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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 study is concerned with morphochemical changes in the metabolism and ultrastructure of the mitochondria and synaptical endings from the cortex of the hemispheres in rats under the influence of cyanide (7mg/kg) following 30 min, 2 hours and 24 hours after its administration. Subfractions of the light and heavy synaptosomes, as well as in the mitochondria of the cell bodies showed changes in the activity of the enzyme systems (cytochromoxidase, K+, Na+-ATPase and Mg2+-ATPase) and disturbances of the ultrastructure of the eliminated organella. After 24 hours the metabolism normalized, which may be explained by a biochemical brain plasticity at the subcellular level under conditions of histotoxic hypoxia.
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PMID:[Effect of cytotoxic hypoxia on the metabolism and ultrastructure of cortical synaptosomes and mitochondria]. 21 78

Rat brain synaptic vesicles exhibit ATP-dependent uptake of gamma-[3H]amino-n-butyric acid ([3H]GABA) and L-[3H]glutamate. After hypotonic shock, the highest specific activities of uptake of both L-glutamate and GABA were recovered in the 0.4 M fraction of a sucrose gradient. The uptakes of L-glutamate and GABA were inhibited by similar, but not identical, concentrations of the mitochondrial uncoupler carbonyl cyanide m-chlorophenylhydrazone and the ionophores nigericin and gramicidin, but they were not inhibited by the K+ carrier valinomycin. N,N'-Dicyclohexyl-carbodiimide and N-ethylmaleimide, Mg2+-ATPase inhibitors, inhibited the GABA and L-glutamate uptakes similarly. Low concentrations of Cl- stimulated the vesicular uptake of L-glutamate but not that of GABA. The uptakes of both L-glutamate and GABA were inhibited by high concentrations of Cl-. These results indicate that the vesicular GABA and L-glutamate uptakes are driven by an electrochemical proton gradient generated by a similar Mg2+-ATPase. The vesicular uptake mechanisms are discussed in relation to other vesicle uptake systems.
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PMID:Comparison of the properties of gamma-aminobutyric acid and L-glutamate uptake into synaptic vesicles isolated from rat brain. 246 84

The first morphological alteration observed in Trypanosoma cruzi different stages upon incubation with crystal violet was mitochondrial swelling. The use of digitonin to solubilize T. cruzi plasma membrane allowed the demonstration of an uncoupling action of crystal violet on epimastigote mitochondria in situ. Low concentrations of crystal violet (20-50 microM) or carbonyl cyanide p-trifluoromethoxyphenylhydrazone (FCCP; 0.5 microM) uncoupled the respiratory control mechanism. The inhibition of State 3 respiration by oligomycin was released by crystal violet or FFCCP. Crystal violet released respiratory control, and enhanced ATPase activity of digitonin-permeabilized epimastigotes. Higher concentrations of crystal violet inhibited mitochondrial respiration. The uncoupled effect of crystal violet was stimulated by inorganic phosphate. In addition, crystal violet inhibited endongenous and glucose-stimulated respiration of the intact epimastigotes, and inhibited the Mg2+-ATPase in the epimastigote mitochondrial fractions. The inhibition of this Mg2+-ATPase increased up to pH 9.0 and decreased with increasing protein concentration. These data indicate that the T. cruzi mitochondrion is apparently the main target of crystal violet toxicity.
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PMID:The mitochondrion of Trypanosoma cruzi is a target of crystal violet toxicity. 254 Apr 35

Sarcoplasmic reticulum vesicles from mammalian skeletal muscle have previously been shown to develop a proton gradient (alkaline inside) of 0.15-0.5 pH units during active Ca2+ uptake. We found that dissipation of this gradient by the proton ionophores gramicidin, nigericin, and carbonyl cyanide p-trichloromethoxyphenylhydrazone caused a rapid transient tension in skinned rabbit psoas muscle fibers. Increases, but not decreases, in medium pH of approximately 0.2 units over the range from pH 6.5 to pH 7.5 also elicited transient tensions. In isolated vesicles, physiological levels of Ca2+ (3.3 microM), inhibited pH-induced Ca2+ release. Dicyclohexylcarbodiimide blocked pH- and ionophore-induced Ca2+ release under conditions in which it could bind to sarcoplasmic reticulum proteins but did not inhibit Ca2+ uptake. We propose that a proton gradient generated across sarcoplasmic reticulum membranes during Ca2+ uptake maintains a Ca2+ release channel in a closed conformation and that dissipation of this gradient permits the Ca2+ release channel to open. We further propose that elevated myoplasmic Ca2+ also causes the Ca2+ channel to close, permitting Ca2+ uptake through Ca2+/Mg2+-ATPase to function effectively. As the proteolipids of sarcoplasmic reticulum bind dicyclohexylcarbodiimide under conditions in which Ca2+ release is blocked and as they have previously been shown to have Ca2+ ionophoric activity, we propose that the Ca2+-release channel either resides in the proteolipids or is controlled by H+ fluxes through the proteolipids.
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PMID:A proton gradient controls a calcium-release channel in sarcoplasmic reticulum. 627 76

Methanobacterium thermoautotrophicum when grown on ordinary culture medium has a tough cell wall which is lysozyme-resistant and difficult to disrupt by physical means. The cell wall, however, can be weakened by the addition of D-sorbitol to the growth medium and the organisms form protoplasts after lysozyme addition. This technique allowed the isolation of two types of intracellular small vesicles: (a) isolated by disruption of the total cell population (lysozyme-sensitive and lysozyme-resistant cells) by ultrafrequency sound and (b) isolated by osmotic lysis of protoplasts. For the first time, a small vesicle fraction isolated as in (a) was capable of synthesizing methane from CO2 and H2 without cytoplasm. There was, however, an absolute requirement for a small, heat-stable, oxygen-sensitive cofactor which was isolated from the cytoplasm. Methane synthesis with this vesicle fraction was inhibited by the detergent deoxycholate, and by the protonophores 2,4-dinitrophenol and carbonyl cyanide m-chlorophenylhydrazone. Mg2+-ATPase appeared to be located on the outer or cytoplasmic surface of the small vesicle fraction isolated as in (b). The results were consistent with a previously made suggestion [Sauer, Erfle & Mahadevan (1981) J. Biol. Chem. 256, 9843-9848] that the interior of the small intracellular vesicles becomes acid during methane synthesis.
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PMID:Methane synthesis by membrane vesicles and a cytoplasmic cofactor isolated from Methanobacterium thermoautotrophicum. 646 20

Uncouplers of mitochondrial oxidative phosphorylation, dinitrophenol (DNP) and carbonyl cyanide p-trifluoromethoxyphenylhydrazone (FCCP), were found to stimulate Mg(2+)-ATPase activity of human erythrocyte membranes in a manner competitive with respect to 2,4-dinitrophenyl-S-glutathione (DNP-SG) which suggested that these compounds may also be substrates of the glutathione-S-conjugate pump. We confirm that the stimulation of erythrocyte membrane ATPase activity by DNP and by another uncoupler, carbonyl cyanide m-chlorophenylhydrazone (CCCP), is competitive with respect to DNP-SG. However, we found no evidence for active transport of DNP and CCCP out of erythrocytes and demonstrate that they inhibit the low-affinity component of DNP-SG transport noncompetitively while stimulating the high-affinity DNP-SG transport (mediated by multidrug resistance-associated protein, MRP1). Implications of these findings may indicate the electrogenic nature of MRP1-mediated transport of glutathione-S conjugates and stimulation of aminophospholipid translocase (flippase) rather than the glutathione-S-conjugate pump by the uncouplers.
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PMID:Uncouplers of mitochondrial oxidative phosphorylation are not substrates of the erythrocyte glutathione-S-conjugate pump. 943 89