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)

Magnesium is an essential cofactor for many enzymatic reactions, especially those involved in energy metabolism. Deficits of magnesium are prevalent due to inadequate intake or malabsorption and due to the renal loss of magnesium that occurs in certain disease states (alcoholism, diabetes) and with drug therapy (diuretics, aminoglycosides, cisplatin, digoxin, cyclosporin, amphotericin B). Protracted deficits of magnesium in humans and animals result in neurological disturbances, including hyperexcitability, convulsions and various psychiatric symptoms ranging from apathy to psychosis, some of which can be reversed with magnesium supplementation, others requiring correction of the dysregulation mechanism. Although the role of magnesium in neuronal function is not completely understood, a lowering of CSF or brain magnesium can induce epileptiform activity and there is an association between decreased CSF magnesium and the development of seizures. CSF concentrations of magnesium are normally higher than magnesium plasma ultrafiltrate (diffusible) concentrations due to the active transport of magnesium across the blood-brain barrier. Under conditions of magnesium deficiency, CSF concentrations decline, although this decline lags behind and is less pronounced than the changes observed in plasma magnesium concentrations. Decreases in CSF magnesium concentrations correlate with the alterations observed in extracellular brain magnesium concentrations in animals following the dietary deprivation of magnesium. CSF magnesium concentrations can readily be repleted following magnesium supplementation, although high dose magnesium therapy, such as that used in the treatment of convulsions in eclampsia, will only increase CSF magnesium concentrations to a very limited degree (approximately 11-18 per cent) above physiological concentrations. Greater increases in CSF magnesium may occur in neonates since neonatal swine, following treatment with magnesium, have CSF magnesium concentrations that are similar to their plasma concentrations. There has been a recent resurgence of interest in magnesium deficiency and its neurological consequences due to the finding that magnesium, at physiological concentrations, blocks N-methyl-D-aspartate (NMDA) receptors in neurones. NMDA receptors are normally activated by glutamate and/or aspartate which represent the principal neurotransmitters for excitatory synaptic transmission in vertebrate CNS. Magnesium deficiency produces epileptiform activity in the CNS which can be blocked by NMDA receptor antagonists. Other mechanisms, including alterations in Na+/K(+)-ATPase activity, cAMP/cGMP concentrations and calcium currents in pre- and postsynaptic membranes, may also be at least partially responsible for the neuronal effects associated with low brain magnesium. Further studies are necessary to increase our understanding of the neurological implications of magnesium deficit in the central nervous system.
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PMID:Brain and CSF magnesium concentrations during magnesium deficit in animals and humans: neurological symptoms. 129 67

The etiology of keratoconus is still unclear. This study presents a new clinical sign, Thalasselis' syndrome, defined as: an association between keratoconus, magnesium deficiency, type-A behavior and allergy. Also, it introduces the hypothesis that magnesium deficiency could affect pathologically the osmotic mechanism of the cornea, specifically the Na-K and/or Ca-ATPase pumps; the collagen structure by alteration of the adenylate cyclase activity; and other mechanisms as well. Furthermore, we propose the Thalasselis' syndrome is compatible with previous theories on keratoconus. In addition to the other therapeutic measures, such as contact lenses and keratoplasty, this study suggests a clinical, nutritional, psychological, and immunological treatment for keratoconic patients.
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PMID:Thalasselis' syndrome and other theories on keratoconus. 258 91

Sprague-Dawley rats were fed a basal AIN-76 diet containing 80, 200, 350, 500 or 650 mg of magnesium per kilogram of diet for 6 wk. Ventricular slices, as well as microsomal fractions, were prepared from the hearts and were used to determine sodium-potassium pump activity. Sodium-potassium pump activity was assessed in the microsomal membranes by determining the ouabain-inhibitable Na+, K+-ATPase activity and [3H]ouabain binding, and in the ventricular slices, by determining ouabain-sensitive 86Rb uptake under K+-free conditions. The ATPase activity increased with increasing dietary magnesium, so that in the hearts of those animals that were fed 500 and 650 mg of magnesium/kg diet, it was significantly greater than the activity in the hearts of the animals fed 80 and 200 mg/kg diet. Similarly, 86Rb uptake by heart slices from rats fed 500 and 650 mg of magnesium/kg diet was significantly greater than the uptake by heart slices from animals fed 80 and 200 mg/kg diet. [3H]Ouabain binding did not change with increasing dietary magnesium. Thus, magnesium deficiency appears to have no effect on the number of sodium-potassium pump sites, but does decrease the activity of the pump. It is suggested that this leads to an increase in intracellular Na+, resulting in a change in the membrane potential, and may contribute to the arrhythmias associated with magnesium deficiency.
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PMID:Effects of dietary magnesium on sodium-potassium pump action in the heart of rats. 282 28

The effects of magnesium supplementation were tested in 20 patients with essential hypertension receiving long-term thiazide diuretic treatment (Th group) and 21 age-matched untreated patients (EHT group). Intra-erythrocyte cations, water content and the ouabain-sensitive sodium efflux rate constant were measured. The Th group received magnesium supplementations as MgO (600 mg Mg/day) for 4 weeks. In the Th group intra-erythrocyte magnesium and the sodium efflux rate constant were lower and red cell sodium was higher than in the EHT group. During magnesium supplementation, there were significant decreases (p less than 0.01) in intra-erythrocyte sodium content and mean blood pressure, and increases (p less than 0.005) in red cell magnesium content and the sodium efflux rate constant. These effects of magnesium were more evident in 9 patients who were unresponsive to diuretic therapy, a definite reduction in mean blood pressure, from 104.8 +/- 2.7 mmHg to 94.4 +/- 2.2 mmHg (p less than 0.001), being observed. In the remaining 11 patients, however, blood pressure remained unchanged. The sodium efflux rate constant was positively correlated with red cell magnesium content and negatively correlated with sodium content (r = 0.61, p less than 0.005 and r = -0.57, p less than 0.01, respectively). These results indicate that long-term diuretic treatment may give rise to intracellular magnesium deficiency and a suppression of cell membrane active sodium transport. The results also suggest that oral magnesium may decrease intracellular sodium, possibly through the activation of Na-K-ATPase, which in turn may contribute to the reduction in blood pressure. Therefore, magnesium supplementation may be a worthwhile additional therapy for diuretics.
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PMID:Intracellular magnesium deficiency and effect of oral magnesium on blood pressure and red cell sodium transport in diuretic-treated hypertensive patients. 322 92

The etiology of keratoconus is still unknown. This project was designed to study, in a group of keratoconic patients and a control group, the following: clinical, endocrinological, immunological, psychological, and ophthalmological factors. We found mean serum magnesium deficiency and type A behavior to be significantly more common in keratoconic patients than in a control group of patients. In addition changes in gluco-mineral corticoids, changes in glucose metabolism, edema of allergic origin, and genetic factors may collaborate in the development of keratoconus. All these factors could affect the osmotic mechanism of the cornea: Na-K and/or Ca ATPase, the collagen structure by alteration of the adenylate cyclase activity, and other mechanisms. This study suggests an association between keratoconus, magnesium depletion, and type A behavior, which together constitute a new clinical syndrome and confirm an association between keratoconus and atopy.
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PMID:Keratoconus, magnesium deficiency, type A behavior, and allergy. 341 70

Comparisons were made between the metabolic activities of whole mitochondria and intact mitochondrial inner membrane preparations from magnesium-deficient and control rats in a basic medium without exogenous magnesium. Magnesium deficiency partially uncoupled oxidative phosphorylation in whole mitochondria and completely uncoupled it with inner membrane preparations. Addition of 1 mM MgCl2 to the medium prevented the total uncoupling of inner membranes and gave ADP:O values similar to those obtained with whole mitochondria from magnesium-deficient rats. No impairment in proton extrusion by intact inner membranes or in ATPase activity by either intact or fragmented inner membranes was detected during magnesium deficiency, but there was evidence of increased membrane permeability to the inward movement of protons. It is concluded that magnesium deficiency probably increases the permeability of the mitochondrial inner membrane and this weakens the coupling between oxidation and phosphorylation.
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PMID:Metabolic activity of liver mitochondria from magnesium-deficient rats. 623 32

Treatment with thiazides and loop diuretics increase the urinary excretion of potassium and magnesium and the body content of these ions are reduced after long-term treatment. The diuretic-induced magnesium deficiency influences the potassium metabolism. Magnesium is a necessary activator of Na-K-ATPase, which supplies the Na-K pump with energy. Lack of magnesium will therefore impair the pumping of sodium out of the cell and of potassium into the cell. The change of the relationship between extra and intracellular potassium may induce cardiac arrhythmias. Certain groups of patients, such as patients on digitalis therapy, patients with secondary hyperaldosteronism, elderly patients with insufficient dietary habits, and heavy drinkers, run an additional risk of developing potassium/magnesium disturbances. In young patients with uncomplicated essential hypertension, the risk is probably very small.
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PMID:Problems with potassium and magnesium in diuretic-treated patients. 632 42

The many causes of clinical magnesium deficiency can be placed into 2 categories: diminished intake of magnesium, and enhanced losses of magnesium, either through the gastrointestinal tract or through the kidneys. Examples of the first category include alcoholism, starvation, anorexia due to neoplastic disease and/or chemotherapy. Examples of the second category include severe diarrhoeal states, gastrointestinal fistulae, malabsorption, diuretic therapy and gentamicin therapy. Estimates of the prevalence of clinical hypomagnesaemia range from 6 to 11% in hospitalised patients. Serum predictors of associated clinical magnesium depletion include hypokalaemia (42%), hyponatraemia (23%), hypophosphataemia (22%) and hypocalcaemia (20%). Experimental and clinical observations strongly support the view that magnesium and potassium are closely linked at the cellular level. Magnesium has been demonstrated to be important in cell energetics (Mg++-activated ATPase), in maintenance of the integrity of cell membranes, retardation of cell loss of potassium, as well as enhancing repletion of cell potassium. While translation of these experimental observations into clinical terms encompasses a wide spectrum of illnesses, there is special relevance in considering the role of magnesium in repletion and maintenance of cell potassium in 2 clinical instances: (a) patients treated with digitalis and diuretics; and (b) hypertensive patients. In these types of patients not only potassium but also magnesium should be administered together to avoid the problem of cell potassium depletion and refractory potassium repletion associated with coexisting and uncorrected magnesium depletion.
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PMID:Magnesium deficiency. Causes and clinical implications. 649 96

Body potassium status is often dosed on serum potassium determinations. However, this parameter is not an adequate guide to the body potassium status, unless several factors are taken into consideration, e.g. acid-base balance and serum creatinine level. Muscle magnesium content is another factor, probably operative through its activation of Na-K-ATPase, which produces the energy necessary for the active transport of potassium into the cell. Magnesium has a membrane-stabilizing effect as well, diminishing the outward movement of potassium from the cell. In case of magnesium deficiency, potassium cannot be transported into the cell in sufficient amounts and the result is an imbalance between the intra- and the extracellular potassium concentration, which in turn may lead to cardiac dysrhythmias.
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PMID:Intra-/extracellular shifts of potassium after the administration of Mg in patients with cardiovascular diseases. 653 41

Magnesium may influence the incidence of cardiac arrhythmias by 1) a direct effect 2) an effect on potassium metabolism 3) an effect as a calcium blocking agent. In the event of a magnesium deficiency the cell cannot attract potassium against the transmembrane concentration gradient. The reason may be that a magnesium deficiency interferes with the function of membrane ATPase, and thus the pumping of sodium out from the cell and potassium into the cell is impaired. The interference from a magnesium deficiency on the equilibrium of potassium between the intra- and extracellular spaces may result in changes in the resting membrane potential, changes in potassium conductance across the cell membrane as well as disturbances in the repolarization phase.
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PMID:Relation between potassium, magnesium and cardiac arrhythmias. 694 39


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