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)

Fetal liver was examined in rats, whose mothers during pregnancy received Turinal (firm: Chemical Works of Gedeon Richter LTD Budapest, Hungary) in a dosage of 0.5 mg/kg BW in the experimental group I and 1 mg/kg BW in the experimental group II. Reaction to the activity of succinate dehydrogenase, lactic dehydrogenase, acid phosphatase, glucose-6-phosphatase, PAS-reaction (Periodic acid Schiff reaction) and hematoxylin-eosin staining were carried out. Changes in the activity of examined enzymes and PAS-reaction in fetal liver depending on dosage were observed. These changes testify to a large influence of administered hormone on metabolism of developing fetal liver.
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PMID:[Effect of progestagens administered during pregnancy on histochemical reaction in fetal liver]. 167 38

Monocrotaline, a pyrrolizidine alkaloid, caused changes in most of the biochemical parameters in rats 12 days after a single dose of 120 mg/kg. These included significantly increased activities of hepatic succinate dehydrogenase, acid ribonuclease, acid phosphatase, gammaglutamyl transpeptidase and 5'-nucleotidase and decreased in the activities of glucose-6-phosphatase and cytochrome P450. The levels of DNA, RNA and glycogen in liver and albumin and protein in serum decreased while serum bilirubin increased. The histopathological changes in liver were characterized by diffused hepatocyte alterations in the form of ballooning, granular cytoplasm, indistinct cell outlines, nuclear changes, focal necrosis, and vascular damage. When picroliv, a standardized iridoid glycoside fraction of Picrorhiza kurroa, was administered orally in a dose of 25 mg/kg simultaneously with monocrotaline, alterations in most of the biochemical parameters along with the histopathological changes in liver caused by monocrotaline were prevented.
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PMID:Picroliv protects against monocrotaline-induced hepatic damage in rats. 190 81

The uptake of L-[14C]glycine and the activities of intracellular marker enzymes of enterocytes were studied in ligated small intestinal segments of rabbits during experimental cholera induced by intra-intestinal injection of pure cholera toxin (CT). No significant difference was observed in the active uptake of L-[14C]glycine between the CT-injected small intestinal segments and the saline-injected control segments, indicating that there is an intact active transport system for intestinal absorption of L-[14C]glycine during experimental cholera in rabbits. Apart from a significant increase in the activity of a brush border marker enzyme (alkaline phosphatase), there was no significant difference between the activities of marker enzymes for lysosomes (acid phosphate), microsomes (glucose-6-phosphatase), mitochondria (succinate dehydrogenase), and a cytosol enzyme (proteinase) in mucosal homogenates of CT-injected small intestinal segments compared to controls. The finding of an intact mitochondrial marker enzyme together with intact L-[14C]glycine absorption provides a scientific basis for considering the use of glycine and other monoamino monocarboxylic amino acids in "improved" oral rehydration solutions for the treatment of acute diarrhea, including cholera.
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PMID:Effect of cholera toxin on L-[14C]glycine uptake and intestinal cell enzymes in rabbit. 194 84

Haemonchus contortus, incubated in 10 micrograms/ml and 50 micrograms/ml concentrations of Nilzan and albendazole in Tyrode solution were stained for histoenzymatic demonstration of various phosphatases, oxido-reductases and esterases. The intestine showed major alterations after drug treatments. The alkaline phosphatases (AkPase), adenosine triphosphatase (ATPase), glucose-6-phosphatase, succinic dehydrogenase (SDH), glutamate dehydrogenase (GDH), reduced nicotinamide adenine dinucleotide phosphate diaphorase and reduced nicotinamide adenine dinucleotide diaphorase showed a decreased activity in intestine after Nilzan treatment, whereas lactic dehydrogenase (LDH), glucose-6-phosphate dehydrogenase (G-6-PD) and monoamine oxidase resisted increased reaction. The albendazole treatment resulted in altered distribution pattern of the AkPase, ATPase, SDH, and GDH; while LDH, G-6-PD, and non-specific esterases exhibited slightly enhanced activity in the epithelium. The functional significance of these changes has been fully discussed.
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PMID:Effect of Nilzan and albendazole on the absorptive surfaces of Haemonchus contortus (Nematoda)--a histoenzymic study. 196 79

It was established that acrylonitrile (AN) toxic action resulted in changes in the morphofunctional characteristics of white blood cells. Deviations were found in the activity of the marker enzymes of alkaline phosphatase neutrophil secretory granules and myeloperoxidase. Other changes were established in the markers of acid phosphatase lysosomes, the enzyme of plasma membrane--5 nucleotidase, in the endoplasm network of glucose-6-phosphatase, in succinate dehydrogenase mitochondria, and in alpha-glycerolphosphate dehydrogenase. Along with a considerably lowered succinate dehydrogenase activity, lymphocyte cell deformation against the activity of this enzyme was detected. The data obtained specified newly revealed changes in the blood at AN intoxication and indicated to innovated means of its prophylaxis.
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PMID:[Study of the activity of membrane-bound leukocyte enzymes in chronic acrylonitrile poisoning in experimental studies and occupational environment]. 196 27

The neurochemical changes induced by malathion, an organophosphate compound, were determined in rats. Maximal changes were found in the brain 2 h after the administration of malathion in a dose of 500 mg/kg ip. The activities of cholinesterase and succinic dehydrogenase were reduced whereas those of glycogen phosphorylase, phosphoglucomutase, and hexokinase were increased; the lactate content of brain was also increase. In malathion treated adrenalectomized animals, changes in the activities of cerebral cholinesterase and succinic dehydrogenase were still present; other changes were, however, abolished by adrenalectomy. Activities of certain enzymes, glucose-6-phosphatase, glucose-6-phosphate dehydrogenase, and lactate dehydrogenase were not significantly altered by malathion in normal or adrenalectomized animals. The results indicate that cerebral cholinergic mechanism in malathion treated animals was not modified by adrenalectomy which, however, abolished or reduced changes in the activities of certain glycolytic and glycogenolytic enzymes that are involved in the utilization or metabolism of glucose. The brain lactate content in malathion treated adrenalectomized animals was, also, not significantly different from the control values, suggesting that modification of induced changes by adrenalectomy.
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PMID:Modification of malathion induced neurochemical changes by adrenalectomy in rats. 209 80

Chronic infection of woodchucks with woodchuck hepatitis virus (WHV) was associated with the development of hepatitis, foci of altered hepatocytes and hepatocellular adenomas and carcinomas. The cytomorphological and cytochemical analysis permitted the identification of three different types of focal lesions; namely, glycogen-storage foci, mixed-cell foci and intermediate-cell foci, each showing a characteristic pattern. The cells of the glycogen-storage foci had clear to acidophilic cytoplasm, and were overloaded with glycogen. They showed a marked elevation in the activity of glucose-6-phosphate dehydrogenase (G6PDH) and malate dehydrogenase (MDH), increased activity of succinate dehydrogenase (SDH), glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and glycerol-3-phosphate dehydrogenase (G3PDH), reduction in the activity of glycogen phosphorylase (PHO), glucose-6-phosphatase (G6Pase), adenosine triphosphatase (ATPase) and adenyl cyclase (ADC), and unchanged activity of glycogen synthase (SYN) and gamma-glutamyl transferase (GGT). The mixed-cell foci mainly consisted of basophilic cells poor in glycogen, but were intermingled with cells containing glycogen. These foci were characterized by a marked decrease in activity of PHO, SYN, G6Pase, G6PDH, ATPase and ADC, and increased activity of GGT, SDH, MDH and GAPDH. The intermediate-cell foci consisted of cells with both basophilic and glycogenotic cytoplasmic compartments, and showed a similar enzyme histochemical profile to the mixed-cell foci, with slight differences in the degree of elevation or reduction of some enzymes. The phenotypic similarities and the close spatial relationship between the foci of altered hepatocytes, and the hepatocellular adenomas and carcinomas in WHV-infected woodchucks, suggest that these lesions are preneoplastic. The focal morphological and metabolic aberrations emerging during hepatocarcinogenesis in WHV-infected woodchuck, are in principle similar to those identified in the course of chemical hepatocarcinogenesis in various species. The focal metabolic aberrations apparently represent a general biological response of the liver parenchyma to oncogenic agents and are closely linked to neoplastic transformation of the hepatocytes.
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PMID:Phenotypic patterns of preneoplastic and neoplastic hepatic lesions in woodchucks infected with woodchuck hepatitis virus. 215 41

To evaluate changes in liver metabolic zonation during development of juvenile cirrhosis, zonal activities of succinate dehydrogenase, glutamate dehydrogenase, glucose-6-phosphatase, and nicotinamide adenine dinucleotide phosphate (NADPH) dehydrogenase were measured by quantitative cytochemistry in the liver of developing rats intoxicated with carbon tetrachloride and phenobarbitone. During treatment, activities were most decreased in perivenular zones and subsequently at the periphery of the cirrhotic nodules for succinate dehydrogenase and glucose-6-phosphatase, whereas glutamate dehydrogenase and NADPH dehydrogenase were less affected. In the periportal zones, enzyme activities decreased less. After stopping intoxication, the rats remained cirrhotic, but enzyme activities returned to control perivenular levels at the periphery of the cirrhotic nodule and to control periportal levels at its center. It is concluded that a metabolic zonation persists in carbontetrachloride/phenobarbitone-induced juvenile cirrhosis and that enzyme activities can recover despite persisting cirrhosis. In this model, afferent vessels seem to be located at the center of the cirrhotic nodules, and efferent vessels, at their periphery. A different metabolic zonation may exist in other human and animal liver cirrhosis that could be related to the site of initial liver damage.
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PMID:Adaptative changes of metabolic zonation during the development of cirrhosis in growing rats. 216 52

In the female urethra, the activity and distribution of 15 enzymes was determined by using both conventional and special histochemical methods. The enzymatic equipment differed according to the type of epithelial lining whose variation is characteristic for the female urethra. In the stratified squamous epithelium of the urethra, alkaline phosphatase, beta-glucuronidase, acetyl-beta-D-glucosaminidase, thiamine pyrophosphatase, and glucose-6-phosphatase exhibited but minimal or no activity, yet the other 10 enzymes studied displayed activity particularly in basally situated cells. Nearer to the lumen of the urethra, the activity in the epithelium kept decreasing and was mostly absent in superficial and desquamated cells. In the pseudostratified columnar and in the transitional epithelium of the urethra, the majority of enzymes showed an evenly distributed activity at all epithelial levels. In the apical parts of the most superficially situated cells bounding the lumen of the urethra, a distinct narrow zone of higher activity was observed. It was seen not only on determining the majority of dehydrogenases but also on examining acid phosphatase and naphthyl esterase. The endocrine cells occurring in the uroepithelial lining of the female urethra displayed, yet always with the exception of squamous epithelium (Zaviacic et al. 1983), distinct activity of acid hydrolytic enzymes, and of the enzymes studied it was particularly acid phosphatase. The majority of the demonstrated enzymes, of the dehydrogenases priority, is to be given to succinate dehydrogenase, enabled to differentiate readily between the highly active striated muscle fibers located in the most peripheral parts of the excisions along the urethral circumference and the smooth musculature of the urethral wall with a lower or only minimal activity.
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PMID:The adult human female urethra. Enzyme-histochemical study. 242 Jan 38

Inositol 1,4,5-trisphosphate [Ins(1,4,5)P3], arising from hydrolysis of phosphatidylinositol 4,5-bisphosphate [PtdIns(4,5)P2], is proposed as the link between membrane-receptor activation and mobilization of Ca2+ from intracellular sites in hormone-secreting cells. The location of Ins(1,4,5)P3-sensitive membranes was investigated in cultured neonatal beta-cells. Membranes were obtained after lysis of cells attached to positively charged Sephadex. After lysis the presence of the enzyme markers 5'-nucleotidase, glucose-6-phosphatase, NADH-cytochrome c reductase, UDP-galactosyltransferase and succinate dehydrogenase indicated the mixed nature of the preparation. After sonication, however, UDP-galactosyltransferase and succinate dehydrogenase activities were undetectable, but 4.8% of total cellular glucose-6-phosphatase and 3.4% of total cellular NADH-cytochrome c reductase remained with 5'-nucleotidase in the preparation, indicating endoplasmic-reticulum association. ATP-dependent 45Ca2+ accumulation was shown in this preparation (410 +/- 24 pmol/mg of protein at 150 nM free Ca2+) and was inhibited by vanadate (100 microM). Ca2+ release was effected by Ins(1,4,5)P3, with half-maximal release at 0.5 +/- 0.14 microM-Ins(1,4,5)P3, t1/2 11.2 +/- 1.1 s. GTP- and guanosine 5'-[beta gamma-imido]triphosphate (p[NH]ppG)-promoted release of 45Ca2+ was demonstrated in this preparation, but the kinetics of release (half-maximal Ca2+ release at 5.4 +/- 0.7 microM, with t1/2 77.3 +/- 6.9 s, and at 51.1 +/- 4.2 microM, with t1/2 19.0 +/- 2.2 s, for GTP and p[NH]ppG respectively), and the ability of neomycin sulphate to block p[NH]ppG-induced release only, are indicative of separate release mechanisms after treatment with these agents. A close association between plasma membrane and elements of the endoplasmic reticulum is indicated in this model, providing a possible mechanism for local alterations in free Ca2+ in the sub-plasma-membrane region.
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PMID:GTP- and inositol 1,4,5-trisphosphate-induced release of 45Ca2+ from a membrane store co-localized with pancreatic-islet-cell plasma membrane. 245 19


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