Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.6.3.1 (Mg2+-ATPase)
 1,484 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The article deals with oxidation of different substrates, intensity of glycolytic and glycogenolytic processes in mitochondria and homogenates of dog liver with its 2-hour exclusion from circulation under conditions of endotracheal ether-oxygen narcosis. It was established that already 30-60-minute ischemia causes a decrease in intensity of succinate, alpha-ketoglutarate oxidation and acceptor respiration, inhibiton in the activity of the citrate cycle enzymes; succinate dehydrogenase, alpha-ketoglutarate dehydrogenase, isocytrate dehydrogenase. The activity of NAD-dependent malate dehydrogenasedehydrogenase and Mg2+-ATPase as well as intensity of NADN oxidation in mitochondria increase. After 2-hour ischemia the activity of Mg2+-ATPase, cytochrome oxidase and peroxidase lowers. A sharply developed glycogenolysis is accompanied by inhibition of phosphorylase activity and a two-fold stimulation of the glycolytic reactions. Peculiarities in regulation of enzymatic reactions under conditions of ischemia and their role in origin of metabolism disturbances in the liver are under discussion.
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PMID:[Carbohydrate metabolism in the liver in acute ischemia]. 17 60

It is established that at the early stage of total heart ischemia in rats (5-10 min) the oligomycin-sensitive ATPase activity of mitochondria measured in heart homogenates in the medium and containing no Mg2+ decreases considerably, whereas the activity of respiratory chain, the value of respiratory control and Mg2+-ATPase activity are practically unchanged. The hypothetic trigger mechanism is suggested for Mg2+ ejection from mitochondria under conditions of respiration cessation. It is supposed to be a defence reaction of cells aimed to prevent ATP hydrolysis by mitochondria under ischemia.
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PMID:[Mg2+ release from heart mitochondria in ischemia: is it the defense mechanism or damage?]. 252 29

An examination was made of the effects of ganglioside GM1 (i.m.) on the losses of membrane fatty acids (palmitic, stearic, oleic, linoleic, and arachidonic), the plasma membrane enzyme Na+, K+-ATPase, and the mitochondrial membrane enzyme Mg2+-ATPase, associated with global ischemia 24 hr after permanent unilateral occlusion of the carotid artery in Mongolian gerbils. While there was a significant loss of fatty acids in saline controls, no loss was detected in membranes from GM1-injected gerbils. Rather, we found an increase in membrane fatty acid content, indicative of altered turnover. A 38% loss of Na+, K+-ATPase and a 36% loss of mitochondrial Mg2+-ATPase observed in membranes from saline controls was reduced in membranes from GM1-injected animals to losses of 15% and 8% respectively. These effects are further described by analyses of enzyme kinetics (apparent Vmax and apparent Km). After 1 week of storage, the activities of both membrane ATPases from saline controls decreased substantially more than from GM1-injected animals, suggesting that the GM1 membranes were better "preserved." Since there was a minimal loss in protein content after 24 hr of ischemia, these results indicate that systemically injected GM1 may protect structure and function of plama membranes during the acute phases of ischemic injury.
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PMID:GM1 ganglioside treatment after global ischemia protects changes in membrane fatty acids and properties of Na+, K+-ATPase and Mg2+-ATPase. 253 6

A monoclonal antibody (mAb 4B4) was raised against purified sarcoplasmic reticulum vesicles from canine myocardium, and shown to inhibit Ca2+ uptake by microsomes isolated from cardiac, skeletal, and smooth muscle. The amount of mAb 4B4 needed to inhibit the Ca2+ uptake 50% at a given membrane concentration correlated with the amount of Ca2+ pump protein in the microsomal preparation. This is consistent with the observation the mAb 4B4 binds specifically to the sarcoplasmic/endoplasmic reticulum Ca2+ pump (Mr 100 kDa), but has no effect on the T-tubule Mg2+-ATPase. Changes in the binding of mAb 4B4 to crude microsomes isolated from dog heart after various durations of global ischemia showed that the decrease in microsomal Ca2+ transport during the first 15 min of ischemia correlated with a loss of active Ca2+ pump molecules. The monoclonal antibody mAb 4B4 may therefore serve as a specific marker for the sarcoplasmic/endoplasmic reticulum Ca2+ pump system in various cells, and can provide quantitative information about the loss of active Ca2+ pump proteins under pathological conditions.
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PMID:Monoclonal antibodies to dog heart sarcoplasmic reticulum as markers of endoplasmic reticulum. 254 29

Isolated spontaneously beating rat hearts were perfused in the Langendorff mode and divided into four groups, i.e., control (aerobic), hypoxic (95% N2-5% CO2), ischemic, and ischemic reperfused. After a total of 90 min of perfusion, the sarcolemma was isolated and enzymatically characterized. Ouabain-sensitive Na+-K+-ATPase was inhibited in all three experimental groups, whereas K+-stimulated phosphatase activity was decreased only in the ischemic and reperfused groups compared with control. 5'-Nucleotidase activity was inhibited (P less than 0.05) only in the ischemic group. Mg2+-ATPase activity was not different from control. Passive Ca2+ uptake and Ca2+ efflux were not significantly altered by any of the interventions. Na+-Ca2+ exchange rate, but not capacity, was decreased (by 32-42%) in the ischemic group but this was partially reversed on reperfusion. These results suggest that changes secondary to lack of flow rather than O2 play a major role in the etiology of ischemic damage to the membrane and that a 15-min period of reperfusion after 60 min of ischemia does not exacerbate this damage.
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PMID:Sarcolemmal enzymes and Na+ -Ca2+ exchange in hypoxic, ischemic, and reperfused rat hearts. 614 98

To investigate the mechanism underlying postischemic contractile dysfunction (myocardial stunning) we examined myocardial sulflhydryl group content, myofibrillar Ca2+-dependent Mg2+-ATPase activity and protein profile after global ischemia and reperfusion. The Langerdorff-perfused rabbit hearts were subjected to 15 min normothermic ischemia followed by 10 min reperfusion and myofibrils were isolated from homogenates of left ventricular tissues. Depressed contractile function during reperfusion was accompanied by a decrease in total sulfhydryl group content. However, myofibrillar protein profile was unchanged and Western immunoblotting analysis showed no significant differences in troponin I immunoreactive bands between control and stunned hearts. Likewise, myofibrillar Mg2+-ATPase activity was unaltered after ischemia and reperfusion. We conclude that myocardial stunning is not caused by altered myofibrillar function and protein degradation but may be partly due to the oxidative modification of as yet undefined proteins.
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PMID:Effect of myocardial stunning on thiol status, myofibrillar ATPase and troponin I proteolysis. 1208 69

Functional properties of myofibrils from chronically ischemic canine myocardium were evaluated. Ischemia was produced by tight stenosis of left anterior descending artery (LAD), followed by 40 min acute ischemia with prior preconditioning. Animals of the first group were sacrificed after 8 weeks. In the second group, angioplasty of LAD was performed after 8 weeks of ischemia and animals were kept alive for other 4 weeks. Control animals were sham operated. Activity and kinetic parameters of myofibrillar Ca2+-stimulated Mg2+-ATPase were measured in myofibrils isolated from anterior and posterior parts of all hearts. We did not find any differences in maximal velocity (Vmax), half-maximal activation constant for calcium (K(Ca2+)50) and cooperativity coefficient (n(hill)) of myofibrils from different experimental groups as compared to controls, either at pH 7, pH 6.5 (acidosis) or pH 7.5 (alkalosis). K(Ca2+)50 increased in medium simulated acidosis (12.6-33.5 times) and n(hill) decreased significantly in all groups as compared with values obtained at pH 7. These results indicate that activity and Ca2+-sensitivity of myofibrillar Mg2+-ATPase remain unchanged despite deteriorated heart function 8 weeks after LAD obstruction. Experiments have confirmed that Ca2+-stimulated-ATPase from canine heart myofibrils responded to pH decrease by a decreased sensitivity to Ca2+ and a decreased cooperativity. However, sensitivity of the enzyme to the pH changes is unaltered by 8 weeks of chronic ischemia.
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PMID:Myofibrillar Ca2+-stimulated Mg2+-ATPase from chronically ischemic canine heart. 1216 24

Sarco(endo)plasmic reticulum Ca2+ (SERCA) pumps are important for cell signaling. Three different genes, SERCA1, 2, and 3, encode these pumps. Most tissues, including vascular smooth muscle, express a splice variant of SERCA2 (SERCA2b), whereas SERCA3a is widely distributed in tissues such as vascular endothelium, tracheal epithelium, mast cells, and lymphoid cells. SERCA2b protein is readily inactivated by peroxynitrite that may be formed during cardiac ischemia reperfusion or during immune response after infection. Here, we compared the peroxynitrite sensitivity of SERCA2b and SERCA3a by using microsomes prepared from HEK-293T cells overexpressing the pumps. We incubated the microsomes with different concentrations of peroxynitrite and determined Ca2+ uptake, Ca2+-Mg2+-ATPase, Ca2+-dependent formation of acylphosphate intermediate, and protein mobility in Western blots. Ca2+ uptake, Ca2+-Mg2+-ATPase, and Ca2+-dependent formation of acylphosphate intermediate were inactivated for both SERCA2b and SERCA3a, but the latter was more resistant to the inactivation. Western blots showed that SERCA2b and SERCA3a proteins oligomerized after treatment with peroxynitrite, but each with a slightly different pattern. Compared with monomers, the oligomers may be less efficient in forming the acylphosphate intermediate and in conducting the remainder of the steps in the reaction cycle. We conclude that the resistance of SERCA3a to peroxynitrite may aid the cells expressing them in functioning during exposure to oxidative stress.
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PMID:Effects of peroxynitrite on sarco/endoplasmic reticulum Ca2+ pump isoforms SERCA2b and SERCA3a. 1460 79

Brief episodes of myocardial ischemia-reperfusion (IR) employed during reperfusion after a prolonged ischemic insult may attenuate the total ischemia-reperfusion injury. This phenomenon has been termed ischemic postconditioning. In the present study, we studied the possible effect of ischemic postconditioning on an ischemic reperfusion (IR)-induced myocardium oxidative injury in rat model. Results showed that ischemic postconditioning could improve arrhythmia cordis, reduce myocardium infarction and serum creatin kinase (CK), lactate dehydrogenase (LDH) and aspartate transaminase (AST) activities in IR rats. In addition, ischemic postconditioning could still decrease myocardium malondialdehyde (MDA) level, and increased myocardium Na+-K+-ATPase, Ca2+-Mg2+-ATPase, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and glutathione reductase (GR) activities. It can be concluded that ischemic postconditioning possesses strong protective effects against ischemia reperfusion-induced myocardium oxidative injury in IR rats.
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PMID:Protective effect of ischemic postconditioning against ischemia reperfusion-induced myocardium oxidative injury in IR rats. 2245 31