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)

To clarify the effect of chronic cadmium exposure on muscles, 29-day-old female ICR strain mice were separated into 7 groups and various diets were given to each group. Group I a commercial diet (Intact), Group II a diet low in calcium and low in vitamin D, Group III a diet low in Ca, low in D and low in vitamin E, Group IV a low in Ca, low in D and 20ppm cadmium-added diet, Group V a low in Ca, low in D and 40ppm Cd diet, Group VI a low in Ca, low in D, low in E and 20ppm Cd diet and Group VII a low in Ca, low in D, low in E and 40ppm Cd diet. The levels of vitamin D and vitamin E were designed to be low in each diet but their amounts fulfilled the minimum nutritional requirements. The experimental period was long, ranging from 29 days to 24 months. Using a microscope, two skeletal muscles, the soleus (red muscle) and the gastrocnemius (white muscle) of mice with chronic Cd effects were observed after staining with H. E. and analyzed after enzyme histochemical reaction to ATPase. Using ATPase stain, type I muscle fibers were distinguished from type II muscle fibers. The long-term effects of cadmium. 1) Comparisons among groups II, IV and V. After 18 months it was found in group IV that myopathic muscle damage (increased random variation of fiber size [Size] and widening of interstitial tissue [Widening]) were more prominent that in group II. In group V myopathic muscle damage (Size and Widening) and type II atrophy were more prominent that in group IV. At 24 months it was found in group IV that myopathic muscle damage (Size, internal nuclei [IN] and Widening) and type I and type II atrophy were more prominent than in group II. In group V myopathic muscle damage (Size, IN and Widening) and type I and type II atrophy were more prominent than in group IV. 2) Comparisons among group III, VI and VII.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[The effects of long-term intake of restricted calcium, vitamin D, vitamin E and cadmium-added diets on the skeletal muscles of mice: an enzyme histochemical study]. 747 99

Non-therapeutic toxic dose (250 mg/kg) of acetaminophen (paracetamol), in vivo to albino rats significantly decreased red cell reduced glutathione (GSH) content and activity of (Na+, K+)-ATPase enzyme, whereas osmotic fragility (O.F.) was increased. However, no change was observed in the activity of glutathione reductase (GR) after acetaminophen treatment, while acetaminophen plus vitamin E treated rats showed significant increase in GR activity. Supplementation of vitamin E to the drug treated rats effectively brought the GSH content, (Na+, K+)-ATPase activity and O.F. back to almost normal. The results suggest that acetaminophen toxic dose treatment induces metabolic and membranal alterations making red cells prone to hemolysis, while vitamin E which is an antioxidant shows its ameliorating role to these changes.
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PMID:In vivo effects of acetaminophen on rat RBC and role of vitamin E. 755 83

The effects of non-esterified arachidonic acid (AA) on erythrocyte membrane ion permeability have been studied using 86Rb flux measurements. [14C]AA was used to quantify membrane incorporation of AA and to show AA removal by albumin washing. The actions of vitamin E and other antioxidants on the effects of AA were examined. Reversible membrane incorporation of 700-2000 nmol AA per ml cells was achieved without significant haemolysis or morphological change. AA incorporation caused a reversible mean increase in bumetanide-sensitive Rb influx of 34% (S.E.M. 4.5, n = 23). This action could be partially prevented by co-incubation with vitamin E, but not by Trolox or dithioerythritol. AA incorporation caused an irreversible mean increase in residual Rb permeability (bumetanide and ouabain insensitive) of 130% (S.E.M. 22, n = 20), associated with a rise in intracellular Na and a fall in intracellular K concentrations. This action was also partially prevented by co-incubation with vitamin E. The effects of AA incorporation on Na,K-ATPase function were difficult to quantify because of the concomitant rises in intracellular Na but the data are consistent with approximately 20% inhibition of activity. Modulation of membrane ion permeability by AA appears to be partially mediated by lipid peroxidation and may have pathophysiological significance.
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PMID:Actions of arachidonic acid on erythrocyte membrane Rb permeability. 758 78

It is established that acetaminophen exhibits oxidative behaviour. The effects of acetaminophen (0.3-14.5 microM) on methemoglobin levels, superoxide dismutase and Na(+)-K+ ATPase activities of normal and vitamin E or vitamin C pretreated erythrocytes were investigated. In acetaminophen incubated erythrocytes, methemoglobin concentration and superoxide dismutase activity were increased in a dose and incubation-time dependent manner, the activity of Na(+)-K+ ATPase was decreased by acetaminophen treatment. Vitamin E (1mg/dl of erythrocyte suspension) or vitamin C (1mg/dl of erythrocyte suspension) provided partial protection of hemoglobin, superoxide dismutase and Na(+)-K+ ATPase against acetaminophen action. Vitamin E was more effective than vitamin C.
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PMID:Effects of acetaminophen on methemoglobin, superoxide dismutase and Na(+)-K+ ATPase activities of human erythrocytes. 762 22

Cadmium chloride (CdCl2)-induced biochemical changes were characterized in male, CD-1 mouse testes. CdCl2 inhibited the testes microsomal Na+,K(+)-ATPase activity in vitro and in vivo. The inhibitory range was 30-50 microns and the concentration for half maximal inhibition (IC50 value) was 90 microns over 5 min preincubation. CdCl2 (2mg/kg/day, s.c.) for 2 days significantly inhibited testes Na+,K(+)-ATPase (near 90% inhibition). The content of testicular GSH and the ratio of reduced glutathione (GSH)/GSSG (oxidized glutathione) decreased in CdCl2-treated groups. Using salicylate as a trapping agent and high pressure liquid chromatography with electrochemical detection (LCED), we measured the OH production in vivo. 2,5-dihydroxybenzoic acid (2,5-DHBA) and 2,3-dihydroxybenzoic acid (2,3-DHBA) as indices of hydroxyl free radical formation significantly increased after 5 days CdCl2 exposure. Pretreatment with vitamin E (20 mg/kg, s.i.d., i.m., 7d) protected CdCl2-induced increase in OH. generation in testes. From this study, it was demonstrated that CdCl2 induced testicular toxicity could possibly be mediated by a significant increase in hydroxyl free radical formation and a reduction in GSH content and Na+,K(+)-ATPase activity. Vitamin E seems to prevent the CdCl2 induced increase in hydroxyl free radical generation.
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PMID:Na+, K(+)-ATPase, glutathione, and hydroxyl free radicals in cadmium chloride-induced testicular toxicity in mice. 766 26

The amyloid beta-peptide (A beta) that accumulates as insoluble plaques in the brain in Alzheimer's disease can be directly neurotoxic and can increase neuronal vulnerability to excitotoxic insults. The mechanism of A beta toxicity is unclear but is believed to involve generation of reactive oxygen species (ROS) and loss of calcium homeostasis. We now report that exposure of cultured rat hippocampal neurons to A beta 1-40 or A beta 25-35 causes a selective reduction in Na+/K(+)-ATPase activity which precedes loss of calcium homeostasis and cell degeneration. Na+/K(+)-ATPase activity was reduced within 30 min of exposure to A beta 25-35 and declined to less than 40% of basal level by 3 hr. A beta did not impair other Mg(2+)-dependent ATPase activities or Na+/Ca2+ exchange. Experiments with ouabain, a specific inhibitor of the Na+/K(+)-ATPase, demonstrated that impairment of this enzyme was sufficient to induce an elevation of [Ca2+]i and neuronal injury. Impairment of Na+/K(+)-ATPase activity appeared to be causally involved in the elevation of [Ca2+]i and neurotoxicity since suppression of Na+ influx significantly reduced A beta- and ouabain-induced [Ca2+]i elevation and neuronal death. Neuronal degeneration induced by ouabain appeared to be of an apoptotic form as indicated by nuclear condensation and DNA fragmentation. The antioxidant free radical scavengers vitamin E and propylgallate significantly attenuated A beta-induced impairment of Na+/K(+)-ATPase activity, elevation of [Ca2+]i and neurotoxicity, suggesting a role for ROS. Finally, exposure of synaptosomes from postmortem human hippocampus to A beta resulted in a significant and specific reduction in Na+/K(+)-ATPase and Ca(2+)-ATPase activities, without affecting other Mg(2+)-dependent ATPase activities or Na+/Ca2+ exchange. These data suggest that impairment of ion-motive ATPases may play a role in the pathogenesis of neuronal injury in Alzheimer's disease.
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PMID:Amyloid beta-peptide impairs ion-motive ATPase activities: evidence for a role in loss of neuronal Ca2+ homeostasis and cell death. 766 6

Among aging disabilities, the one associated with the progressive decline of vision is functionally most disadvantageous. Cataracts are one of the more common causes of such visual disability. Several predisposing factors have been identified in the genesis of this disease. While it is perhaps a multifactorial process, significant developments have taken place in recent years suggesting that oxygen radicals are involved in the development of this aging manifestation. Antioxidant enzymes, such as catalase and superoxide dismutase, have been demonstrated to protect the lens cell membrane from oxidative stress as reflected by the prevention of the Na(+)-K(+)-ATPase-dependent pump deterioration due to oxyradical-dependent oxidation of its proteins and lipids. From the nutritional point of view, antioxidants such as ascorbate and vitamin E also offer significant protection to the lens against damage due to oxidative stress. Evidence regarding the protective effect of these nutrients has been based on lens organ culture studies in the presence of active oxygen, generated photochemically as well as enzymatically. The experiment involving photochemical environs simulate the status of the eye during the photopic vision. In vivo, the effectiveness of ascorbate against cataracts has been tested in rat pups developing cataracts under the oxidative influence of sodium selenite. Certain antioxidants produced metabolically also may be useful in protecting against cataracts. Pyruvate produced in glucose metabolism seems to be an important antioxidant. The efficacy of this compound has been tested within in vitro organ culture as well as in vivo, the latter experiments being done with selenite-treated rats. There is a hope that these and other nutritional and metabolic antioxidants may one day be useful in delaying or even preventing cataract formation in human beings.
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PMID:Prevention of cataracts by nutritional and metabolic antioxidants. 774 71

Adriamycin (AD)-Fe3+ caused the inactivation of Na(+)-, K(+)-ATPase and Ca(2+)-ATPase of erythrocyte membranes during lipid peroxidation. AD-Fe3+ also induced the formation of fluorescent substances from the membranes with lipid peroxidation. The fluorescent substances were little extracted by chloroform-methanol, indicating that they were retained in the membranes. Butylated hydroxytoluene and trolox strongly inhibited both the inactivation of these ATPases and the formation of fluorescent substances with lipid peroxidation. Another antioxidant, vitamin E, slightly prevented the damage of the membranes. However, p-nitrophenyl phosphatase activity and acetylcholine esterase have lower or no susceptibility to the membrane lipid peroxidation. These results indicated that the ATPases were very sensitive to lipid peroxidation and that the membranes were modified during the peroxidation reaction.
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PMID:Adriamycin-Fe(3+)-induced inactivation of enzymes in erythrocyte membranes during lipid peroxidation. 774 51

Ozone (5 mumol.min-1) inhibited the human erythrocyte membrane Na(+)-K+ ATPase (EC.3.6.1.39) activity in a time dependent manner. Inhibition was more pronounced for the first 5 min of ozone exposure in the directly ozone exposed membranes than in the membranes prepared from ozone exposed erythrocytes. However, Na(+)-K+ ATPase activities of both preparations were inhibited to the same extent (about 70%) at the end of 10 min ozone exposure. It was also determined that there was a close relationship between the decrease of enzyme activity and the increase in the thiobarbituric acid reactive substances in both types of preparations. Na(+)-K+ ATPase was inhibited by ozone even at the presence of vitamin E or vitamin C. However, the degree of the inhibitions and the amounts of thiobarbituric acid reactive products formed were smaller than the corresponding values found in the absence of these vitamins.
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PMID:Effects of ozone on the activity of erythrocyte membrane Na(+)-K+ ATPase. 780 27

Twelve dogs were subjected to cardiopulmonary bypass with membrane oxygenator for 120 minutes. The effect of lipid peroxide injury on red blood cells was studied by measurement of plasma and erythrocyte membrane lipid peroxide, deformabioity of erythrocyte, plasma free hemoglobin, superoxide dismutase, Na(+)-K(+)-ATPase and Ca(2+)-Mg(2+)-ATPase of erythrocytes. The effect of vitamin E on red blood cells was also investigated. The findings indicated that vitamin E might protect red blood cells from lipid peroxide injury during extracorporeal circulation. The mechanism of damage effect of lipid peroxide and the protective effect of vitamin E on red blood cells were briefly discussed.
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PMID:[Lipid peroxidation injury to red blood cells during extracorporeal circulation: mechanism and protection]. 786 7


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