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 protective action of aspartic acid on isolated and perfused rat liver was studied. In case of D-galactosamine intoxication the GOT, GPT and SDH activity and the lactate and pyruvate concentration in the perfusion medium were less augmented and the glycogen level in hepatic tissue was less diminished in animals treated with aspartic acid, as compared to controls. The histochemical applied (PAS reaction for glycogen, nucleic acids, NADH2-diaphorase, glucose-6-phosphatase and membrane-ATP-ase), also stated a protecting effect in the treated animals. The protective action of aspartate is hypothetically considered to be exerted by its capacity to reestablish the cellular deficit of pyridine nucleotides and thus to improve the synthesis of nucleic acids, glycoprotein and glycolipids or/and by its participation in various metabolic pathways.
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PMID:Protecting action of aspartate on the hepatic changes induced by D-galactosamine. 18 87

Rats were made to drink D2O mixed water (30: 70) for 6 weeks in order to study the biological effects of orally administered D2O on the liver. Heavy water administration results in gradual decrease in the body weight whereas the liver showed marginal increase in weight throughout the experimental period. Phosphatases and dehydrogenases were analyzed biochemically. Acid phosphatase, glucose-6-phosphatase and adenosine triphosphatase registered fall in contrast to alkaline phosphatase, SDH and LDH, all of which showed a definite increase. Lipids, nucleic acids and proteins, estimated biochemically, gradually decreased throughout the experimental period in response to D2O feeding.
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PMID:Biologic effects of orally administered deuterium oxide on rat liver. 19 33

The aim of the present work was to study by means of histochemical and chemical methods the 7-day course of changes in carbohydrate metabolism in the liver of male rats induced by a single dose of isoprenaline of 50 mg/kg administered subcutaneously. A statistically significant reduction was seen both in the level of free glycogen and lactate within 24 hours. The decrease of pyruvate level was not so marked. At the same time, there was increased, and within the hepatic lobules also extended activity of enzymes catalyzing glycogenolysis, i.e. alpha-glucan phosphorylase and particularly the branching Q-enzyme, glucose-6-phosphatase and LDH, whereas the level of malate and activity of SDH, which are constituents of the Krebs cycle, were found to be reduced. Cytochrome oxidase activity was changed after 24 hr compared to the controls. The obtained results indicate that an extensive glycogenolysis occurs in the liver of rats in the 24 hr following s.c. administration of isoprenaline, the major part of liver glycogen being degraded through glucose-6-phosphate to blood glucose and its metabolism via the Krebs cycle reduced. The observed metabolic changes are of reversible character and tend to normalize over the 2nd and 3rd day following isoprenaline administration.
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PMID:Study of histochemical and biochemical changes in the liver of rats induced by high doses of isoprenaline. 20 78

In native cryostat tissue sections of adult female albino rat liver the activities of succinate dehydrogenase (E. C. 1.3.99.1), glucose-6-phosphatase (E. C. 3.1.3.9) and malic enzyme (E. C. 1.1.1.40) were histochemically demonstrated and planimetrically determined. The areas of the enzymes with a maximum activity in the periportal regions, namely SDH and G-6-Pase, were respectively 34% and 41% of the whole parenchyma. Malic enzyme showed a maximum activity in the perivenous region, which consisted of about 53% of the total parenchyma. The zonal distribution of enzyme activities is related only to the terminal vessels; in the vicinity of the preterminal vessels an irregular distribution pattern was found. The results further support the assumption of the bifunctionality of liver parenchyma.
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PMID:[Quantitative investigations of the zonal distribution of SDH, G6Pase and malic enzyme activity in liver parenchyma (author's transl)]. 21 84

Microsome, cytosol and serum malathion carboxylesterase (MaCEst) activity was assessed in rats after single i.p. administration of carbon tetrachloride (CCl4) in doses ranging from 0.05 to 1 ml kg-1. MaCEst activities were compared with those of glucose-6-phosphatase (G6-Pase) as an indicator of endoplasmic reticulum damage and serum glutamate dehydrogenase (GLDH) and sorbitol dehydrogenase (SHD) as indicators of liver cytolysis. The data showed a dose-dependent increase in GLDH and SDH serum activities (175% and 68%) from 0.05 ml kg-1; an increase in serum G6-Pase (31%) and a decrease in microsomal G6-Pase (38%) was apparent only after 0.5 or 1.0 ml kg-1 doses. MaCEst activity was unaffected. The results demonstrate that, under these experimental conditions, serum and subcellular measurements of MaCEst activity failed to reveal the liver toxicity of CCl4.
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PMID:Difference in liver and serum malathion carboxylesterase and glucose-6-phosphatase in detecting carbon tetrachloride-induced liver damage in rats. 166 44

One hundred and five sexually mature male hamsters were divided in different groups. In the first experiment hamsters were administered gossypol, 10 mg/kg and 20 mg/kg/body weight/day, for twenty and thirty days. In the second experiment hamsters were administered gossypol, 5, 10 and 20 mg/kg/body weight/day, for sixty days. In the third experiment, hamsters were administered gossypol 5 mg, 10 mg, 20 mg and 40 mg/kg body weight/day for 45 days. Animals in all the groups were given gossypol by oral intubation every day. No significant effect on the body weight of hamsters following gossypol treatment was observed. At low doses the weights of testis and accessory sex organs were not statistically different from those of the controls. A significant decrease in testis and epididymis weight was however observed following high doses of gossypol. Low doses of gossypol treatment did not affect the motility of the vas deferens spermatozoa. The vas deferens spermatozoa were however immotile after 40 mg/kg/day gossypol treatment. Gossypol treatment induced a series of histological changes in the seminiferous epithelium of the hamster testis. The earliest sign of drug effect was seen in spermatids and with the increase in doses the effects became more pronounced and extended to the spermatocytes. At 40 mg/kg dose an almost complete arrest of spermatogenesis was observed. Quantitatively, the ratio of pachytene spermatocytes: resting spermatocytes and step 7 spermatids: pachytene spermatocytes decreased significantly. The step 7 spermatids did not mature to step 19 spermatids at all. Histochemically activities of ATPase, SDH and LDH decreased with the increasing doses of gossypol, the activity of 3B hydroxysteroid dehydrogenase was not affected by gossypol treatment. In testis the glucose-6-phosphatase activity was not affected significantly but the activities of fructose 1, 6-diphosphatase and glucose-6-phosphate isomerase decreased significantly with the increasing doses of gossypol. Amylase activity rose significantly at higher doses. Marked changes in LDH and LDH-X were however observed with the increase in gossypol dose. In liver the activity of glucose-6-phosphatase increased significantly while the activities of fructose 1, 6-diphosphatase, glucose-6-phosphate isomerase and amylase were not affected following gossypol treatment. The glycogen contents however increased significantly following high doses of gossypol. No changes in testosterone production and plasma levels of testosterone were observed following gossypol treatment.
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PMID:Response of hamster to the antifertility effect of gossypol. 170 27

The following enzymes have been studied (subcellular fractions are shown between parentheses): NAG and beta-glucuronidase (lysosomes); SDH (mitochondrial); glucose-6-phosphatase (endoplasmic reticulum); 5'-nucleotidase and (Na+, K+)Mg2+ ATPase (plasma membranes). Alterations on their activities were observed after subcutaneous injection of sex hormones, compared with controls. NAG activity from liver was always significantly decreased in lysosomal and microsomal fractions after the hormonal treatment. In the same conditions, NAG from brain was always increased. beta-Glucuronidase behaves like NAG in brain; in liver it was not modified by testosterone and it was slightly increased in lysosomal fraction after oestradiol treatment. SDH activity was not modified in mitochondrial fractions from liver, but this activity was always significantly increased in brain. Glucose-6-phosphatase activity was always significantly decreased in microsomal fractions from liver. It was increased in brain after oestradiol and testosterone injection, but medroxyprogesterone treatment caused a decreased activity. 5'-Nucleotidase and (Na+, K+)Mg2+ ATPase from brain were significantly increased in microsomal fractions by oestradiol and testosterone. Medroxyprogesterone, however, caused an increase in ATPase, but did not affect 5'-nucleotidase. Both activities in liver were decreased by oestradiol and increased by testosterone, but medroxyprogesterone caused (Na+, K+)Mg2+ ATPase to rise and 5'-nucleotidase to fall.
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PMID:Effects of oestradiol, testosterone and medroxyprogesterone on subcellular fraction marker enzyme activities from rat liver and brain. 298 29

The effect of subcutaneous injection of hydrocortisone and corticosterone on the activity values of some subcellular fractions marker enzymes from rat liver and brain was investigated and compared with controls (without treatment with hormones). The following enzymes were studied (subcellular fraction are shown between parentheses): N-acetyl-beta-D-glucosaminidase and beta-glucuronidase (lysosomes); succinate dehydrogenase = SDH (mitochondria); glucose-6-phosphatase (endoplasmic reticulum); 5'-nucleotidase and Na+-K+-Mg2+ ATPase (plasma membrane). The specific activity of lysosomal enzymes from liver showed no change when rats were injected either with hydrocortisone or corticosterone. The same enzymes from brain showed significant increases in their activities with both hydrocortisone or corticosterone except beta-glucuronidase; this enzyme gave activity values remaining between the control levels, after treatment with corticosterone. The activity of mitochondrial SDH was increased after corticosterone injection either in liver or brain. After hydrocortisone injection, its activity rises significantly in brain (72%), but it falls in liver compared to the control values. Glucose-6-phosphatase behaves similarly in brain or liver fractions; its activity increases always after corticosterone treatment and decreases by hydrocortisone. The plasma membrane marker enzymes did not change practically in brain fractions, excepted Na+-K+-Mg2+ ATPase which tends to rise its activity after hydrocortisone injection. In liver fractions, both 5'-nucleotidase and Na+-K+-Mg2+ ATPase activities increase either by corticosterone or hydrocortisone treatment, except 5'-nucleotidase which specific activity decreases in liver after hydrocortisone treatment.
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PMID:Alterations in the activities of subcellular fractions marker enzymes in rat liver and brain by hydrocortisone and corticosterone treatment. 298 17

The influence of extraneous supplementation of L-ascorbic acid in chronic chlordane toxicity has been studied in rats. Oral administration of chlordane brings about a marked growth retardative effect, stimulates vitamin C synthesis in the system, elevates the vitamin C status of the liver and kidney tissues and also the urinary excretion. It inhibits the activities of acid and alkaline phosphatases, SDH and Mg2+-ATPase of both hepatic and renal tissues. The activities of serum and mitochondrial GOT, serum alkaline phosphatase, and glucose-6-phosphatase of both hepatic and renal tissues are markedly stimulated. The normal histological patterns of both liver and kidney tissues are grossly altered under chlordane toxicity condition. There occurs marked increase in the hepatic lipid composition. Supplementation of L-ascorbic acid in high doses to the chlordane treated rats can effectively counteract some of these alterations in respect of enzyme activities, morphological characteristics and of hepatic lipid composition.
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PMID:Studies on the protective effects of L-ascorbic acid in chronic chlordane toxicity. 731 25