Gene/Protein Disease Symptom Drug Enzyme Compound
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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.
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PMID:Effects of monensin on selenium status and related factors in genetically hypo- and hyperselenemic growing swine. 146 9

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.
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PMID:A syndrome in commercial turkeys in California and Oregon characterized by a rear-limb necrotizing skeletal myopathy. 148 64

Quail were fed monensin to determine liver damage, as measured by changes in activities of serum enzymes and liver microsomal enzymes. Monensin fed at a therapeutic level of 110 ppm for 2 weeks produced an increase in cytochrome P-450 and cytochrome b5 and induction of the activities of benzphetamine N-demethylase, aminopyrine N-demethylase, and aniline hydroxylase, with no changes in the activities of serum sorbitol dehydrogenase (SDH), alanine aminotransferase (ALT), and aspartate aminotransferase (AST). On the other hand, quail fed 110 ppm, 220 ppm, and 330 ppm monensin in feed for 6 weeks showed a significant rise in SDH and AST activities at 330 ppm but not at 110 ppm and 220 ppm. The manifestations of liver toxicity observed at 330 ppm were accompanied by a significant decrease in all the aforementioned hepatic microsomal mixed-function oxidases. In contrast, quail fed monensin at 110 ppm and 220 ppm for 6 weeks produced no change in these parameters except for benzphetamine N-demethylase, aminopyrine N-demethylase, and aniline hydroxylase, which were significantly increased in birds fed 220 ppm of monensin.
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PMID:Toxicity of dietary monensin in quail. 224 82

Twenty beef calves weighing approximately 180 kg were allotted to 3 groups. In group A, 6 calves were given 25 mg of mycelial monensin/kg of body weight orally and were evaluated at 1, 2, and 4 days for clinical, ECG, clinicopathologic, and pathologic alterations. In group B, 7 calves were given a single dose of monensin (40 mg/kg) and 5 were given a 2nd 40 mg/kg dose on day 7; calves were evaluated at days 1, 2, 4, 7, 8, 9, and 11. In group C, 2 calves served as controls. Monensin-treated calves developed anorexia, diarrhea, and lethargy after day 1. One group B calf died on day 7 with lesions of congestive heart failure. Electrocardiographic abnormalities were not observed in group A calves; in group B, prolongation of Q-T and QRS intervals occurred from days 2 to 11 and first degree heart block was seen from days 7 to 11. Clinicopathologic alterations included: increased serum activities of aspartate aminotransferase and creatine kinase in group B calves after day 2; decreased serum K+, Na+, and Ca2+ concentrations in both groups, and postdosing occurrence of leukocytosis. Calves were euthanatized sequentially and the lesions of monensin toxicosis were present in the heart, skeletal muscles, and rumen in groups A and B. Disseminated pale yellowish-brown areas of necrosis were present in the ventricular myocardium of 6 of 12 group B calves. Gross lesions were not present in the skeletal muscles or rumen. Microscopically, the myocardial and skeletal muscular lesions were characterized by sarcoplasmic vacuolation from mitochondrial swelling and lipid accumulation in calves killed after day 1 in groups A and B, and by myocardial necrosis with contraction bands, but without calcification, in group B calves killed by day 4. Acute rumenitis was present in groups A and B calves. Myotoxic effects of monensin may be related to its action as an ionophore producing altered intracellular ion concentrations and initiating degeneration and necrosis in striated muscle fibers.
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PMID:Clinical, clinicopathologic, and pathologic alterations in acute monensin toxicosis in cattle. 665 Sep 60

Monensin was administered orally to 3 sheep at dosages of 12 (the LD50), 16, and 24 mg/kg of body weight, respectively. Clinical signs of monensin toxicosis were observed in the sheep in 24 to 36 hours of administration. Clinical signs included CNS depression, anorexia, diarrhea, and stiffness. Increased serum creatine phosphokinase and aspartate aminotransferase activities identified possible muscle damage. Sheep were euthanatized at 54 hours after dosing; at necropsy, there were skeletal muscle hemorrhages, pale myocardium, and pulmonary edema. Ultrastructural lesions were in the liver, diaphragm, and myocardium; diaphragm and myocardium were most severely affected. Mitochondrial swelling and cristolysis, swollen sarcoplasmic reticulum, and disruption of myofibrillar architecture were prominent. These ultrastructural changes are consistent with the hypothesis that monensin causes muscle cell necrosis due to its ionophorous properties and disruption of cellular Na+:Ca2+ balance. It is proposed that this upset of normal ionic processes allows increased intracellular calcium, which directly leads to the functional and structural mitochondrial changes observed.
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PMID:Acute monensin toxicosis in sheep: light and electron microscopic changes. 674 73

Monensin and lead were administered separately or concurrently at different toxic doses to broiler chicks. Administration of lead alone did not result in a significant depression of haematological parameters. Administration of higher levels of monensin caused a reduction in haematocrit and an increase in blood serum levels of alanine aminotransferase, aspartate aminotransferase and cholesterol. Concurrent administration of monensin and lead caused a severe depression of haematological profiles which indicated the existence of an interaction between the two substances. It was concluded that concurrent administration of monensin and lead potentiated the toxic effects of each other.
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PMID:Oral administration of monensin and lead to broiler chicks: effects on haematological and biochemical parameters. 781 Mar 94

Monensin and selenium (sodium selenite) at different toxic levels were administered orally to the broiler chickens for variable periods. A depression in haematological parameters and biochemical ones such as alanine and aspartate aminotransferase, serum total protein and cholesterol were recorded in acute and subacute toxicosis of these substances. The present experiments led to the conclusion that concurrent administration of selenium and monensin at toxic levels resulted in exasperated toxic response in broiler chickens which in turn had been produced by embellishment of toxicosis inducing properties of both examined substances.
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PMID:Effects of concurrent oral administration of monensin and selenium on some haematological and biochemical parameters in broiler chickens. 812

The effects of monensin on the energy metabolism of dairy cows in early lactation were investigated in a large clinical trial that was randomized and double-blinded. A total of 1010 Holstein cows and first lactation heifers were allocated to receive a controlled-release capsule of monensin or a placebo at 3 wk prior to expected calving date. Treatments were randomized across 25 dairy farms located near Guelph, Ontario, Canada. Serum samples obtained at the time of treatment administration and at wk 1, 2, 3, 6, and 9 postcalving were analyzed for beta-hydroxybutyrate, glucose, aspartate aminotransferase, urea, total protein, calcium, and phosphorus. Cows were also assigned a body condition score at the time each sample was obtained. Monensin treatment significantly reduced serum beta-hydroxy-butyrate concentrations at wk 1, 2, and 3 postpartum and significantly raised serum glucose concentrations during wk 1 and 2 of lactation. In addition, monensin treatment significantly reduced the loss of body condition score and decreased serum activity of aspartate aminotransferase during the postpartum period. Concentrations of serum urea were significantly higher during wk 2 and 3 postpartum for the cows that were treated with monensin. Monensin treatment had no effect on the concentrations of calcium, phosphorus, or total protein.
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PMID:Effect of prepartum administration of monensin in a controlled-release capsule on postpartum energy indicators in lactating dairy cows. 978 26

Choline and monensin may be supplemented during the transition period with the objectives of aiding in fat metabolism and improving energy balance, respectively. The objectives of this study were to determine the effects of supplementing rumen-protected choline (RPC) and monensin in a controlled-release capsule (CRC) on metabolism, dry matter intake, milk production, and liver function in transition dairy cattle. Three weeks before expected calving, 182 Holsteins were randomly assigned to receive one of the following: a monensin CRC, 56 g/d of RPC until 28 d in milk, CRC + RPC, or neither supplement (control). Blood samples were collected at enrollment, 1 wk before calving, and in the first and second weeks after calving. Liver biopsies were obtained from multiparous cows randomly selected from each treatment group within 24 h and again 3 wk postpartum. Daily milk production was recorded through 60 d in milk. There were no interactions of the effects of RPC and CRC on any of the outcomes measured. Overall, cows that received RPC produced 1.2 kg/d more milk in the first 60 d of lactation, but this effect was attributable to an increase in milk production of 4.4 kg/d among cows with a body condition score > or =4 at 3 wk before calving; fat cows that received RPC ate 1.1 kg of DM/d more from wk 3 before calving through wk 4 after calving. Monensin supplementation significantly increased serum concentrations of glucose and urea, lowered concentrations of beta-hydroxybutyric acid and aspartate aminotransferase in the peripartum period, and increased liver glycogen content at 3 wk into lactation. The metabolic effects of CRC are consistent with previous studies, and the effects on liver are novel. The mechanism by which RPC increased milk production was not revealed in this study and merits further research.
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PMID:Effects of rumen-protected choline and monensin on milk production and metabolism of periparturient dairy cows. 1710 12

Toxic effects of monensin, a polyether antibiotic mainly used as a coccidiostat, have been described in a wide range of animals. The present study was performed to investigate the toxic effects of monensin in goats. Seven adult goats were administered sodium monensin, 13.5 mg kg(-1), daily for five consecutive days via gastric gavage. Monensin toxicity was evaluated by clinical signs, serum biochemistry and pathology. Monensin exposure caused diarrhea, tachycardia and reduction in ruminal movements and body temperature. Significant increase of creatine kinase, lactate dehydrogenase, aspartate aminotransferase, total bilirubin, blood urea nitrogen, creatinine and erythrocyte superoxide dismutase were observed in monensin exposed goats. Reduction of erythrocyte glutathione peroxidase and elevation of serum malondialdehyde and troponin I were inconsistent. In necropsy, there were effusions in body cavities, vacuolar degeneration and coagulative necrosis in cardiac and skeletal muscles and renal tubular necrosis. These findings suggested that monensin intoxication in goats leads to cardiac, skeletal and renal damage and a wide range of biochemical abnormalities. Oxidative stress may be involved in the pathogenesis of monensin poisoning.
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PMID:Clinical, laboratory and pathological findings in sub-acute monensin intoxication in goats. 2556 13


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