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)

Subcutaneous injection of iron dextran resulted in a hepatic siderosis within 2 weeks in rats, as previously reported for mice. Hepatic carcinomas as well as neoplastic nodules in rats were entirely or mainly free of stainable iron and, thus, could be readily identified histologically. In addition, early carcinogen-induced altered foci were resistant to iron accumulation. In rats fed 0.02% N-2-fluorenylacetamide (FAA) for 13 weeks, the number of iron-resistant foci identified following iron injection was the same as that observed with dietary iron overload. Histochemical investigation of enzymatic markers that have been used to identify foci in rats revealed that foci characterized by enzymatic reactions of positive gamma-glutamyl transpeptidase and decreased adenosine triphosphatase and glucose-6-phosphatase corresponded to those characterized by resistance to iron accumulation. However, in quantitative analysis of the early carcinogen-induced foci in rats given iron dextran following a diet containing 0.02% 2-FAA for 13 weeks, more lesions were detected by resistance to iron accumulation than by any of these other properties. There was considerable phenotypic heterogeneity among foci for the enzyme markers. It is concluded that resistance to iron accumulation is a more sensitive and reliable marker for early carcinogen-induced altered hepatocellular foci than is any other histochemical property.
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PMID:The sensitivity and heterogeneity of histochemical markers for altered foci involved in liver carcinogenesis. 22 50

D-Galactosamine (800 mg/kg, intraperitoneally) caused significant decrease in the activities of 5'-nucleotidase, glucose-6-phosphatase and cytochrome P450 and increase in activities of gamma-glutamyl transpeptidase, succinate dehydrogenase, acid phosphatase and acid ribonuclease in liver after 24 hr. The levels of RNA, protein and glycogen decreased while total lipids, phospholipids, cholesterol and lipid peroxides increased. It also increased the serum levels of transaminases, alkaline phosphatase and bilirubin while protein concentration decreased significantly. Oral administration of Picroliv (12 mg/kg/day for 7 days), a standardised iridoid glycoside fraction of Picrorhiza kurroa, significantly prevented the biochemical changes in liver and serum of galactosamine-toxicated rats. Kutkoside (12 mg/kg/day for 7 days) also protected against changes in most of the hepatic and serum constituents studied. Another iridoid glycoside from Picroliv, Picroside I, at the same dose level could only prevent toxicant-induced changes in acid phosphatase, phospholipids and lipid peroxides in liver and alkaline phosphatase in serum. Mixture of Picroside I and Kutkoside in the ratio of 1:1.5 at 12 mg/kg dose elicited lesser response than Picroliv.
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PMID:Picroliv and its components kutkoside and picroside I protect liver against galactosamine-induced damage in rats. 133 78

The efficacy of Picroliv, a standardized iridoid glycoside fraction of Picrorhiza kurroa, was studied against the Amanita phalloides-induced biochemical changes in rat liver. A phalloides (50 mg.kg-1) caused significant increases in the activities of hepatic 5'-nucleotidase, gamma-glutamyl transpeptidase, acid ribonuclease, and succinate dehydrogenase, but a decrease in glucose-6-phosphatase. The level of cytochrome P-450 in microsomal fraction and content of glycogen in liver showed significant depletions. Picroliv (25 mg.kg-1.d-1 x 10 d) provided significant restorations of all the biochemical changes poisoned by A phalloides except cytochrome P-450 and glycogen. These results demonstrated the protective effect of Picroliv against A phalloides-induced hepatotoxicity in rats.
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PMID:Effects of picroliv, the active principle of Picrorhiza kurroa, on biochemical changes in rat liver poisoned by Amanita phalloides. 135 30

Na-coupled D-glucose transport in rabbits with cis-diamminedichloride platinum (CDDP; cisplatin) induced acute renal failure (ARF) has been studied. ARF occurred at 3 days after injection of CDDP (3 mg/kg i.v.). Na-coupled D-glucose transport into brush-border membrane vesicles (BBMV) from both outer cortex (OC) and outer medulla (OM) of ARF rabbits under zero-trans condition was decreased. Increased Km (i.e., decreased affinity of transport carrier for D-glucose) in OC and decreased Vmax (i.e., decreased number of glucose carrier) in OM were observed in CDDP-induced ARF rabbits. Decrease glucose transport was also observed under equilibrium exchange condition. Intravesicular volume of BBMV from OC and OM of ARF rabbits was decreased. In homogenate and BBMV from OC and OM of ARF rabbits, activities of gamma-glutamyl transpeptidase and alkaline phosphatase (marker enzymes of brush-border membrane) were decreased. Activities of succinate dehydrogenase, glucose-6-phosphatase, and Na-K ATPase (marker enzymes of mitochondria, endoplasmic reticulum, and basal lateral membrane, respectively) were not affected by CDDP administration. These results suggested that one of the main target sites of CDDP in kidney is brush-border membrane (BBM) along the proximal tubule, that is, not only Na-coupled D-glucose transport carrier protein but also other proteins in BBM.
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PMID:Decreased sodium dependent D-glucose transport across renal brush-border membranes in cis-diamminedichloride platinum induced acute renal failure. 156 86

Primary cultures of renal rabbit proximal tubule cells were initiated from a pure suspension of proximal tubule fragments. Proximal tubule cells were grown in a hormone-supplemented, serum-free medium containing low concentrations of antibiotics. Confluent monolayers exhibited multicellular dome formation, indicating the presence of transepithelial solute and water transport. Ultrastructural examination revealed a monolayer of polarized epithelial cells with tight junctions and sparse membraneous microvilli facing the culture medium. Time course biochemical characterization was performed using a palette of 12 enzymes, representative of important metabolic functions or pathways. Brush-border-associated enzymes (gamma-glutamyl transpeptidase and alanine aminopeptidase) were moderately reduced throughout the culture whereas alkaline phosphatase was markedly decreased at confluency. Mitochondrial and lysosomal marker enzymes were well preserved over the culture period. Glutathione-S-transferase activity remained stable during the 16-day culture period investigated. Glycolysis enzyme activities (lactate dehydrogenase and hexokinase) were enhanced, as a function of culture age. Na(+)-K(+)-ATPase activity rise was concomitant with the increase of glycolysis marker enzymes. In contrast, the gluconeogenesis marker enzyme, glucose-6-phosphatase, fell dramatically to reach a low level equivalent to 4% of the activity measured in isolated proximal tubules. Primary cultures exhibited several differentiated functions of the proximal tubule cell: (a) PTH alone was able to induce a significant stimulation of adenylate cyclase activity, unlike isoproterenol, thyrocalcitonin, and arginine vasopressin, and (b) sodium-dependent alpha-methylglucoside (AMG) transport was detected. This AMG uptake was selectively inhibited by phlorizin (5 X 10(-3) M), which is a competitive inhibitor of glucose uptake at the apical membrane. Complete characterization made it possible to investigate hitherto unexplored aspects of in vitro cultured proximal tubule cells. This primary culture model could provide a useful and reliable tool to investigate in vitro renal proximal tubule function, under normal conditions or after a drug-induced toxicity.
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PMID:Biochemical, functional, and morphological characterization of a primary culture of rabbit proximal tubule cells. 167

The significance of glucose-6-phosphatase (G6P) expression by bile duct-like cells proliferating during hepatocarcinogenesis in the histogenesis of hepatocellular carcinoma is not clear. To this end, we measured the histochemical and biochemical activity of G6P in normal rat liver, and in rat livers in which bile duct-like proliferation was induced by either hyperplastic (bile duct ligation for 14 days or feeding alpha-naphthylisothiocyanate for 28 days) or neoplastic (feeding a choline-devoid diet containing 0.1% ethionine for 60 days) regimens. In normal, hyperplastic, and preneoplastic livers, G6P histochemical activity was confined to the hepatocytes; proliferated bile duct-like cells, like normal bile ducts, did not display visible G6P staining. When the enzyme activity was determined biochemically, however, hydrolysis of glucose-6-phosphate was observed in both parenchymal and nonparenchymal liver cells isolated from all experimental animals. In elutriated nonparenchymal fractions, G6P activity was directly proportional to the number of cells positive for gamma-glutamyl transpeptidase and cytokeratin no. 19 (markers of bile duct cells) and inversely proportional to the number of cells positive for vimentin (marker of mesenchymal cells). These results indicate that, while by light microscopy hepatic G6P histochemical activity is detectable only in the hepatocytes, the biochemical activity is also expressed in proliferating bile duct-like cells. However, the nonparenchymal activity is observed during both neoplastic and hyperplastic liver growth, thus indicating that the presence of this enzyme in bile duct-like cells proliferating during hepatocarcinogenesis should not necessarily be construed as supporting their stem cell nature nor their neoplastic commitment.
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PMID:Distribution of glucose-6-phosphatase activity in normal, hyperplastic, and preneoplastic rat liver. 168 20

We describe the successful isolation and maintenance of primary cultures of dog gallbladder epithelial cells. The surgically removed gallbladder was treated with trypsin/EDTA for 45 minutes and epithelial cells were collected and resuspended in Eagle's minimum essential medium with 10% fetal calf serum, and plated on Vitrogen-coated culture dishes. Each gallbladder yielded approximately 12 to 15 x 10(6) columnar epithelial cells, greater than 95% of which were viable by trypan blue exclusion. In culture, cells maintained their polarity. They were arranged and grew in small and tight clusters that coalesced at confluency. When examined using transmission electron microscopy, prominent and numerous microville were identified on the apical portion of the plasma membrane. Cells were connected by well-formed desmosomes. Scanning electron microscopy revealed clusters of polyhedral cells with numerous papillary projections. Immunohistochemical studies demonstrated uniform staining of cells to keratin 35BH11 and AE1. Histochemical studies were positive for gamma-glutamyl transpeptidase and negative for glucose-6-phosphatase and albumin. Cells incorporated [3H]uridine into intracellular proteins and [14C]glucosamine into tissue and secreted mucous glycoproteins linearly over 2 to 24 hours. Flow cytometry studies demonstrated a consistent and reproducible number of cells (10 to 12%) at S-phase. However, the number of cells at S-phase was dramatically reduced to almost negligible as cells reached confluency. This method of culturing primary dog gallbladder epithelial cells is highly reproducible and reliable. These cells preserve their state of differentiation, polarity, histochemical and immunohistochemical profile, morphologic, and metabolic integrity with repeated passaging or after being frozen. [3H]Thymidine uptake is well maintained, although doubling time shows a trend of decreased cell duplication with time. This technique offers the opportunity to study the electrophysiologic, metabolic, and immunologic properties of epithelial cells.
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PMID:Long-term culture and partial characterization of dog gallbladder epithelial cells. 170 26

Several pharmaceutical agents, manufacturing chemicals, and environmental contaminants were found to act primarily as promoting agents in an initiation-promotion paradigm. The phenotypic distribution of four enzyme markers--placental glutathione-S-transferase (PGST), gamma-glutamyl transpeptidase (GGT), canalicular ATPase (ATPase), and glucose-6-phosphatase (G6Pase)--was analyzed in altered hepatic foci (AHF) by quantitative stereology. The number and volume distribution of AHF were determined for each promoter tested. For phenobarbital and 2,3,7,8-tetrachloro-p-dioxin, PGST and GGT together scored 100% of the AHF; for 1-(phenylazo)-2-naphthol (CI solvent yellow 14) and chlorendic acid, PGST alone marked 90% of the AHF; after chronic administration of WY-14,643, ATP and G6Pase were the predominant markers. In rats fed tamoxifen, G6P scored more than half of the AHF. Differences in the number of AHF promoted by each of these agents and in their phenotypic distributions may reflect the differentially responsive nature of individual initiated hepatocytes to the action of specific promoters. Since the chronic bioassay of suspected carcinogens does not allow one to differentiate between weak complete carcinogens and those carcinogenic agents that act in a reversible manner to promote the growth of previously initiated cells, the partial hepatectomy, altered-hepatic-focus model of cancer development is proposed as a supplement to the chronic bioassay for the identification of those carcinogenic agents that are primarily, if not exclusively, promoting agents in rat liver.
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PMID:An initiation-promotion assay in rat liver as a potential complement to the 2-year carcinogenesis bioassay. 185 24

Histochemistry is a valuable tool in the analysis of altered hepatic foci. These lesions contain alterations in the activities of certain enzymes, including gamma-glutamyl transpeptidase (GGT), placental glutathione-S-transferase (PGST), glucose-6-phosphatase (G6Pase), and ATPase, or in certain cellular functions, such as the ability to store iron. The appearance of altered hepatic foci has been found to correlate with the later appearance of hepatocellular carcinomas in rodents. The markers PGST and GGT are the most sensitive at detecting altered hepatic foci induced by most chemicals, but are unable to detect altered hepatic foci induced by some agents, such as peroxisome proliferators. Other markers, such as ATPase or G6Pase, should therefore be used in combination with PGST or GGT in identifying altered hepatic foci. The strain of rat used and the type of diet fed also influence the number of altered hepatic foci induced and the enzyme markers seen. The number of foci per cm2 and the diameters of altered hepatic foci in histochemically-stained tissue sections can easily be quantified. The number of foci per cm2, however, does not give a reliable estimate of the number of altered hepatic foci induced because larger altered hepatic foci are more likely to be transected. The equations of quantitative stereology therefore should be used to transform the data to obtain the number of foci induced per cm3 or per liver, the average volume of individual foci, and the percent of the liver volume occupied by altered hepatic foci. In conclusion, the use of histochemistry to identify preneoplastic lesions and the use of quantitative stereology to estimate their number and volume allow accurate and sensitive quantitation of altered hepatic foci.
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PMID:Histochemical and stereological analysis of putative preneoplastic hepatic lesions. 194 71

In order to evaluate the usefulness of key gluconeogenic enzymes, in relation to the markers commonly used (alkaline phosphatase and gamma-glutamyl transpeptidase) for the diagnose of cholestasis the serum activity of phosphoenolpyruvate carboxykinase, fructose 1,6-bisphosphatase and glucose-6-phosphatase has been measured in rats with bile-duct ligation. Among the gluconeogenic enzymes studied only phosphoenolpyruvate carboxykinase activity increased significantly in the first 48 hours after cholestasis, decreasing thereafter to normal values. Both alkaline phosphatase and gamma-glutamyl transpeptidase activities showed a very significant increase which persisted throughout the experiment. These results seem to indicate that in spite of the high organ specificity of these enzymes they do not appear to be useful for the diagnosis of cholestasis.
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PMID:Evaluation of key gluconeogenic enzymes in experimental biliary obstruction. 198 72


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