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)

Selenium deficiency has been implicated as a cause of hepatic injury, possibly from accentuated lipoperoxidation due to decreased activity of the selenoenzyme, glutathione peroxidase. Because of possible clinical and biochemical links between selenium and alcohol, we performed nutritional assessment and assayed red blood cell, plasma, and whole blood selenium by spectrofluorometry in 27 normals (group I), 30 asymptomatic alcoholics on admission to a detoxification unit, (group II) and 16 alcoholics with severe liver disease (group III). We found a mean (+/- SD) whole blood selenium of 0.109 micrograms/ml +/- 0.014 for group I vs 0.076 +/- 0.010 for group II (P less than 0.001), and 0.047 +/- 0.006 for group III (P less than 0.001 vs group I and II). For plasma, the mean (+/- SD) selenium was 0.095 micrograms/ml +/- 0.016 for group I versus 0.065 micrograms/ml +/- 0.012 in group II and 0.038 micrograms/ml +/- 0.007 in group III (All P less than 0.001). Calculated red blood selenium levels were also significantly reduced in alcoholics versus controls. Whole blood and plasma selenium correlated directly with serum albumin. For whole blood selenium versus albumin, r = 0.73 (P less than 0.01), and for plasma selenium versus albumin, r = 0.71 (P less than 0.01). A significant inverse correlation was noted between whole blood selenium and the height of the total serum bilirubin (r = -0.46), alkaline phosphatase (r = -0.50), and AST (r = -0.51) (P less than 0.01 for all). Among alcoholics admitted for detoxification, selenium was diminished despite the absence of severe malnutrition, as determined by standard nutrition assessment parameters.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Low blood selenium levels in alcoholics with and without advanced liver disease. Correlations with clinical and nutritional status. 402 13

A number of plasma biochemical parameters were examined in five outbreaks of runting in broiler chickens. In four of the five outbreaks, runts showed consistent elevations in plasma amylase activity and reductions in glutathione peroxidase activity. In two of the five outbreaks the plasma vitamin E concentration was reduced, as was the activity of plasma alkaline phosphatase. A highly significant number of runted chickens were found to have pancreatic degeneration, elevated plasma amylase activity and reduced plasma glutathione peroxidase activity, compared with non-runted chickens. The implications of these changes are discussed in relation to the aetiology of runting and stunting syndrome and, in particular, the possible involvement of selenium.
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PMID:Pancreatic degeneration in broilers with runting and stunting syndrome. 608 56

The serum concentration of selenium was decreased by 17 and 48% in non-cirrhotic and cirrhotic alcoholics, respectively, as compared to healthy controls. In these alcoholics the serum selenium correlated positively with the serum albumin and plasma prothrombin time and inversely with the serum bilirubin, alkaline phosphatase and gamma-glutamyl transpeptidase. Abstinence from ethanol for two weeks was without effect on the serum selenium level in non-cirrhotic alcoholics and acute alcohol intake did not change the serum selenium concentration in non-alcoholic volunteers. In patients with primary biliary cirrhosis the serum concentration of selenium was similar to that in the alcoholic cirrhotics. In patients with hypoalbuminaemia of renal origin the serum selenium was normal. In conclusion our results show that the deterioration of liver function, irrespective of its aetiology, leads to the decrease in serum selenium levels. Whether a defect in removal of lipoperoxides is associated with this decrease in serum selenium concentration remains to be decided by further studies.
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PMID:Decreased serum selenium in alcoholics--a consequence of liver dysfunction. 613 17

Plasma, whole blood, and red blood cell selenium levels were determined by spectrofluorometry in 30 patients with chronic heavy ethanol ingestion (group I) and 20 normal controls (group II). Nutritional and general medical evaluations were also performed. The mean plasma selenium level was 0.065 microgram/ml +/- 0.012 (SD) for group I versus 0.100 +/- 0.016 for group II (p less than 0.0001). Whole blood levels were 0.076 microgram/ml +/- 0.011 versus 0.114 +/- 0.015 (p less than 0.0001), and red blood cell levels were 0.092 microgram/ml +/- 0.016 compared with 0.130 +/- 0.025 (p less than 0.0001), respectively. Mean triceps skin fold was 8.2 mm +/- 3.5 for group I males versus 12.3 mm +/- 5.0 (p less than 0.005) for group II males but was not well correlated with whole blood selenium status (r = 0.33). Nutritional parameters of percentage of ideal body weight, midarm muscle circumference, serum albumin, and total lymphocyte count revealed no differences. Mildly elevated serum aspartate aminotransferase and/or alkaline phosphatase values occurred in 53% of alcoholics, but selenium levels in these patients were no different from those with normal liver tests. We conclude that depressed blood selenium levels occur frequently in patients with chronic heavy ethanol ingestion even in the absence of overt malnutrition. Since selenium deficiency can produce a spectrum of organ injury which resembles that associated with chronic alcoholism, the relationship of selenium deficiency to alcohol-induced organ injury deserves further study.
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PMID:Diminished blood selenium levels in alcoholics. 639 3

Studies on albino rats showed that high doses of tetracycline-induced damages of the liver evident from increased activity of serum enzymes (alanine aminotransferase, aspartate aminotransferase and alkaline phosphatase) and inhibition of bile secretion, synthesis and secretion of bile acids and cholesterol excretion. Administration of vitamin E, sodium selenite, infusion of Astragalus L. and especially vitamin E combinations with sodium selenite markedly or completely arrested the occurrence of hepatotoxic properties of tetracycline. It is suggested that the use of vitamin E combinations with selenium-containing preparations is advisable in the prophylaxis and treatment of tetracycline-induced damages of the liver.
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PMID:[Vitamin E and selenium-containing preparations in the prevention treatment of tetracycline-induced lesions of the liver]. 663 74

The inhibitory effect of selenium (Na2SeO3) on 1,2-dimethylhydrazine (DMH)-induced colon carcinogenesis in male Sprague-Dawley rats is presented. A 4-ppm selenium supplement to the drinking water was provided concurrently with DMH treatment and continued until death or sacrifice. Rats were administered 10 weekly injections of 10 mg DMH per kg body weight. Thirtyone weeks following the tenth DMH injection, all surviving animals were sacrificed. At sacrifice, the colon tumor incidence in DMH-only controls was 8 of 28 (29%). Selenium supplementation significantly (p less than 0.01) reduced the colon tumor incidence to 1 of 37 (3%). The cumulative colon tumor incidence for all animals found dead or sacrificed was also significantly (p less than 0.05) reduced from 11 of 40 in DMH controls to 3 of 40 in DMH-selenium-supplemented rats. The total number of colon tumors was reduced from 13 to 3, and the average number of tumors per rat from 1.2 to 1.0 by supplemental selenium. The majority (greater than 65%) of all tumors were located in the distal colon. The serum glutamic oxaloacetic transaminase, alkaline phosphatase, and complete blood count were normal and equivalent for the DMH only, DMH-selenium, and untreated control groups in this study. The glutathione S-transferase activity in liver cytosol preparations was increased from 39.6 +/- 7.3 (S.D.) microM product/min/mg (DMH only) to 67.6 +/- 5.8 microM product/min/mg by selenium only and to 54.3 +/- 10.6 microM product/min/mg in selenium-DMH-treated rats. Protection by selenium may in part be attributed to enhanced detoxification of carcinogenic electrophiles.
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PMID:Selenium inhibition of 1,2-dimethylhydrazine-induced colon carcinogenesis. 683 12

The role of selenium in protection against nephrotoxicity and hepatotoxicity of cadmium in rats was investigated. The administration of Cd (3 mg/kg, s.c.) for 3 days enhanced the urinary excretion of lactic dehydrogenase (LDH), glutamic oxaloacetic transaminase (GOT) and total proteins, decreased the renal activity of GOT and alkaline phosphatase (ALP) and increased the renal level of Cd, Cu and Zn. Cadmium also increased the serum GOT and glutamic pyruvic transaminase (GPT), decreased the hepatic activity of GOT and GPT and increased the hepatic level of Cd and Zn. The concomitantly administered Se (2 mg/kg, i.p.) initially reduced most of these Cd-induced alterations. The results show protection by Se against nephrotoxicity and hepatotoxicity of Cd on the 4th day of the commencement of Cd administration, but the signs of Cd intoxication were observed on the 8th day.
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PMID:Time-dependent protective effect of selenium against cadmium-induced nephrotoxicity and hepatotoxicity. 715 Dec 36

The biochemical and clinical effects of selenium (Na2SeO3) on 1,2-dimethylhydrazine (DMH)-induced colon carcinogenesis in male Sprague-Dawley rats are presented. A 4-ppm selenium supplement to the drinking water was provided before, during, and after 20 weekly injections of 20 mg DMH per kg body weight. Immediately after the 20th DMH injection, part of the rats were sacrificed. The incidences of colon tumors in groups provided selenium before DMH, before and during DMH, and only during DMH treatment were reduced to 39, 43, and 36%, respectively. The incidence in the DMH only control was 63%. Other rats in all treated and control groups were maintained up to 5 months post-DMH treatment. At 10-week intervals throughout the study, selected blood and tissue components were analyzed. The following hematological changes correlated with DMH treatment. (a) Serum glutamic oxalacetic transaminase increased 2-fold (normal, 66 +/- 14 g/dl). (b) Serum alkaline phosphatase increased 24% (normal, 166 +/- 56 units/liter). (c) Serum protein decreased 14% (normal, 6.77 +/- 0.48 g/dl). (d) White blood count increased 2- to 3-fold (normal, 7.7 +/- 2.7 X 10(3)/cu mm). And (e) hemoglobin decreased 67% (normal, 18.1 +/- 1.3 g/dl). The magnitude of these changes varies with each selenium treatment group and with each 10-week analysis period. Provision of 4 ppm selenium doubled both liver and blood selenium levels compared to unsupplemented controls. The effects of selenium and DMH treatments on glutathione peroxidase and beta-glucuronidase activities and on sialic acid are presented. Possible mechanisms by which selenium protects against DMH-induced neoplasia are discussed.
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PMID:Biochemical and clinical effects of selenium on dimethylhydrazine-induced colon cancer in rats. 730 70

Pluripotent embryonic stem (ES) cell cultures provide an efficient method for genome manipulation with many applications in marine biotechnology. To develop this technology we have been working to derive fish ES cell lines for in vitro studies of embryo cell growth and differentiation and for the generation of transgenic fish. Zebrafish embryonal cell cultures were derived from blastula-stage embryos in LDF medium supplemented with fetal bovine serum, trout serum, trout embryo extract, selenium, insulin, and leukemia inhibitory factor. Cultures derived under these conditions on feeder layers of zebrafish embryonic fibroblasts possessed a diploid karyotype and exhibited an ES-like morphology with elevated levels of alkaline phosphatase enzyme activity. Injection of primary cell cultures derived from embryos of transgenic fish carrying neo produced chimeric fish detected by polymerase chain reaction analysis. Embryo cells cultured on poly-D-lysine substrate in the presence of retinoic acid or Buffalo rat liver cell-conditioned medium (BRL-CM) and a reduced serum concentration differentiated into neuronal cell types exhibiting elevated levels of acetylcholinesterase enzyme activity and expression of neurofilament and glial fibrillary acidic protein.
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PMID:ES-like cell cultures derived from early zebrafish embryos. 767 May 94

Caco-2 cell human colon adenocarcinoma cell line was used to study the hormonal regulation of small intestinal epithelial cell differentiation. We had previously shown that insulin-transferrin-selenium and triiodothyronine (5 x 10(-8) M)-supplemented medium can best replace serum after 2 days of culture for both the maintenance and differentiation of Caco-2 cells. The present study demonstrates that precoating petri dishes with complete serum allows the growth and differentiation of Caco-2 cells seeded directly in serum-free medium. On the other hand, precoating with dialyzed serum inhibits alkaline phosphatase and dipeptidyl-dipeptidase IV activities by more than 50%. The results obtained with complete serum-precoated culture plates indicate that there is no synergy between insulin and triiodothyronine because cells maintained in transferrin-selenium and triiodothyronine-supplemented medium, with or without insulin, express comparable enzyme activities. Moreover, large increases in alkaline phosphatase and dipeptidyl-dipeptidase IV activities were observed when triiodothyronine was added to the culture medium by the time confluency was reached. In contrast, gamma-glutamyltransferase was lowered to a greater extent when triiodothyronine was present from the beginning of culture. These findings show that triiodothyronine preferentially stimulates alkaline phosphatase and dipeptidyl-dipeptidase IV activities during the differentiation period whereas it selectively inhibits gamma-glutamyltransferase during the proliferation phase. Triiodothyronine acts in a dose-dependent manner.
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PMID:Alkaline phosphatase and peptidase activities in Caco-2 cells: differential response to triiodothyronine. 788 29


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