatase levels between both groups.
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PMID:[Vitamin E therapy in viral hepatitis]. 377 99

The present study was carried out to investigate the efficacy of liposome-associated alpha-tocopherol in treating pulmonary damage caused by paraquat exposure. alpha-Tocopherol liposomes (8 mg alpha-tocopherol/kg body weight) or plain liposomes were intratracheally instilled into the lungs of rats 24 h after paraquat treatment (20 mg/kg, ip); treated animals were killed 8, 24 or 48 h after administration of the liposomal preparations. Lungs of animals exposed to paraquat were extensively damaged as evidenced by an increase in lung weight and decreases in pulmonary angiotensin converting enzyme and alkaline phosphatase activities. Also, paraquat treatment resulted in a significant reduction in glutathione (GSH) concentration in the lung and an elevation in microsomal lipid peroxidation levels, as measured by the formation of diene conjugates. Treatment of paraquat-injected rats with plain liposomes did not significantly alter paraquat-induced changes of all parameters examined. On the other hand, treatment of rats with alpha-tocopherol liposomes, 24 h after paraquat administration, resulted in a significant increase in pulmonary alpha-tocopherol concentrations as well as a reduction in paraquat-induced changes in lipid peroxidation, GSH concentration, and lung angiotensin converting enzyme and alkaline phosphatase activities. The results of the present study suggest that alpha-tocopherol, administered directly to the lung in a liposomal form, may serve as a potentially effective pharmacological agent in the treatment of paraquat-induced lung injury.
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PMID:Liposomal alpha-tocopherol alleviates the progression of paraquat-induced lung damage. 777 11

Effects of dietary aflatoxin (AF) and supplemental vitamin E (d-alpha-tocopherol) were evaluated in growing crossbred pigs. Nine barrows (3 replicates of 3 each, mean body weight, 14.0 kg) per group were assigned to 1 of 4 treatment groups (for a total of 36 barrows): 0 IU of supplemental vitamin E and 0 mg of AF/kg of feed (control); 2,400 IU of vitamin E divided into equal doses and administered IM on days 1 and 16; 2.5 mg of AF/kg of feed; or 2.5 mg of AF/kg of feed plus 2,400 IU of vitamin E administered similarly to treatment 2. Barrows were administered their respective treatment for 32 days. Evaluations were made for group production performance and for serum biochemical, immunologic, hematologic, pathologic, serum and tissue tocopherol, and serum retinol variables. Body weight was reduced by AF-alone and AF plus vitamin E treatments, compared with control and vitamin E-alone treatments. Liver weight was increased for the AF alone-treated and the AF plus vitamin E-treated barrows, compared with control barrows. The AF alone-treated barrows had alterations in:serum values of alkaline phosphatase, gamma-glutamyltransferase, albumin, glucose, phosphorus, calcium, cholesterol, total iron, unsaturated iron-binding capacity, total iron-binding capacity, and urea nitrogen; RBC numbers, hematocrit, hemoglobin concentration, and prothrombin time; and mitogen-induced lymphoblastogenic responses. With the exception of some slight ameliorating effects on hematologic measurements, supplemental treatment with vitamin E did not prove beneficial against the toxicosis-associated AF treatment. The AF alone-treated barrows had decreased serum tocopherol and retinol concentrations, compared with control and pretest values, and decreased tocopherol concentration in cardiac tissue. High parenterally administered doses of vitamin E did not have sparing effect on AF-induced reductions of serum tocopherol or retinol concentration; however, compared with pretest values, serum tocopherol concentration was increased by vitamin E-alone treatment. Tocopherol concentration in cardiac tissue of the AF plus vitamin E-treated barrows was increased over that of the AF alone-treated barrows, indicating an ameliorating effect on AF-induced tissue concentrations reductions. These data indicate that vitamin E may not have a sparing effect on AF-induced toxicosis and that AF may reduce serum retinol and serum and tissue tocopherol concentrations.
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PMID:Influence of vitamin E on aflatoxicosis in growing swine. 801 6

The toxicity of nickel, chromium (III) and (VI), vanadium and aluminium was compared in an immortalized neonatal rat osteoblast cell line using the MTT assay and a novel index of cytotoxicity, alkaline phosphatase (ALP) activity. Where toxicity was observed, ALP was a consistently more sensitive detection method than the MTT assay. The toxicity of the metals increased in the order aluminium < chromium (III) < vanadium < nickel < chromium (VI). alpha-Tocopherol partially prevented nickel-induced toxicity (as assessed by ALP activity), whereas ascorbic acid had no protective effect. Chromium (VI) was more toxic than (III), with significant toxicity observed at 0.5 microM. It is thought that Cr (III) cannot readily penetrate the cell membrane and this may account for the lower toxicity. Aluminium had a stimulatory effect on cell growth at low concentrations (0.5 microM). The combination of immortalized rat osteoblasts and the ALP activity test provides a powerful tool for in vitro testing of orthopaedic materials.
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PMID:Interactions of orthopaedic metals with an immortalized rat osteoblast cell line. 880 83

Reactive oxygen species are known to play a key role in the development of acute lung injury, and such injury can be alleviated by pretreating the lung with a suitable antioxidant preparation. In this study, we evaluated and compared the antioxidant efficacy of two liposomal preparations: liposomes containing only alpha-tocopherol versus bifunctional liposomes containing both alpha-tocopherol and glutathione (GSH). alpha-Tocopherol liposomes (2 mg alpha-tocopherol/animal) or liposomes containing both alpha-tocopherol and GSH (2 mg alpha-tocopherol and 10 mumol GSH/animal) were intratracheally instilled into the lungs of rats 30 min prior to a challenge with paraquat dichloride (30 mg/kg, i.p.); animals were killed 24 hr post-paraquat challenge. Lungs of paraquat-challenged animals were damaged extensively as evidenced by increases in lung weight, indicative of edema, and decreases in lung activities of angiotensin converting enzyme (ACE) and alkaline phosphatase (AKP), indicative of endothelial and alveolar type II epithelial cell injuries, respectively. While the pretreatment of rats with alpha-tocopherol liposomes or liposomes containing both alpha-tocopherol and GSH significantly attenuated paraquat-induced changes in lung ACE activity to more or less the same extent, the bifunctional liposomal preparation conferred additional protection to alveolar type II epithelial cells, as evidenced by a significantly higher pulmonary AKP activity. Our results also showed that both liposomal preparations failed to ameliorate paraquat-induced lung edema despite a significant protection of pulmonary endothelial cells, suggesting that paraquat-induced edema formation may be independent of endothelial cell damage. In conclusion, liposome-associated antioxidants can protect the lung against an oxidant challenge, and the extent of protection appears to be related to the characteristics of each antioxidant formulation.
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PMID:Alleviation of paraquat-induced lung injury by pretreatment with bifunctional liposomes containing alpha-tocopherol and glutathione. 893 65

In a replicated 2-yr study, 32 Holstein cows in midlactation were fed diets containing tall fescue hay that was free of or infected with endophyte and with or without added vitamin E in a 7-wk trial to examine the effect of vitamin E supplementation on symptoms associated with fescue toxicosis. Treatments were 1) uninfected tall fescue, 2) tall fescue infected with endophyte, 3) infected tall fescue plus 1000 IU of vitamin E/d, and 4) infected tall fescue plus 2000 IU of vitamin E/d. Feed intake, milk yield, rectal temperature, and body weight change were not significantly altered by dietary treatment. Concentration of prolactin in plasma was lower for cows fed the infected tall fescue than for those fed the uninfected tall fescue. No differences in alkaline phosphatase content of plasma were detected because of tall fescue or vitamin E treatment. Vitamin E supplementation had no effect on symptoms that were associated with fescue toxicosis in lactating dairy cows fed tall fescue hay that was infected with endophyte.
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PMID:Effect of dietary supplementation with vitamin E for lactating dairy cows fed tall fescue hay infected with endophyte. 909 8

1. alpha-Tocopherol (alpha-T) and gamma-tocotrienol (gamma-T) were supplemented continuously for 8 weeks in the diets of normal rats and rats chemically induced with cancer using diethylnitrosamine (DEN), 2-acetylaminofluorene (AAF) and partial hepatectomy. Hepatocarcinogenesis was followed by determining the plasma gamma-glutamyl-transpeptidase (GGT) and alkaline phosphatase (ALP) activities as well as placental glutathione S-transferase (PGST) and GGT activities histochemically, at 4-week intervals. 2. Male Rattus norvegicus were supplemented alpha-T and gamma-T at two different doses of 30 and 300 mg/kg diet. The supplementation was started at three different times: simultaneously with DEN administration; 4 weeks; and 8 weeks after DEN administration. 3. Elevation of plasma GGT activities and formation of PGST and GGT positive foci were attenuated significantly (P < 0.05) when alpha-T and gamma-T were supplemented simultaneously with cancer induction. Supplementation begun 4 and 8 weeks after cancer induction did not affect plasma enzyme activities and formation of enzyme-positive foci. 4. alpha-T was more effective than gamma-T, and a lower dose of 30 mg/kg was found to be more effective in reducing the severity of hepatocarcinogenesis.
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PMID:Different starting times of alpha-tocopherol and gamma-tocotrienol supplementation and tumor marker enzyme activities in the rat chemically induced with cancer. 914 29


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