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)

Molar extinction coefficients of precipitated lead sulfide (PbS) and polymerized diaminobenzidine (polyDAB) have been determined at wavelengths of 450 nm and 480 nm, respectively, for quantitative histochemical analysis of phosphatase reactions. These values are essential for the conversion of cytophotometric (mean integrated) absorbance values to absolute units of substrate converted per unit time and volume of tissue. This conversion allows direct comparison of histochemical and biochemical data. The molar extinction coefficient of PbS at 450 nm was found to be 3,800 and therefore, per mole phosphate liberated, the molar extinction coefficient is 5,700 because 3 moles phosphate are captured by 2 moles lead at neutral or alkaline pH. Parallel experiments with the cerium-DAB method revealed that the molar extinction coefficient of polyDAB at 480 nm is 5,500 with respect to liberated phosphate. The molar extinction coefficients were applied for comparison of data from biochemical and histochemical assays of glucose-6-phosphatase activity in rat livers. A significant correlation was found between both sets of data. The values were in the same order of magnitude with histochemical values approximately 1.4 times higher than biochemical values.
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PMID:Molecular extinction coefficients of lead sulfide and polymerized diaminobenzidine as final reaction products of histochemical phosphatase reactions. 133 96

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.
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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

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

Treatment of female C57BL/6 x DS-F1 mice with 3'-methyl-4-dimethylaminoazobenzene (3'-Me-DAB) neonatally resulted in the development of adenomatous nodules and glucose-6-phosphatase (G-6-Pase) deficient foci at 8 and 6 months of age, respectively. Ovariectomy of these mice at 1 month of age hastened the development and increased the incidences of these lesions. Subcutaneous implantation of estradiol-17 beta (E2) with ovariectomy at 1 month of age markedly decreased the incidences of adenomatous nodules and G-6-Pase deficient foci at 10 or 12 months of age, but subcutaneous implantation of progesterone did not reduce their incidences. Subcutaneous implantation of E2 into ovariectomised mice at 6 months of age resulted in significant decreases in the incidences of adenomatous nodules and G-6-Pase deficient foci at 10 months of age, but implantation of E2 into the spleen of ovariectomised mice of the same age had no effect on their incidences. The present results suggest that E2 suppresses the development of adenomatous nodules and G-6-Pase deficient foci induced in the mouse liver by 3'-Me-DAB by actions on tissues other than the liver.
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PMID:Suppression by oestrogen of hepatocellular tumourigenesis induced in mice by 3'-methyl-4-dimethylaminoazobenzene. 839 4

Thick biological specimens prepared as whole mount cultured cells stained with histochemical reactions, such as thiamine pyrophosphatase, glucose-6-phosphatase, cytochrome oxidase, acid phosphatase, DAB reactions demonstrating specific cell organelles such as Golgi apparatus, endoplasmic reticulum, mitochondria, lysosomes, peroxisomes and pinocytotic vesicles, were observed by ultrahigh voltage electron microscopy at accelerating voltages of 400-1000 kV producing stereo-pairs. As a result, those cell organelles were observed 3-dimensionally and the relative relationships between these organelles demonstrated.
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PMID:Three dimensional observation of whole mount cultured cells stained with histochemical reactions by ultrahigh voltage electron microscopy. 853 71

The procedures recently developed in our laboratory to observe three-dimensional structures of cell organelles in thick biological specimens by means of high voltage electron microscopy are reviewed. Thick biological specimens such as whole mount cultured cells seeded and grown on grid meshes in culture vessels or thick sections cut from embedded tissues and stained by histochemical reactions can be readily observed three-dimensionally by high voltage transmission electron microscopy at 400-1000kV. Cultured cells used were both primary cultures from animal tissues and established cell lines maintained in our laboratory. The livers of adult Wistar rats were isolated by collagenase perfusion, and hepatocytes were suspended in a Leibovitz medium and seeded on formval coated gold grid meshes in Petri dishes, incubated in a CO(2) incubator in a humidified atmosphere containing 5% CO(2) in air at 37 degrees C for a few days. Established cell lines, CHO-K1 cells, were cultured in Ham's F12 medium, while HeLa cells were cultured in Eagle's MEM under the same condition. Some of the cells were cultured under experimental conditions such as hepatocyte culture in the medium containing peroxisome proliferating agents such as clofibrate or bezafibrate and some of them were labeled with (3)H-thymidine, (3)H-uridine, (3)H-labeled precursors and (14)C-bezafibrate. Also some cells were incubated in medium containing HRP to induce pinocytosis. All the whole mount cultured cells on grid meshes were prefixed in buffered 2.5% glutaraldehyde, stained with various histochemical reactions and postfixed in 1% osmium tetroxide. The histochemical reactions used were glucose-6-phosphatase (G-6-Pase), thiamine pyrophosphatase (TPPase), cytochrome oxidase, acid phosphatase (AcPase), DAB, ZIO, PA-TCH-SP reactions and radioautography was performed after labeling with radiolabeled compounds. The whole mount cultured cells were dried in a critical point dryer and were observed with JEOL JEM-4000EX or Hitachi H-1250M high voltage electron microscopes at 400-1000kV. By tilting the specimens' stereo-pair micrographs were recorded and they were observed with stereoscopes. Rat liver, mouse intestine and pancreas tissues, fixed and stained as above, were embedded in Epoxy resin, thick sectioned at 1-2 microm and were observed as for the whole mount cultured cells at 1000kV. Stereo-pairs were further analyzed with an image analyzer JEOL JIM-5000 (JEOL, Tokyo, Japan), producing two contour lines plotted from the micrographs at a thickness of 0.2 microm and were observed with anaglyph type glasses, demonstrating the depth or heights of respective cell organelles. The results show that whole mount cultured cells and thick sections stained with histochemical reactions reveal cell organelles corresponding to marker enzymes, such as G-6-Pase in endoplasmic reticulum, TPPase and ZIO in Golgi apparatus, cytochrome oxidase in mitochondria, AcPase in lysosomes, DAB in peroxisomes and pinocytotic vesicles, PA-TCH-SP in secretory granules, (3)H-thymidine and (3)H-uridine in nuclei, (3)H-animo acids in endoplasmic reticulum and secretory granules, (14)C-bezafibrate around ER and peroxisomes. The ultrastructure of these cell organelles as well as the structural relationship between them can be demonstrated three-dimensionally with stereo-pair images. Overall, these procedures are useful for analyzing stereologically the ultrastructure of cell organelles in cells and tissues.
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PMID:Three-dimensional high voltage electron microscopy of thick biological specimens. 1107 Mar 59