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)

The alterations in the distribution and activity of certain key enzymes, viz. alkaline phosphatase, acid phosphatase, glucose-6-phosphatase, cholinesterase and lipase, have been determined in the liver of rats (Rattus rattus albino) after experimental poisoning with hexavalent chromium. The histochemical and biochemical observations presented herewith provide visual evidence of chromium-induced inhibition of all these enzymes except lipase, which was found to be stimulated insignificantly. The results have been interpreted in terms of changes in the micro-environment of the cell, formation of apo-enzymes, metal-protein complexes, oxidative phosphorylation and finally with liver function.
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PMID:Dysenzymia induced by hexavalent chromium in rat liver. 299 22

The intraperitoneal (IP) treatment of rats with diazinon (40 mg/kg) resulted in a variety of changes in the brain. Glycogen was depleted, but there was an increase in the activities of glycogen phosphorylase, phosphoglucomutase, hexokinase, lactate dehydrogenase, and fructose 1,6 diphosphatase. The activity of glucose-6-phosphatase was unaffected while that of cholinesterase was significantly reduced. Lactic acid content was increased, while that of pyruvate was not altered. Animals developed tremors and convulsions, which were maximal two hours after treatment. The induced changes may be compensatory mechanisms to provide extra energy to cerebral tissue as a result of the stimulatory effects in diazinon-treated animals.
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PMID:Cerebral glucose and glycogen metabolism in diazinon-treated animals. 350 78

Effect of diazinon (10,20 and 40 mg/kg, i.p.) on the level of blood glucose in rats was investigated. Hyperglycaemia peaked 2 h after i.p. treatment with 40 mg/kg diazinon. The cerebral acetylcholinesterase activity was significantly reduced. The blood level of pyruvic acid was unchanged while that of lactic acid was significantly increased. Convulsions and biochemical changes caused by diazinon (40 mg/kg) were prevented by diazepam injected immediately after diazinon. In diazinon-treated hyperglycaemic animals, the glycogen content of the brain was depleted, the activities of glycogen phosphorylase, phosphoglucomutase and hexokinase were significantly increased and the activity of glucose-6-phosphatase remained unchanged. Lactate dehydrogenase activity was also increased by treatment with diazinon. The induced changes may compensate for the energy requirement of stimulatory effects caused by diazinon.
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PMID:Changes in cerebral glycogenolysis and related enzymes in diazinon treated hyperglycaemic animals. 362 68

Prostaglandins E1 and E2 are specifically bound by particulate fractions from bovine adrenal medulla. The subcellular localization of these binding sites has been investigated by comparing their distribution in subcellular fractions obtained by differential and gradient centrifugation to those of marker enzymes for various organelles. Prostaglandin E2 binding sites were purified about 16-fold with respect to the homogenate in a fraction which was highly enriched in plasma membranes on the basis of the activities of the marker enzymes acetylcholinesterase and calcium-dependent ATPase, which were both purified by about 12-fold in this fraction. The plasma membrane fraction contained relatively low activities of marker enzymes for mitochondria (monoamine oxidase), lysosomes (acid phosphatase), endoplasmic reticulum (glucose-6-phosphatase), Golgi (galactosyl transferase) and chromaffin granule membranes (dopamine beta-hydroxylase). The only other fractions enriched in prostaglandin E2 binding sites were those for the endoplasmic reticulum and the Golgi, in which the binding sites were purified about 4-fold and 7-fold, respectively. This is probably due mainly to contamination with plasma membranes, since calcium-dependent ATPase and acetylcholinesterase were each purified to a similar extent in these two fractions. These data suggest that the high-affinity prostaglandin E2 binding sites of the adrenal medulla are localized primarily on the plasma membranes of the medullary cells.
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PMID:Subcellular localization of prostaglandin E2 binding sites in bovine adrenal medulla. 614 8

Although zinc in traces is essential for the growth and well being of the animal, however a long-term treatment has been found equally toxic to the liver and kidney. Present report describes its effects on few key enzymes viz. alkaline phosphatase, acid phosphatase, 5-nucleotidase, lipase, glucose-6-phosphatase, and cholinesterase in the liver of rat, Rattus rattus albino. Histochemical observations have provided visual evidences on Zn-induced dysenzymia. The results have further been interpreted in terms of its effects on cellular organelle, levels of enzyme protein and microenvironment of the hepatic parenchyma.
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PMID:A note on dysenzymia in the liver of rats fed on zinc, an essential metal. 629 52

Chronic dieldrin administration to rats (5 mg/kg/day) produced pathological changes in liver and kidney tissues. Dieldrin treated rats showed high levels of liver ascorbic acid and increased activities of inorganic pyrophosphatase in brain and glucose-6-phosphatase in liver. The activities of Mg2+-ATPase in liver and acetylcholinesterase in brain were decreased under toxic doses of dieldrin. L-Ascorbic acid supplements in treated animals could partially prevent the pathological alterations, as observed histologically in liver and kidney tissues. Administration of this vitamin could also prevent alterations in some enzyme activities produced by toxic dieldrin doses.
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PMID:Effects of L-ascorbic acid supplementation on dieldrin toxicity in rats. 714 87

Enzymological data on alkaline phosphatase, acid phosphatase, glucose-6-phosphatase, cholinesterase and lipase obtained in the kidney of rats, fed on molybdenum (Mo) and copper (Cu), are reported. Antagonistic or synergistic behaviour has been determined by feeding the rats simultaneously on these two metals. Molybdenum inhibited all other enzymes except acid phosphatase and lipase. Complete inhibition of alkaline phosphatase was recorded after copper treatment. The combined treatment with molybdenum and copper exhibited reversible enzyme changes, however, cholinesterase activity remained inhibited.
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PMID:Effect of molybdenum and copper on key enzymes of rat kidney with special reference to physiological antagonism. 724 24

Chronic oral administration of ammonium molybdate in rats markedly retarded the growth rate of rats and high protein diet could partially reverse this condition. The activities of several enzymes viz. acid phosphatase, alkaline phosphatase, glucose-6-phosphatase, succinic dehydrogenase, glutamate oxaloacetate transaminase, inorganic pyrophosphatase and acetylcholinesterase in different tissues and serum levels of luteinizing hormone, follicle stimulating hormone, prolactin and cortisol are altered due to the toxicity conditions and high protein diet fed group of animals showed almost normal values in respect of a few of these parameters. Normal histological pattern of both liver and kidney tissues were altered under molybdenum toxicity condition. Significant increase of basophilic substances are observed in the cytoplasm of the liver cells of the toxic group of animals which is counteracted by feeding high protein diet.
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PMID:Biochemical studies on molybdenum toxicity in rats: effects of high protein feeding. 732 62

To investigate the pathogenesis of retina lesions caused by intraocular pressure elevation, activities and distribution of enzymes in retina including lactic dehydrogenase (LDH), succinate dehydrogenase (SDH), adenosinetriphosphatase (AT-Pase), acid phosphatase (ACP), cholinesterase (ChE), cytochrome oxidase (CCO), nucleotidase (5'-Nase) and glucose-6-phosphatase (G6Pase) were determined histochemically in 30 rabbits. It was found that 1) in the early stage of intraocular pressure elevation, the activities of LDH, SDH, ATPase, ACP, and ChE in retina were increased, while the activities of CCO, 5'-Nase decreased; 2) in the late stage of intraocular pressure elevation, the activities of all these enzymes but ACP, which showed a reduced activity, were close to the normal level; 3) in superoxide dismutase.(SOD-CCE) treated group, except the slight increase of LDH and G6Pase activities, the activities of the remaining enzymes were near to normal. Our results suggest that the various histochemical changes in retina induced by intraocular pressure elevation were compensatory in the early stage and were beneficial to the supply of energy needed in retinal tissue and cellular metabolism; while in the late stage, the lesion of retina cells developed due to decompensation. SOD-CCE could alleviate the retinal lesions caused by intraocular pressure elevation, and can be used as auxiliary drug for the treatment of intraocular pressure elevation.
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PMID:Enzymatic histochemistry of retina with experimental intraocular pressure elevation in rabbits. 873 48

Synaptic plasma membrane (SPM) vesicles represent a membrane fraction very useful in studying non-vesicular neurotransmitter release. The procedure described here to isolate SPM vesicles from a crude synaptosomal fraction of sheep brain cortex is quick, simple (ultracentrifugation in a discontinuous density gradient of dextran T110), and combines a high yield (130 micrograms/g brain) with a satisfactory grade of purification. The preparation of SPM vesicles consists of vesicles (approximately 0.54 +/- 0.8 micron diameter) delimited by a single membrane with the native orientation. We are able to ascertain these characteristics on the basis of morphology studies (electron microscopy observations), enzyme activities (Na+/K(+)-ATPase, Ca2+/Mg(2+)-ATPase, acetylcholinesterase and glucose-6-phosphatase), biochemical composition (lipid and protein analysis) and the tetrodotoxin sensitivity of the veratridine-induced gamma-aminobutyric acid (GABA) release. Isolating the SPM vesicles by the proposed procedure permits manipulating the ionic gradients across the membrane by changing the ion concentrations on either side or by utilizing specific ionophores. The vesicles retain their various activities, including their capacity for neurotransmitter uptake and release assays for at least 3 months, when preserved at -70 degrees C. Furthermore, the vesicles permit depicting the electrochemical gradients across the membranes into chemical and electrical components. We describe the use of the tetraphenylphosphonium cation (TPP+) to dissipate the membrane potential (delta psi) of the vesicles, while preserving ionic gradients. The characteristics of the lipid-soluble cation TPP+ allows a massive inflow of this cation into vesicular compartments and a consequent depolarization.
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PMID:Membrane potential manipulation in synaptic plasma membrane vesicles for studying neurotransmitter uptake and release. 938 41


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