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 effect of LC(50) and a sublethal concentration of lead nitrate on the activities of alkaline phosphatase, acid phosphatase, glucose-6-phosphatase, lipase and urease in the kidneys and ovaries of a teleost fish, Channa punctatus has been examined after 96 hr and 30 days respectively. The results show that all the five enzymes in the two tissues are inhibited significantly at both the experimental stages. However, the inhibition produced after 30 days by the sublethal concentration ish higher indicating the cumulative action of lead. Further, the inhibition of enzymes is, more marked in kidney than in the ovary.
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PMID:Effects of lead nitrate on the activities of a few enzymes in the kidney and ovary Heteropneustes fossillis. 22

Thiamine pyrophosphatase (TPPase), nucleoside diphosphatase (NDPase), and glucose-6-phosphatase (G-6-Pase) were localized by the cerium technique in guinea pig pinealocytes and compared with the corresponding lead technique. NDPase and TPPase were also compared at different pH values using the cerium technique. Vibratome sections of perfusion-fixed tissue were incubated with cerium chloride or lead nitrate. Substrates used were thiamine pyrophosphate (for TPPase), sodium inosine diphosphate (NDPase), and disodium glucose-6-phosphate (G-6-Pase). The 1-2 trans saccules of the Golgi apparatus showed TPPase and NDPase activity but none for G-6-Pase. The endoplasmic reticulum (ER) cisternae and perinuclear space had NDPase and G-6-Pase activity but not TPPase. The abluminal plasmalemma of endothelial cells and the plasmalemma of Schwann cells demonstrated TPPase and NDPase activity but the luminal plasmalemma of the endothelial cells and the plasmalemma of pinealocyte processes showed only NDPase activity. TPPase was active at all pH values tested, but NDPase was most active at pH values of 6.5 and 7.0. Lead phosphate precipitate was frequently seen in nuclei, perinuclear space, ER cisternae, and "synaptic" vesicles when lead was used as the capturing agent. These sites were usually not labeled when cerium was used.
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PMID:Ultrastructural localization of phosphatase activity in the guinea pig pineal gland by the cerium technique. 215 98

Male Wistar rats were given a single i.v. injection of lead nitrate (10 mumol/100 g body wt) and were killed with matched controls 24, 48, 72 h and 20 days after the treatment. Changes of liver carbohydrate metabolism were studied histochemically testing the following parameters: glycogen content, activities of glycogen synthase (SYN), glycogen phosphorylase (PHO), glucose-6-phosphatase (G6PASE), glucose-6-phosphate dehydrogenase (G6PDH), 6-phosphogluconate dehydrogenase (6PGDH), glyceraldehyde-3-phosphate dehydrogenase (GAPDH). In addition, gammaglutamyltransferase (GGT) activity was demonstrated. Between 24 and 48 h after lead nitrate injection there was a nearly complete loss of liver glycogen. Seventy-two hours later the polysaccharide reappeared in single hepatocytes and after 20 days the livers of the lead-treated animals not only had replenished their glycogen stores but contained even more glycogen than the matched controls. SYN and PHO activities were diminished from 24 to 72 h, but returned to control values after 20 days. G6PASE and GGT remained elevated up to 72 h before dropping to normal at 20 days after treatment. The pentose phosphate pathway enzymes G6PDH and 6PGDH showed the most remarkable changes in livers treated with lead nitrate. G6PDH was already elevated at 24 h, but only in Kupffer cells. At 48 and 72 h, when hepatocytes exhibited a highly increased mitotic rate, the levels of G6PDH, 6PGDH and GAPDH were elevated. After 20 days dehydrogenase activities were comparable to those of controls. The results of this study suggest that a single dose of lead nitrate not only stimulates proliferation of hepatocytes but also induces considerable changes in rat liver carbohydrate metabolism, especially between 24 and 72 h after administration. During that period glycogen metabolism undergoes a strong reduction, whereas gluconeogenesis and particularly the pentose phosphate pathway respond with a remarkable increase. This metabolic profile is most likely associated with lead biotransformation as well as with liver cell proliferation. It corresponds only partially to that found in preneoplastic and neoplastic liver lesions observed in chemical carcinogenesis, and is reversible, in contrast to the persistent alterations associated with neoplastic transformation.
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PMID:Effect of lead nitrate on liver carbohydrate enzymes and glycogen content in the rat. 217 37

Promastigotes of Leishmania mexicana amazonensis possess an elaborated system of cytoplasmic membranes which is clearly visualized when the cells are fixed in a glutaraldehyde solution containing Ca++ and post-fixed in an osmium tetroxide solution containing Ca++ and potassium ferricyanide. When the parasites are incubated in a medium containing glucose-6-phosphate and lead nitrate, reaction product indicative of glucose-6-phosphatase activity is seen in the membrane system confirming that it corresponds to the endoplasmic reticulum (ER). A large concentration of profiles of the ER was observed at the anterior region of the cell, close to the flagellar pocket, appearing as a 'proliferative focus'. Profiles of the ER radiate toward the periphery of the cell penetrating between the subpellicular microtubules and reaching the plasma membrane.
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PMID:Fine structure and cytochemistry of the endoplasmic reticulum and its association with the plasma membrane of Leishmania mexicana amazonensis. 402 Sep 25

The effect of two new chelating agents-Tiron (4,5-dihydroxy-1,3-benzene disulphonic acid disodium salt) and succinic acid--on the mobilization of beryllium was studied. Animals were exposed to beryllium nitrate (1 mg kg(-1) i.p.) daily for 21 days. Administration of beryllium nitrate showed a marked decrease in haemoglobin percentage, blood sugar, serum alkaline phosphatase and serum protein and a significant increase in the activity of transaminases. Tissue protein and glycogen contents and the activity of alkaline phosphatase, adenosine triphosphatase and succinic dehydrogenase showed significantly decreased values, but beryllium nitrate provoked a considerable increase in the activity of acid phosphatase and glucose-6-phosphatase in the vital and reproductive organs. Significant improvement in the haematological and biochemical parameters was observed with Tiron but no therapeutic effect was seen with succinic acid. Atomic absorption spectrophotometry (AAS) also showed a decreased level of beryllium concentration in the liver and kidney after Tiron therapy.
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PMID:Influence of chelating agents on the toxicity and distribution of beryllium in rats. 980 33

The efficacy of Tiron (4,5-dihydroxybenzene 1,3-disulfonic acid disodium salt) was examined in the treatment of beryllium-induced maternal and developmental toxicity in rats. Single administration of beryllium nitrate at a dose of 50 mg/kg (i.m.) on day 13 of gestation caused reductions in fetal and placental weights, the number of implantation sites and number of corpora lutea, as well as causing post-implantation loss, stunted growth, increase in the number of resorptions, and also a disturbed sex ratio. Maternal toxicity was demonstrated by reduction in body weight gain. Administration of beryllium also showed significant alteration in the hematological and biochemical indices of the mother as well as the fetus. Marked decreases were recorded in hemoglobin percentage, blood sugar levels, serum protein contents and serum alkaline phosphatase activity. By contrast, significant elevation was found in the activity of transaminases (aspartate aminotransferase and alanine aminotransferase). Tissue protein contents, glycogen contents, activities of alkaline phosphatase, adenosine triphosphatase and succinic dehydrogenase of kidney, lungs and uterus, and maternal and fetal liver all showed significantly decreased values after beryllium exposure, and remarkable elevation was observed in acid phosphatase, glucose-6-phosphatase and hepatic lipid peroxidation. These parameters were restored considerably with administration of 471 mg/kg i.m. Tiron from days 14 to 18 of gestation. Atomic absorption spectrophotometry also revealed a high concentration of beryllium in different organs of pregnant rats. Interestingly, a small amount of metal ion was also detected in the fetus and reduced accumulation of beryllium was noticed after Tiron treatment.
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PMID:Protective effect of Tiron (4,5-dihydroxybenzene-1,3-disulfonic acid disodium salt) against beryllium-induced maternal and fetal toxicity in rats. 1218 11

The present study was conducted to evaluate the therapeutic effectiveness of chelating agents [glutathione, 2,3 dimercapto propane sulfonic acid (DMPS) and D-penicillamine (DPA)] in combination with antioxidant (sodium selenite) in beryllium induced toxicity in female rats. A bolus dose of 50mg/kg-beryllium nitrate was administered singly followed by chelation therapy with GSH, DMPS + Se and DPA + Se at various durations of 1,3 and 7 days respectively. Results revealed a significant fall in the glycogen content, whereas, a marginal fall in the protein was also observed. The enzymatic activity of alkaline phosphatase and adenosine triphosphatase was depleted; on the contrary, there was a significant rise in the acid phosphatase and glucose-6-phosphatase pattern. A rise in the hepatic lipid peroxidation activity is a direct indication of oxidative damage resulting in free radical generation. The distribution of the metal by atomic absorption spectrophotometry revealed an increased concentration of beryllium in liver and kidney, followed by lung and uterus. The relative ability of three chelating agents to act as antagonists, for acute beryllium poisoning, have been examined in liver, kidney, lungs and uterus. The appreciable change in the beryllium concentration in various organs is duration dependent during the entire period being highly significant at 7 days regimen. Biochemical and distribution studies reveal that DPA + Se was the most effective therapeutic agent followed by DMPS + Se and GSH.
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PMID:Role of chelating agents and antioxidants in beryllium induced toxicity. 1262 5

Influence of adjuvants i.e., alpha-tocopherol (25 mg/kg, p.o.) and piperine (10 mg/kg, p.o.) on therapeutic potential of chelator tiferron (300 mg/kg, i.p.) was evaluated to encounter toxicogenic events of beryllium exposure. Albino rats were exposed to beryllium nitrate (1 mg/kg, i.p.) daily for 28 days followed by treatment of aforesaid therapeutic agents for 5 consecutive days. Results were considered to be significant at p < or =0.01 and p < or =0.05. Exposure to beryllium increased its concentration in liver, kidney and serum causing significant alterations in the activity of CYP-450 2E1 system, microsomal lipid peroxidation and protein; alkaline phosphtase, lactate dehydrogenase, gamma-glutamyl transpeptidase, bilirubin, creatinine and urea in serum; activity of acid phosphatase, alkaline phosphatase, adenosine triphosphatase, glucose-6-phosphatase and succinic dehydrogenase in liver and kidney. Beryllium exposure also induced severe alterations in histopathology and ultramorphology of liver and kidney proving its toxic consequences at cellular level. Tiferron along with adjuvants dramatically reversed alterations of all variables more towards control rather than individual treatment. Study concluded that tiferron in combination with alpha-tocopherol and piperine respectively was beneficial in diluting beryllium induced systemic toxicity; however, combination of tiferron and piperine presented more pronounced therapeutic potential.
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PMID:Amelioration of beryllium induced alterations in hepatorenal biochemistry and ultramorphology by co-administration of tiferron and adjuvants. 1727 10

Uranium, the heaviest of the naturally occurring elements is widely present as environmental contaminant from natural deposits, industrial emissions and most importantly from modern weapons. Histopathological examinations revealed that uranyl nitrate (UN) exposure caused severe damage to pars recta of renal proximal tubule. However, biochemical events involved in cellular response to renal injury are not completely elucidated. We hypothesized that UN exposure would severely damage kidney tissues and alter their metabolic functions. Rats were treated with a single nephrotoxic dose of UN (0.5mg/kg body weight) i.p. After 5d, effect of UN was studied on the activities of various enzymes of carbohydrate metabolism, brush border membrane (BBM) and oxidative stress in different kidney tissues. Activity of lactate dehydrogenase increased whereas activities of isocitrate, succinate and malate dehydrogenases, glucose-6-phosphatase and fructose-1,6-bisphosphatase significantly decreased by UN exposure. Activity of glucose-6-phosphate dehydrogenase decreased whereas that of NADP-malic enzyme increased. The activities of BBM enzymes were significantly lowered and after dissociation from BBM excreted in urine. Lipid peroxidation and the activities of superoxide dismutase and glutathione peroxidase increased whereas catalase activity decreased by UN. UN treatment caused specific alterations in the activities of metabolic and membrane enzymes and perturbed antioxidant defenses.
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PMID:Effect of uranyl nitrate on enzymes of carbohydrate metabolism and brush border membrane in different kidney tissues. 1834 12

Synergistic therapeutic potential of ferritin (5mg/kg, i.p.) and propolis (honeybee hive product; 200mg/kg, p.o.) was analyzed to encounter the beryllium induced biochemical and ultra morphological alterations. Female albino rats were exposed to beryllium nitrate (1mg/kg, i.p.) daily for 28 days followed by treatment of above mentioned therapeutic agents either individually or in combination for five consecutive days. Exposure to beryllium increased its concentration in serum, liver and kidney and significantly altered the activities of CYP2E1 and CYP1A2 enzymes, microsomal lipid peroxidation and microsomal proteins. Activities of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, lactate dehydrogenase, gamma-glutamyl transpeptidase, bilirubin, protein, creatinine and urea in serum as well as hemoglobin and blood glucose level; activity of acid phosphatase, alkaline phosphatase, adenosine triphosphatase, glucose-6-phosphatase and succinic dehydrogenase, total triglycerides, total cholesterol, total protein contents, glycogen contents, lipid peroxidation and glutathione level in liver and kidney were significantly altered after beryllium administration. Beryllium exposure severely altered ultramorphology of liver and kidney that proved its toxic consequences at cellular level. Ferritin in combination with propolis dramatically reversed the alterations of these variables towards control in a synergistic manner concluding its beneficial effects over monotherapy in attenuating beryllium induced systemic toxicity.
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PMID:Synergistic effects of ferritin and propolis in modulation of beryllium induced toxicogenic alterations. 1862 18


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