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 effect of nicophesone on the processes of cojugation and alkaline phosphatase was studied in tests staged on albino rats and rabbits poisoned with carbon tetrachloride (CCl4). Nicophesone is shown to stimulate conjugation of bilirubin with glucoronic and sulphuric acids and to depress the activity of alkaline phosphatase. The data obtained are considered inasmuch as they concern the hypobilirubinemic action of nicophesone.
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PMID:[Mechanism of the hypobilirubinemic action of nicofezon]. 14 7

Cytochemical changes of glycogen and alkaline phosphatase were studied under sequential effect of p-dimethylaminoazobenzene (DAB) feeding and CCl4 injections. It has been found that in liver cells of experimental animals, the concentration of glycogen and the activity of alkaline phosphatase were decreased.
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PMID:Cytochemical studies of rat liver glycogen and alkaline phosphatase under the effect of hepatocarcinogens. 19 31

The effect of carbon-tetrachloride poisoning and the protection caused by AMP were studied. A single dose of CCl4 has resulted in a rapid development of a fatty liver, a considerable increase in serum enzymes, glutamic oxalacetic and pyruvic transaminases as well as serum-alkaline phosphatase. Total serum protein showed a tendency to decrease accompanied by a decrease in A/G ratio. Administration of adenosine-5-monophosphate prevented the increase in serum-alkaline phosphatase and increased the A/G ratio. There was, however, a slight but significant decrease in serum GOT and GPT within the 24-hrs. period of study, but it remained still higher than that of the control. AMP lowered liver fat without complete protection against the development of fatty liver.
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PMID:Effect of AMP on acute carbon-tetrachloride hepatotoxicity. 20 15

Activity of alanine and aspartate aminotransferase, alkaline phosphatase, adenosine, desaminase and AMP-aminohydrolase was determined in rats in the process of the liver regeneration under acute and chronic lesion with CCl4. It is shown that under chronic lesion of the liver with CCl4, in contrast to the acute one, changes in the aminotransferase activity in blood serum are not expressed in the liver, the activity is essentially decreased. A steady increase was observed in the activity of adenosine desaminase, AMP-aminohydrolase and alkaline phosphatase in the liver and blood serum. It is concluded that the normal regenerative process is accompanied by short-term shifts of the enzymes activity in the liver and blood serum. The development of a chronic process results in a characteristic increase in the activity of adenosine desaminase, AMP-aminohydrolase and alkaline phosphatase in the liver and blood serum.
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PMID:[Enzyme activity during regeneration under acute and chronic liver lesion with CCL4]. 68 74

The influence of phenobarbitone givenin ten repeated doses simultaneously with small doses of CCl4 on serum enzymes was investigated in albino rats. The same experiment was repeated to investigate the influence of propionyl-promazine (phenothiazine derivative). The results proved that SGPT is a more specific and sensitive index than SGOT of hepato-cellular injury. The activity ratio between serum GOT and GPT in the normal control group was 2.44. The activity of SGPT increased nearly 6.1 fold after CCl4 administration and thus the activity ratio between GOT and GPT is sharply reduced to 0.56. The activity of serum GPT when CCl4 and phenobarbitone were administered together showed value of about 1/2 of the value when CCl4 was administered alone, while it remained high when CCl4 administration was combined with propionyl-promazine. Serum GOT and alkaline phosphatase increased significantly in all the groups. Regarding the pathological examination of the liver it was found that marked fatty necrosis could be demonstrated when high values of SGPT was found, which is not the case with serum GOT. It is concluded that in the present experimental conditions phenobarbitone protected the liver from the hepatotoxic effect of CCl4, while propionyl-promazine did not.
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PMID:Effect of phenobarbitone and propionyl-promazine on serum enzymes in carbon-tetrachloride hepatotoxicity. 69 49

Glutathione reductase activity of both serum and liver tissue homogenates was measured in normal controls and in cases of hepatic parenchymatous diseases, and the results were compared with those from animal experiments in which hepatic damage was produced by CCl4 injection. Glutathione reductase showed a different attitude from those of transaminases and alkaline phosphatases under these clinical and experimental conditions. Glutathione reductase activity increased in both serum and liver in patients with hepatic damage, and this increase occurred earlier than the changes in alkaline phosphatase activity.
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PMID:Glutathione reductase activity in serum and liver tissue of human and rat with hepatic damage. 115 81

It has been shown in experiments on white rats that chronic (for one month) intoxication with CCl4 and C2H5OH results in liver injury. It manifests by activation of aminotransferases (ALT, AST) and alkaline phosphatase in blood serum, initiation of lipid peroxidation, depletion of the liver pool of reduced glutathione, and suppression of bile production. The liver preparations (sirepar and vitohepat) reduce hepatotoxicity of the poisons in question. The use of vitohepat and sirepar in combination with carsil potentiated hepatoprotective and antioxidative activity of the liver preparations.
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PMID:[The efficacy of vitogepat and sirepar in combination with karsil in chronic liver lesions]. 130 40

Individual serum bile acids (SBA) are emerging as potentially useful early indicators of liver injury. This study was undertaken to compare the usefulness of individual SBA with the routinely used assays for detecting the effects of the hepatotoxicants carbon tetrachloride (CCl4) and chloroform (CHCl3). Serum samples were assayed for liver injury by determination of alanine aminotransferase (ALT), aspartate amino-transferase (AST), alkaline phosphatase (ALP), bilirubin and total bile acid (by enzymatic kit). These results were compared with levels of individual SBA measured by high performance liquid chromatography (HPLC). Liver samples from CCl4-treated rats were taken for light and electron microscopic examination. The highest dose for each chemical caused increases in serum ALT and AST but not ALP. Chloroform at the highest dose increased bilirubin. Total SBA levels as assayed by the kit were elevated in response to CCl4 and CHCl3 at doses below which serum enzymes and bilirubin were increased. Some individual SBA were increased at a still lower dose for each of these two chlorinated solvents. At the lowest dose of CCl4 tested no consistent light microscopic or ultrastructural changes were found. At all the higher doses periacinar cells displayed typical accumulation of lipid droplets and degranulation and dilation of rough endoplasmic reticulum. The extent of the ultrastructural changes were dose-dependent. Thus individual SBA assayed by HPLC may be considered as a very sensitive indicator of liver injury induced by the classical hepatotoxicants carbon tetrachloride and chloroform.
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PMID:Individual serum bile acids as early indicators of carbon tetrachloride- and chloroform-induced liver injury. 145 31

The effects of (4R)-hexahydro-7,7-dimethyl-6-oxo-1,2,5-dithiazocine-4- carboxylic acid (SA3443), a novel cyclic disulfide compound, on the development of chronic liver injury were studied in rats, using two types of models, carbon tetrachloride (CCl4)-induced chronic liver injury and heterologous serum (swine serum)-induced liver fibrosis. SA3443 (30-100 mg/kg, p.o.) significantly suppressed increases in serum transaminase and alkaline phosphatase activity induced by CCl4-treatment for 10 weeks. This compound also inhibited increases in hepatic lipids and hydroxyproline content in CCl4-treated rats. In the histopathological studies, treatment with SA3443 resulted in a decrease in the degree of hepatic necrosis, fibrosis and steatosis. On the other hand, 8-weeks treatment with swine serum revealed hepatic fibrosis without appearance of necrosis or fatty accumulation. In this model, SA3443 (30 mg/kg, p.o.) reduced the hepatic hydroxyproline level, and diminished the formation of connective tissue in the liver. These findings indicate that SA3443 protects the liver against chronic liver injuries induced by CCl4 and heterogeneous serum.
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PMID:The protective effects of SA3443, a novel cyclic disulfide, on chronic liver injuries in rats. 174 24

The present study examined the effects of (1-[(2-thiazolin-2-yl)amino]-acetyl-4-(1,3-dithiol-2-ylidene)-2,3, 4,5- tetrahydro-1H-1-benzazepin-3,5-dione hydrochloride (KF-14363) on liver fibrosis in rats with chronic liver injury induced by carbon tetrachloride (CCl4). Liver injury in male rats was induced by repeated administration of CCl4 at 0.5 ml/kg twice a week. The progression of liver fibrosis was checked in the 4th, 6th, 8th and 10th weeks using the relative amount of hepatic 4-hydroxy proline (4-hyp) to total proteine as an index of hepatic collagen. The relative amount of hepatic 4-hyp in these rats exceeded significantly that in rats not administered CCl4 by the 4th week. This progressed in proportion to the duration of CCl4 administration. In groups concurrently administered KF-14363 at 30 and 100 mg/kg/d from the 5th or 8th week of the CCl4 administration, the relative amount of hepatic 4-hyp was found to be lower in the 10th week than at the start of the KF-14363 administration. The inhibition of liver fibrosis was also observed histopathologically. The concurrently co-administration with CCl4 or KF-14363 at 30 and 100 mg/kg for 2 or 5 weeks inhibited the increases in serum transaminases and alkaline phosphatase induced by CCl4. The results show that KF-14363 inhibits liver fibrosis in a dose dependent fashion in rats with progressive liver injury.
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PMID:Effects of KF-14363 on liver fibrosis in rats with chronic liver injury induced by carbon tetrachloride. 181 77


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