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

Methylxanthines (MX) inhibit cell division in sea urchin and clam eggs. This inhibitory effect is not mediated via cAMP. MX also inhibit respiration in marine eggs, at concentrations which inhibit cleavage. Studies showed that no changes occurred in ATP and ADP levels in the presence of inhibitory concentrations of MX, indicating an extra-mitochondrial site of action for the drug. Subsequent studies revealed decreased levels of NADP+ and NADPH, when eggs were incubated with inhibitory concentrations of MX, but no change in levels of NAD+ and NADH. MX did not affect the pentose phosphate shunt pathway and did not have any effect on the enzyme NAD+ -kinase. Further studies showed a marked inhibitory effect on the glutathione reductase activity of MX-treated eggs. Reduced glutathione (GSH) could reverse the cleavage inhibitory effect of MX. Moreover, diamide, a thiol-oxidizing agent specific for GSH in living cells, caused inhibition of cell division in sea urchin eggs. Diamide added to eggs containing mitotic apparatus (MA) could prevent cleavage by causing a dissolution of the formed MA. Both MX and diamide inhibit a Ca2+-activated ATPase in whole eggs. The enzyme can be reactivated by sulfhydryl reducing agents added in the assay mixture. In addition, diamide causes an inhibition of microtubule polymerization, reversible with dithioerythritol. All experimental evidence so far suggests that inhibition of mitosis in sea urchin eggs by MX is mediated by perturbations of the in vivo thiol-disulfide status of target systems, with a primary effect on glutathione levels.
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PMID:Effects of caffeine and other methylxanthines on the development and metabolism of sea urchin eggs. Involvement of NADP and glutathione. 1 15

The activity of the intraerythrocytary enzymes glucose-6-phosphate dehydrogenase, pyruvate kinase, glutathione reductase and ATPase was measured before and after splenectomy in 13 patients with congenital hemolytic anemia and 3 patients suffering from chronic thrombocytopenia. All patients were treated successfully, as reflected by clinical and basal hematological parameters. Glucose-6-phosphate dehydrogenase and pyruvate kinase were significantly depressed after splenectomy. It was not possible to set up prognostic criteria of splenectomy from the intraerythrocytary enzymes.
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PMID:Intra-erythrocytary enzymes before and after splenectomy. 12 29

A disruption of calcium homeostasis, leading to a sustained increase in cytosolic calcium levels, has been associated with cytotoxicity in response to a variety of agents in different cell types. We have observed that administration of a single high dose or multiple lower doses of the carcinogenic nephrotoxin ochratoxin A (OTA) to rats resulted in an increase of the renal cortex endoplasmic reticulum ATP-dependent calcium pump activity. The increase was very rapid, being evident within 10 min of OTA administration and remained elevated for at least 6 hr thereafter. The increase in calcium pump activity was inconsistent with previous observations that OTA enhances lipid peroxidation (ethane exhalation) in vivo, a condition known to inhibit the calcium pump. However, no evidence of enhanced lipid peroxidation was observed in the renal cortex since levels of malondialdehyde and a variety of antioxidant enzymes including catalase, DT-diaphorase, superoxide dismutase, glutathione peroxidase, glutathione reductase and glutathione S-transferase were either unaltered or reduced. In in vitro studies, addition of OTA to cortex microsomes during calcium uptake inhibited the uptake process although the effect was reversible. Preincubation of microsomes with NADPH had a profound inhibitory effect on calcium uptake but inclusion of OTA was able to reverse the inhibition. Changes in the rates of microsomal calcium uptake correlated with changes in the steady-state levels of the phosphorylated Mg2+/Ca(2+)-ATPase intermediate, suggesting that in vivo/in vitro conditions were affecting the rate of enzyme phosphorylation.
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PMID:Alterations in ATP-dependent calcium uptake by rat renal cortex microsomes following ochratoxin A administration in vivo or addition in vitro. 141 61

Glutathione (GSH) and GSH-related enzymes, glutathione reductase (GR), gamma-glutamyl cysteine synthetase (gamma-GCS), gamma-glutamyl transpeptidase (gamma-GTP), glutathione S-transferase (GST) and adenosine triphosphatase (ATPase) enzymes were analysed to study the effect of busulfan on the defence mechanisms of the lens. All these enzymes were found to increase significantly except GSH which showed only 7.9% increase as compared to controls in precataractous stage. These results affirm that busulfan is capable of evoking a response from the enzymes involved in the various pathways of GSH enabling the lens to prolong its clarity. The cataractous lenses showed significant decrease in all these parameters. Here, the impairment of the defense mechanism (GST, GR) and the total ATPase may be attributed to the cumulative action of the drug which can react with -SH groups of these enzymes, ultimately causing opacification.
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PMID:Glutathione and glutathione-related enzymes in busulfan treated rat lens. 191 43

The effect of oral administration of endosulfan (12.5 mg/kg body weight), daily for 4 days was investigated on erythrocytes of female rats of 4 different age groups i.e. 15, 30, 70 and 365 days old. Erythrocyte membrane Na+, K(+)-ATPase and Mg2(+)-ATPase activities were significantly inhibited in all the age groups of rats. However, percent inhibition was maximum in the youngest animals. A significant decrease in the activity of erythrocyte glutathione reductase was observed in 30 and 70 days old rats whereas a significant increase in the activity of glucose-6-phosphate dehydrogenase (G-6-PD) was observed in these groups. The increase in G-6-PD activity may be a physiological response to compensate for decrease in the reduced glutathione level which results from decrease in the activity of glutathione reductase.
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PMID:Age related toxic effects of endosulfan on certain enzymes of rat erythrocytes. 227 57

Bacterial plasmids have genes that confer highly specific resistances to As, Bi, Cd, Cu, Cr, Hg, Pb, Te, Zn, and other toxic heavy metals. For each toxic cation or anion, generally a different resistance system exists, and these systems may be "linked" together on multiple resistance plasmids. For Cd2+, AsO2-, AsO4(3)-, Hg2+, and organomercurials, DNA sequence analysis has supplemented direct physiological and biochemical experiments to produce sophisticated understanding. The cadA ATPase of S. aureus plasmids is a 727 amino acid membrane ATPase that pumps Cd2+ from the cells as rapidly as it is accumulated. This polypeptide is related by sequence to other cation translocating ATPases, including the membrane K+ ATPases of Escherichia coli and Streptococcus faecalis, the H+ ATPases of yeast and Neurospora, the Na+/K+ ATPases of vertebrate animals, and the Ca2+ ATPases of rabbit muscle. The conserved residues include the aspartyl residue that is phosphorylated, the lysine involved in ATP binding, and the proline within a membrane translocating region. The arsenate and arsenite translocating ATPase consists of 3 polypeptides (from DNA sequence analysis), including a recognizable ATP binding protein (arsA), an integral membrane protein (arsB gene), and a substrate specificity subunit (arsC gene). Inorganic mercury and organomercurial degradation is carried out by a series of about 6 polypeptides, including 2 soluble intracellular enzymes (organomercurial lyase and mercuric reductase). The latter is related by sequence and function to glutathione reductase and lipoamide dehydrogenase of prokaryotes and eukaryotes. These enzymes are dimeric, FAD-containing, NAD(P)H-dependent oxidoreductases. Other recognizable polypeptides in the mer system include a DNA-binding regulatory protein from the merR gene and a Hg2+ transport system consisting of a periplasmic Hg2(+)-binding protein (merP gene) and a membrane protein (merT gene) in gram negative systems.
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PMID:DNA sequence analysis of bacterial toxic heavy metal resistances. 248 81

Previous studies from this laboratory have shown that the normal lens can tolerate exposure to 0.05 mM H2O2 without apparent damage and that this is due in part to an active glutathione redox cycle. The present studies were designed to investigate the role of glutathione reductase in protecting cation transport systems in the lens against potentially damaging effects of peroxide. Pre-treatment of rabbit lenses with 0.5 mM 1.3-bis(2-chloroethyl)-1-nitrosourea (BCNU), a relatively specific inhibitor of glutathione reductase, brought about a 71% inhibition of the enzyme in the capsule-epithelia of the lenses. Subsequent exposure of the lenses for 3 hr to a constant level of 0.05 mM H2O2 in culture medium produced significant accumulation of oxidized glutathione (GSSG) in the lens epithelium and severe effects on the electrolyte balance in the lens, on the activity of Na, K-ATPase and on the accumulation and efflux of 86Rb. The effects included a 35% decrease in activity of Na, K-ATPase, a 10 mM increase in the concentration of Na+ and an 8 mM decrease in K+. BCNU-H2O2 treatment also resulted in loss of transparency of the lenses in the form of vacuoles present in the anterior, subcapsular region, encircling the entire periphery of the organ near the germinative zone of the epithelium. Treatment with either BCNU or 0.05 mM H2O2 alone had only minimal effects on accumulation of GSSG in the epithelium, on lens transparency and on the parameters of cation transport which were investigated. When lenses were treated with 0.05 mM H2O2 alone and then placed in normal medium to measure the accumulation of 86Rb it was found that the cation pump was stimulated 20% above the normal level of activity. Levels of H2O2 higher than 0.05 mM without BCNU pre-treatment produced significant inhibition of Na, K-ATPase and the effects of 0.3 mM H2O2 on cation transport and GSSG accumulation were comparable to those of BCNU-0.05 mM H2O2. While inhibition of the activities of glutathione reductase and Na, K-ATPase in the lenses was found to be irreversible, a partial recovery of the Na+ level and nearly complete recovery of the K+ level were observed when treated lenses were cultured in normal medium for an additional 6 hr. In addition, the rate of efflux of 86Rb which was significantly faster from the BCNU-H2O2-treated lenses compared with the controls, was found to return to the control value during the recovery period.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Peroxide-induced effects on lens cation transport following inhibition of glutathione reductase activity in vitro. 282 Jul 73

Some indices of erythrocyte metabolism (EM): activity of lactate dehydrogenase (LDH), glucose-6-phosphate dehydrogenase (G-6-PD), glutathione reductase (GR) and common adenosinetriphosphatase (ATPase) activity were studied in 102 patients with acute viral hepatitis (AVH). The suppression of erythrocyte enzymatic activity (EE) was revealed. It was most noticeable at the peak of average and severe AVH. In a decrease of jaundice and during reconvalescence G-6-PD, GR and ATPase activity reduced up to the control level. The suppression of LDH activity was more noticeable, maintained at discharge and was of prognostic value in investigation at early periods of disease in cases of prolonged reconvalescence. Changes in EE activity showed correlation with indices of liver function (levels of certain bilirubin fractions and transaminase activity). In cases of developing deficiency of erythrocyte G-6-PD activity there was a high correlation between a degree of cytolysis and the suppression of erythrocyte LDH activity. The importance of erythrocyte metabolic derangements revealed in AVH pathogenesis was discussed.
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PMID:[Lactate dehydrogenase, glucosephosphate dehydrogenase, glutathione reductase and adenosine triphosphatase activities in the erythrocytes of patients with acute viral hepatitis]. 295 83

Erythrocyte membrane (EM) abnormalities in a 16-yr-old boy with hypoalphalipoproteinemia resembling fish eye disease (FED-LS) were investigated. The proband's erythrocytes had markedly decreased osmotic fragility with target cells observed in the peripheral film. Analysis of his EM lipids revealed normal cholesterol and phospholipid content but a marked increase in phosphatidylcholine with concomitant decreases in phosphatidylethanolamine and sphingomyelin. Of the EM enzymes examined, acetylcholinesterase and superoxide dismutase activities were decreased while those of Na+-K+ ATPase, catalase and glutathione reductase were normal. 51Cr erythrocyte survival in the patient was slightly decreased. The observed changes in a number of structural and functional properties of erythrocytes in this disorder are indistinguishable from those previously described in homozygotes for familial lecithin:cholesterol acyltransferase (LCAT) deficiency. Thus, it is possible that in both of these disorders an abnormality of plasma LCAT activity causes, either directly or indirectly, functional and structural changes in the erythrocyte membrane.
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PMID:Erythrocyte abnormalities in a hypoalphalipoproteinemia syndrome resembling fish eye disease. 341 11

We have studied the effects of adriamycin (doxorubicin HCl) on human red blood cells. The peroxidizing effect of adriamycin on the thiols of red cell constituents resulted in decreased glutathione stability, and oxidation of hemoglobin and membrane protein components 1, 2, and 3, forming large molecular weight complexes. Membrane lipids were also peroxidized. Adriamycin itself did not inhibit the enzymes of the reductions system (glucose-6-phosphate dehydrogenase, 6-phosphogluconic dehydrogenase, glutathione reductase, glutathione peroxidase, catalase, superoxide dismutase) of the red cells. Because adriamycin has the potential of inhibiting ATPase, including both Na-K-dependent ATPase and ouabain insensitive ATPase, at concentrations not inhibitory to other enzymes, the net sodium content increased, and potassium content decreased after incubation of red cells with adriamycin at high concentrations. The experimental results described with adriamycin may serve as a model for the possible mechanism of cardiotoxicity observed in its clinical use, and also explain the potential hemolyzing effect on red cells. There was greater oxidizing effect on glucose-6-phosphate dehydrogenase (G-6-PD) deficient than on normal erythrocytes. It is suggested that adriamycin be used with caution in individuals with G-6-PD deficient red cells.
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PMID:The effects of adriamycin (doxorubicin HCl) on human red blood cells. 625 23


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