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)

An attempt has been made to study the protective effect of a new chelating agent named p-amino salicylic acid oxine azo dye complex and metallic zinc on the Ccl4 induced hepatic injury in squirrels. This is probably the first multidisciplinary approaching (histological, histochemical and biochemical), report, employing this chelating agent and zinc together in the cure of a hepatic tissue. Apart from a pathological support, biochemical estimation of two enzymes noticed: Viz glucose-6-phosphatase dehydrogenase and beta-glucuronidase were treated as enzymatic denominators in liver cure. It further claims the suitability of the drug for clinical use. However, a detailed mechanism of action of this chelating agent remains practically unknown. It is hypothesized, that chelation of zinc facilitates the peneteration of a drug complex in the hepatic cells. Further zinc serves the purpose of drug transporter. The chelating agent masks the toxic substances (metabolites of Ccl4), which are eventually excreted, but still bound to it. The regeneration progresses speedily after the biomembranes are stabilized.
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PMID:Simultaneous protective effect of a new chelating agent and zinc, on the carbon tetrachloride induced hepatic injury in squirrels. 89 57

Inflammation, induced by turpentine (0.1 ml i.m.), protected against carbon tetrachloride (CCl4)-induced hepatotoxicity based on serum activities of sorbitol dehydrogenase. Inflammation was confirmed by elevated serum ceruloplasmin activities, and was associated with high hepatic levels of metallothionein, a zinc protein proposed to protect against CCl4-induced injury. Inflammation suppressed cytochrome P-450 activities, but this was not associated with protection against CCl4-promoted liver microsomal injury as assessed by glucose-6-phosphatase activity loss. Thus, protection against plasma membrane injury did not result primarily from depressed microsomal activation of CCl4. Each effect of inflammation reported here resembled effects of zinc injections. This similarity strengthens the hypothesis that metallothionein protects against CCl4-induced hepatic plasma membrane injury.
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PMID:Inflammation, an inducer of metallothionein, inhibits carbon-tetrachloride-induced hepatotoxicity in rats. 131 82

We studied the development of liver tumors in male transforming growth factor alpha (TGF-alpha) transgenic mice of the CD1 strain and examined the expression of the transgene by immunohistochemistry and in situ hybridization. Livers of 4-5-week-old transgenic mice contained areas of centribobular hypertrophy with low glucose-6-phosphatase activity. These areas progressively expanded, and hypertrophy and dysplasia became generalized in livers of mice at 10-12 months of age. The expression of the transgene, determined by either immunohistochemistry or in situ hybridization, was uneven in animals that were 10 weeks old or older. The positive hepatocytes formed patches with a predominant centrilobular distribution. We studied a total of 23 liver tumors (7 hepatocellular carcinomas and 16 adenomas) obtained from 11 mice at 13-15 months of age and from one 7-month-old animal which received zinc sulfate to induce the transgene. The carcinomas were well differentiated tumors, without glucose-6-phosphatase or gamma-glutamyltranspeptidase activity, that developed from the dysplastic parenchyma and occasionally within an adenoma. In all carcinomas and in 56% of the adenomas there was overexpression of the transgene in relationship to the surrounding tissue. The majority of the tumors that overexpressed TGF-alpha were alpha-fetoprotein positive, while alpha-fetoprotein staining was not detected in tumors (all adenomas) that did not show excessive transgene expression. We conclude that TGF-alpha functions as a promoter of liver carcinogenesis through its effect as an autocrine inducer of hepatocyte proliferation. Further, the data indicate that TGF-alpha overexpression may favor tumor progression.
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PMID:Development of liver tumors in transforming growth factor alpha transgenic mice. 132 2

Extreme copper deficiency has been shown to enhance CCl4-induced injury in rats. CCl4 hepatotoxicity was studied in rats with copper deficiency moderated by limiting deficiency periods to 5 or 6 weeks, using minimally adequate dietary zinc and including a marginal copper diet. Also, housing some rats in groups of six, rather than individually, was found to moderate the effects of low copper intake. Weanling male rats were fed copper at either 6, 2, or 0.2 mg/kg diet (adequate, marginal, deficient). Copper-zinc superoxide dismutase activity levels for singly and group-housed marginal rats were 80% and 93%, respectively, of adequate values. Values for deficient rats were 35% (singles) and 47% (group). In singly housed rats, a CCl4 dose of 400 microliters/kg intraperitoneally increased serum sorbitol dehydrogenase activities, indicators of cell membrane hepatotoxicity, in inverse proportion to dietary copper. A lower dose (100 microliters/kg) also produced smaller sorbitol dehydrogenase increases in adequate rats compared with deficients, but produced lowest increases in the marginals. The latter pattern also occurred in group-housed rats given the higher CCl4 dose, but the difference for adequate and marginal rats was not significant. The higher CCl4 dose, in singly housed rats, decreased liver glucose-6-phosphatase activities independently of copper intake. These activities are inversely proportional to microsomal lipid damage. In conclusion, moderate copper deficiency enhanced CCl4 hepatotoxicity, but the effect depended on injury criteria, CCl4 dose, and actual copper status as assessed by copper-zinc superoxide dismutase activities.
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PMID:Effects of moderate copper deficiency on carbon tetrachloride-induced hepatotoxicity in rats. 185 May 23

The effect of regucalcin, a calcium-binding protein isolated from rat liver cytosol, on glucose-6-phosphatase in the microsomes of rat liver was investigated. Addition of Ca2+ up to 2.5 microM to the enzyme reaction mixture caused a significant increase of glucose-6-phosphatase activity in hepatic microsomes, while Ni2+, Zn2+, Cd2+, Cu2+, Mn2+ and Co2+ (20 microM) did not have an appreciable effect. Vanadate (V5+) markedly inhibited the enzyme activity; a significant inhibitory effect was seen at 10 microM V5+. The Ca2+-induced increase of glucose-6-phosphatase activity was reversed by the presence of regucalcin; the effect was complete at 1.0 microM of the protein. Regucalcium had no effect on the basal activity of the enzyme. Meanwhile, the inhibitory effect of V5+ (10-100 microM) on glucose-6-phosphatase was not appreciably blocked by the presence of regucalcin (up to 2.0 microM). The present data suggest that hepatic microsomal glucose-6-phosphatase is uniquely regulated by Ca2+ and V5+, of various metals, and that the Ca2+ effect is reversed by regucalcin. The present study supports the view that regucalcin plays an important role as a regulatory protein in liver cell function related to Ca2+.
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PMID:Effects of Ca2+ and V5+ on glucose-6-phosphatase activity in rat liver microsomes: the Ca2+ effect is reversed by regucalcin. 254 64

In order to determine the specific action of cadmium on bone metabolism, the effect of cadmium on alkaline phosphatase activity, a marker enzyme of osteoblasts, was compared with that of other divalent heavy metal ions, i.e., zinc, manganese, lead, copper, nickel and mercury (10 microM each), using cloned osteoblast-like cells, MC3T3-E1. Cadmium had the strongest inhibitory effect on alkaline phosphatase activity of the cells among the metals tested. At the same dose, however, cadmium failed to inhibit cellular glucose-6-phosphatase and lactate dehydrogenase activities, suggesting that the inhibitory effect of cadmium on alkaline phosphatase was specific and was not dependent on cell injury. Cadmium treatment caused a significant decrease in cellular zinc level, but mercury treatment had no such effect at the dose inhibiting alkaline phosphatase activity. There was a good correlation between decrease of cellular zinc level and inhibition of alkaline phosphatase activity in cadmium-treated cells. Concomitant treatment of the cells with zinc prevented the cadmium-induced inhibition of alkaline phosphatase activity. However, this was not the case in the mercury-induced inhibition. Cadmium also inhibited the mineralization of osteoblasts. When 10 or 20 microM zinc was concomitantly added to the cultures, the inhibition of mineralization was prevented. These data suggest that the inhibitory effect of cadmium in osteoblasts may be closely related to its influence on the cellular zinc metabolism.
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PMID:Preventive effects of zinc on cadmium-induced inhibition of alkaline phosphatase activity and mineralization activity in osteoblast-like cells, MC3T3-E1. 274 54

Cadmium causes hyperglycemia, activation of hepatic and renal gluconeogenic enzymes such as glucose-6-phosphatase and fructose-1,6-diphosphatase, increases hepatic and renal zinc, renal copper and decreases hepatic and renal iron levels in rats. Glibenclamide, a hypoglycemic agent, significantly reversed most of the Cd effects, enhanced fecal excretion of Cd and potentiated urinary and fecal elimination of Cd by calcium trisodium diethylenetriaminepentaacetate (CaNa3DTPA), a commonly used metal chelator. However, the restoration of Cd-induced alterations in carbohydrate metabolism was not related to elimination of Cd from the tissues.
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PMID:Influence of glibenclamide on the efficacy of calcium trisodium pentetat as an antidote for cadmium toxicity. 283 34

Ultracytochemical reactions for the demonstration of acid phosphatase, glucose-6-phosphatase and thiamine pyrophosphatase, as well as zinc iodide-osmium tetroxide impregnation, revealed the existence of GERL (Golgi apparatus-Endoplasmic Reticulum-Lysosomes) in pinealocytes of the Mongolian gerbil (Meriones unguiculatus). The spatial arrangement of this structure was studied on thick sections using a goniometric stage. Although it was not possible to determine whether GERL in pinealocytes belongs to the Golgi apparatus or to endoplasmic reticulum, it can be concluded that its presence in studied cells signifies that they are considerably more active synthetically than has been believed to date.
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PMID:Ultracytochemical evidence for the presence of GERL in pinealocytes of the Mongolian gerbil (Meriones unguiculatus). 302 41

Zinc, lead and cadmium in the form of chloride salts when added to a standard assay system containing 80 X 10(-6) ejaculated washed human spermatozoa caused a dose and duration-dependent inhibition of their motility. The activity of certain key enzymes of carbohydrate and energy metabolism, viz, glycogen phosphorylase, glucose-6-phosphatase, fructose-1, 6-diphosphatase, glucose-6-phosphate isomerase, amylase, Mg2+- dependent ATPase and lactic and succinic acid dehydrogenases were also found to be inhibited. The order of inhibitory effects of the heavy metals were zinc less than lead less than cadmium. The metal chelating agent, ethylene diamine tetra-acetic acid (EDTA, disodium salt) also interfered with the spermatozoal motility and inhibited the enzyme activities.
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PMID:Effect of selected metal ions on the motility and carbohydrate metabolism of ejaculated human spermatozoa. 314 74

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


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