Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
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Gene/Protein
Disease
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Enzyme
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Target Concepts:
Gene/Protein
Disease
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Drug
Enzyme
Compound
Query: EC:3.1.3.9 (
glucose-6-phosphatase
)
3,081
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The histochemical characteristics of liver cell foci in woodchucks were investigated. The foci appeared to be distributed throughout the liver and were observed only in the woodchuck hepatitis virus (WHV)-positive animals, including all 19 woodchucks with hepatocellular carcinoma(HCC), and 7 without HCC. No foci appeared in 11 WHV-negative animals. Histochemical studies revealed that liver cell foci and carcinoma cells were characterized by positive gamma-glutamyl transpeptidase (GGT) enzymatic reactions and decreased
glucose-6-phosphatase
enzyme activity compared to non-neoplastic liver. Furthermore, serum GGT was significantly elevated in almost all of the animals which had larger carcinomas. Ultrastructural findings of foci showed some resemblance to carcinoma cells, being characterized by abundant free ribosomes within the cytoplasm and undeveloped endoplasmic reticulum. These results suggest that the liver cell foci are potential precursors of HCC in WHV-infected animals, and that serum GGT may be a useful marker for indicating the development of carcinoma.
Jpn J
Cancer
Res 1988 Apr
PMID:Enzyme-altered liver cell foci in woodchucks infected with woodchuck hepatitis virus. 289 65
A rapid increase in the fraction of small liver cells was observed in the liver of rats during the early stage of hepatocarcinogenesis by 3'-methyl-4-dimethylaminoazobenzene (3'-Me-DAB). The change in cell population was represented by the decrease in
glucose-6-phosphatase
activity and by the increase in number of gamma-glutamyltranspeptidase-positive cells. When DNA synthesis of liver cells from rats fed 3'-Me-DAB was measured by autoradiography in primary culture, it began to increase 2 weeks after the start of the carcinogen feeding, reaching a plateau level after 3 weeks. Liver cells from rats fed 3'-Me-DAB for 2 weeks or over demonstrated a remarkable resistance to the cytotoxic effect of the carcinogen (0.24 mM) in primary culture. Furthermore, liver cells from rats fed 3'-Me-DAB for 3 weeks or over proliferated in the presence of the carcinogen in primary culture. When liver cells from 3'-Me-DAB-fed and control rats were transplanted into syngeneic rat spleens, the former cells proliferated more vigorously than did the latter. The growth potential of liver cells from 3'-Me-DAB-fed rats tended to be enhanced with time in the carcinogen feeding. Hepatocellular carcinomas developed in the host spleens implanted with liver cells from a rat fed 3'-Me-DAB for 8 weeks. As described above, liver cells from rats fed 3'-Me-DAB demonstrated much greater proliferative ability than normal control cells in vivo and in vitro.
J
Cancer
Res Clin Oncol 1989
PMID:In vivo and in vitro test for growth potential of liver cells from rats during early stage of hepatocarcinogenesis by 3'-methyl-4-dimethylaminoazobenzene. 292 Dec 69
Neoplastic liver cell colonies were induced in the livers of isogeneic F344 rats by intraportal injection of a hepatic cell suspension from diethylnitrosamine-treated donor rats. Examination of the livers 12 days after cell implantation revealed well-demarcated groups of liver cells. The colonies showed alterations of the normal hepatocyte phenotype, which were clearly demonstrated by histologic, cytochemical, and electron microscope techniques. The hepatocytes were markedly deficient in
glucose-6-phosphatase
and bile canalicular ATPase activities, and they contained numerous mitotic figures. Scanning and transmission electron microscopy allowed characterization of hepatocyte interfaces and the shape of sinusoids and the biliary network. The nodular colonies displayed disorganized, thickened trabeculae separated by dilated sinusoids. In these colonies the hepatocytes proliferated intensely and formed, inside the host parenchyma, revascularized, integrated nodular structures. However, these hepatocytes showed ultrastructural anomalies: large nuclei with prominent nucleoli, many free polysomes, and areas of proliferated smooth endoplasmic reticulum in connection with unfolded cisternae of the rough endoplasmic reticulum. All of these features agreed with the hypothesis previously proposed that the colonies may be precursors of the hepatocarcinomas that ultimately develop in animals given injections of treated liver cells. Direct confirmation, however, still is needed.
J Natl
Cancer
Inst 1985 Sep
PMID:Ultrastructural and cytochemical study of the early stages of liver colonization by transplanted neoplastic hepatocytes. 299 29
Cultured hepatocytes from adult Fischer 344 rats were transformed by virion or cloned simian virus 40 (SV40) DNA using the calcium phosphate method. Transformation by SV40 occurred in either serum-supplemented medium or chemically defined medium (CDM). The frequency was greatest in serum-supplemented medium but transformants did not remain differentiated. In contrast, SV40 transformants developed less frequently in CDM, but retained differentiated functions. The frequency of transformation was enhanced by treatments that stimulated cell proliferation, in particular supplementing CDM with epidermal growth factor. Hepatocytes transformed in CDM were epithelial in morphology, secreted albumin, transferrin, hemopexin, and expressed the enzyme
glucose-6-phosphatase
, all characteristics of normal liver. Transformants did not produce detectable levels of alpha-fetoprotein, a marker of fetal or abnormal liver. We conclude that (a) hepatocytes can be transformed by transfection with SV40 DNA; (b) the frequency of transformation is enhanced by stimulating DNA synthesis; and (c) the transformed cells retain specific functions of normal hepatocytes in situ. Using this system it will be possible to study transformation of hepatocytes by viral and cellular oncogenes and to determine their effects on hepatocellular differentiation.
Cancer
Res 1986 Aug
PMID:Transformation of rat hepatocytes by transfection with simian virus 40 DNA to yield proliferating differentiated cells. 301 81
Preneoplastic liver lesions were produced in female Wistar rats by oral administration of 2-acetylaminofluorene for 165 days succeeded by a carcinogen-free standard diet up to 420 days. During the treatment numerous altered hepatic foci (AHF) and hyperplastic nodules (HN) were detected histochemically by a focal decrease or lack of adenosine-5-triphosphatase and
glucose-6-phosphatase
(
G-6-Pase
) activities. In addition, the immunohistochemically demonstrable amount of L-type pyruvate kinase was clearly reduced. The histochemically demonstrated decrease of
G-6-Pase
was substantiated by microbiochemical determination of the enzyme activity in microdissected material. Moreover, during the experimental period a continuous decrease in glucokinase and an increase in hexokinase was detected microbiochemically within AHF and HN. These alterations indicate a shift in the carbohydrate metabolism from gluconeogenesis to glucose utilization and pentose-phosphate-pathway for biosynthesis of nucleic acids. Beside other oncofetal markers, HK may be used as indicator of the early stages of liver carcinogenesis.
J
Cancer
Res Clin Oncol 1987
PMID:Decrease in glucokinase and glucose-6-phosphatase and increase in hexokinase in putative preneoplastic lesions of rat liver. 304 Jul 65
The clonality of chemically induced altered hepatocellular foci was examined in rat liver. Chimeric rats composed of two histologically distinguishable cell lineages were placed on an initiation-promotion protocol for liver cancer induction. This resulted in multiple lesions of altered enzyme expression. These altered hepatocellular foci are generally considered to be initiated sites susceptible to
cancer
formation. The cellular origins of these lesions were determined by aligning sections demonstrating cell lineage with serial sections stained for altered enzyme expression. Analysis included 110 areas of deficient ATPase (EC 3.6.1.3) activity and 59
glucose-6-phosphatase
(
EC 3.1.3.9
; G-6-Pase) deficient lesions, 744 foci of re-expression of gamma-glutamyl transpeptidase (EC 2.3.2.2; gamma-GT), and decreased glycogen mobilization (187 lesions). Of the 1100 focal enzyme alterations, 1054 were shown to be composed entirely of cells from a single lineage of the two lineages present in the mosaic tissue. Multiple alterations occurred within given lesions. Lesions with up to four phenotypic alterations were found to consist of cells of a single lineage. These results suggest that individual enzyme-altered foci are clonal in origin and that phenotypic heterogeneity within altered hepatocellular foci is due to lesion progression within a clonal population and not to a multicellular derivation.
...
PMID:Clonality of preneoplastic liver lesions: histological analysis in chimeric rats. 319 1
A hepatocellular carcinoma cell line, LMH, has been established from a hepatocellular carcinoma induced in a male leghorn chicken by diethylnitrosamine. The cell line is characterized by well-differentiated morphological and biochemical features including the expression of
glucose-6-phosphatase
and canalicular ATPase activities and triploid karyotype with six marker chromosomes. The cells have been continuously propagated in culture for 5 yr and are now at about the 120th passage. Morphological change occurred in culture associated with gradual increase in growth rate at about the 40th passage. However, the biochemical and chromosomal features remained constant. This is the first established domestic fowl epithelial cell line and will allow comparative investigation of a number of parameters relevant to chicken hepatocarcinogenesis.
Cancer
Res 1987 Aug 15
PMID:Establishment and characterization of a chicken hepatocellular carcinoma cell line, LMH. 360 75
Sequential studies on levels of glycogen and lactic acid as well as activities of
glucose-6-phosphatase
, fructose-1, 6-diphosphatase aldolase, aspartic and ornithine transcarbamylase, arginase and xanthine oxidase were carried out in liver and tumour tissue of mice fed with 0.03% thioacetamide in normal stock diet. It was observed that significant decrease in glycogen content and activities of gluconeogenic enzymes was apparent at the age of 4 months, i.e. 2 months after thioacetamide treatment. Alterations in the other parameters studied were observed later, i.e. at the age of 9 months. Maximum changes were observed in the hepatomas, i.e. at the age of 17 months.
Br J
Cancer
1970 Sep
PMID:Studies on progressive metabolic alterations in thioacetamide induced hepatocarcinogenesis. 431 41
Activities of
glucose-6-phosphatase
, fructose 1,6-diphosphatase, ornithine transcarbamylase, arginase and xanthine oxidase were measured in thioacetamide induced primary hepatoma and its tumour cell suspension. It was observed that the percentage decrease in the activities of all the enzymes in tumour cell suspension was far more than that observed in tumour tissue. However, in these studies no qualitative difference was observed between the parenchymal cells and the tumour cells.
Br J
Cancer
1970 Dec
PMID:Enzyme studies on tumour cell suspensions. 432 28
Comparative studies of enzyme activities during the dedifferentiation of hepatic cells and through their development into overt hepatomas are few and contradictory. This study was designed to investigate the histochemical, biochemical and morphologic features of the altered liver cells with particular emphasis on the importance and validity of the histoenzymatic behavior of
glucose-6-phosphatase
(
G6Pase
) as a marker for the detection of precancerous hepatic cells. Serum and hepatic levels of
G6Pase
were analyzed and compared with the histoenzymatic behavior of this enzyme. The use of other enzymes, such as adenosine triphosphatase (ATPase) and gamma glutamyl-transpeptidase (GGT) as histochemical markers for
malignancy
was also tested. The activities of a variety of enzymes commonly used as diagnostic tools were also evaluated in both the liver homogenates and sera of rats treated with 2 mg diethylnitrosamine (DENA)/kg body weight for 2-28 weeks. Using
G6Pase
as a histoenzymatic marker, precancerous cells appeared after 4 weeks of exposure to DENA in the form of small islets devoid of
G6Pase
activity. These
G6Pase
free cells increased in number forming larger islands and finally appeared as tumor nodules after 28 weeks of treatment. The histoenzymatic behavior of ATPase was identical to that of
G6Pase
. The precancerous cells, as well as the tumor cells appeared devoid of ATPase activity. The application of GGT as a marker, showed significantly increased activity in the altered liver and tumor cells. Increased serum levels of
G6Pase
were noted after 10 weeks and were greatly elevated in the late stages of the evolution of the precancerous cells.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Serum and hepatic enzyme activity in rats treated with diethylnitrosamine. 610 Feb 19
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