Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P20020 (adenosine triphosphatase)
 3,299 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Homogeneous preparations of cytoplasmic membrane isolated from Staphylococcus aureus 6538P exhibited membrane-associated adenosine triphosphatase (ATPase) activity. Membrane ATPase activity was activated by divalent cations (4.0 mM: Mg2+ greater than Mn2+ greater than Co2+ greater than Zn2+), and ATP was hydrolyzed more readily than other nucleoside triphosphates and phosphorylated substrates. The pH optimum for the membrane ATPase was 6.5. The ATPase could not be released from the membrane by differential osmotic treatments, but detergent treatment effectively solubilized active enzyme. The nonionic detergent Triton X-100 (1%) released a protein with ATPase activity, after substrate-dependent staining in polyacrylamide gels, that differed slightly in electrophoretic migration when compared to the active enzyme solubilized with sodium dodecyl sulfate (0.1%). Membrane-associated ATPase activity was inhibited by N,N'-dicyclohexylcarbodiimide (0.001 to 1 mM) and NaF (50% inhibition at 5 mM NaF). Azide and trypsin inhibited activity, whereas ouabain had a slight inhibitory effect. Diethylstilbestrol showed appreciable activation of the membrane ATPase over the range employed (0.001 to 1 mM).
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PMID:Staphylococcus aureus adenosine triphosphatase: inhibitor sensitivity and release from membrane. 645 44

Freshly ejaculated human semen samples of proven motility were studied to test the hypothesis that inhibition of sperm motility after gossypol treatment (a polyphenolic pigment isolated from cottonseed) is caused by decreased adenosine triphosphatase (ATPase) activity and/or imbalance in the molecules of biological significance. When sperm were incubated with 10 and 100 mcg of gossypol acetic acid for different time periods at 37 degrees centigrade, a marked reduction in motility was abserved. The motility was reduced from 83-4% after 210 minutes (P .001). Also, a significant decrease in the activities of calcium ion and magnesium ion activated ATPase in the sperm was observed after incubation in gossypol (P .005). Zinc ion concentration also showed a change, but it was not statistically significant. These data indicate that sperm motility inhibition after gossypol treatment is due to inhibition of ATPase activity in the sperm. This research was conducted in India.
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PMID:Studies on the male antifertility agent-gossypol acetic acid. II. Effect of gossypol acetic acid on the motility and ATPase activity of human spermatozoa. 645 65

Disturbance of central serotoninergic system has been suggested in Down's syndrome (DS). In this syndrome the 5-HT concentration in blood platelets is below normal, but the mechanism behind this has been controversial. Recently, evidence has accumulated indicating a decreased active transport of 5-HT possibly due to lowered activity of Mg++-dependent Na+-K+-stimulated adenosine triphosphatase. In the present study the kinetic analysis of 5-HT uptake by blood platelets from DS patients revealed a decreased Vmax, suggesting decreased transport function but an unchanged affinity to the uptake receptors, as indicated by normal Km values. The controls were mentally retarded patients from the same institute. The uptake continued in a linear fashion up to 20 min., suggesting an unchanged storage of 5-HT. Also the effect of zinc on the 5-HT uptake was studied; plasma zinc levels have been noted to be lowered in DS infants. In vitro zinc caused a dose-dependent inhibition of uptake at 10(-5) and 10(-4) M. In vivo, after 2 weeks treatment 135 mg/day orally no significant effect was noted.
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PMID:Nature of lowered 5-hydroxytryptamine uptake by blood platelets of patients with Down's syndrome. 645 3

Adverse effects on hematopoiesis and renal function have been reported in both animals and humans exposed to high doses of lead for a protracted period of time, but little is known about the interrelationship between these two target organ systems. The present study examines rats exposed via drinking water to high dose (5000 mg/L) or low dose (100 mg/L) lead, either continuously or discontinuously, for periods ranging from 1 to 12 months. In addition to blood lead, indices of hematological abnormalities included hematocrit, zinc protoporphyrin (ZPP) and red blood cell (RBC) membrane sodium-potassium-activated adenosine triphosphatase (Na-K-ATPase). Renal function abnormalities were assessed by measurements of glomerular filtration rate (GFR) by the single injection 125-I-iothalamate technique and urinary excretion of the proximal renal tubular enzyme, ligandin. Blood lead and GFR correlated positively during the first 6 months of lead administration, reflecting a stimulatory effect of lead on renal hypertrophy and GFR during this time period. When this distorting effect was factored out, there were few residual correlations between renal and hematological abnormalities. The only significant relationship between GFR and hematological parameters of lead toxicity was a negative correlation between GFR and RBC membrane Na-K-ATPase in animals treated with high dose lead for 6 months and observed at the end of 12 months (discontinuous group).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Experimental model of lead nephropathy. IV. Correlation between renal functional changes and hematological indices of lead toxicity. 780 24

Trypanosoma cruzi survives in vertebrate and invertebrate hosts and has developed mechanisms that allow it to adapt to changes in the microenvironment such as temperature, pH, and ionic composition. Most of its calcium is concentrated in an organelle named the acidocalcisome, which is acidified by a (V-H+)-adenosine triphosphatase and has H+/Ca2+ counter-transportation for calcium uptake. In this work, acidocalcisomes were examined using different transmission electron microscopy techniques. In thin sections of different stages, acidocalcisomes presented a circular shape with an electron-dense inclusion containing P3-, Ca2+, Na+, Mg2+, K+, and Zn2+. They could be distinguished from gold-labeled albumin-containing reservosomes in whole epimastigotes, and a morphometric analysis showed higher amounts of these organelles in amastigotes as compared with epimastigotes and trypomastigotes. It is possible that this variation in the amount of acidocalcisomes in the different evolutive stages could reflect adaptation mechanisms used by the parasite to survive and multiply in different environmental conditions.
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PMID:The fine structure of acidocalcisomes in Trypanosoma cruzi. 1083 11

The Arabidopsis thaliana AtHMA3 protein belongs to the P(1B)-adenosine triphosphatase (ATPase) transporter family, involved in heavy metal transport. Functional expression of AtHMA3 phenotypically complements the Cd/Pb-hypersensitive yeast strain Deltaycf1, but not the Zn-hypersensitive mutant Deltazrc1. AtHMA3-complemented Deltaycf1 cells accumulate the same amount of cadmium as YCF1-complemented Deltaycf1 cells or wild-type cells, suggesting that AtHMA3 carries out an intracellular sequestration of Cd. A mutant of AtHMA3 altered in the P-ATPase phosphorylation domain did not complement Deltaycf1, suggesting that metal transport rather than chelation is involved. The fusion protein AtHMA3::green fluorescent protein (GFP) is localized at the vacuole, consistent with a role in the influx of cadmium into the vacuolar compartment. In A. thaliana, the mRNA of AtHMA3 was detected mainly in roots, old rosette leaves and cauline leaves. The expression levels were not affected by cadmium or zinc treatments.
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PMID:AtHMA3, a plant P1B-ATPase, functions as a Cd/Pb transporter in yeast. 1501 46

In the present study an attempt has been made to evaluate the effect of Tiron along with Zinc, Selenium and Vitamin E against vanadium intoxication in female albino rats. Toxicant caused significant increase in the activities of serum transaminases, serum alkaline phosphatase and lactate dehydrogenase. Significant decrease was observed in blood sugar, serum albumin and triglyceride levels whereas serum proteins, cholesterol and urea levels increased significantly during toxicity (p </= 0.001). Hepatic lipid peroxidation increased significantly, whereas significant depletion was observed in reduced glutathione after vanadium administration. The activity of glucose-6-phosphatase in the liver was also inhibited significantly after vanadium administration. A significant rise was observed in glycogen content of liver and kidney after toxicant exposure. Activities of alkaline phosphatase, adenosine triphosphatase and succinic dehydrogenase were inhibited significantly on the contrary activity of acid phosphatase elevated in kidney. Histopathological examination of the liver and kidney using light and ultramicroscopic study also substantiated the above findings. It was found that therapy with Tiron was effective but significant recovery in all the parameters was found with Tiron + Se followed by Tiron+ VitE and Tiron +Zn.
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PMID:Effect of tiron and its combination with nutritional supplements against vanadium intoxication in female albino rats. 1753 42

Propolis is a natural product produced by bees that was discovered through the study of traditional cures and knowledge of indigenous people throughout the world. It is rich in vitamins A, B, C, and E, and in amino acids, copper, iron, manganese, and zinc. The investigators studied the duration-dependent hepatoprotective effects of propolis extract (200 mg/kg, orally) against carbon tetrachloride (CCl 4; 1.5 mL/kg, intraperitoneally)-induced liver damage in rats. Administration of CCl 4 caused a sharp elevation in the activity of serum transaminases and serum alkaline phosphatase. A significant depletion in hepatically reduced glutathione was observed with significantly enhanced hepatic lipid peroxidation. After CCl 4 administration, glycogen contents and activities of alkaline phosphatase, adenosine triphosphatase, and succinic dehydrogenase were significantly decreased, whereas total protein contents and activity of acid phosphatase were increased in the liver and kidney. Propolis extract reversed alterations in all parameters when administered within 6, 12, and 24 h of toxicant exposure. Propolis therapy produced duration-dependent protection, with maximal protection achieved at 24 h after CCl 4 exposure. It is believed that propolis in its natural form has general pharmacologic value and marked hepatoprotective potential because of its composition of minerals, flavonoids, and phenolic compounds.
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PMID:Duration-dependent hepatoprotective effects of propolis extract against carbon tetrachloride-induced acute liver damage in rats. 1802 40

Wilson's disease is an infrequent, autosomic recessive pathology, resulting from a loss of function of an adenosine triphosphatase (ATP7B or WDNP), secondarily to a change (more than 60 are described currently), insertion or deletion of the ATP7B gene located on the chromosome 13q14.3-q21.1, which involves a reduction or an absence of the transport of copper in the bile and its accumulation in the body, notably the brain. Wilson's disease is transmitted by an autosomic recessive gene located on the long arm of chromosome 13. The prevalence of the heterozygote is evaluated at 1/90 and the homozygote at 1/30,000. Consanguinity, frequent in the socially geographically isolated populations, increases the prevalence of the disease. The toxic quantities of copper, which accumulate in the liver since early childhood and perhaps before, remain concentrated in the body for years. Hence, cytological and histological modifications can be detected in the biopsies, before the appearance of clinical or biological symptoms of hepatic damage. The accumulation of copper in the liver is due to a defect in the biliary excretion of metal and is accompanied invariably by a deficit in ceruloplasmin; protein synthesized from a transferred ATP7B gene, which causes retention of the copper ions in the liver. The detectable cellular anomalies are of two types: hepatic lesions resulting in acute hepatic insufficiency, acute hepatitis and finally advanced cirrhosis and lesions of the central nervous system responsible for the neurological and psychiatric disorders. In approximately 40-50% of the patients, the first manifestation of Wilson's disease affects the central nervous system. Although copper diffuses in the liver towards the blood and then towards other tissues, it has disastrous consequences only in the brain. It can therefore cause either a progressive neurological disease, or psychiatric disorders. Wilson's disease begins in the form of a hepatic, neurological, or psychiatric disease in at least 90% of the patients. In some rare cases, the first manifestations of the disease can be psychiatric which, according to the literature, accounts for only 10% of the cases. The disease can be revealed by isolated behavioral problems, an irrational syndrome, a schizophrenic syndrome, or a manic-depressive syndrome. Damage to the central nervous system can be more severe, thus, several differential diagnoses have been discussed: a psychotic disorder of late appearance; a depressive state; a mental confusion disorder. The clinical syndrome is complex. Indeed, it is the polymorphism, which dominates in the description of the psychiatric demonstrations of the disease. This can lead to prejudicial diagnostic wandering, particularly since heavy sedative treatment may be required to suppress behavioral problems. Clinically, Wilson's disease generally appears between the age of 10 and 20. It rarely remains masked until after the age of 40. The first manifestations are hepatic (40% of the cases), neurological (35%) or psychiatric (10%). The inaugural disorder can finally take on a haematological, renal, or mixed form in approximately 15% of the cases. We have detailed the principal clinical elements. In approximately 40-50% of the patients, the first manifestation of the disease affects the central nervous system, where it can cause either a progressive neurological disease, or psychiatric disorders. The ophthalmologic disorder is dominated by Kayser-Fleischer's ring, representing a green or bronze colored ring on the periphery of the cornea. It occupies the higher pole of the cornea, then the lower pole, and extends to the whole circumference. It is generally only visible under examination with a slit lamp. It disappears on average within 3-5 years following copper chelating therapy. Kayser-Fleischer's ring has been described other than in Wilson's disease, in exceptional cases of prolonged cholestasis. On haematological level, the hyperhaemolysis is due to the toxicity of the ionic copper, released massively in the plasma by hepatocellular necrosis. The other manifestations can be found in the following organs: renal, osteoarticular, cardiac, endocrine, cutaneous, and in the teguments. Until 1952, the diagnosis was evoked only on clinical symptomatology. It can henceforth be marked unambiguous, even in the absence of any symptom, by the description of a ceruloplasmin plasma concentration of less than 200 ml/l, and of a Kayser-Fleischer's ring. Hepatic copper on sample is constantly increased during the disease (from 3 to 25 micromol/g of dry weight). On the other hand, the absence of a reduction in the plasma ceruloplasmin does not make it possible to exclude the diagnosis. Conversely, a reduction in ceruloplasmin can exist other than in Wilson's disease (nephritic syndrome, malabsorption syndrome, or severe hepatic insufficiency). Kayser-Fleischer's ring is quasiconstant among patients with neuropsychiatric demonstrations (thus, its absence represents a very strong argument against the diagnosis). It can on the other hand be lacking during hepatic forms, and in this case, its absence is not an argument against the diagnosis. Magnetic resonance imaging can reveal abnormal signals of the grey cores. A genetic study is conducted by liaison analysis in the event of a family history of the disease. When it is not treated, Wilson's disease induces lesions of the tissues, the outcome of which is always fatal. Treatment relies on the regulation of copper chelation, which improves the prognosis, and zinc, which captures the copper in a nontoxic form. The severe psychiatric disorders observed during Wilson's disease may require tranquilizers, but care should be taken because of potential neurological or hepatic side effects. Lithium seems an interesting treatment and remains theoretically indicated, taking into account the scarcity of the extrapyramidal symptoms and the hepatic dysfunction among patients at the stage of cirrhosis, since it is not metabolized in the liver. Although rare, it is important to approach Wilson's disease in psychiatry because the psychiatric manifestations can precede the somatic disorders and help to pose the diagnosis. We stress the importance of the early diagnosis of the pathology, the outcome of which is fatal in the absence of specific treatment.
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PMID:[The onset of psychiatric disorders and Wilson's disease]. 1878 84

Low-temperature-induced biochemical changes in bud and root band zone of the sugar cane set suppress sprouting, which is responsible for drastic yield decline in ratoon crops. This study was undertaken to modulate these low-temperature-induced biochemical changes using potassium, zinc, and Ethrel to enhance the sprouting of buds at 5 and 10 degrees C. Potassium, zinc, and Ethrel led to 80, 50, and 40% improvement in bud sprouting at 5 degrees C, respectively. An increase in reducing sugars and a decrease in sucrose contents were recorded with treatment of potassium, zinc, and Ethrel. Acid invertase, adenosine triphosphatase, indoleacetic acid oxidase, and nitrate reductase in vivo activities were also enhanced. However, treatments led to a significant decline in indoleacetic acid, total phenols, and superoxide dismutase activity, which rendered the in situ toxicity buildup in sets at low temperatures.
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PMID:Modulation of low-temperature-induced biochemical changes in bud and root band zones of sugar cane sets by potassium, zinc, and Ethrel for improving sprouting. 1903 60


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