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)

A cell line, HuH-28 was established in vitro from a patient with cholangiocellular carcinoma (CCC). This cell line has been in continuous culture over 10 month period with slow growth potential. HuH-28 was composed of spindle-shaped cells as major population besides a small percentage of polygonal-shaped cells. Chromosome number of the cells were distributed near the hypotriploid region on the 3rd passage. HuH-28 cells were not transplantable into nude mice, but secreted some tumor markers including alkaline phosphatase (ALP), gamma glutamyltranspeptidase (GGT), beta 2-microglobulin (BMG), ferritin, elastase-1 and tissue polypeptide antigen (TPA). This HuH-28 cell line will represent a good model for the investigation of carcinogenesis, histogenesis+ and diagnosis of CCC.
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PMID:[Establishment and characterization of a human cholangiocellular carcinoma cell line]. 285 43

Chemopreventive agents are compounds that inhibit carcinogenesis when administered prior or subsequent to a course of carcinogen administration. The effects of dietary administration of crocin dyes on the hepatic damage induced by aflatoxin B1 (AFB1) and dimethylnitrosamine (DMN) in rats were investigated. Female Sprague-Dawley rats were treated with different dosages of AFB1 (0.9 or 4.5 mg/kg) or DMN (8 or 20 mg/kg) by i.p. administration, and the different degrees of hepatic damage were revealed by the elevations of levels of serum marker enzymes such as aspartate amino-transferase, alanine aminotransferase, alkaline phosphatase, gamma-glutamyl transpeptidase and lactic dehydrogenase. Pre-treatment of the animals with crocin dyes 50 mg/kg daily for three consecutive days, the enzyme elevations were significantly suppressed. This suggested that the crocin dyes possessed chemopreventive effects on the early acute hepatic damage induced by AFB1 or DMN. Feeding experiments demonstrated that crocin dyes at 0.1% in the diet could suppress partially the chronic hepatic damage induced by multiple dosages of AFB1 or DMN, but at a higher concentration of 1% crocin dye failed to do so because of their host toxicity. Crocin dyes are extracted from the fruits of Gardenia jasminoides and consist of carotenoids and geniposides as active principles. The protective mechanisms of crocin dyes may be attributed to their carotenoids which are converted metabolically to retinoids in rats.
Carcinogenesis 1986 Apr
PMID:Protection of crocin dyes on the acute hepatic damage induced by aflatoxin B1 and dimethylnitrosamine in rats. 287 Aug 20

An in vivo model of liver hyperplastic noduligenesis was induced in rats by long-term administration of thioacetamide (TAM) (50 mg/kg/day i.p.). Three doses of 50 mg/kg of an antitumoral Rh(III) complex were administered at 14, 9 and 5 days before the end of TAM treatment. Plasma and urine were obtained from either TAM or Rh(III) complex or TAM plus Rh(III) complex treated rats to determine the interactions of both substances with the biochemical parameters related to liver function. The rise in alkaline phosphatase (ALP), leucine aminopeptidase (LAP), gamma-glutamyl transferase (GGT) and the unchanged activities in the aspartate and alanine aminotransferases (AST, ALT) in plasma of TAM-treated rats indicated that the disease induced by this substance can be considered as a chronic obstructive biliary disease with indices of cell proliferation and tumors. The increased concentration of bilirubin both in the plasma and urine of TAM-treated rats suggested liver cholestasis and hepatobiliary obstruction. The very low values of creatinine clearance indicated that there was some degree of kidney failure due to the effect of TAM. The increased concentration of ammonia both in plasma and urine were probably a consequence of the decreased flux in the urea cycle in the liver. The Rh(III) complex alone did not produce significant changes in the plasma enzyme activities. The only significant changes were found in the concentrations of uric acid and ammonia in the urine. When the Rh(III) complex was administered to TAM-treated rats, significant restoration of the following parameters were observed: plasma enzymatic activities, blood bilirubin and ammonia, uric acid and creatinine in the urine and the creatinine clearance. These results suggest that the altered liver function induced by TAM can be restored by Rh(III) complex. The mechanisms by which this complex acts to counteract the TAM-induced changes are not yet established.
Carcinogenesis 1987 Nov
PMID:Effect of a rhodium complex on alterations of hepatic function in thioacetamide-induced hyperplastic noduligenesis in rats. 288 38

The administration of [3H]BPDE-DNA, whether by i.p. or i.v. injection, to male Wistar rats resulted in the majority of the radioactivity being recovered in the faeces. Excretion was rapid: within 24 h post-injection, 45% of the applied dose was recovered in the faeces. H.p.l.c. analysis of radioactive material extracted from the faeces by methanol showed that it contained a single component which co-chromatographed with [3H]BPDE-dGuo and which was not affected by treatment with alkaline phosphatase, aryl sulphatase or beta-glucuronidase. To determine if this phenomenon occurs after topical application of BP to a target tissue, such as mouse skin, animals were treated with [3H]BP and their faeces collected. After an extensive extraction procedure involving differential solubility in organic solvents, Sephadex LH-20 chromatography and h.p.l.c., a product was isolated from mice faeces which had characteristics consistent with a [3H]BPDE-dGuo adduct. These findings are discussed in relation to detection of BPDE adducts in human populations.
Carcinogenesis 1987 Sep
PMID:Topical treatment of mice with benzo[a]pyrene or parenteral administration of benzo[a]pyrene diol epoxide-DNA to rats results in faecal excretion of a putative benzo[a]pyrene diol epoxide-deoxyguanosine adduct. 311 51

N-Methyl-N'-nitro-N-nitrosoguanidine (MNNG) dissolved in distilled water (5 g/l) was administered orally once by gastric tube at a dose of 0.25 ml/10 g body weight to 5-day-old or 28-day-old Wistar Furth (W/Fu) or ACI rats. Gastric tumors in the glandular stomach were found in 58% of 5-day-old ACI rats, but none were found in the rest of the groups. Forestomach tumors were found in both strains of rats at both age groups with incidences of 68-100%. Lung tumors were induced in 64% of 5-day-old and 6% of 28-day-old W/Fu rats, but not in ACI rats. Besides the tumors, a high frequency of hepatic cysts was also noted in ACI rats. Intestinal metaplastic foci with alkaline phosphatase activity were found in the group of 5-day-old ACI rats and none in the rest of the groups. The results showed that the incidences and the locations of tumors in rats induced by MNNG are greatly influenced by both strain and age.
Carcinogenesis 1988 Jul
PMID:Effect of age and strain on N-methyl-N'-nitro-N-nitrosoguanidine tumorigenesis in ACI and Wistar Furth rats. 338 48

The incidence, distribution, size, and histopathology of small and large bowel tumors induced by parenteral administration of 1,2-dimethylhydrazine were examined in rats given 1% or 2% sodium butyrate dissolved in drinking water. Although previous in vitro reports on colon cancer cell lines have suggested that sodium butyrate might have a role to play as a chemotherapeutic "differentiating agent," the results of this in vivo study indicate that sodium butyrate treatment enhanced the development of colonic neoplasia and was associated with increased fecal butyric acid concentrations. In contrast, no changes were seen in the incidence of small bowel tumors, luminal butyric acid concentrations, mucosal morphology, or brush-border enzyme activities (i.e., sucrase, alkaline phosphatase). This study suggests that dietary butyrate has an important, possibly indirect, regulatory role in carcinogenesis associated with an experimental animal model of colonic neoplasia.
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PMID:Effects of differing concentrations of sodium butyrate on 1,2-dimethylhydrazine-induced rat intestinal neoplasia. 373 64

The use of gas chromatography-mass spectrometry (GC-MS) for characterization of free radical-induced base damage to DNA is presented. Damage introduced to DNA by reactive oxygen species such as hydroxyl radicals appears to play an important role in mutagenesis, carcinogenesis and aging. Elucidation of the chemical nature of such DNA lesions is necessary for the assessment of their biological consequences and enzymatic repair. DNA exposed to radiation-generated hydroxyl radicals in aqueous solution was hydrolyzed to 2'-deoxyribonucleosides with a mixture of DNase I, venom and spleen exonucleases and alkaline phosphatase. The hydrolysate was subsequently trimethylsilylated and analyzed by GC-MS. A large number of DNA lesions were separated and identified. Mass spectra obtained were interpreted on the basis of the typical fragmentation pathways of trimethylsilylated nucleosides. The use of GC-MS with selected-ion monitoring facilitated the detection of these lesions at the very low quantities and radiation doses (below 10 Gray) that might be relevant to those in biological systems.
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PMID:Characterization of free radical-induced damage to DNA by the combined use of enzymatic hydrolysis and gas chromatography-mass spectrometry. 378 50

Aflatoxin carcinogenesis appears to relate to multiple factors. This includes bulky adduct formation at DNA guanine N-7. The process also requires more extensive physiological degradation, possibly by the toxin alone as the active principle, but in instances also involving other assaults (e.g., hepatitis B virus). Since aflatoxin carcinogenesis involves complex effects, we have undertaken to define the range of influence of this common food contaminant upon a susceptible model, the broiler-type chick. Aflatoxicosis in two treated groups was indicated by jaundice, coagulopathy, dehydration of combs and shanks, retardation of body weight, and decrease in bursa weight. Blood clotting time, hemoglobin content, erythrocyte and packed-cell volume were affected. Hepatocytes were swollen and had undergone fatty degeneration. Bile duct hyperplasia was evident. Total serum protein, alkaline phosphatase, creatine, lactate dehydrogenase, serum glutamic oxalacetic transaminase and glutamyl transpeptidase were similarly abnormal in birds receiving the contaminated (0.5 and 2.5 micrograms/g aflatoxin B1) feed rations. The aflatoxin B1 and its metabolites were isolated by HPLC from chick serum, liver and muscle.
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PMID:Clinical and biochemical effects of aflatoxin in feed ration of chicks. 392 39

A new class of phosphate-esterified alpha-hydroxyalkyl-alkyl-nitrosamines is described. Here we report the synthesis of these compounds. The mechanism of their formation from the corresponding alpha-acetoxy compounds, and starting from alpha-hydroperoxy compounds is studied by monitoring the reactions in the u.v.-spectrophotometer, by reaction with alkaline phosphatase and by determination of aldehydes generated during degradation of the N-nitrosoacetylesters. Their stability in aqueous solution and their phosphatase-induced degradation was determined. It was found that alpha-phosphate-nitrosamines are more stable in aqueous solution than the alpha-acetates or the parent alpha-hydroxy compounds. Therefore their role as intermediates in nitrosamine metabolism is discussed.
Carcinogenesis 1986 Mar
PMID:N-nitroso-hydroxyalkyl-alkylamine phosphate esters--a new class of N-nitroso compounds. 394 22

The effects of the hepatocarcinogenic peroxisome proliferating hypolipidemic agents clofibrate (CF) and nafenopin (NF) on rat liver carcinogenesis initiated by N-2-fluorenylacetamide (FAA) were studied and compared with that of the neoplasm promoter phenobarbital (PB). Male F344 rats were fed 0.02% FAA for 8 weeks to induce hepatocellular altered foci, and were then given no chemical or equimolar amounts (0.03 mmol/kg diet) of the chemicals for 24 weeks in the diet. In groups of animals killed sequentially, 0.07% PB had a marked enhancing effect on FAA-induced foci, while 0.073% CF produced only slight enhancement and 0.093% NF produced none. At the end of the experiment, only PB increased the incidence and multiplicity of liver neoplasms. NF suppressed histochemical gamma-glutamyltranspeptidase activity in the abnormal hepatocytes of foci as well as in periportal hepatocytes. In homogenates of livers from rats fed NF, gamma-glutamyl-transpeptidase activity was reduced, and this occurred to a lesser degree with CF, whereas PB enhanced activity. NF also induced alkaline phosphatase activity in hepatocytes throughout the lobule, but not in altered hepatocytes, thereby making foci demonstrable in sections reacted for alkaline phosphatase. These findings thus reveal significant cell membrane effects of NF and CF and suggest that their involvement in hepatocarcinogenesis is more complex than a promoting action.
Carcinogenesis 1984 Dec
PMID:Effects of the hepatocarcinogenic peroxisome-proliferating hypolipidemic agents clofibrate and nafenopin on the rat liver cell membrane enzymes gamma-glutamyltranspeptidase and alkaline phosphatase and on the early stages of liver carcinogenesis. 614 19


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