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)

Among various beryllium (Be) compounds, beryllium oxide (BeO) has so far been noted as a causative substance which introduce chronic pulmonary berylliosis. In our study, chronic pulmonary berylliosis was experimentally evoked by using two species of BeO with individual purity and fired temperature (A group: 95.0% in purity, and 1,300 degrees C or above in fired temperature, B group: 99.9% in purity, and 800-1,000 degrees C in fired temperature), and demarcation of prepared Be concentration involving in the genesis of the disorder was examined. BeO with various concentrations ranging from 200 micrograms to 0.1 micrograms were mixed with 0.1% agar solution and infused into right thorax cavity of male guinea pig, following which variation of the body weight was checked and pulmonary histo-pathological findings, peripheral hematological tests, and sero-biochemical tests were carried out on a periodical basis at 8 weeks, 16 weeks, and 32 weeks. The results obtained are outlined herein. 1) Body weights of test animals in both A group and B group were significantly decreased as compared with that of the control. 2) Pulmonary histo-pathological findings revealed the genesis of epitheloid-cell granuloma in the lungs where non-infusion sides were included, which resembled to non-caseating granuloma in the human pulmonary berylliosis. 3) The frequency in the genesis of epithelaid-cell granuloma was 1/36 (2.8%) in A group and 4/35 (11.4%) in B group, granuloma formation being marked in the latter. 4) Examination of the frequency in terms of BeO dosages revealed no results suggesting the dose-response relationship between pulmonary granuloma formation and the dosage. 5) There were no changes worthy of note in peripheral hematological tests. 6) Sero-biochemical tests revealed that alkaline phosphatase value together with total protein in each was significantly decreased in B group at 32 weeks following the infusion.
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PMID:[Studies on the effects of beryllium oxide in purity and fired temperature to the occurrence of chronic pulmonary berylliosis]. 687 88

The effects of meso-2,3-dimercaptosuccinic acid (DMSA) and 2,3-dimercaptopropane sulphonate (DMPS) on body beryllium burden, hepatic lipid peroxidation, glutathione, alkaline and acid phosphatase and some biochemical variables of porphyrin metabolism were studied in beryllium-poisoned rats. It was observed that beryllium poisoning is associated with a slight increase in lipid peroxidation, significant depletion of alkaline phosphatase and elevation of acid phosphatase activities in the liver and increased beryllium concentration in blood and other soft organs. Evidence is presented that both DMSA and DMPS during concomitant administration prevented most of the above beryllium-induced biochemical alterations. Tissue beryllium concentration and histopathological lesions in liver and kidneys were also significantly less marked following simultaneous administration of DMPS compared to beryllium-exposed controls; DMSA was comparatively less effective.
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PMID:Beryllium-induced biochemical alterations and their prevention following co-administration of meso-2,3-dimercaptosuccinic acid or 2,3-dimercaptopropane sulphonate in rats. 796 38

The present study was conducted to evaluate the therapeutic effectiveness of chelating agents [glutathione, 2,3 dimercapto propane sulfonic acid (DMPS) and D-penicillamine (DPA)] in combination with antioxidant (sodium selenite) in beryllium induced toxicity in female rats. A bolus dose of 50mg/kg-beryllium nitrate was administered singly followed by chelation therapy with GSH, DMPS + Se and DPA + Se at various durations of 1,3 and 7 days respectively. Results revealed a significant fall in the glycogen content, whereas, a marginal fall in the protein was also observed. The enzymatic activity of alkaline phosphatase and adenosine triphosphatase was depleted; on the contrary, there was a significant rise in the acid phosphatase and glucose-6-phosphatase pattern. A rise in the hepatic lipid peroxidation activity is a direct indication of oxidative damage resulting in free radical generation. The distribution of the metal by atomic absorption spectrophotometry revealed an increased concentration of beryllium in liver and kidney, followed by lung and uterus. The relative ability of three chelating agents to act as antagonists, for acute beryllium poisoning, have been examined in liver, kidney, lungs and uterus. The appreciable change in the beryllium concentration in various organs is duration dependent during the entire period being highly significant at 7 days regimen. Biochemical and distribution studies reveal that DPA + Se was the most effective therapeutic agent followed by DMPS + Se and GSH.
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PMID:Role of chelating agents and antioxidants in beryllium induced toxicity. 1262 5

Efforts have been made to minimize the toxic effect caused by beryllium. Adult cyclic rats of Sprague Dawley strain were administered a bolus dose of 50mg/kg beryllium nitrate intramuscularly. The chelation therapy with glutathione (GSH), dimercapto propane sulfonic acid (DMPS)+ selenium (Se) and D-Penicillamine (DPA) + Se was given for 3 days followed by a rest of 1,3 and 7 days respectively. The results revealed a significant fall in the blood sugar level, serum alkaline phosphatase activity, serum proteins. A significant rise in the transaminases i.e. aspartate aminotranferase and alanine aminotranferase pattern is indicative of leakage of enzymes from liver resulting in alterations in the cell permeability. A rise in the hepatic lipid peroxidation activity is a direct indication of oxidative damage resulting in free radical generation. Results of the distribution studies by atomic absorption spectrophotometry reveal an increased concentration of beryllium in liver and kidney followed by lung and uterus. The relative ability of 3 chelating agents to act as antagonists for acute beryllium poisoning have been examined in liver, kidney, lungs and uterus. The appreciable change in the beryllium concentration in various organs is duration-dependent during the entire period being highly significant after 7 days rest. From the biochemical assays, and distribution studies it can be assumed that DPA+Se was the most effective therapeutic agent followed by DMPS+Se and GSH. Thus it can be concluded that DPA+Se is a better therapeutic agent as compared to DMPS+Se and GSH.
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PMID:Analysis of time-dependent recovery from beryllium toxicity following chelation therapy and antioxidant supplementation. 1557 30