Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.3.9 (glucose-6-phosphatase)
 3,081 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 3 fish species (Labeo rohita, Clarias batrachus and Channa punctatus) subjected to a sublethal concentration (0.035 mg/l) of DDT continuously for 20 days both hepatic and renal acid and alkaline phosphatases were elevated, whereas the rise in glucose-6-phosphatase and fructose-1,6-diphosphatase was restricted to hepatic tissue. The variations in phosphatase levels were more pronounced in L. rohita than in the other two species.
Toxicol Lett 1982 Sep
PMID:DDT toxicity: gluconeogenic enzymes and non-specific phosphomonoesterases in three teleosts. 629 22

The endoplasmic reticulum (ER) and its contribution to the endomembrane system (i.e., membranes of cell organelles) in the neuron have been investigated in brains of mice by applying electron microscopic enzyme cytochemistry for demonstration of glucose-6-phosphatase (G6Pase) activity. The phosphohydrolytic activity of G6Pase is a well-known cytochemical marker for the ER in numerous cell types. Of the different substrates employed, glucose-6-phosphate and mannose-6-phosphate were the only two with which G6Pase reaction product was seen in the neuronal ER and organelles related morphologically to the ER. G6Pase activity in cell bodies and dendrites was localized consistently within the lumen of the nuclear envelope, rough and smooth ER, lamellar bodies, hypolemmal and subsurface cisternae, and frequently in the cis saccules of the Golgi apparatus. The G6Pase reactive ER appeared as a network of saccules and tubules pervading the cell body and its dendrites. Possible membrane continuities were identified between the ER and the other reactive structures, including the cis half of the Golgi apparatus. Neither G6Pase activity nor reactive ER was associated with the trans Golgi saccules or GERL. G6Pase activity thus serves as a reliable marker for the perikaryal and dendritic ER and related structures. These observations support the theory that the ER is an integral component of the neuronal endomembrane system associated with the transfer of membrane or membrane molecules among intracellular compartments, the packaging and transport of exportable protein, and energy metabolism. G6Pase activity in the ER of axons and terminals is considered in detail in part two of this study.
J Histochem Cytochem 1983 Sep
PMID:The neuronal endoplasmic reticulum: its cytochemistry and contribution to the endomembrane system. I. Cell bodies and dendrites. 630 51

Glycogen storage disease type Ib has all the clinical manifestations of glycogen storage disease type Ia such as hepatomegaly, growth retardation, bleeding tendency, hypoglycemia, hyperlactacidemia, hyperuricemia, hyperlipidemia, impaired platelet function plus neutropenia. The overall glucose-6-phosphatase activity in disrupted microsomes from liver is normal whereas glucose-6-phosphate translocase, the first enzyme in the glucose-6-phosphate transport system is absent. There is no glucose-6-phosphatase activity in vivo. Recent results show that in granulocytes the glucose-6-phosphate-dependent hexosemonophosphate-shunt is impaired.
Eur J Pediatr 1983 Sep
PMID:Glycogen storage disease type Ib. 631 72

The alarming hazardous nature of asbestos makes it the foremost among toxic fugitive dusts. The biochemical mechanisms responsible for the diverse biological effects of asbestos, such as fibrosis, asbestos bodies, pleural plaques, respiratory difficulty, cancer, and cytotoxicity, are being studied in this laboratory. As asbestosis progresses in guinea pigs, along with reticulum formation, lysosomal enzymes are released from membrane-bound latent state to active free form, initiating degradative changes. Considerable alterations take place in the pulmonary metabolic machinery. Mitochondria in lung cells were found to be important loci for the toxic effect of asbestos. A profile of mitochondrial activity, in control and asbestotic animals, revealed specific enzymic changes such as increased cytochrome c oxidase during the disease. The functional organization of mitochondria was also altered, since the organelles from asbestotic lungs were swollen as measured by spectrophotometry. Glutamate dehydrogenase activity of mitochondria became exposed in asbestosis. The maleate dehydrogenase shunt which is involved in transport of the redox potential across the membrane was enhanced in cytosol and mitochondria. The involvement of microsomal enzymes in asbestosis was indicated by alterations in glucose-6-phosphatase and tyrosine transaminase and aniline hydroxylase. Changes in the biotransformational capacity of lung, due to asbestos, could be an important aspect in toxicity, especially the carcinogenic effect. Considerable alterations were encountered in the levels of different phospholipids and in mucopolysaccharide constituents. On the basis of the above, the molecular mechanisms in asbestos toxicity are explained as an integrated model. Interactions of dust constituents with those of membranes and the ensuing metabolic adjustments are thus important in the etiology of asbestosis.
Environ Health Perspect 1983 Sep
PMID:Biochemical mechanisms in asbestos toxicity. 631 71

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.
Exp Cell Res 1984 Sep
PMID:A diploid epithelial cell line from normal adult rat liver with phenotypic properties of 'oval' cells. 646 34

Chicks were given biotin-deficient diets containing either suboptimal (low) or supraoptimal (high) concentrations of protein from 1-d-old until they were used during their fourth week of life. The low-protein diet predisposed chicks to develop fatty liver and kidney syndrome and the high-protein diet to develop classical biotin deficiency signs. Two other groups, as controls, received biotin-supplemented rations. Low dietary protein increased lipogenesis by isolated hepatocytes but had little effect on gluconeogenesis compared to high dietary protein. Low dietary protein decreased activities of hepatic isocitrate dehydrogenase (EC 1.1.1.42), fructose-1,6-bisphosphatase (EC 3.1.3.11) and glucose-6-phosphatase (EC 3.1.3.9; GP) and increased activities of fatty acid synthase (FAS), citrate cleavage enzyme (EC 4.1.3.8; CCE) and malate dehydrogenase (decarboxylating) (EC 1.1.1.39). When biotin deficiency was superimposed, the rate of lipogenesis by isolated hepatocytes (from fed birds) was decreased. Gluconeogenesis from lactate and glycerol was also depressed. Activity of GP was further decreased by biotin deficiency on the low-protein regimen and FAS and CCE were further increased. PK activity was increased by biotin deficiency.
Br J Nutr 1983 Sep
PMID:The effect of biotin deficiency and dietary protein content on lipogenesis, gluconeogenesis and related enzyme activities in chick liver. 661 62

Trans unsaturated fatty acids are formed during hydrogenation of edible oils and their consumption in the United States has increased with increasing utilization of margarines. The effect of elaidic acid and trielaidin on atherosclerosis in cholesterol-fed rabbits were studied many years ago by Weigensberg and McMillan, who found these fatty acids to be significantly more hypercholesterolemic but not more atherogenic. Jackson et al. have found that trans fatty acids are not inordinately atherogenic in swine. We have fed rabbits semipurified, cholesterol-free diets containing either 3.2 or 6.0% of trans fatty acid. The diets were slightly hyperlipidemic but no more atherogenic than the control diet. We measured the activities of five hepatic enzymes (glucose-6-phosphatase, fatty acid synthetase, malate dehydrogenase, beta-hydroxybutyrate dehydrogenase, and monoamine oxidase [EC 1.4.3.4]). The diets affected only the activity of monoamine oxidase, which was lower in the livers of rabbits fed 6.0% trans fatty acid. Vervet monkeys were fed the same diets either for 1 year or for 6 months and then returned to the control diet for 6 months. The dietary manipulations had no effect on serum or lipid levels or aortic sudanophilia. Trans fatty acid levels of the serum reflected dietary concentration. Six months after cessation of feeding of the trans fat the levels of trans fatty acids in serum were virtually normal. Trans fatty acids appear to exert a hypercholesterolemic effect but do not influence aortic atherosclerosis in rabbits or aortic sudanophilia in vervet monkeys.
Fed Proc 1982 Sep
PMID:Trans fatty acid effects in experimental atherosclerosis. 681 29

Kinetics of hepatocarcinogenesis was evaluated in 15-day-old male C57BL/6J X C3HeB/FeJ F1 mice using a nontoxic carcinogenic dose range of diethylnitrosamine (DEN). The carcinogen was injected i.p. once, and the animals were killed according to the protocol. Two studies were carried out sequentially over a period of 4 years. In the first study, groups of mice were treated with 0.625, 1.25, 2.5, and 5.0 micrograms of DEN per g of body weight, and subgroups of eight mice were killed at 10-week intervals, the first at 10 weeks following carcinogenic treatment. The dose-response relationship, transformation probabilities, and the dose versus time to 50% incidence of the early (basophilic foci) and later appearing focal and nodular hepatocellular lesions were evaluated. In the second study, groups of mice were treated with 0.312, 0.625, 1.25, 2.5, and 5.0 micrograms of DEN per g of body weight, and subgroups of 8 to 20 animals were killed at 10, 16, 20, 24, 30, 34, 40, 45, 50, 55, 60, 65, 70, 75, 80, 85, 90, 95, 100, and 110 weeks after carcinogenic treatment. The numbers of induced basophilic foci and hepatocellular carcinomas per number of liver cells at risk (transformation probabilities) were used to evaluate dose-response, time-response, and time-dose kinetics. In both studies, the kinetics of hepatocarcinogenesis was evaluated from data plotted on the double logarithmic scale. Regardless of the dose used, DEN induced four distinct morphological entities: basophilic (glucose-6-phosphatase deficient) foci; hyperplastic nodules; hepatocellular adenomas; and hepatocellular carcinomas in all animals. The first study demonstrated a positive dose-response relationship and constancy (k) of the product of single dose (d) and the time to 50% (t50%) incidence (d . tn50% = k) for each of the four morphological entities. The numerical value of the power of time (n) increased from 2.6 to 2.7, 3.4, and 5.7 for the above four lesions, respectively. The second study showed first-order kinetics regarding the induction of basophilic foci and hepatocellular carcinomas. The transformation probability of development of basophilic foci was up to three orders of magnitude greater than that observed for development of hepatocellular carcinomas, suggesting a qualitative difference between these two types of hits. The time-response kinetics showed that the development of basophilic foci and carcinomas was related to the time factor by powers of 2 and 4 for these two lesions, respectively. The time-dose relationship to a fixed number of lesions per number of liver cells at carcinogenic risk showed a negative slope with an n value of 2 for the induction of basophilic foci (d . t28/10(7) = k) and an n value of 4 for the induction of hepatocellular carcinomas (d . t40.08/10(7) = k). The data indicated that at least two critical events are needed for the induction of basophilic foci and at least four events are required for the induction of hepatocellular carcinomas...
Cancer Res 1983 Sep
PMID:Kinetics of diethylnitrosamine hepatocarcinogenesis in the infant mouse. 687 63

Individuals with type Ia glycogen storage disease (glucose-6-phosphatase deficiency) frequently develop hepatic adenomas. Potential complications involving these adenomas include malignant transformation and hemorrhage. Five of 9 patients with this disease had evidence of hepatic filling defects on radionucleotide liver scan when first evaluated at our hospital. Dietary therapy aimed at preventing hypoglycemia was begun in 7 of the 9 patients. Prevention of hypoglycemia resulted in the correction of all of the metabolic abnormalities (lactic acidosis, hyperlipidemia, hyperuricemia, and growth retardation). Treatment also corrected the marked elevation in plasma glucagon concentrations. A disappearance of the hepatic lesions occurred in 2 of the treated patients, and a marked reduction in size of the adenoma occurred in the third patient. The hepatic filling defects remained present in the two untreated patients. None of the affected patients receiving dietary therapy have developed hepatic adenomas. One of these patients is now 22 yr old and has received dietary therapy for 7 yr. Early dietary therapy seems to be effective in preventing development of adenomas as well as inducing their resolution.
Gastroenterology 1981 Sep
PMID:Regression of hepatic adenomas in type Ia glycogen storage disease with dietary therapy. 694 8

The effect of daily intraperitoneal administration of Mn2+(4 mg/kg) was investigated on the metabolism of carbohydrates and certain enzymes involved in the oxidation of glucose in the rat liver and blood at the intervals of 30, 60 and 90 days after exposure. Mn2+ had no effect on the contents of blood reducing sugars and proteins, however the levels of pyruvic and lactic acids were reduced at 60 and 90 days after the metal treatment. The contents of liver glycogen and proteins remained unaffected while pyruvic acid content was decreased in Mn2+ treated rat liver throughout the experimental period. The activities of glycogen phosphorylase and lactate dehydrogenase decreased while that of phosphoglucoisomerase and glucose-6-phosphatase increased in the post mitochondrial supernatant at 60 and 90 days of Mn2+ exposure. The levels of hexokinase decreased and FDP-aldolase and fructose-1, 6-diphosphatase increased throughout the experimental period. The magnitude of alteration was found to be greater with the increase in the duration of Mn2+ treatment. Several of the mitochondrial enzymes in the liver were inhibited in the manganese exposed rats which may be responsible to inhibit the rate of dehydrogenation of Kreb cycle's intermediates along with the linked respiratory chain and eventually oxidation in the rat liver.
Acta Pharmacol Toxicol (Copenh) 1982 Sep
PMID:Effects of manganese on carbohydrate metabolism and mitochondrial enzymes in rats. 713 26


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