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:3.6.1.3 (ATPase)
65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The activities of Ca2(+)- and Na+, K(+)-ATPases were studied in liver plasma membranes from CCl4-cirrhotic rats and from livers of rats treated with silymarin in addition to CCl4. CCl4 chronic treatment produced significant decreases in Na+, K(+)- and Ca2(+)-ATPase activities; however, the animals treated with silymarin along with CCl4 showed no differences in ATPase activities as compared to controls. The lipid analysis performed in plasma membranes revealed increases in the cholesterol/phospholipid (CH/PL) and sphingomyelin/phosphatidylcholine (SM/PC) ratios in the cirrhotic group. Again, the membranes isolated from rats receiving CCl4 + silymarin showed normal CH/PL and SM/PC values. Considering that CH/PL and SM/PC ratios are related to membrane microviscosity, this study suggests that a lower fluidity of the membrane may be responsible for the observed decreases in ATPase activities in the cirrhotic group. Additionally, the role of silymarin to improve liver function in CCl4-cirrhosis can be attributed partially to its action at membrane level by preventing the increases in CH/PL and SM/PC ratios.
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PMID:The role of membrane composition in ATPase activities of cirrhotic rat liver: effect of silymarin. 216 6

Rat hepatocyte plasmatic membrane damages caused by the administration of tetrachloromethane of heliotrine was investigated. Phospholipid content in plasmatic membranes decreased. Heliotrine caused complete and CCL4 twofold inhibition of Na, K-ATPase. Intraperitoneal administration of egg yolk phosphatidylcholine liposomes had a reparative effect on the damaged membranes consisting in the restoration of phospholipid content and enzyme activities.
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PMID:[Reparation of the hepatocyte plasma membrane using phosphatidylcholine liposomes]. 217 98

To investigate whether the impairment of mitochondrial function in cirrhosis is due to a reduction in liver cell mass or whether mitochondrial function is altered specifically, we analyzed mitochondrial volume and surface density of mitochondrial membranes in control and cirrhotic rats by stereological means. Cirrhosis was induced by long-term exposure to phenobarbital and CCl4. Hepatocellular and mitochondrial volumes were reduced to a similar extent, by 39% and 40%, respectively, in cirrhotic animals (p less than 0.01). Thus the fraction of hepatocytes occupied by mitochondria did not differ between the two groups. Both total outer (31 +/- 3 vs. 19 +/- 6 m2; p less than 0.01) and inner (87 +/- 24 vs. 45 +/- 12 m2; p less than 0.01) mitochondrial membranes were significantly reduced. Membrane surface was normal per unit of mitochondrial volume, however, suggesting intact mitochondrial structure. Matrix and outer membrane enzyme activities expressed per compartment did not differ between control and cirrhotic animals. Inner membrane, in contrast, had an increased enzyme content per unit area both for cytochrome oxidase (10.3 +/- 2.9 vs. 13.0 +/- 1.6; p less than 0.05) and ATPase (13.7 +/- 1.4 vs. 21.2 +/- 2.9; p less than 0.01). Basal oxygen consumption measured in the perfused liver in situ was significantly reduced in cirrhotic livers (1.6 +/- 0.1 vs. 1.1 +/- 0.4 mumol/min-1/gm-1) but was unchanged when expressed per square meter of inner membrane. Our results demonstrate that impaired mitochondrial function is mainly due to loss of hepatocellular mass. Increased enzyme activity per unit surface area of inner mitochondrial membrane may be important to maintain mitochondrial function of the cirrhotic liver.
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PMID:Mitochondrial structure and function in CCl4-induced cirrhosis in the rat. 220 57

Recently, we have shown that taurocholate transport is impaired in hepatocytes isolated from CCl4 cirrhotic rats. Na+,K+-ATPase activity depends on the lipid composition of the surrounding membrane. Therefore, we performed this study in order to detect differences in plasma membrane composition and membrane functions between livers of CCl4 cirrhotic (n = 17) and of control rats (n = 15). After biochemical characterization of the animals we isolated basolateral and canalicular membrane vesicles and determined membrane enzyme activities, transport functions and lipid composition. We found no differences in the isolation characteristics of the plasma membranes between the two groups. The lipid composition of the membrane fractions was not altered, except for a lower cholesterol content in the canalicular membranes of the cirrhotic group (200 +/- 15 vs. 246 +/- 18 micrograms/mg protein, P less than 0.05). Taurocholate transport into basolateral membrane vesicles and marker enzyme activities of the membrane fractions were also equal in control and cirrhotic animals. We conclude that the plasma membrane composition and membrane enzyme/transport activities have returned to normal in CCl4 cirrhotic rats 14 days after cessation of exposure to CCl4. Thus, a disturbed transport system is not the cause for the observed decreased taurocholate transport into hepatocytes from cirrhotic rats. Even a cirrhotic liver has a high potential for recovery after acute CCl4 intoxication.
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PMID:Taurocholate transport by liver plasma membrane vesicles is not altered in cirrhotic rats. 254 20

The incubation of isolated rat hepatocytes with 0.172 mM carbon tetrachloride caused a rapid decrease in the calcium content of both mitochondrial and extramitochondrial compartments. However, the release of Ca2+ from the intracellular stores was not associated with an increase in the cytosolic Ca2+ levels as measured by activation of phosphorylase alpha or by Quin-2 fluorescence. A rapid rise in hepatocyte free calcium was only observed with concentrations of CCl4 higher than 0.172 mM. The lack of activation of phosphorylase alpha was not due to the inhibition of the enzyme by CCl4, since in CCl4-treated hepatocytes the phosphorylase activity could be stimulated by glucagon, butyryl--cAMP or by the increase of cell calcium induced by the addition of A23187. Ca2+-dependent ATPase of plasma membranes was only slightly affected in the early phases of poisoning with CCl4 when both mitochondrial and extramitochondrial calcium pools were already lowered. This led to the conclusion that calcium released from intracellular organelles could be extruded from the cells in sufficient amounts to prevent the increase of the cytosolic levels. A rise in hepatocyte free calcium was observed during the second hour of incubation with CCl4, concomitantly with the appearance of both LDH leakage and plasma membrane blebbing. The addition of EGTA to the medium prevented both the increase in cytosolic Ca2+ and the blebbing suggesting that they were a consequence of an influx of calcium into the cells. However, neither EGTA nor the addition of inhibitors of calcium-dependent phospholipase A2 or non-lysosomal proteases were able to protect against cell death. These latter results suggested that the alterations of calcium distribution induced by CCl4 in isolated hepatocytes were not a primary cause of the toxic effects, although they did not exclude that a sustained rise in cytosolic Ca2+ could contribute in the progression of cell injury.
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PMID:Effects of carbon tetrachloride on calcium homeostasis. A critical reconsideration. 276 92

The activities of Na+,K+-, and Ca2+-ATPases were determined in plasma membranes obtained from livers of rats treated acutely and chronically with CCl4. Twenty-four hours after a single oral dose of CCl4 the ATPases decreased below 50% of control values. The activity of Ca2+-ATPase returned to normal after 4 days, and Na+,K+-ATPase activity returned to normal values after 12 days. One week after initiation of the chronic intraperitoneal treatment with CCl4, the Na,K+-ATPase decreased to 40% of control values and continued to decrease further until reaching values below 1%. Ca2+-ATPase followed a pattern similar to that obtained with Na+,K+-ATPase, except that the decrease was not as severe. Colchicine treatment prevented the modifications in ATPases when given simultaneously with CCl4 and reverted the alterations in ATPase activities of the CCl4-cirrhotic animals. Because ATPases are known to be modulated by the lipid composition of the membrane, we also determined the cholesterol to phospholipid ratio in all the isolated membranes. The ratios were increased in membranes with low ATPase activity due to an increase in the total concentration of cholesterol. Plasma membranes of cirrhotic rats treated with colchicine showed a low concentration of cholesterol, a decreased cholesterol to phospholipid ratio, and Na+,K+-ATPase activity was almost normal. When plasma membranes of cirrhotic rats were fused with phosphatidyl serine-containing liposomes, the cholesterol to phospholipid ratio decreased and the ATPase activity increased. The ATPase activity of normal plasma membranes decreased below 20% of control values when enriched with cholesterol. Our results suggest that the decrease in the plasma membrane Na+,K+-ATPase activity of the cirrhotic rat is due in part to an increase in its cholesterol concentration and in the cholesterol to phospholipid ratio.
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PMID:Cryptic adenosine triphosphatase activities in plasma membranes of CCl4-cirrhotic rats. Its modulation by changes in cholesterol/phospholipid ratios. 299 43

Altered transport of nuclear RNA sequences is an early response to carcinogens. Nuclear envelopes (NE) were isolated and assayed for nucleoside triphosphatase activity (NTPase), on the premise that this enzymatic activity participates in RNA transport. A common feature of the action of five different carcinogens (thioacetamide, 2-acetylaminofluorene, 3'-methyl-4-dimethylaminoazobenzene, dimethylnitrosamine, and aflatoxin B1), at low doses without significant toxicity, was to increase NE NTPase activity and to increase RNA transport, as assessed by the appearance of rapidly labeled RNA in the cytoplasm and by in vitro assay. The increases in NTPase were specific for the NE fraction, and early toxic effects of higher doses initially masked the increases. The induced increases in NE NTPase were long-lived. In contrast, increases in NE NTPase were observed only during the regenerative phase of CCl4 intoxication; the CCl4-induced increase was short-lived and returned promptly to control levels. These changes in NTPase activity were not associated with parallel changes in phosphorylation/dephosphorylation of NE proteins. Increases in NE NTPase and alterations in RNA transport, without attendant nuclear replication, may relate to altered nuclear RNA restriction. This change in a regulatory phenomenon may make these cells more susceptible to further modification, potentially playing a role in the initiation phase of carcinogenesis.
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PMID:Increased nucleoside triphosphatase activity of rat liver nuclear envelope is associated with hepatocarcinogen exposure. 620 70

Our study shows evidences that CCl4 administration (at the dose of 2,5 ml/kg b.w. "per os") increased ATPase activities in rat liver plasmamembranes 1 and 2 hours after treatment. Conversely we found that CCl4 poisoning decreased ATPase activities in microsomal membranes of rat liver at the same tested times. Therefore we suggest that ATPase activities were differently influenced by CCl4 treatment with respect to different subcellular distribution of those enzymes.
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PMID:[Changes in adenosinetriphosphatase activity in rat liver after CC14 poisoning]. 621 84

The ATPase activity (proton ATPase) of rat liver mitochondria was studied 2, 24, 28, 96 and 168 h after acute tetrachloromethane poisoning. It is established that the tetrachloromethane poisoning. It is established that the tetrachloromethane poisoning is accompanied by a considerable activation of mitochondrial H+-ATPase and a decrease of the DNP and Ca+, Na+ and K+ activating influence on it. Maximum changes in the H+-ATPase activity is observed 24 h after poisoning. Changes in the H+-ATPase properties are accompanied by a fall in the alpha-ketoglutarate dehydrogenase and succinate dehydrogenase activities and by disturbance of the liver mitochondria contractile properties. The electrochemical membrane potential of the mitochondria under the effect of tetrachloromethane is supposed to be reduced due to a primary damage of the phospholipid matrix of the coupling membrane and an increase in its proton conductivity.
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PMID:[ATPase activity of rat liver mitochondria in acute tetrachloromethane poisoning]. 646 Mar 65

Earlier work has shown increased hepatocellular free Ca2+ levels in rats receiving a single subtoxic dose of CCl4 after dietary pretreatment with nontoxic (10 ppm, 15 days) levels of chlordecone (CD), indicating a significant perturbation of Ca2+ homeostasis in the interactive toxicity of CD + CCl4 combination treatment. In the present study, the mitochondrial and microsomal ability to sequester Ca2+ as well as plasma membrane translocase activity was investigated, since it is known that cells maintain normal Ca2+ homeostasis by these mechanisms. Hepatic plasma membrane Ca(2+)-ATPase (high and low affinity components) as well as 45Ca uptake by mitochondria and microsomes was measured using a range of calcium concentrations in Ca(2+)-EGTA-buffered medium at different time points after a single ip administration of CCl4 (100 microliters/kg). Male Sprague-Dawley rats were maintained for 15 days either on a normal diet or on a diet containing 10 ppm CD prior to CCl4 injection. Hepatic plasma membranes, devoid of microsomal and mitochondrial contamination, were prepared using polyethyleneimine-coated beads. CD treatment alone did not significantly decrease the plasma membrane Ca(2+)-ATPase activity. Similarly, CCl4 treatment alone did not alter Ca(2+)-ATPase in hepatic plasma membranes at any concentration of free Ca2+ in assay medium employed in this study. The interactive combination treatment, however, resulted in significant, irreversible, and specific inhibition of the high affinity component of the hepatic plasma membrane Ca(2+)-ATPase at early time points. Low affinity Ca(2+)-ATPase was not affected with any treatment protocol. CD pretreatment alone significantly inhibited 45Ca uptake by mitochondria and microsomes when incubated at 10 microM and higher, concentrations much higher than normal cytosolic levels, but not at lower concentrations of Ca2+. CCl4 administration to both normal and CD-pretreated rats resulted in significant inhibition of microsomal and mitochondrial 45Ca uptake as early as 1 hr at all concentrations of free calcium. While the extent of inhibition was greater and irreversible after CD + CCl4 treatment, it was reversible after normal diet + CCl4 treatment. Phosphorylation of proteins was determined in order to investigate if the inhibition of microsomal 45Ca uptake during CD + CCl4 toxicity might be correlated to decreased phosphorylation of any particular protein involved in Ca2+ transport. SDS-polyacrylamide gel electrophoresis of microsomal protein revealed at least 30 Coomassie blue stainable bands. Of these, 6 bands were phosphorylated when microsomes were incubated with [32P]ATP.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Loss of calcium homeostasis leads to progressive phase of chlordecone-potentiated carbon tetrachloride hepatotoxicity. 769 Sep 97


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