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)

1 The specific [3H]-ouabain binding to microsomal fractions derived from cat heart, liver, spleen, and kidney increased significantly following chronic administration of ethanol. 2 Since ouabain binds exclusively to cell membrane (Na+ + K+)-adenosine triphosphatase ((Na+ + K+)-ATPase), these results provide evidence for an increase in number of (Na+ + K+)-ATPase macromolecules during chronic alcoholism. 3 The importance of the increase in number of (Na+ + K+)-ATPase molecules in the adaptive increase in ethanol metabolism and cardiac myopathy in chronic alcoholism is discussed.
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PMID:[3H]-Ouabain binding to peripheral organs of cats: effect of ethanol. 14 33

The histopathology of muscle in cerebral palsy has not been elucidated because correlated morphologic and biochemical data on normal pediatric muscles are insufficient to allow adequate correlation of pathologic findings. One hundred and eight muscle biopsies were taken during reconstructive operations on 85 patients. Normal values for pediatric muscles were obtained from a literature review and supplemented with our data on normal patients. Fiber sizes are normally different for children of different ages. Histochemical staining of enzyme systems demonstrate that adenosine triphosphatase staining, pre-incubated at pH 9.4, 4.6, AND 4.3 WAS USED FOR FIBer typing and fiber size. Depending on the muscle biopsied and the clinical status of the patient, there is a variety of patterns of type I and type II fiber atrophy, hypertrophy, and myopathy. In some cases, denervation changes are present to suggest nerve entrapment. Correlated clinical observations suggest type I fiber predominant muscles do not re-educate well when surgically transferred to perform a specified function.
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PMID:Pathology of spastic muscle in cerebral palsy. 15 52

A case of non-progressive congenital myopathy is described in which there was absence of muscles and scapulo-peroneal distribution of weakness. The muscle biopsy showed preferential atrophy of Type I fibers and subsarcolemal bodies. These bodies were composed of an acidic protein with sulphahydryl groups which showed acid stable adenosine triphosphatase activity. The possibility of a maturational arrest as a cause is presented.
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PMID:Department of Neurology, Northwestern University Medical School, Chicago, Illinois. 19 43

1 (-)Emetine (0.25-2.0 mg/kg i.p.) was administered to rats for up to 220 days. 2 At doses of 1.0 mg/kg or less, the animals continued to gain weight but more slowly than the untreated control animals. The physiological changes in the muscles from these animals were minimal; there was a small reduction in both the resting membrane potential and in the maximum rate of rise of the action potential. There was no atrophy or loss of muscle fibres although in the occasional muscle, hyaline fibres, necrotic fibres and split fibres were observed. There was a focal loss of myofibrillar adenosine triphosphatase (ATPase) and nicotinamide adenine dinucleotide tetrazolium reductase (NADH-TR) in Type II and Type III fibres, but no such loss in Type I fibres. 3 The animals receiving 2.0 mg/kg of (-)emetine gained weight slowly for up to 20 days but then rapidly lost weight and by 30 days they were weak and emaciated. The muscles from these animals were severly atrophied and the total muscle wet weight was reduced by almost 20%. 4 The strength of the muscles from these animals was measured in vitro using direct stimulation. They were weaker than normal both in absolute terms and when expressed in terms of tension developed/unit wet weight. 5 There was no evidence of either functional or structural denervation but surgically denervated muscles from animals in this group were indistinguishable from denervated muscles from normal rats. 6 Severe structural damage was obvious in the fibres of both extensor digitorum longus and soleus. Necrotic, hyaline and splitting fibres were common and the focal loss of myofibrillar ATPase and NADH-TR activity was extensive and occurred in Type I fibres as well as in Type II and Type II fibres. 7 It is concluded that the muscular weakness induced by (-)-emetine is due to a direct effect on the muscle fibres and that this occurs at a subcellular level. There is no evidence that functional or structural denervation plays any role in the aetiology of emetine myopathy in the rat.
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PMID:Emetine myopathy in the rat. 127 39

The response of rat quadriceps muscle fibers to chronic streptozotocin (STZ) diabetes was studied. Transverse sections of rectus femoris muscle from diabetic and weight-matched control rats were assayed for myofibrilar adenosine triphosphatase (ATPase) and nicotinamide adenine dinucleotide-tetrazolium reductase (NADH-TR). A quantitative analysis was carried out by an automatic interactive analysis system focused on the fiber type size and distribution. STZ-induced diabetes caused important effects in this muscle, with changes in the distribution of oxidative enzyme reactions, type I fiber hypertrophy, and type II fiber atrophy, which was greater in type IIB than in type IIA. It is concluded that hypoinsulinism produces morphological alterations in proximal skeletal muscle fibers that are similar to those of neurogenic myopathy. Thus the pathological changes in these mammalian muscle fibers could explain the clinical syndrome seen in diabetic patients called "diabetic symmetrical proximal motor neuropathy," perhaps the least understood of the major neuropathic complications of diabetes.
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PMID:Proximal skeletal muscle alterations in streptozotocin-diabetic rats: a histochemical and morphometric analysis. 182 78

In this communication, the results of an enzyme histochemical study on m. gluteus medius of horses, sensitive to exertional myopathy, during attacks of rhabdomyolysis are presented. The activity and location of about 25 enzymes were examined. In the present report, the early metabolic changes are discussed. Within 6 min after an attack, some large rounded fibres (approximately 2%) were seen, which showed an intense red staining in the haematoxylin and eosin sections. These hypercontracted fibres showed an increase in activity of mitochondrial adenosine triphosphatase, indicating the presence of uncoupling and/or loose coupling of the mitochondria. This finding may point to a deficient production of ATP in the m. gluteus medius of horses sensitive for exertional myopathy and this deficiency may lead to pathological alterations in the skeletal muscles. The pathological fibres revealed a changed activity of other mitochondrial enzymes as well.
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PMID:[Histochemical changes in skeletal muscles of racehorses susceptible to rhabdomyolysis after exertion. I. Early myopathological changes]. 253 41

Macroscopic, histopathologic, and histochemical investigations were made on a group of eight neonatal Angus X Hereford calves, selected from an ongoing outbreak of crooked calf disease among calving heifers. Arthrogryposis of the forelimbs was seen to varying degrees in all eight animals, and torticollis was present in six calves. Histopathology, using hematoxylin and eosin stain, did not reveal any striking or consistent lesion in the affected animals; the majority of the tissues sampled were normal. Muscle samples were processed for adenosine triphosphatase (ATPase) and NADH-tetrazolium reductase (NADH-tr) histochemistry, and the data suggest that a primary myopathy is not responsible for the congenital anomalies in the affected calves.
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PMID:Crooked calf disease: a histological and histochemical examination of eight affected calves. 381 Nov 38

Total calcium uptake, but not the initial rate, and non-calcium-stimulated (basic) adenosine triphosphatase activity of rat gastrocnemius microsomal fractions 3, 7 and 14 days after denervation increased compared with contralateral controls. Microsomal sphingomyelin also increased but phosphatidylcholine plus choline plasmalogen was unchanged in amount. These results are contrasted with those reported for vincristine myopathy.
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PMID:Calcium transport and phospholipid composition of microsomal fractions from denervated rat gastrocnemius. 427 77

Our previous studies indicate that impaired function of skeletal muscle limits the exercise tolerance of patients with end-stage renal failure who are either maintained on dialysis or undergo renal transplantation. To study the morphology of the condition, muscle biopsies were performed on eight patients with renal failure-associated myopathy. Control samples were taken from seven healthy athletes undergoing knee surgery and from five otherwise healthy but untrained subjects. Tissues were examined by routine light and transmission electron microscopy. Histochemical staining of frozen sections for myosin adenosine triphosphatase and quantitative computer-assisted morphometry of the fiber type and size was performed. The mean (+/- SD) size for type I fibers in patients was 61.2 +/- 11.8 microns, while type II fibers measured 46.7 +/- 11.4 microns. The mean percentage of type II fibers was 67% +/- 12%. These values are within the normal population range and were not different from controls. Significant changes were found on light microscopy of patient samples. These included fiber splitting, internalized nuclei, nuclear knots, moth-eaten fibers, fiber degeneration and regeneration, increased content of lipid droplets, and fiber-type grouping. Electron microscopy showed a large variety of nonspecific abnormalities, including mitochondrial changes, Z-band degeneration, myofilament loss, and accumulation of intracellular glycogen. Ten of 12 control subjects showed no such changes; minor abnormalities were noted on both light and electron microscopy in the remaining two subjects. Muscle oxidative capacity (19.5 +/- 5.1 microL O2/min) for patients with end-stage renal failure was not different from values for those who had undergone renal transplantation, but was lower than values found in trained athletes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Morphologic features of the myopathy associated with chronic renal failure. 823 13

Ouabain, a cardiac glycoside, binds to the Na(+)-K(+)-adenosine triphosphatase (Na+ pump) and prevents active transport of Na+ and K+ across cell membranes. We used [3H]ouabain to quantify the number and affinity of Na+ pumps in skeletal muscle from Quarter Horses with the muscular disorder hyperkalemic periodic paralysis (HYPP). [3H]Ouabain-binding properties of gluteal muscle from clinically normal and affected horses were used to determine whether altered Na+ pump number or affinity could contribute to the pathologic features of muscle in affected horses. Foals and adult horses with HYPP were compared with age-matched clinically normal horses. The number of [3H]ouabain-binding sites in adult gluteal muscle was not different between the 2 types of horses (85.7 +/- 8.9 pmol of [3H]ouabain-binding sites/g [wet muscle weight] in horses with HYPP vs 100.2 +/- 8.8 pmol/g in clinically normal adult horses). Gluteal muscles in HYPP-affected and clinically normal foals also contained a similar number of [3H]ouabain-binding sites (222.3 +/- 21.0 pmol/g vs 225.3 +/- 24.2 pmol/g, respectively). The affinity of these binding sites for ouabain was not different, between adults or foals, in clinically normal or affected horses. Our results indicate that membrane events underlying the periodic episodes of paralysis in horses with HYPP are not attributable to quantitative changes in Na+ pump number or affinity. Our data cannot exclude the possibility that the specific activity of the Na+ pump is altered in muscle from HYPP-affected horses.
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PMID:[3H]ouabain binding in skeletal muscle from horses with hyperkalemic periodic paralysis. 839 Dec 30


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