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 metabolic effects of ethanol are due to a direct action of ethanol or its metabolites, changes in the redox state occurring during its metabolism, and modifications of the effects of ethanol by several nutritional factors. Ethanol causes hyperglycemia or hypoglycemia depending whether or not glycogen stores are adequate, inhibits protein synthesis, and results in a fatty liver and elevations in serum triglyceride levels. Increases in serum lactate, results from the increased reduced nicotinamide-adenine dinucleotide/nicotinamide-adenine dinucleotide + (NADH/NAD+) ratio, and hyperuricemia probably occurs owing to the increased turnover of adenine nucleotides after ethanol ingestion. Ethanol decreases thiamine absorption and decreases the enterohepatic circulation of folate. Acetaldehyde, the major metabolite of ethanol, increases the degradation of pyridoxal 5'-phosphate by displacing it from its binding protein and making it susceptible to hydrolysis by membrane-bound alkaline phosphatase. Chronic ethanol administration also results in decreased vitamin A stores and reduced bone mass and blood levels of 25-hydroxyvitamin D. The mechanism whereby ethanol affects these vitamins and their associated enzymes is unknown.
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PMID:The effect of ethanol and its metabolites on carbohydrate, protein, and lipid metabolism. 329 39

Alcoholic subjects (453) were randomly assigned to disulfiram or placebo therapy and followed for up to 12 months for drinking. Drinking status was determined from interviews of the subject and a household contact each 2 months and from the analysis of eight blood samples or 39 urines submitted at intervals during the year. Liver status was monitored each 2 months by obtaining serum alkaline phosphatase, bilirubin, and AST. Sensitive criteria were arbitrarily selected to identify about 1/5 of the patients with episodic elevations of liver tests. There was no relationship of liver test elevations to disulfiram treatment. However, the elevated AST related significantly to drinking status (p = 0.004) as did elevated bilirubin (p = 0.044), but not elevated alkaline phosphatase (p = 0.146). Two hundred one patients had liver test elevations at least one time and were continued on drug, four were dropped. One hundred seventy-nine of these patients were drinking, 22 were abstinent, and four were indeterminant. It is concluded that patients on disulfiram with minor liver test abnormalities are usually drinking.
Alcohol Clin Exp Res 1987 Jun
PMID:Liver toxicity encountered in the Veterans Administration trial of disulfiram in alcoholics. 330 98

We recently presented preliminary data indicating the presence of antibodies against acetaldehyde adducts in sera of over 70% of alcoholic patients. To assess the respective roles of liver disease and alcohol consumption as well as the specificity of this immune response, 141 patients in various stages of alcoholic and nonalcoholic liver diseases were tested by a hemagglutination assay. Sixty-three (73%) of 86 alcoholics had antibody titers above control levels (p less than 0.0001). Alcohol consumption of these individuals was significantly higher (p less than 0.001) than that of those alcoholics with normal titers. Twenty-two patients (39%) with nonalcoholic liver diseases also had elevated levels of antibodies against acetaldehyde adducts (p less than 0.0005); of these, 8 had primary biliary cirrhosis (7 in Stages III and IV), 9 had chronic active hepatitis (6 with cirrhosis) and 5 had acute (virus- or drug-induced) hepatitis. Antibody titers did not correlate with levels of transaminase or alkaline phosphatase activity, nor with bilirubin, and albumin. However, in 52 alcoholics and in nonalcoholic patients with biopsy-confirmed liver disease, the highest titers were seen in the more advanced stages of liver damage. Thus, in addition to alcohol consumption, severity of liver disease may play a role in the appearance of circulating antibodies against acetaldehyde adducts.
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PMID:The role of alcoholism and liver disease in the appearance of serum antibodies against acetaldehyde adducts. 337 72

(1) The acute effects of ethanol on protein synthesis by liver and skeletal muscle were investigated in young (95-100 g) rats. Rats were injected intraperitoneally with ethanol, 75 mmol/kg body wt; controls were injected with isovolumetric 0.15 M NaCl. After 140 min rates of protein synthesis were measured by injection of a large dose of L[4(3)H]phenylalanine and at 150 min rats were killed. (2) Fractional rates of protein synthesis in control animals were approximately four to five times greater in liver than muscle. Absolute rates were, however, comparable in liver and skeletal muscle. Ethanol reduced the fractional rate of liver protein synthesis by 5-20%; the response for muscle was relatively greater (25-30%). The decrease in the amount of protein synthesized by muscle was also greater than that by liver. (3) After 150 min, plasma gamma-glutamyl transferase, alanine aminotransferase, alkaline phosphatase, lactate dehydrogenase and creatine kinase activities were all decreased by 25-60%. Aspartate aminotransferase activity was increased by 42%, though this was not statistically significant. (4) Increased plasma glucose and triglycerides in ethanol-dosed rats indicated that limitations in substrate supply were not mediating factors in reducing protein synthesis. Ethanol was also able to exert its effects in the presence of elevated insulin levels. A direct effect of ethanol, or its metabolites, on protein synthesis, is therefore implied.
Alcohol Alcohol 1988
PMID:Comparison of the acute effects of ethanol on liver and skeletal muscle protein synthesis in the rat. 339 Feb 39

The determination of myo-inositol trisphosphate by an enzymatic fluorometric assay is presented. The method involves the acid extraction of water-soluble inositol polyphosphates followed by separation by anion-exchange chromatography. Samples are subsequently neutralized by passage over a Dowex Cl- resin and elution with lithium chloride. Samples are then desalted with ethanol. Following dephosphorylation with alkaline phosphatase, free myo-inositol is measured enzymatically via the NAD-dependent oxidation to scyllo-inosose with myo-inositol dehydrogenase. The efficiency of recovery, assay specificity, and an application to the measurement of inositol polyphosphates in hormone-stimulated tissue are discussed.
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PMID:Enzymatic fluorometric assay for myo-inositol trisphosphate. 349 10

The EXPERT consultation system-building tool, a knowledge-based artificial intelligence program developed at Rutgers University, has been applied to the development of a laboratory consultation system facilitating sequential laboratory testing and interpretation. Depending on the results of a basic panel of laboratory tests, the system requests that specific secondary tests be performed. Input of these secondary findings can result in requests for tertiary testing, to complete the database necessary for interpretation. Interpretation of all results is based upon final inferences from the collected findings through a series of rules, a hierarchical network that yields an efficient production system not easily obtained through conventional programming. The rules included in this model are based upon initial results for total protein, calcium, glucose, total bilirubin, alkaline phosphatase, lactate dehydrogenase, aspartate aminotransferase, thyroxin, hemoglobin, mean corpuscular volume, and the concentrations of four drugs. Pertinent clinical history items included are jaundice, diabetes, thyroid disease, medications, and ethanol. Implementing this system in a laboratory-based accelerated testing program involving outpatients maximized the effective use of laboratory resources, eliminated useless testing, and provided the patient with low-cost laboratory information.
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PMID:Application of the EXPERT consultation system to accelerated laboratory testing and interpretation. 352 78

We studied a consecutive series of 204 patients who were admitted to a hospital for addictive diseases during 40 months and who had a liver biopsy. Parenteral drug abusers (n = 34) were significantly younger than alcohol abusers (n = 23) or abusers of both (n = 147) and had lower levels of serum alkaline phosphatase, total bilirubin, and aspartate aminotransferase than the other two groups. Chronic active hepatitis and chronic persistent hepatitis were more frequent (p less than 0.001) in abusers of parenteral drugs alone, whereas cirrhosis was found most often (p less than 0.001) in abusers of both alcohol and parenteral drugs. Cirrhosis was present in 10 of 39 (26%) simultaneous abusers of alcohol and parenteral drugs compared with 58 of 96 (60%) alcohol-abusing former parenteral drug abusers (p less than 0.001). Methadone maintenance treatment was not associated with cirrhosis. Thus, methadone-maintained patients who abuse alcohol and develop cirrhosis should remain in methadone maintenance treatment and receive concomitant alcoholism treatment. Also, these data further support the hypothesis that abusers of both alcohol and parenteral drugs have an increased risk of developing cirrhosis.
Alcohol Clin Exp Res 1986 Oct
PMID:Chronic liver disease in abusers of alcohol and parenteral drugs: a report of 204 consecutive biopsy-proven cases. 354 73

We have recently shown that rat liver 60 S ribosomal subunits active in protein synthesis can be reconstituted from inactive core particles lacking 30% of the total proteins, mainly L10a, L12, L22, L24, A33 and the acidic phosphoproteins P1-P2, obtained by treatment of 60 S subunits with dimethylmaleic anhydride [(1987) Eur. J. Biochem. 163, 15-20]. In this study, an ethanol extract of the 60 S subunit which contains only P1 P2 was also shown to be effective in reconstitution with the DMMA-core-particles: it strongly stimulated the EF-2-dependent GTP hydrolysis and, to a lesser extent, polyphenylalanine synthesis; like the DMMA wash it shifted the thermal denaturation curve of the DMMA-core particles towards that of control subunits. Prior dephosphorylation of the ethanol extract by alkaline phosphatase inhibited the reconstruction process.
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PMID:Role of acidic phosphoproteins in the partial reconstitution of the active 60 S ribosomal subunit. 358 68

Patients with alcoholic hepatitis with plasma B12 levels above 800 pg/ml have overt clinical manifestations of liver disease including severe hepatocellular damage. High plasma B12 levels significantly correlate (P less than 0.0001) with standard liver function tests, e.g. bilirubin, cholylglycine, alkaline phosphatase, AST and prothrombin time as an index of the severity of hepatic damage. Decrease in plasma B12 to normal titres implies a decrease in the severity of alcoholic liver disease, whereas increased plasma B12 levels relate to increased severity and mortality.
Alcohol Alcohol 1987
PMID:Plasma vitamin B12 titres as indicators of disease severity and mortality of patients with alcoholic hepatitis. 359 79

The anti-inflammatory activity of Cassia occidentalis leaf powder and an ethanol extract of Cardiospermum halicacabum aerial parts were assayed in male albino rats using carrageenan-induced rat paw edema. C. occidentalis was maximally active at a dose of 2000 mg/kg, while the C. halicacabum extract was maximally effective at a dose of 500 mg/kg. In the cotton pellet granuloma assay, these drugs were able to suppress the transudative, exudative and proliferative components of chronic inflammation. Further, these drugs were able to lower the lipid peroxide content and gamma-glutamyl transpeptidase and phospholipase A2 activity in the exudate of cotton pellet granuloma. The increased alkaline phosphatase activity and decreased A/G ratio of plasma in cotton pellet granulomatous rats were normalized after treatment with these drugs. C. occidentalis powder and C. halicacabum extract were able to stabilize the human erythrocyte membrane against hypotonicity-induced lysis. It is likely that these drugs may exert their anti-inflammatory activity by inhibition of phospholipase A2, resulting in the reduced availability of arachidonic acid, a precursor of prostaglandin biosynthesis, and/or by stabilization of the lysosomal membrane system.
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PMID:Biochemical modes of action of Cassia occidentalis and Cardiospermum halicacabum in inflammation. 361 9


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