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Query: UNIPROT:P17174 (
aspartate aminotransferase
)
14,872
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Monensin is an ionophoretic antibiotic, which selectively transports alkali metal cations across biological membranes. In growing swine, monensin toxicosis causes acute, degenerative cardiac and skeletal
myopathy
resembling vitamin E-selenium deficiency. Selenium is an essential trace element incorporated in glutathione peroxidase (GSH-Px), an antioxidant enzyme system that protects subcellular membranes. In our study, we examined the effects of monensin on body weight, Se balance, antioxidant status, and serum concentrations of selected minerals in growing pigs that were genetically hypo- or hyperselenemic (hypo-Se and hyper-Se, respectively). Three groups of eight 8-week-old pigs, each comprised of 4 hypo-Se and 4 hyper-Se pigs (76.4 +/- 3.0 and 106.3 +/- 10.3 ng of Se/ml of serum, respectively), were fed standard diets containing 0.1 mg of supplemental Se/kg of body weight, and either 0, 200, or 400 mg of monensin/kg for a 77-day period, followed by a 28-day monensin withdrawal period. On days 0, 7, 28, 56, 70, and 98, all pigs were weighed and blood was collected for determination of serum GSH-Px, creatine phosphokinase, and
aspartate transaminase
values, as well as serum concentrations of vitamin E, Se, Ca, Cu, Fe, K, Mg, Na, P, and Zn. Significance of main effects of monensin treatment, genetic Se status, and their interactions was tested by Fisher's variance ratio test, followed by conditional comparison of treatment means with a Bonferroni test. Signs of monensin toxicosis were not observed and monensin consumption had no effect on body weight, or serum creatine phosphokinase,
aspartate transaminase
, or Se values. However, pigs consuming monensin had consistently higher serum GSH-Px activities, possibly because of increased synthesis of this adaptive antioxidant enzyme. Interactions were not found between monensin and genetic Se status. Hyperselenemic pigs were heavier and had higher serum Se and GSH-Px values than hypo-Se pigs. Furthermore, hypo-Se and hyper-Se pigs were hypo- and hypercupremic, respectively, suggesting genetic regulation of copper status. It is likely that pigs with inadequate antioxidant status (hyposelenemia, hypocupremia) are more susceptible to diseases associated with cellular membrane damage, such as vitamin E-Se deficiency disease and monensin toxicosis.
...
PMID:Effects of monensin on selenium status and related factors in genetically hypo- and hyperselenemic growing swine. 146 9
Twenty-three biochemistry parameters and hematocrit were followed during 10 days in a 13 months old Arabian Oryx (Oryx leucoryx) during capture
myopathy
. An increase was found in bilirubin, creatine-kinase, alanine aminotransferase, and
aspartate aminotransferase
levels, but not in potassium level. Most of the parameters analyzed were the first given for this species.
...
PMID:Biochemical parameters following capture myopathy in one Arabian oryx (Oryx leucoryx). 147 80
A necrotizing skeletal
myopathy
of rear limbs was diagnosed in 17 flocks of commercial turkeys. The mean mortality attributed to the
myopathy
was 2.29% (range = 0.13-9.7%) over a mean period of 9.6 days (range = 6-14 days). The mean age of the birds at the time of onset was 7.4 weeks (range = 4-10.5 weeks). Clinically, birds experienced an episode of watery droppings and high-pitched crying, followed by rear-limb paresis or paralysis. Creatine kinase and
aspartate aminotransferase
were markedly elevated in birds with the
myopathy
. Grossly, a few birds had pale streaking in the muscles of the thighs and legs. Histologically, acute and subacute degeneration was present in myofibers of the legs, abdomen, thighs, back, and tail. The subacute lesion was characterized by marked sarcolemmal cell proliferation. Feed analyses ruled out selenium deficiency and the presence of mycotoxins as etiologies. Monensin was present in approved usage or only slightly elevated levels. A known potentiating antibiotic was being used concurrently with monensin in only one flock.
...
PMID:A syndrome in commercial turkeys in California and Oregon characterized by a rear-limb necrotizing skeletal myopathy. 148 64
Infused beta 2 agonists have been shown to cause focal myocardial necrosis. Serum creatine kinase activity was compared in 13 patients with brittle asthma currently being treated with subcutaneous terbutaline and an age and sex matched control group of patients with moderate asthma having inhaled treatment only. The median serum total creatine kinase activity for patients receiving subcutaneous terbutaline (211 units/l) was greater than that for the control group (120 units/l). The cardiac specific isoenzyme component of creatine kinase was not raised in either group, and the electrocardiograms and serum
aspartate aminotransferase
activity were normal. Electromyograms in five patients receiving subcutaneous terbutaline with high creatine kinase activity showed changes consistent with myositis in two, one of whom was subsequently shown to have a metabolic
myopathy
, which is thought to be long standing. No pathological changes were seen in the myocardium at necropsy in a patient who died from an acute attack of asthma while taking subcutaneous terbutaline. These results suggest that the raised creatine kinase activity seen in patients receiving this treatment is unlikely to be myocardial in origin.
...
PMID:Creatine kinase activity in patients with brittle asthma treated with long term subcutaneous terbutaline. 192 27
Acute muscle pain with stiffness developed in a patient with latent hypothyroidism after administration of clofibrate. Serum creatine kinase (CK),
aspartate aminotransferase
, and lactate dehydrogenase were markedly elevated, but returned to normal one and a half months after the discontinuation of clofibrate. Clofibrate challenge (750 mg/day) for three days caused muscle pain and an elevation in serum CK. Hypothyroidism may be a predisposing factor in the development of clofibrate-induced
myopathy
.
...
PMID:Clofibrate-induced myopathy in a patient with primary hypothyroidism. 208 82
Serum activity of alanine aminotransferase (ALT) was consistently increased in dogs with canine X-linked muscular dystrophy (CXMD), a primary
myopathy
characterized by profound and on-going skeletal muscle necrosis. In order to determine whether the ALT was of liver origin, serum activity of creatine kinase (CK),
aspartate aminotransferase
(
AST
), ALT, and sorbitol dehydrogenase (SDH) obtained from dystrophic dogs was compared with enzyme activity present in clinically normal dogs. In dystrophic dogs at all ages tested, serum activity of CK,
AST
, and ALT was increased, and significant increases were present in dogs four weeks or older. In contrast, SDH activity in dystrophic dogs was not statistically different from values in clinically normal dogs. Ultrastructural examination of liver tissue revealed no evidence of hepatic degeneration in dystrophic dogs. It was concluded that increased serum activity of ALT in the dog may be associated with severe skeletal muscle degeneration, without concurrent hepatocellular necrosis.
...
PMID:Increased serum alanine aminotransferase activity associated with muscle necrosis in the dog. 236 22
Salinomycin poisoning occurred in a flock of 700 point-of-lay turkeys; 400 birds died over 7 days as a result of consuming feed contaminated with 50 ppm salinomycin. No gross lesions were detected. Histologic evidence of a
myopathy
was most readily detected in leg muscles of turkeys 5 to 7 d after ingesting salinomycin. Feeding trials were undertaken and individual susceptibility to the drug was found to vary greatly. In affected birds the plasma concentrations of creatine kinase (CK) and
aspartate aminotransferase
(
AST
) were found to be in the range of 500,000 to 2,500,000 IU/l and 9000 to 25,000 IU/l, respectively. The marked increase in the plasma activities of these enzymes preceded histological evidence of segmental muscle necrosis.
...
PMID:Salinomycin poisoning in point-of-lay turkeys. 281 61
Blood samples were collected twice weekly over a nine month period from 24 Thoroughbred racehorses in training at Newmarket to study the effects of daily training schedules and stage of oestrous cycle on serum enzyme levels and clinical signs of equine exertional
myopathy
. The sampling period extended from November to July and was performed between 16:00 h and 18:00 h so as to be at least 6 h after exercise. Serum creatine kinase,
aspartate aminotransferase
and plasma progestogen concentrations were measured. All horses were subjected to a similar traditional training programme. The study demonstrated marked fluctuations in serum muscle enzyme concentrations which were more pronounced in two-year-old fillies than three-year-old fillies and colts. There was no correlation, however, with the stage of oestrous cycle. It was concluded that some degree of muscle cell damage, which results in a variable increase in serum creatine kinase levels, occurs in all horses following light exercise after a rest day. Traditional flat race training may not be ideal in this respect and it is suggested that, for horses with an observed tendency towards exertional
myopathy
, more consistent and longer periods of less strenuous exercise may be advantageous.
...
PMID:Changes in serum muscle enzyme levels associated with training schedules and stage of the oestrous cycle in Thoroughbred racehorses. 376 82
The effect of halothane-induced hypotension on the development of postanesthetic
myopathy
was studied, using 6 healthy adult horses. Horses were anesthetized with halothane in oxygen for 3.5 hours on each of 2 occasions. Intermittent positive-pressure ventilation was used to maintain PaCO2 of 45 to 55 mm of Hg throughout both anesthetic exposures. By regulating the inspired halothane concentration, a mean arterial blood pressure of 85 to 95 mm of Hg (normotension) was maintained throughout the 1st anesthetic exposure, and a mean arterial blood pressure of 55 to 65 mm of Hg (hypotension) was maintained during the 2nd anesthetic exposure. All horses recovered uneventfully from normotensive anesthesia, but all had some muscle dysfunction after prolonged hypotensive anesthesia. Because of apparent animal discomfort and lameness involving more than 1 limb, 3 horses were euthanatized soon after they recovered from hypotensive anesthesia. The 3 other horses showed a degree of lameness. In addition, 1 horse had raised, swollen plaques over the hip, rib, and facial areas which were in contact with the surgical table, and another had evidence of facial nerve paralysis. One hour after the 6 horses stood after hypotensive anesthesia was completed, values obtained for
aspartate transaminase
and creatinine were significantly (P less than 0.05) greater than those obtained after normotensive anesthesia was completed. Aspartate transaminase, total bilirubin, and creatinine values were significantly (P less than 0.05) increased when compared with those obtained before horses were anesthetized. A large increase was measured in creatine kinase. Twenty-four hours after hypotensive anesthesia was completed, creatine kinase and lactate dehydrogenase in the 3 surviving horses were significantly (P less than 0.05) greater than those values after normotensive anesthesia was completed.
...
PMID:Arterial hypotension and the development of postanesthetic myopathy in halothane-anesthetized horses. 382 55
Three patients with opiate self-poisoning developed acute muscle damage with elevated serum
aspartate aminotransferase
and creatine kinase activities, increased serum myoglobin concentrations, raised plasma creatinine concentrations, hypocalcaemia and hyperphosphataemia. These abnormalities gradually resolved over 7-10 days, but recovery was complicated due to the development of acute renal failure (requiring haemodialysis) in one patient. Plasma drug concentrations, shortly after admission, in the patients taking dihydrocodeine and morphine were grossly elevated (184 and 60 micrograms/l respectively). Clinical evidence of
myopathy
was minimal in all three patients and muscle biopsy of one patient was normal at 7 days.
...
PMID:Opiate-induced rhabdomyolysis. 398 9
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