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:3.1.3.9 (glucose-6-phosphatase)
3,081 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Characteristic enzyme alterations have been demonstrated during the stages of experimental hepatocarcinogenesis in rats. The activity of gamma-glutamyl transpeptidase (GGTPase) in hyperplastic and neoplastic hepatocytes is usually increased, whereas that of canalicular adenosine triphosphatase (ATPase) and of glucose-6-phosphatase (G6Pase) is more variable. The activities of these marker enzymes were studied by histochemical techniques in 10 human hepatocellular carcinomas (HCCs), 1 liver cell adenoma, and 1 cholangiocarcinoma of liver. In 9 cases, the nontumorous liver was also examined. All HCCs, but not the liver cell adenoma, displayed enzyme patterns that differed from normal. GGTPase activity was markedly increased in 8 HCCs, whereas the activities of G6Pase and ATPase were lost in 6 and 8 HCCs, respectively. These enzyme alterations occurred as 5 of 7 possible combinations, resulting in significant heterogeneity of enzyme phenotypes, similar to that in experimental hepatocarcinogenesis.
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PMID:Enzyme patterns in human hepatocellular carcinoma. 624 71

Enzyme deviation patterns were examined in primary rat hepatomas induced by short-term sequential administration of two chemical carcinogens from among 2-fluorenylacetamide (FAA), diethylnitrosamine (DENA), and 3'-methyl-4-dimethylaminoazobenzene (3'-Me-DAB) or by FAA or 3'-Me-DAB followed by phenobarbital as a promoter. The purpose was to discern how the patterns are influenced by different administration schedules of carcinogens and which of the two carcinogens in the sequence affects the pattern more. Biochemical differentiation of hyperplastic hepatic nodules and hepatomas was determined by simultaneous assays of activities and isozyme composition of glucose-adenosine triphosphate phosphotransferase, pyruvate kinase, glucose-6-phosphatase, fructose-1,6-bisphosphatase, and gamma-glutamyltransferase with consideration of histological classification of nodules and tumors. Poorly differentiated hepatomas were predominantly induced by 3'-Me-DAB followed by FAA or DENA except for hepatomas induced by 3'-Me-DAB followed by phenobarbital, which were mainly well and moderately differentiated; well and moderately differentiated hepatomas were predominantly induced by FAA followed by 3'-Me-DAB or phenobarbital. The degree of enzyme deviation of the hepatomas induced by DENA as the first carcinogen was intermediate between those of hepatomas induced by FAA or 3'-Me-DAB, although the degree tended to increase with increased dose or term of DENA. These results indicate that deviations of some enzymes, such as pyruvate kinase and fructose-1,6-bisphosphatase, as well as histological differentiation of the primary hepatomas are more strongly influenced by the first carcinogen than by the second under our administration schedules and that the degree of enzyme deviation shown by hepatomas produced by a particular carcinogen treatment regimen principally related to the potential of that regimen to induce the more anaplastic tumors.
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PMID:Enzyme deviation patterns in primary rat hepatomas induced by sequential administration of two chemically different carcinogens. 626 36

A diploid epithelial cell line (termed WB-F344) was isolated from the liver of an adult male Fischer-344 rat and the phenotypic characteristics of the cells were studied. These cells measure approximately two-fifths the volume of freshly isolated hepatocytes. They are histochemically negative for glucose-6-phosphatase and weakly positive for gamma-glutamyl transpeptidase. They produce extensive intercellular reticulin fibers which stain immunocytochemically for fibronectin, and they synthesize both alpha-fetoprotein and albumin, but they do not accumulate glycogen particles. Ultrastructurally, they are polygonal cells with numerous intercellular desmosomes and nexus junctions, and they are partially surrounded by basement membrane-like material. Cytoplasmic organelles include few, but sometimes dilated profiles of rough endoplasmic reticulum, lysosomes, abundant free ribosomes, sparse smooth endoplasmic reticulum and Golgi membranes, microbodies, and small, pleomorphic mitochondria. They express A and C isozymes of aldolase, K isozyme of pyruvate kinase, LDH2 to LDH5 isozymes of lactate dehydrogenase, and 'fetal liver'-type alkaline phosphatase isozyme. When compared with the phenotypes of isolated and purified normal hepatocytes, biliary epithelial (ductular) cells and 'oval' cells isolated from livers treated with chemical carcinogens, the phenotypic properties of the liver epithelial cell line in culture most resemble those of the 'oval' cells.
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PMID:A diploid epithelial cell line from normal adult rat liver with phenotypic properties of 'oval' cells. 646 34

The hypothesis that during the promotion phase of carcinogenesis a second rare event leads to a promoter-independent tumour cell was tested in an initiation-promotion-initiation type of experiment. Precancerous (island) cells induced in rat liver by 10 mg/kg N-nitrosodiethylamine given 24 h after partial hepatectomy were promoted by a protocol consisting of 2-acetylaminofluorene/partial hepatectomy. Administration of 25-100 mg/kg N-ethyl-N-nitrosourea served as second initiater. Microscopic foci of neoplastic cells were observed within the precancerous islands 66 days later; no such foci were noted in the appropriate controls. Deficiency of adenosine triphosphatase and glucose-6-phosphatase marker enzymes in the foci was more pronounced than in the surrounding island cells; glycogen storage was decreased and cytoplasmic basophilia slightly increased; gamma-glutamyltranspeptidase staining was negative or decreased with respect to the surrounding island cells, which exhibited a partially positive reaction. We conclude that a secondary change produced by N-ethyl-N-nitrosourea in precancerous island cells leads to focus-forming cells which grow, in the absence of promoter, into foci of neoplastic phenotype. Similar rare, initiation-like events might be involved in the process of tumour promotion in general.
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PMID:Initiation-promotion-initiation. Induction of neoplastic foci within islands of precancerous liver cells in the rat. 653 10

The potential promoting and/or complete carcinogenic activity of a methyl group-deficient (MD) diet lacking methionine, choline, vitamin B12, and folate on liver tumor induction in weanling male F344/NCr rats was examined. Each of 50 rats per group received one injection 20 mg diethylnitrosamine [(DENA) CAS: 55-18-5; N-nitrosodiethylamine]/kg body weight at 4 weeks of age, and then each was maintained on a methyl group-adequate (MA) diet for 52 weeks (groups 2 and 5) or on an MD diet for 15 weeks followed by the MA diet for 37 weeks (group 4). Controls received injections of saline and were maintained on the same two respective diet regimens (groups 1 and 3, respectively). Histologic results from sacrifices at 6, 10, 15, 22, 39, and 52 weeks revealed early development of foci of eosinophilic gamma-glutamyltransferase (GGT)-positive hepatocytes by week 6 in DENA-MD diet-treated rats, with subsequent development of a diffuse hyperplasia of hepatocytes, oval cell proliferation, cholangiofibrosis, nodular cirrhosis, and neoplastic nodule (NN) formation and, at 52 weeks, hepatocellular carcinomas (HCC) in 13 of 15 rats. Similar but significantly fewer lesions were observed at slightly later sacrifice times in the livers of saline-MD diet-treated rats, with development of NN in 5 of 12 rats and an HCC in 1 of 12 rats at 52 weeks. DENA-treated rats on MA diets developed relatively few GGT-positive foci, and none developed any neoplastic lesions. Except for basophilic foci, areas and foci of cellular alteration containing glycogen-rich hepatocytes frequently exhibited diminished uptake of injected iron and decreased glucose-6-phosphatase and ATPase contents focally or throughout. This study indicates that a relatively brief exposure of both untreated and DENA-treated weanling rats to a severely MD diet produces classical preneoplastic and neoplastic lesions in their livers.
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PMID:Profound postinitiation enhancement by short-term severe methionine, choline, vitamin B12, and folate deficiency of hepatocarcinogenesis in F344 rats given a single low-dose diethylnitrosamine injection. 659 43

Oval cells and biliary epithelial cells were isolated from livers of rats fed a choline-deficient diet containing 0.1% ethionine and from normal rat livers, respectively. Nonparenchymal cell suspensions prepared from these livers by collagenase perfusion followed by digestion of undissociated tissue with 0.1% collagenase, 0.1% Pronase, and 0.004% DNase I were separated into six fractions by centrifugal elutriation. Cells in each fraction were characterized histochemically for gamma-glutamyl transpeptidase, peroxidase, alkaline phosphatase, and glucose-6-phosphatase activities, and for albumin and alpha-fetoprotein by immunocytochemical methods. Cells from Fraction 5 of the elutriation procedure had various features predicted for oval cells and were selected for further studies. The cell yield in this fraction, from each preneoplastic liver, was 5.7 X 10(7) cells, 93 +/- 2% of which were gamma-glutamyl transpeptidase positive, 6 +/- 1% peroxidase positive, 61% albumin positive, and 29% alpha-fetoprotein positive. Cells in this fraction have a median diameter of 13.1 micron and are diploid and cycling. The majority of these cells has morphological features characteristic of biliary epithelial cells, although some cells display features intermediate between duct cells and hepatocytes. Nucleic acid hybridization using specific probes revealed that these cells contain albumin and alpha-fetoprotein messenger RNAs, while hepatocytes from normal and preneoplastic liver contain only albumin messenger RNA. Biliary cells obtained from normal livers do not contain albumin messenger RNA. The large-scale purification and characterization of cell populations from preneoplastic livers is an important step in elucidating the cellular derivation of liver tumors.
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PMID:Isolation of oval cells by centrifugal elutriation and comparison with other cell types purified from normal and preneoplastic livers. 669 43

A comparative morphologic, morphometric and enzyme histochemical investigation of lesions induced by short-term application of N-nitrosomorpholine (NNM) and subsequent so-called 'selection pressure' was carried out in order to assess the characteristics of the numbers of induced putative preneoplastic populations and to cast light on reversibility associated with this model. The glycogen storage foci, mixed cell foci and neoplastic nodules observed after 'selection pressure' were in principle similar to those seen after stop experiments, although alterations in morphology and enzyme phenotype of individual cells were usually far more pronounced after short-term induction. It was established that 75% of the lesions were no longer visible 11 weeks after withdrawal of induction stimuli and that a large proportion of these remaining demonstrated heterogeneity in morphological and histochemical markers indicative of reversion to normal phenotype. After a further 10 weeks a slight increase in number of foci associated with decrease in size and enhanced homogeneity in phenotypic markers was established. The behaviour of foci and nodules undergoing reversion was considered with respect to changes in basophilia and glycogen storage and activity of the enzymes glucose-6-phosphate dehydrogenase, glucose-6-phosphatase, glyceraldehyde 3-phosphate dehydrogenase, glycogen phosphorylase and synthase, acid phosphatase and gamma-glutamyl transpeptidase and correlated with location of altered cellular populations within the liver functional acinus.
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PMID:Phenotypic instability in focal and nodular lesions induced in a short term system in the rat liver. 685 Sep 91

Sequential alterations in enzyme histochemical profiles and reaction of hepatocytes to rapid iron overload were examined in male BALB/c mice during chronic, safrole exposure. At 24 weeks after initiation of safrole treatment, foci of enzyme-altered hepatocytes were noted. These foci were composed of cells showing a decrease in reactivity for glucose-6-phosphatase (Glc-6-Pase) and succinate dehydrogenase (SDH) and an increase for gamma-glutamyl transpeptidase (gamma-Glu-T). In control, iron-loaded mice, the livers were intensely siderotic. In safrole-exposed, iron-loaded mice, foci of iron-negative hepatocytes, varying from a few cells to a lobule in diameter, were initially noted at 24 weeks. Both enzyme-altered and iron-negative foci occurred in the livers of exposed mice at all time periods after 24 weeks. After 36, 52, and 75 weeks of safrole treatment, hepatocellular adenomas were noted with altered enzyme histochemical profiles. Hepatocytes from adenomas were characterized by a decreased staining for Glc-6-pase and SDH and increased staining for gamma-Glu-T and glucose-6-phosphate dehydrogenase (Glc-6-PD). In addition, a few nodules showed a decrease in staining for 5'nucleotidase. In iron-loaded mice, hepatocytes of adenomas showed a decreased to negative reaction for iron when the surrounding parenchyma was siderotic. Hepatocellular carcinomas (HPC) occurred in livers of mice exposed to safrole for 52-75 weeks. The cells of HPC displayed similar enzyme histochemical reactions as cells of adenomas. They were decreased for Glc-6-Pase and SDH activity and increased for gamma-Glu-T and Glc-6-PD. In iron-loaded mice, the HPC cells were negative for stainable iron. Foci, adenomas, and HPC displayed some variability in enzyme histochemical reactions. Variability existed between lesions as well as between cells of the same lesion.
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PMID:Biology of hepatocellular neoplasia in the mouse. II. Sequential enzyme histochemical analysis of BALB/c mouse liver during safrole-induced carcinogenesis. 694 76

Histochemical and cytochemical studies were done to further characterize the preneoplastic hepatocytes with extraperoxisomal catalase (EPC-cells) that were found in the livers of rats fed 3'-methyl-4-dimethylaminoazobenzene. Catalase activity was demonstrated cytochemically to be localized in nuclear matrices, hyaloplasm, and peroxisomal matrices of EPC-cells. It is suggested that an impairment of peroxisome formation is involved in the altered intracellular distribution of catalase. Administration of clofibrate increased the catalase activity in EPC-cells. To examine the preneoplastic nature of EPC-cells, activities of glucose-6-phosphatase (G6Pase) and gamma-glutamyl transpeptidase (GGT) were examined, since changes in the activities of these enzymes have been used as markers of putative preneoplastic cells. In the present study, neither weak G6Pase activity nor positive GGT activity was considered to be a consistent feature of EPC-cells. However, available evidence suggests that EPC-cells are one of the carcinogen-induced cell populations with altered phenotypes.
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PMID:Hepatocytes with extraperoxisomal catalase in rats fed 3'-methyl-4-dimethylaminoazobenzene. 711 45

Male inbred Fischer rats were fed a diet containing 5 p.p.m. aflatoxin for 1, 3, 4 1/2 and 6 weeks at which times groups were killed for histological and histochemical study. Aflatoxin produced a scattered individual cell necrosis of parenchymal cells by 1 week. At 3 weeks small basophilic proliferative foci were seen which increased in size and abundance to 6 weeks. These foci showed starvation-resistant glycogen, variable depletion of glucose-6-phosphatase, succinic dehydrogenase, aniline hydrogenase, membrane ATPase and acid phosphatase. At 6 weeks the foci showed the presence of gamma glutamyl transpeptidase and glucose-6-phosphate dehydrogenase. The basophilic foci were not preceded by other focal histological and histochemical change. The basophilic proliferative lesions are observed when an irreversible change has been induced in the liver. The role of such lesions in the histogenesis of hepatocellular carcinoma is discussed.
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PMID:Histochemical studies on the early proliferative lesion induced in the rat liver by aflatoxin. 724 Dec 69


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