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)

Differences in skeletal muscle characteristics, metabolic profiles and functional performance between males and females were investigated using young (15--24 yrs) male and female twins as subjects. The comparison included such variables as anthropometry, muscle strength, mechanical power, maximum oxygen uptake, electrical activation of muscle, muscle fibre composition (m. vastus lateralis), and activities of several skeletal muscle enzymes. The results disclosed the following primary differences between males and females: In the various functional tests the performance of females was from 61.1 to 84.6% of that in males; distribution of slow twitch fibres in m. vastus lateralis of the females (49.1 +/- 7.7%) was lower (p less than .05) than that of the males (55.9 +/- 11.9); activities of enzymes Ca2+ stimulated ATPase, CPK, phosphorylase and LDH1a leads to py were higher (p less than .05--0.1) in the males, whereas the distribution pattern of LDH-1 isozyme was higher (p less than .05) in the females. A pronounced difference between the two groups was a almost 100% longer rise time of isometric force in females. It is concluded that the males as compared to the females demonstrate higher aerobic and strength performance capacity, more efficient neuromotoric output during contraction, more slow twitch muscle fibres and more pronounced contractile and glycolytic profiles in the skeletal muscles.
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PMID:Skeletal muscle fibre types, enzyme activities and physical performance in young males and females. 15 Jan 96

Paraoxon in doses of one LD50 (0.426 mg/kg), eight times and eighty times LD 50 was applied s.c. to female Sprague-Dawley rats. After 3, 6, 10, 24 and 36--48 h the activities of enzymes GOT, GPT, GLDH, SDH, CPK and ChE were measured, once after i.m. antidote application of Toxogonin only, of Toxogonin + atropine and the next one after application of combination Toxogonin + atropine + Solcoseryl (low-molecular components of deproteinized blood from young calves. The values obtained showed that in spite of treatment with Toxogonin or Toxogonin + atropine the activities of the enzymes increased; this enhancement could be prevented by addition of Solcoseryl to Toxogonin + atropine. The ChE-activity after 36 h was equivalent to that of the control value. The effect of paraoxon in the initial phase of poisoning was discussed in connection with hypoxia and acidosis resulting from a respiratory insufficiency as well as the inhibition of ATPase-activity with restriction of the energy metabolism following: consequently the effect of Solcoseryl was interpreted as an activation of the disturbed energy metabolism.
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PMID:[Phosphoric acid ester poisoned rats after antidote therapy. 2. Determination of serum enzyme activity]. 58 4

Congenital polycystic kidney disease is characterized by the formation of large fluid-filled cysts in kidney tubules. It has been postulated that increased epithelial cell proliferation and altered transtubular fluid transport are necessary for cyst formation. To address the latter problem, we have studied the plasma membrane distribution of the alpha 1 and beta 1 subunits of Na+/K(+)-ATPase during progressive stages of proximal and collecting tubular cyst formation in the CPK mouse, a murine model of autosomal recessive polycystic kidney disease. In both control and cystic proximal tubules, Na+/K(+)-ATPase distribution was restricted to the basal-lateral membrane of cells. However, in newborn through day 5 kidney tissue, 16% of control vs. 47% of cystic outer cortical, 6% of control vs. 46% of cystic inner cortical, and 2% of control vs. 63% of cystic medullary collecting tubules demonstrated apical and lateral membrane distribution of Na+/K(+)-ATPase. In all nephrogenic zones, the percentage of control or cystic collecting tubules demonstrating apical membrane distribution of Na+/K(+)-ATPase decreased over time, but the percentage of cystic collecting tubules with apical membrane Na+/K(+)-ATPase remained significantly greater than in developmentally matched controls. No alterations in the normal distributions of other apical or basal-lateral membrane marker proteins were noted at any stage of control or cystic proximal or collecting tubule development. We conclude that apical-lateral membrane Na+/K(+)-ATPase expression is a normal transient feature of early collecting tubule development. However, apical membrane Na+/K(+)-ATPase persists in cystic kidneys, suggesting that such expression may be a manifestation of the relatively undifferentiated phenotype of epithelial cells lining collecting tubule cysts. The persistence of apical membrane Na+/K(+)-ATPase, if the enzyme is functional, may have pathogenic important in abnormal transtubular fluid transport in polycystic kidney disease.
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PMID:Abnormal sodium pump distribution during renal tubulogenesis in congenital murine polycystic kidney disease. 132 37

m-Nisoldipine 4, 8, 16 nmol/L, nisoldipine 1, 4 nmol/L and nifedipine 4, 8, 16, 50 nmol/L enhanced the recoveries of functional parameters of working rabbit hearts after ischemia-reperfusion, as well as prevented the development of contracture and the release of CPK from the reperfused hearts. m-Nisoldipine 8 nmol/L, nisoldipine 1 nmol/L and nifedipine 8 nmol/L attenuated the reduction of myocardial Na+-K+-ATPase and 5'-nucleotidase activity induced by ischemia-reperfusion. The breakdown of membrane phospholipids and elevation of the myocardial Ca2+-ATPase activity and the free fatty acids level were also prevented.
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PMID:[Protective effects of m-nisoldipine and nisoldipine on myocardial damage in working rabbit hearts after ischemia-reperfusion]. 255 66

Recent studies in a murine model of genetically-determined polycystic kidney disease, the CPK mouse, have suggested that alterations in renal Na-K ATPase activity in concert with tubular epithelial hyperplasia have pathogenic import in proximal tubular cyst formation. In the current study, we therefore studied the relative roles of Na-K ATPase activity, tubular epithelial hyperplasia, and basal lamina alterations during in vitro modulation of proximal tubular cyst regression during serum-free organ culture of newborn CPK kidneys. Under basal in vitro conditions, regression of CPK proximal tubular cysts was demonstrated in association with progressive decreases in Na-K ATPase activity and tubular epithelial hyperplasia. The pattern of proximal tubular cyst regression was modified by: a) Na-K ATPase activity induction with triiodothyronine, which promoted proximal tubular cystogenesis; and b) Na-K ATPase activity inhibition with ouabain, which blocked the effects of T3 on the process of cyst formation. Modulation of proximal tubular cystogenesis by Na-K ATPase induction and inhibition were accomplished without significant changes in proximal tubular epithelial hyperplasia or expression of basal lamina components. We conclude that increased Na pump activity may have a significant role in proximal tubular cyst formation and progressive enlargement in the CPK mouse.
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PMID:In vitro modulation of tubular cyst regression in murine polycystic kidney disease. 255 82

A first Japanese case of an adult polysaccharide storage myopathy (APSM) was reported. A 30-year-old Japanese male was admitted because of weakness of the lower limbs. The onset of the symptoms was at the age of 23. Neurologically he had moderate weakness of proximal limb muscles involving the lower limbs more than the upper and slightly decreased vibratory sense in the feet. His gait was waddling. The following laboratory values were obtained; SGOT 45 I.U., SGPT 83 I.U., CPK 218 I.U., UA 8.3 mg/dl. Ischemic exercise test of the forearm showed a normal rise of venous lactate. EMG revealed a mixture of myopathic and mild neurogenic patterns characterized by motor units of short duration and low amplitude with intermittent high amplitude potentials, fibrillation and fasciculation. There were also prominent myotonic discharges without clinical myotonia. MCV was normal, however sural nerve SCV was slightly slow (lt. 36/m, rt. 38 m/s). Muscle biopsy revealed vacuolar myopathy. Most vacuoles contained basophilic, PAS-positive, diastase-resistant and Lugol's iodine-negative material. With ATPase staining there was type 1 fiber predominance (84%), but the vacuoles were predominantly seen in type 2A fiber. In ultrastructural study, the storage material was located under the sarcolemma and in the areas of the intermyofibrillar network. No delimiting membranes were seen. At higher magnification, these masses were consisted of filaments. Therefore the storage material was considered to be unusual polysaccharide. Glycogen storage disease was suspected, however, biochemical study of the muscle specimen disclosed no enzymatic defect including branching enzyme.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Adult polysaccharide storage myopathy]. 269 Nov 65

In the current study, the pathogenesis of proximal tubular cyst formation was studied in an animal model of polycystic kidney disease, the CPK mouse. The specific roles of (a) sodium-potassium adenosine triphosphatase (Na-K ATPase) activity, determined by an enzyme-linked kinetic microassay, (b) proximal tubular epithelial hyperplasia, determined by calculation of mitotic indices, and (c) altered proximal tubular basal lamina formation, determined by immunohistological localization of basal lamina glycoproteins, were investigated at progressive developmental stages of CPK proximal tubular cyst formation. Increases in renal Na-K ATPase were present at the earliest fetal stages of proximal tubular cyst formation, and subsequently paralleled the course of proximal tubular cyst progression. Proximal tubular epithelial hyperplasia, although not present at the earliest stages of cyst formation, was a consistent feature of progressive proximal tubular cystic enlargement. Abnormalities in basal lamina glycoprotein expression were not present at any stage of proximal tubular cyst development. We conclude that increased Na-K ATPase and tubular epithelial hyperplasia are significant features of proximal tubular cyst formation in the CPK mouse.
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PMID:Congenital murine polycystic kidney disease. II. Pathogenesis of tubular cyst formation. 285 68

Glycerinated rabbit psoas muscle fibers containing native CPK, ATPase, and myokinase activities were used and isometric contraction and relaxation responses to either ADP or ATP + CP or to ATP alone in the presence and absence of P1, P5-di(adenosine-5'-pentaphosphate), a myokinase inhibitor, were compared. In previous (14) work it was shown that CP generated more efficient and faster contraction and relaxation of glycerinated muscle fibers than ATP. The present work deals with the role of myokinase in the differential response of fibers to CP and ATP. Inhibition of the myokinase activity of these fibers caused slight diminution of the rate of contraction at physiological concentrations of ATP. Uninhibited fibers were not able to reach maximum contraction, because the tension began to drop gradually even in the presence of Ca2+. Addition of Ap5A permitted maximum contraction and the ability to stay at the contracted state. In the case of CP + adenosine nucleotides (ATP or ADP), myokinase activity decreased the rate of tension development which was statistically significant after 5-7 sec of contraction. Thus, a higher tension was obtainable when myokinase was inhibited. At high concentration of adenine nucleotides (greater than 2 mM) and in the absence of Ap5A, not only the maximum tension never was reached, but a spontaneous drop in tension was observed before addition of EGTA, as was seen with ATP alone. Relaxation was faster and more complete in the presence of uninhibited myokinase activity except that the ADP was low (125 mM). These observations provide further evidence for a close functional interaction of these three enzymes in the mechanism of contraction and relaxation, giving further support to the notion of the creatine-phosphocreatine energy shuttle.
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PMID:Myokinase and contractile function of glycerinated muscle fibers. 301 Oct 38

The calcium uptake and ATPase activity were studied using fragmented sarcoplasmic reticulum (FSR) vesicles from normal and selenium (vitamin E)--deficient lambs. The latter group was suffering from white muscle disease (WMD). The calcium uptake of FSR vesicles from muscle of WMD lambs was reduced 10-fold as compared to those from normal lambs. An inverse relationship was found with the calcium uptake ability of the FSR vesicles and the severity of WMD. ATPase activity was nonsignificantly lower in vesicles from WMD lambs. The most active FSR vesicles from both normal and WMD lambs banded at 27% when purified on linear sucrose density gradients. The number of protein bands appearing in acrylamide gels of the purified vesicles appeared to be directly proportional to the severity of WMD. The 75Se cosedimented with the calcium uptake and ATPase activity when FSR vesicles from a lamb injected with 75Se-selenite were subjected to linear sucrose density gradient centrifugation, suggesting that selenium is incorporated into these vesicles. Injection of selenium into WMD lambs resulted in significantly greater calcium uptake activity in vesicles 18 and 38 days later as compared with untreated WMD lambs. Injection of selenium in WMD lambs resulted in a marked decrease in plasma CPK activity and a significant increase of glutathione peroxidase activity in the blood.
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PMID:Calcium uptake and ATPase activity of sarcoplasmic reticulum vesicles isolated from control and selenium deficient lambs. 821 48

Various cardiac lesions such as hypertrophy, disarray and fibrosis similar to HCM, were often found in the heart of methamphetamine (MA) abusers. Myolysis, eosinophilic changes, contraction band necrosis and small round cell infiltration were also observed. Male ddy mouse were administered MA 1 mg/kg subcutaneously every day for 4 weeks. Their hearts revealed many cardiac changes such as hypertrophy, myolysis, contraction band necrosis, disarrangement of myofibers, saw-like cytoplasm, side-to-side connection of cardiac cells and vascuolative degeneration microscopically, and crysterosis of mitochondria, enlargement of sarcoplasmic reticulum and hypercontraction electronmicroscopically. These changes are thought to be similar to that of MA abusers, so it is certified that MA has toxic effect on the heart. Moreover, these changes could not be found when beta-blocker or calcium antagonist was premedicated. To elucidate the mechanisms of MA cardiac toxicity, we have designed some experiments. When MA (15 mg or 20 mg/kg) was administered on rats, cardiac lipid peroxidates, as a marker of free radical, increased rapidly. When rats were feeded for 7 weeks with Vitamin E deficient diet, 10 mg/kg MA administration was enough to increase lipid peroxidates. Simultaneous ECG observation revealed various arrhythmia such as VPB, A-V block and intraventricular conduction delay. In the investigation of contractile protein, although we could not find differences in the isozyme pattern of myosin heavy chain between MA groups (1 mg/kg for 8 and 12 weeks) and control group, Mg2+ ATPase activity of myocardial actomyosin at 0.1 microM Ca2+ increased significantly in 12 weeks MA group. We also found MA induced cardiac toxicity in cultured myocytes. Primary cultured adult rat myocytes were exposed to MA (1 x 10(-5) M and 1 x 10(-3) M) for 1 to 24 h in the presence and absence of 1 x 10(-5) M propranolol. After 24-h MA treatment, cellular granulation, swelling and hypercontraction and release of CPK were observed both with and without propranolol treatment. These findings suggest that MA may exert direct toxic effects on the heart.
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PMID:[Cardiac lesions in methamphetamine abusers]. 1190 41


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