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)

Enzyme histochemical and immunohistochemical techniques were used to examine palatine tonsils and aggregated lymphoid follicles (Peyer's patches) of the ileum in 6- to 9-day-old and in 6-month-old pigs. Histochemical techniques were used to detect alpha-naphthyl-acetate esterase (ANAE), alpha-naphthyl-butyrate esterase (ANBE), beta-glucuronidase, adenosine triphosphatase (ATPase), and acid phosphatase (AcP). Nonspecific esterases (ANAE, ANBE) were detected in macrophages, T-cell area lymphocytes, eosinophils, fibroblastic reticular cells (FRC), follicular dendritic cells (FDC), and interdigitating cells (IDC). beta-Glucuronidase reactivity was strong in macrophages, eosinophils, FDC, and IDC, and weaker in FRC. Adenosine triphosphatase reactivity was detected in B-cell area lymphocytes, FDC, FRC, and IDC. Cell types with acid phosphatase reactivity were macrophages, FDC, FRC, and IDC. Nonepithelial cells of tonsils and aggregated lymphoid follicles of the ileum had similar enzymatic reactions. In Peyer's patches, however, epithelial cells were positive for all enzymes studied; in tonsils, only nonspecific esterases were detected. Immunoperoxidase techniques were used to detect S-100 protein and cytoplasmic immunoglobulins (IgG, IgM, and IgA). The S-100 protein was detected in lymphocytes, FDC, and FRC of tonsils and Peyer's patches; in tonsillar epithelial and endothelial cells; and in IDC of Peyer's patches.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Histochemical and immunohistochemical study of the mucosal lymphoid system in swine. 138 98

Use of skeletal muscle for cardiac augmentation is a promising technique for treatment of end-stage cardiac failure. An electrode woven through the latissimus dorsi that recruits nearby nerve fibers is commonly used to pace skeletal muscles both in clinical practice and in the laboratory. A proximally placed nerve cuff electrode offers potential advantages in improved recruitment of muscle fibers and low threshold for stimulation. We tested the effectiveness of a nerve cuff electrode passed directly about the proximal thoracodorsal nerve. Our report looks at the efficacy of nerve cuff electrode stimulation and compares electrical and histologic characteristics of a 180-degree wrap of the thoracodorsal nerve to a 360-degree wrap in dogs over 3 months. Threshold voltage at the commonly used pulse width of 200 microseconds was typically in the range of 400 to 600 mV for each electrode after 3 months. Statistical analysis revealed no significant difference (p < 0.05) in threshold voltage or current between the 180-degree and 360-degree nerve cuff electrode either at acute evaluation or after 3 months. Even contraction of latissimus dorsi was achieved with all implants. Adenosine triphosphatase staining revealed 100% conversion of type II to type I fibers in all stimulated muscles. Histologic examination of the thoracodorsal nerve and latissimus dorsi muscle revealed no abnormalities grossly or by light microscopy. Thus, a carefully applied nerve cuff electrode is an atraumatic, effective method for skeletal muscle stimulation. The 180-degree and 360-degree nerve cuff configurations are equally effective.
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PMID:Comparison of 180-degree and 360-degree skeletal muscle nerve cuff electrodes. 141 88

In the present study, we investigated the toxic response to repeated oral administration of 2-chloroethyl linoleate (2-CEL) in male rats at 250 mg/kg body weight for 2 weeks on alternate days (total 7 doses). Control rats received an equal volume of mineral oil. The five animals from each group were sacrificed on days 1, 7 and 28 following the last dose. No significant changes were observed in body weight, as well as organ-to-body weight ratios due to 2-CEL treatment. The red blood cell counts increased significantly in 2-CEL treated animals at day 28 as compared to the controls. Elevated counts of platelets, monocytes and eosinophils and low counts of basophils and large unstained cells were also observed at some time points in 2-CEL treated rats. Significantly reduced activities of total serum lactate dehydrogenase (LDH), aspartate aminotransferase and alanine aminotransferase were found at most of the time points except for LDH at day 28. Adenosine triphosphatase activity was also significantly reduced in liver mitochondrial fraction at all time points. Histopathological studies showed consistent centrilobular lesions (incidence 4/4) in the liver consisting of hepatocyte vacuolar degeneration and focal necrosis at day 28. A few centrilobular lesions were also observed (incidence 2/4) at day 7, while no changes were observed at day 1. These results indicate that 2-CEL is a hepatotoxin, however, the observed decrease in serum enzyme levels in relation to hepatotoxicity of 2-CEL, needs to be elucidated.
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PMID:Toxic response to repeated oral administration of 2-chloroethyl linoleate in rats. 160 45

Tartrate-resistant acid adenosine triphosphatase activity at pH 6.5, using a lead-salt method, was localized at light and electron microscopic levels in cartilage and bone matrices, osteoclasts, and chondroclasts. Cartilage matrix staining occurred after vascular invasion of the growth plate. In osteoclasts, activity was present in lysosomes, extracellular ruffled border channels, and the underlying cartilage and bone matrices. Staining artifacts occurred at lower pH levels (pH 5.4, 5.0). Adenosine diphosphate, p-nitrophenylphosphate, thiamine pyrophosphate, and alpha-naphthylphosphate also acted as substrates; but no activity was observed when adenosine monophosphate, adenylate-(beta, gamma-methylene) diphosphate, and beta-glycerophosphate were used. The activity was inhibited by NaF, dithionite, and a high concentration of p-chloromercuribenzoic acid, and activated by simultaneous addition of FeCl2 and ascorbic acid, as has been shown in biochemical studies. These histochemical results support the view that the adenosine triphosphate hydrolyzing activity at pH 6.5 is due to tartrate-resistant acid phosphatase (TRAP). There were some differences in ultrastructural localization between TRAP and tartrate-sensitive acid phosphatase (TSAP) activities in osteoclasts: TSAP activity was more intense in lysosomes and Golgi complexes and TRAP was stronger in the cartilage and bone matrices. It is suggested, therefore, that most of TRAP is in an inactive form in cells and is activated when secreted.
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PMID:Ultrastructural localization of tartrate-resistant acid phosphatase (purple acid phosphatase) activity in chicken cartilage and bone. 165 24

Histoenzymological changes in Adenosine triphosphatase (ATPase) activity were studied during folliculogenesis in immature and mature rat ovary. Its presence in oocytes of small follicles and absence in those of large follicles postulate a correlation between their absorptive mechanism during the development of the oocyte. The presence of ATPase activity in the theca, corpora lutea and interstitial gland tissue may be related to the vascular endothelium which is associated with the transport system across the membrane.
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PMID:Histochemical changes in adenosine triphosphatase activity during folliculogenesis and corpus luteum formation and regression in the rat ovary. 184 16

Intact astrocytes cultured from newborn rat cerebral cortex rapidly converted extracellular ATP to ADP. The ATPase responsible was apparently not saturated, even at 750 microM ATP. In contrast, the conversion of ADP to AMP was slow, and the reaction was limiting for the subsequent dephosphorylation process. Adenosine formation was the only fate for AMP. The reaction was catalyzed by 5'-nucleotidase with an apparent Km of 55 microM for AMP and appeared to be inhibited by high concentrations of ATP and ADP. Astrocytes were able to take up adenosine with an apparent Km value of 45 microM. Uptake was inhibited by dipyridamole but not by anti-5'-nucleotidase IgG. The results support the proposal that astrocytes play a role in modulating synaptic events involving ATP and adenosine.
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PMID:Metabolism of extracellular adenine nucleotides by cultured rat brain astrocytes. 191 71

Na+/K(+)-Adenosine triphosphatase-dependent activities of K(+)- return relaxation and 86Rb uptake were studied in pulmonary arteries taken from rats with pulmonary hypertension induced by monocrotaline. Rats were given monocrotaline in drinking water, 20 mg/l, for 4 or more days. Isolated arteries were placed in tissue baths and contracted with norepinephrine or 5-hydroxy-tryptamine under K(+)-free conditions. The arteries relaxed when K+ was "returned" to the bath. Compared to arteries from untreated rats, arteries taken from rats pretreated with monocrotaline developed less force in response to contracting agents and did not relax to the same extent. After 4 days treatment with monocrotaline, the rate of relaxation of the arteries in response to K(+)-return was slower than that of arteries taken from untreated rats. Endothelial trauma or in vitro treatment with ouabain produced a similar decrease in the rate of relaxation. Uptake of radiolabeled Rb by perfused arteries was not altered by 4 days of monocrotaline pretreatment. Isolated lungs taken from monocrotaline-pretreated rats (5 days of ingestion of 20 mg/l of monocrotaline drinking water) accumulated similar quantities of 86Rb+ during 40-sec perfusions. Shorter perfusion times, 10 and 20 sec, resulted in greater rates of uptake of 86Rb- by lungs taken from monocrotaline-treated rats. Monocrotaline produced changes in both the mechanical and biochemical properties of pulmonary arteries after only 4 to 5 days. These changes were associated with ouabain-sensitive processes. It appears, therefore, that one of the early targets in monocrotaline intoxication is the Na+/K+ pump of the pulmonary arteries.
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PMID:Na+/K(+)-adenosine triphosphatase activity of pulmonary arteries after intoxication with the pyrrolizidine alkaloid, monocrotaline. 215 11

Adenosine triphosphatase activity and nucleotide binding affinity of isolated beta-subunit preparations from Escherichia coli F1F0-ATP synthase were studied. The aim was to find out whether isolated beta-subunit would provide an experimental model in which effects of mutations on catalysis per se, unencumbered by complications due to their effects on positive catalytic cooperativity, could be studied. Three types of purified, isolated beta-subunit preparations were studied. Type I-beta was from a strain lacking all F1F0 subunits except beta and epsilon. Type II-beta was from F1 carrying the alpha S375F mutation which blocks positive catalytic cooperativity. Type III-beta was from normal F1. Type I- and II-beta had very low ATPase activity (less than 10(-4) s-1) which was azide-insensitive, aurovertin-insensitive, and unaffected by anti-beta antibody. Type I-beta activity was EDTA-insensitive. We conclude that isolated beta-subunit from E. coli F1F0 has zero or at most very low intrinsic ATPase activity. Type III-beta had low ATPase activity (8.4 x 10(-5) s-1 to 1.1 x 10(-3) s-1 in seven different preparations). This activity was aurovertin-sensitive, but varied in azide sensitivity from 0 to 34% inhibited. The azide-sensitive component, like F1 and alpha 3 beta 3 gamma oligomer, was inhibited by anti-beta and anti-alpha antibodies. The azide-insensitive component was stimulated by anti-beta and unaffected by anti-alpha. We show here that (alpha beta)-oligomer has ATPase activity which is azide-insensitive, aurovertin-sensitive, stimulated by anti-beta, and unaffected by anti-alpha. The intrinsic ATPase activity of Type III-beta could be due to contaminating (alpha beta)-oligomer plus alpha 3 beta 3 gamma-oligomer. Isolated beta had very low affinity for nucleotide as compared to the first catalytic site on F1. Taken together with the very low ATPase activity of isolated beta (even if real), the work shows that isolated beta is not a good experimental model of F1 catalysis.
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PMID:Adenosine triphosphatase and nucleotide binding activity of isolated beta-subunit preparations from Escherichia coli F1F0-ATP synthase. 215 22

The role of the endothelium in response to aggregating platelets was examined in porcine coronary and peripheral (carotid, femoral and renal) arteries from normal and hypercholesterolemic pigs. Male Yorkshire pigs were fed either a normal diet or a 2% high cholesterol diet for 10 weeks. Endothelium-dependent responses were examined in vitro. In all arteries from control animals, aggregating platelets caused endothelium-dependent relaxations, which were augmented by ketanserin (a 5-HT2-serotonergic blocker), attenuated by apyrase (an adenosine diphosphatase and triphosphatase) or methiothepin (a combined 5-HT1 and 5-HT2-serotonergic blocker) and were almost abolished by a combination of apyrase and methiothepin. The platelet-induced relaxations were most pronounced in the coronary arteries. Adenosine diphosphate caused endothelium-dependent relaxations, which were significantly attenuated by apyrase. Serotonin also caused endothelium-dependent relaxations, which were significantly attenuated by methiothepin but augmented by ketanserin. The endothelium-dependent relaxations to adenosine diphosphate were most pronounced in coronary arteries and those to serotonin in coronary and renal arteries. In cholesterol-fed animals, the endothelium-dependent relaxations to aggregating platelets, adenosine diphosphate and serotonin were impaired in all four arteries. These experiments indicate that 1) the endothelium exerts inhibitory effects against aggregating platelets in porcine coronary and peripheral arteries; 2) platelet-induced endothelium-dependent relaxations are achieved by purinergic and 5-HT1-serotonergic receptors on the endothelium; and 3) hypercholesterolemia reduces the endothelium-dependent relaxations to aggregating platelets in a generalized manner because it impairs the relaxations to adenosine diphosphate and serotonin released from the platelets.
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PMID:Hypercholesterolemia causes generalized impairment of endothelium-dependent relaxation to aggregating platelets in porcine arteries. 278 7

The effect of phosphorylation by cyclic GMP-dependent protein kinase (G-kinase) on the activity of the plasmalemmal Ca2+-transport ATPase was studied on isolated plasma membranes and on the ATPase purified from pig erythrocytes and from the smooth muscle of pig stomach and pig aorta. Incubation with G-kinase resulted, in both smooth-muscle preparations, but not in the erythrocyte ATPase, in a higher Ca2+ affinity and in an increase in the maximal rate of Ca2+ uptake. Cyclic AMP-dependent protein kinase (A-kinase) did not exert such an effect. The stimulation of the (Ca2+ + Mg2+)-dependent ATPase activity of the purified Ca2+ pump reconstituted in liposomes depended on the phospholipid used for reconstitution. The stimulation of the (Ca2+ + Mg2+)-ATPase activity by G-kinase was only observed in the presence of phosphatidylinositol (PI). G-kinase, but not A-kinase, stimulated the phosphorylation of PI to phosphatidylinositol phosphate (PIP) in a preparation of (Ca2+ + Mg2+)-ATPase obtained by calmodulin affinity chromatography from smooth muscle, but not in a similar preparation from erythrocytes. Adenosine inhibited both the phosphorylation of PI and the stimulation of the (Ca2+ + Mg2+)-ATPase by G-kinase. In the absence of G-kinase the (Ca2+ + Mg2+)-ATPase was stimulated by the addition of PIP, but not by PI. In contrast with previous results of Furukawa & Nakamura [(1987) J. Biochem (Tokyo) 101, 287-290], no convincing evidence for a phosphorylation of the (Ca2+ + Mg2+)-ATPase was found. Evidence is presented showing that the apparent phosphorylation occurs in a contaminant protein, possibly myosin light-chain kinase. It is proposed that G-kinase stimulates the plasmalemmal Ca2+ pump of smooth-muscle cells indirectly via the phosphorylation of an associated PI kinase.
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PMID:Cyclic GMP-dependent protein kinase stimulates the plasmalemmal Ca2+ pump of smooth muscle via phosphorylation of phosphatidylinositol. 285 Aug 1


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