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)

(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.
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PMID:Comparison of the acute effects of ethanol on liver and skeletal muscle protein synthesis in the rat. 339 Feb 39

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 nutritional factors. Ethanol causes hyperglycemia or hypoglycemia depending on whether glycogen stores are adequate, inhibits protein synthesis, and results in fatty liver and in elevations in serum triglyceride levels. Increases in high-density lipoprotein cholesterol after ethanol ingestion may explain the lower risk of myocardial infarction and death from coronary disease after moderate drinking. Increases in serum lactate, resulting from the increased NADH/NAD+ ratio, and hyperuricemia, most likely the result of increased turnover of adenine nucleotides, are common transient effects of ethanol ingestion. Causes of vitamin deficiencies in alcoholism are decreased dietary intake, decreased intestinal absorption, and alterations in vitamin metabolism. Ethanol decreases thiamine absorption and decreases the enterohepatic circulation of folate. Acetaldehyde 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. Ethanol decreases hepatic vitamin A concentration and its conversion to active retinal, and modifies renal metabolism of vitamin D.
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PMID:Metabolic effects of alcohol. 388 Dec 85

Effect of chronic ethanol administration on some enzyme activities was studied in plasma membranes, brain homogenate cytoplasmic reticulum and cytosol, liver homogenate and microsomal fractions and blood serum. Ethanol was ingested as a constituent of isocaloric "semiliquid" diet. The investigation was carried out to estimate the diagnostic value of certain enzymes in evaluation of alcohol intoxication. In male rats ethanol caused remarkable hyperlipidemia, accumulation of lipids in liver tissue and elevation of gamma-glutamyl transpeptidase activity in blood serum and brain tissue. In liver tissue moderate induction of glucose-6-phosphatase, NADPH-cytochrome c reductase and alkaline phosphatase was observed. The putative mechanism of elevation of organospecific enzyme activities in blood serum during chronic ethanol consumption is discussed.
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PMID:[Effect of chronic administration of ethanol on the enzyme activity of rat serum, liver and brain]. 614 65

Pregnant rats were fed individual liquid diets throughout gestation and lactation. The diets contained either 2 or 10 micrograms zinc/ml diet with or without 30% of the kilocalories supplied from ethanol. The low zinc diet produced a moderate zinc deficiency in dams evidenced by decreases in tissue zinc content, serum alkaline phosphatase activity and urinary zinc concentration. Despite the presence of high zinc content in the diet, ethanol antagonized the maternal zinc status to a level typical of that produced by the low zinc diet. The lowest zinc status, however, was found when low dietary zinc and ethanol were combined. The maternal interaction between ethanol and zinc also depressed offspring serum zinc and alkaline phosphatase activity in a similar manner. Ethanol, however, did not affect tissue content of calcium, magnesium or phosphorus, which indicates that ethanol is a specific antagonist of zinc utilization during gestation and lactation.
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PMID:Interaction between ethanol and low dietary zinc during gestation and lactation in the rat. 649 58

In this study we measured some parameters that are associated with ethanol damage to the liver. The method allowed us to determine the injury that chronic and acute ethanol treatments produce at the cellular level without interference from homeostatic or compensatory mechanisms. The system used is a hepatic fetal human cell line, WRL-68, which retains, in culture, many of the liver-specific functions. WRL-68 cells do not metabolise ethanol, and consequently we could evaluate the effect of ethanol alone. We explored two different conditions: 30 days with 0.1 M ethanol (chronic treatment) and 24 h in the presence of 0.5 M ethanol (acute treatment). 1. The transmission electron microscopy studies revealed, in both treatments, the presence of granules not usually present in the cytoplasm of control cells and morphological mitochondrial alterations in chronically treated cells. 2. Lipid peroxidation, measured as the rate of malondialdehyde production, increased three and a half times in acutely treated cells and about twofold in chronically treated cells. 3. The percentage of total activity (activity in the medium/(activity in the medium + activity of the cells). 100) and the enzymatic activity in the culture medium of gamma glutamyl transpeptidase (GGT), alanine amino transferase (ALAT), aspartate amino transferase (ASAT) and alkaline phosphatase (AI-P), increased. 4. We measured some parameters related to the transport of sodium across the membrane. Cells chronically treated with ethanol had higher rate constants and effluxes than control cells. There was no difference between the total and passive efflux. Ethanol treated cells apparently lacked the ouabain sensitive pathway. In acutely treated cells, the total sodium efflux and the rate constant were enhanced. Sodium pools in the acutely treated cells were diminished and active sodium pumping was seven times higher than in control cells. 5. We determined the number of high affinity ouabain binding sites per cell. Ethanol did not alter the number of pumps, rather it seems to induce a functional alteration. Our results indicate that ethanol per se induces lipid peroxidation, alters enzymatic activities, sodium transport systems, sodium pools and cellular morphology, and that all these changes may be partly responsible for ethanol-induced hepatotoxicity. The data compare favourably with those reported in the literature for many different systems. Therefore our model for studying the mechanism of alcohol effects appears to be valid, with the advantage of being able to compare experiments that can be done in the same system and under the same conditions.
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PMID:The effect of chronic and acute ethanol treatment on morphology, lipid peroxidation, enzyme activities and Na+ transport systems on WRL-68 cells. 759 92

The effects of protein malnutrition on haematological and serum biochemical values were evaluated in gossypol-treated rats which were simultaneously fed with ethanol. Gossypol caused anaemia, leucopenia and thrombocytopenia in malnourished animals, suggesting a depression of bone marrow activity. Gossypol also caused a significant elevation of serum alkaline phosphatase and alanine aminotransferase activities and increases in the concentrations of Mg++ and Ca++ with reduced albumin, regardless of the nutritional status. These changes were more severe with malnutrition. Ethanol alone caused a thrombocytopenia but no other significant haematological changes. However, it appeared to cause derangement of lipid and protein metabolism as reflected in serum cholesterol and urea. The toxic effects seen in gossypol-treated rats were significantly reduced in animals simultaneously given ethanol. As the livers of gossypol-treated rats were significantly heavier than in these animals, it seems possible that ethanol consumption enhances the ability of the liver to metabolize gossypol, thereby reducing its accumulation and consequently its toxicity. However, further studies are needed to determine the mechanisms responsible.
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PMID:Haematological and serum biochemical changes in the rat due to protein malnutrition and gossypol-ethanol interactions. 788 58

Ethanol administration to rats for 30 days and 90 days followed by paracetamol administration resulted in liver injury indicated by the significant increase in the serum GOT and GPT levels. The ethanol treatment to rats and the administration of paracetamol to the normal and alcoholic rats also caused a significant increase in the activity of serum acid and alkaline phosphatase. The hepatotoxicity of ethanol and paracetamol were indicated by the histological alterations in this study. The content of lipid peroxidation products-malondialdehyde, hydroperoxides and conjugated dienes were increased in the liver, heart, kidney and brain of the acute and chronic ethanol treated and paracetamol treated rats. The activities of the antiperoxidative enzymes-SOD and catalase decreased in the ethanol and paracetamol treated rats. The changes in the activities of the antiperoxidative enzymes in alcoholism and drug toxicity suggests increased peroxidation, increased synthesis of ecosonoids and increased damage to the tissues. The glutathione levels were decreased in the rats administered ethanol for 30 days, while the glutathione levels increased in the 90 days ethanol treated rats. The paracetamol treatment caused a decrease in the glutathione levels in the normals and the ethanol treated rats.
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PMID:Role of lipid peroxides, glutathione and antiperoxidative enzymes in alcohol and drug toxicity. 835 54

Ethanol consumption has a toxic effect on the epithelium of the small bowel, but enterocyte maturity is very difficult to measure under these circumstances. However, when ethanol intake is combined with enterectomy, enterocyte immaturity is greater, permitting an easier separation of these two effects. In a group of rats (13 male Wistar rats weighing approximately 220 g) fed a liquid diet containing 35% ethanol for 4 weeks after resection of the proximal jejunum, the residual small intestine brush border maltase, sucrase, and lactase activities were similar to those of a pair-fed control group (13 animals). However, alkaline phosphatase activity was decreased in the mucosa and in the enterocyte brush border, probably because of the lower activity of this enzyme in the jejunum-ileum remnant of the alcoholic group.
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PMID:Effect of chronic ethanol consumption on the activities of residual small bowel brush-border enzymes after proximal jejunum resection in the rat. 865 45

The habitual consumption of alcoholic beverages is clearly associated with low bone mass and an increased prevalence of skeletal fractures. Microscopic analysis of skeletal tissue from alcoholic patients reveals reduced osteoblast number and suppressed bone formation activity with a relative sparing of resorptive indices. The decreased number of osteoblasts observed in alcoholic subjects results from either impaired proliferation or accelerated senescence. Polyamines and ornithine decarboxylase (ODC), the rate-limiting enzyme for polyamine synthesis, are essential for cell proliferation in a variety of cell types. To determine if the adverse effect of ethanol on osteoblast number involves modulation of polyamine biosynthesis, we examined the effect of ethanol on parameters of cell growth and ODC activity in a human osteoblast-like osteosarcoma cell line (TE-85). Ethanol markedly impaired DNA synthesis and cell proliferation in a dose-dependent fashion, but alkaline phosphatase activity (a marker of differentiated osteoblast function) remained intact, and accelerated apoptosis was not evident. Thus, the reduced osteoblastic cell number was a result of a direct effect on proliferative processes rather than a nonspecific toxic effect of ethanol to accelerate cell death. Induction of ODC activity was impaired in ethanol-exposed cell cultures in a dose-dependent fashion that paralleled the antiproliferative effects. Finally, supplemental polyamine administration substantially improved DNA synthesis in ethanol-exposed UMR 106-01 cell cultures. These data confirm a direct inhibitory effect of ethanol on osteoblast proliferation without overt cellular toxicity that may, in part, explain the reduced bone mass observed in those who consume excessive amounts of alcohol.
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PMID:Ethanol inhibits human osteoblastic cell proliferation. 872 57

The expression of caprine arthritis-encephalitis virus capsid protein was studied in seropositive naturally infected asymptomatic goals (10< seropositive naturally infected encephalitic kids (12) and goats (4), and noninfected control goats (3). Rabbit antiserum to recombinant viral capsid and matrix proteins were used in a biotin-streptavidin-alkaline phosphatase complex immunohistochemical method on sections of formalin- and ethanol-fixed tissue specimens. Macrophages in inflamed areas of the lung (8/12), in the brain (5/16), and in the spinal cord (4/16) from encephalitic animals harbored viral antigens, as revealed by immunohistochemistry and use of a capsid protein-specific antiserum. Altogether 12/16 encephalitic animals tested positive for viral antigen. Viral antigens were found in 5/10 seropositive asymptomatic goals in macrophages located in the lung (3), the udder (1), and the medulla of lymph nodes (4). None of the control animals tested positive for viral antigen. Ethanol fixation showed highest sensitivity, and the lowest antigen concentration that revealed a positive signal discernible from background was twofold higher in ethanol-fixed specimens than in formalin-fixed specimens. The evaluation was performed on artificial antigen substrates embedded with defined concentrations of recombinant viral capsid protein. Immunohistochemistry is a valuable supplement to the methods presently available for diagnosis in cases suspicious of caprine arthritis-encephalitis.
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PMID:Immunohistochemical identification of caprine arthritis-encephalitis virus in paraffin-embedded specimens from naturally infected goats. 916 73


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