Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.6.1.3 (ATPase)
 65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Total smooth microsomes from rat liver isolated on a Cs(+)-containing sucrose gradient were concentrated and subsequently fractionated by zone centrifugation on a stabilizing sucrose gradient. The prerequisite for fractionation is to prepare total smooth microsomes in a nonaggregated condition, as well as to utilize a procedure which counteracts enzyme inactivation. The median equilibrium density of the various smooth microsomal vesicles ranges from 1.10 to 1.18. The phospholipid/protein ratio is identical in all subfractions, but cholesterol, on a PLP basis, is enriched in the subfractions with the highest sedimentation velocity. The enzyme distribution pattern reveals a pronounced heterogeneity. A number of NADH- and NADPH-oxidizing enzymes are concentrated in the upper part of the gradient and exhibit a certain degree of separation from G6Pase. Mg(++)-ATPase and AMPase are enriched in the lower part of the gradient. No specific enrichment of newly synthesized NADPH-cytochrome c reductase activity occurs in any of the subfractions after phenobarbital treatment. These data demonstrate that smooth microsomes, by adequate fractionation procedure, can be separated into subfractious of heterogeneous composition.
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PMID:Subfractionation of smooth microsomes from rat liver. 439 31

The ultrastructural localization of AcPase, AlkPase, ATPase, TPPase, NDPase and G-6-Pase in rat pancreatic B-cells is studied. The plasmolemma is reactive to AlkPase, ATPase, and NDPase. The concave part of the Golgi complex and the lysosomes show AcPase and TPPase activity. In the halo of some beta-granules located near to the Golgi area the AcPase activity is also present. The cisterns of the endoplasmic reticulum are positive for G-6-Pase. So each of the phosphatases has a well expressed ultrastructural localization. It is assumed that this enzyme specificity is connected with the specific organelle's metabolism. Some considerations are made for the possible role of each enzyme in the B-cell physiology.
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PMID:Ultrastructural study on the enzymes in the pancreatic B-cells of the rat. 611 12

Hepatocellular growth inhibition and restorative hyperplasia were studied in 80 young male Buffalo rats that were fed .02% 2-AAF for up to four weeks. Between 30 and 58 days of age, the control rats tripled their body weights and more than doubled their liver weights. But these increases were respectively inhibited by 25 and 22% in 2-AAF fed rats. Because the rats were in a phase of rapid growth, it was necessary to evaluate the age-related hepatic changes in control animals prior to analyzing the experimental data. Thirty-seven-day-old control rats had 3H-thymidine labeling indices of hepatocytes that were two to five times higher than in 58-day-old rats. A replicative gradient was also noted in the hepatic acini. At three ages of sacrifice (37, 44 and 58 days), the control hepatocytes in the periportal regions (Zone 1) had labeling indices that were at least three times higher than those surrounding the terminal hepatic veins (Zone 3). Histochemical GGTase activity also showed age-related zonal changes. Particularly prominent was the decrease with age in the enzyme activity of the most actively replicating Zone 1 hepatocytes. GGTase activity was observed in hepatocytes occupying 7.6% of tissue section areas in rats sacrificed at 30 days of age, but this decreased to 0.3% by the fourth week of the study. After four weeks of feeding the carcinogen toxic growth inhibition was most impressive in midzonal (Zone 2) hepatocytes, which also showed decreased glycogen, and decreased cytoplasmic RNA. The localization of injury to acinar midzones is particularly noteworthy in view of the extreme rarity of the finding in the hepatic toxicology literature. Growth inhibition was already apparent after only one week of 2-AAF feeding, when the 3H-thymidine labeling indices of Zone 2 hepatocytes were 90% lower (0.9%) than in control rats (8.6%). Hepatocellular hyperplasia, presumably a restorative response to the midzonal growth inhibition, was prominent in Zone 1, but also noted in Zone 3, after four weeks of the study. However, most of the Zone 1 hyperplastic cells showed canalicular GGTase activity, while none of the Zone 3 hyperplastic cells showed this phenotype. Occasional discrete foci of hyperplastic hepatocytes that were considered putatively premalignant because of their very high GGTase activity and low G6Pase and ATPase activities were also noted after four weeks of 2-AAF feeding. The foci were usually in close physical association with hyperplastic Zone 1 hepatocytes, but could be distinguished by their higher GGTase and lower G6Pase activities.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Hepatocellular injury, hyperplasia and putative premalignancy in rats fed 2-acetylaminofluorene. 614 61

Intraperitoneal administration of Thimet (0.6 mg/kg) on alternate days for a period of 30 days produced various pathological and biochemical changes in the liver and testes of male gerbils. Histology of the liver showed necrosis, enlarged hepatocytes and fatty degeneration. Histological changes seen in the testes were enlarged interstitium, pyknotic spermatogenic cells, reduction in tubular size and atrophy of Leydig cells. The activities of alkaline and acid phosphatases increased in both liver and testes while that of ATPase decreased significantly. The activity of G-6-Pase decreased in liver but increased significantly in testes. Partial recovery was seen 15 days after termination of Thimet treatment. The activities of acid phosphatase, ATPase of liver and alkaline phosphatase, acid phosphatase, and ATPase of testes did not return to their normal values up to 15 days after stopping the injections.
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PMID:Histopathological and biochemical changes in the liver and testes of desert gerbil, after repeated exposures of Thimet (phorate). 645 90

The effect of feeding mycotoxins, i.e. aflatoxin B1 (1.25 ppm from 3 to 38 days of age) and ochratoxin A (0.5 ppm from 3 to 38 days of age) along with inclusion body hepatitis virus (IBHV) inoculation (at 10 days of age) singly and in combination was studied in broiler chicks. Birds in combined treatment groups, i.e. aflatoxin fed and virus inoculated and ochratoxin fed and virus inoculated, showed more changes in activities of phosphatases (AKPase, ATPase, G-6-Pase and ACPase) in liver and kidney tissues than their respective individual treatment groups with a few exceptions. Reduction in the activities of oxido-reductases in liver and kidney tissues were almost comparable in different treatment groups. The increase in muco-polysaccharides reaction was more marked in both the combined treatment groups than the single treatment groups. Intensity of lipid reaction was more in ochratoxin virus combination group than either alone.
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PMID:Histochemical/histoenzymic studies in broiler chicks fed aflatoxin, ochratoxin and inoculated with inclusion body hepatitis virus singly and in concurrence. 802 44

In 10 Wistar male rats, partial hepatectomy was performed and followed by intraperitoneal injection of DEN (30 mg/kg) once and giving drinking water containing 80 ppm sodium fluoride (36 ppm F) for 14 weeks. By stereologic method of enzyme histochemistry, it was observed for the first time that the foci of hepatocytic precancerous enzyme alterations (gamma-GT positive, ATPase negative and G-6-Pase negative) were significantly increased in number and size compared with the negative control group. The results suggest that sodium fluoride promoted the growth of precancerous lesions of the liver induced by DEN in rats, and this has provided some data to the understanding of the relationship between fluorosis and neoplasms.
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PMID:[Promotive action of sodium fluoride on precancerous lesions of hepatocellular carcinoma induced by diethylnitrosamine (DEN) in rats--stereologic study of enzyme histochemistry]. 816 99

The experimental rats were randomly divided into three groups: i.e. control group; endotoxic shock group (the model of endotoxic shock was induced by intravenous administration of E. Coli endotoxin, 16 mg/kg); and electroacupuncture (EA) group ("Renzhong" or "Zusanli" acupoint was stimulated for 15 minutes at 1 hr after injection of endotoxin). The experimental rats were decapitated at 75 minutes after injecting endotoxin. Their livers were taken out for cryostat section, and histochemical observation. The results were as follows: 1) The glycogen in the hepatic cells of endotoxic shocked rats were almost completely depleted. The activities of SDH Mg(++)-ATPase and G-6-Pase and 5'-Nase were decreased; especially the activities of 5'-Nase in the biliary canaliculi and sinusoids were apparently reduced. 2) The content of hepatic glycogen in EA group was increased, but some of them was still depleted. The activities of SDH, Mg(++)-ATPase and G-6-Pase were slightly increased as compared with that of the endotoxic shock group. The activity of 5'-Nase was obviously increased after EA. The preliminary results indicated that EA at "Renzhong" or "Zusanli" acupoint of rats with endotoxic shock might play certain role on improving the hepatic metabolism and promoting the membrane transport action.
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PMID:[Histochemical observation of the effect of electroacupuncture on the livers of rats with endotoxic shock]. 875 27

The study was performed on rats divided into 9 groups. Groups 1-3 served as controls. In groups 4 and 5 rat livers were subjected to 90-min ischemia followed by 12- or 24-hour reperfusion. In groups 6 and 7 rats were injected with intraperitoneal chlorfenvinphos (2 mg/kg b.w.) and sacrificed after 12 or 24 hours. In groups 8 and 9 rat livers were subjected to 90-min ischemia, 12- or 24-hour reperfusion and then rats were injected with chlorfenvinphos (2 mg/kg b.w.). Liver sections were evaluated morphologically, histochemically (SDH, LDH, G6Pase, glycogen, Mg2+ ATPase and AcP). The microsomal fraction of the liver was evaluated for cytochrome P450 content and NADPH-cytochrome P-450 reductase activity. It has been found that liver ischemia and reperfusion result in extensive necrosis, enzymatic disturbances, particularly in acinar zone 3. Ischemia as well as reperfusion decrease the cytochrome P450 content of hepatocytic microsomes and the activity of NADPH-cytochrome P-450 reductase. Intraperitoneal injection of chlorfenvinphos during ischemia and reperfusion dramatically intensifies damage to the liver, although chlorfenvinphos alone produces only mild nonspecific effects on the morphological and enzymatic structure of the liver.
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PMID:Effect of chlorfenvinphos on rat liver subjected to ischemia and reperfusion. 947 88

Our study investigated the effects of Corylus avellana extract on acetaminophen and carbon tetrachloride intoxicated liver of young rats. Hepatocytolysis was determined by measuring the level of serum transaminases (GPT and GOT), steatosis by Sudan black staining, histological structures by hamatoxylineosin staining and the activity of enzymes such as SDH, GtDH, G-6-Pase and ATPase. Comparatively, the most serious lesions appeared in CCl4 intoxication. Corylus avellana extract had some beneficial effects in CCl4 toxicosis: it reduced hepatocytolysis as well as histological lesions and returned the activity of some enzymes to normal values.
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PMID:Effects of Corylus avellana in acetaminophen and CCl4 induced toxicosis. 1019 Jan 84

Determining both the mechanism by which 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) acts as a tumor promoter and the shape of the dose-response curve at low doses remains an important goal of risk-assessment-directed research. In this report, we extend previous mechanistic and descriptive work done on the effect of TCDD on promotion in the two-stage model of hepatocarcinogenesis, to include lower, more clinically relevant doses. After initiation [PH + 10 mg diethylnitrosamine (DEN)/kg], groups of female Sprague-Dawley rats were administered TCDD in one of four doses: 0.01, 0.1, 1.0, or 10 ng/kg/day for 1, 3, or 6 months. Early increases in liver weight (19-69%) due to hepatocyte hypertrophy were resolved after 3- or 6-months exposures to TCDD, and were not associated with the effects of TCDD on promotion. Non-focal cell proliferation in DEN-treated groups was significantly reduced after 1 or 3 months of exposure to 0.1 ng/kg/day TCDD, leading to U-shaped dose-response curves. TCDD effects on non-focal cell proliferation were not associated with effects on promotion. GSTP-positive AHF represented approximately 97% of the total AHF. Significant increases in both the volume fraction and the number of altered hepatic foci (AHF) were observed at the highest dose (10 ng/kg/day) for GSTP-positive AHF in DEN-treated groups. Increases in the number of G6Pase- and ATPase-deficient AHF/cm3 were observed at TCDD doses as low as 0.01 ng/kg/day. This is the lowest tumor-promoting dose of TCDD reported to date. This study represents an unusually complete data set for further dose-response analysis and simulation or mathematical modeling of TCDD-mediated promotion in the rat liver.
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PMID:Quantitative analysis of dose- and time-dependent promotion of four phenotypes of altered hepatic foci by 2,3,7,8-tetrachlorodibenzo-p-dioxin in female Sprague-Dawley rats. 1054 23


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