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:2.6.1.1 (aspartate aminotransferase)
21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. For methods of vitamin E and selenium supplementation were evaluated using thirty-nine pregnant ewe-lambs fed on a ration containing 0.043 mg Se/kg and 25 mg vitamin E/kg. Treatments were control, fortified mineral mix (ESe salt) (300 mg vitamin E, 3 mg Se), ruminal Se pellets (505 mg Se), drench (300 mg vitamin E, 3 mg Se) and intramuscular injection (600 mg vitamin E, 3 mg Se). Only ewes supplemented, commencing approximately 50 d before parturition. 2. Birth weights were similar for all treatments and live-weight gains of lambs to 56 d of age were improved in all supplemented groups (P less than 0.05). There were no clinical cases of nutritional muscular dystrophy. 3. Se concentrations in whole blood were more than doubled in both lambs and ewes drenched or injected; responses to ESe salt and pellets were much smaller. 4. Plasma tocopherol levels were increased in injected dams and their lambs (P less than 0.001). 5. Haemoglobin concentration and erythrocyte counts were significantly higher (P less than 0.01) in control ewes and lambs than in treated lambs. 6. Lactate dehydrogenase (EC 1.1.1.27), creatine kinase (EC 2.7.3.2) and aspartate aminotransferase (EC 2.6.1.1) activities were increased in lambs from control, ESe salt and pellet groups (P less than 0.001). Glutathione peroxidase (EC 1.11.1.9) activity responded to Se supplementation in both ewes and their lambs (P less than 0.001) and the response was highest in the injected group, followed in order, by the drench, pellet, Ese salt and control groups. 7. These studies indicated that in terms of the haematological and blood chemistry changes investigated, the intramuscular injection was most effective, followed by the oral drench. Ruminal pellets and fortified salt were less satisfactory.
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PMID:Haematological and blood chemistry changes in ewes and lambs following supplementation with vitamin E and selenium. 69 59

Pigs which were deficient in vitamin E and/or selenium had the following parameters weekly determined from six to 13 weeks of age: Packed cell volume, hemoglobin concentration, red cell and white cell counts, red cell indices, reticulocyte count, serum iron, serum total iron binding capacity, myeloid: erythroid ratio, serum glutamic-oxaloacetic transaminase and creatine phosphokinase activities and body weight. Except for the myeloid:erythroid ratio and serum creatine phosphokinase activity, these parameters were not found to be significantly affected by either vitamin E deficiency, selenium deficiency or deficiency of both. The myeloid:erythroid ratio was increased (p less than 0.01) in association with selenium deficiency, which tends to indicate decreased erythropoiesis but was not reflected in the peripheral red cell picture. Evidence of dyserythropoiesis was not found to be a significant feature in serial bone marrow aspiration biopsies of vitamin E and/or selenium deficient pigs. Even if the serum glutamic-oxaloacetic transaminase activities were not found to be significantly affected by either vitamin E deficiency, selenium deficiency or deficiency in both as compared to replete animals, a few animals, especially in the group deficient in both vitamin E and selenium, presented quite marked transient increases of serum glutamic-oxaloacetic transaminase activity which was interpreted to reflect the occurrence of acute episodes of hepatosis dietetica. Serum creatine phosphokinase activities were found to be increased in association with vitamin E deficiency (p less than 0.01), selenium deficiency (less than 0.05) and the interaction was also significant (p less than 0.01). It was concluded that the serum creatine phosphokinase activity increases reflect the occurrence of subclinical muscular dystrophy and that vitamin E and selenium deficiencies have marked additive effects in the induction of skeletal muscular dystrophy.
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PMID:Studies on vitamin E and selenium deficiency in young pigs. I. Hematological and biochemical changes. 83 88

The effect of Trichostrongylus colubriformis on lambs maintained on a ration containing a low level of selenium and on animals receiving vitamin E and Se supplementation was investigated. The pathological changes seen in control animals slaughtered at the start of the experiment and in the animals which died during the course of the investigation revealed a high level of nutritional muscular dystrophy (NMD) in the lambs. There were no marked haematological changes in the control or infested sheep. Infestation was characterized by slight hypoalbuminaemia and gamma-globulinaemia. Serum levels of the enzymes AAT and CPK, which are important indicators of muscle necrosis and NMD, were greatly increased in sheep infested with T. colubriformis and not receiving supplementary Vit. E + Se. Data from this study therefore indicates that trichostrongylosis may aggravate the degree of muscle necrosis in lambs prone to the development of NMD.
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PMID:Haematological changes caused by Trichostrongylus colubriformis in lambs fed a dystrophogenic diet. 91 93

Effects of intramuscular injections of selenium and vitamin E on lesions in pigs with selenium-vitamin E deficiency syndrome were determined in 2 factorial experiments, using a total 69 pigs. The pigs were fed a selenium-vitamin E deficient, 22.3% protein ration, supplemented with methionine, minerals, and vitamins. Weekly intramuscular injections of isotonic saline solution, vitamin E, selenium, or vitamin E and selenium were given to the respective treatment groups. Selenium-vitamin E deficiency lesions occurred only in pigs that were given saline injections. Weekly intramuscular injections of either selenium (as selenous acid buffered to pH (7.3) at the rate of 0.05 mg/kg of body weight or vitamin E at the rate of 20 IU/kg of body weight or the combination of selenium and vitamin E prevented cardiac and skeletal myodegeneration, hepatic necrosis, and death. Significant increases of serum aspartate aminotransferase activity values were noted in pigs with liver, heart, or skeletal muscle lesions, but these increases were not correlated with the extent of the lesions. Vascular lesions, epicardial and endocardial hemorrhages, and yellow discoloration of body fat were not features of this experimentally induced disease. These lesions may be related to factors other than the deficiency of selenium, vitamin E, or selenium and vitamin E in rations previously used in reported studies.
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PMID:Effects of intramuscular injections of selenium and vitamin E on selenium-vitamin E deficiency in young pigs. 93 Nov 31

1. Rats were given moderate-selenium (4-5 mg/kg) or low-Se (0-5 mg/kg) diets during gestation and lactation. Their young were given diets with high (10 mg/kg), moderate or low Se contents from weaning, and groups of rats were killed at intervals during the 14-week experimental peroid. 2. Compared with young rats which received the low-Se diet, those which received the moderate- or high-Se diets had a high incidence of liver lesions and there were changes in liver Se content, haemoglobin concentration, packed cell volume, prothrombin activity, fibrinogen content, spleen weight, body water and serum glutamic-oxaloacetic and glutamic-pyruvic transaminas (L-aspartate : 2-oxoglutarate aminotransferase; EC 2.6.1.1 and L-alanine : 2-oxoglutarate aminotransferase; EC 2.6.1.2 respectively) and alkaline phosphatase (EC 3.1.3.1) activities. In those rats which received the high-Se diet the changes were more pronounced than in those which received the moderate-Se diet. 3. In young rats from dams given moderate-Se diets, which were themselves given the moderate-Se diet, the liver Se content decreased continuously, whereas rats given the same diet but from dams which had received the low-Se diet, the liver Se content increased continuously. There was a slight improvement of symptoms of Se toxicity in all groups by the 5th week of the experimental peroid. 4. The results suggest that there was an adaptation to chronic Se intake.
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PMID:Effects of ingestion of organic selenium in adapted and non-adapted rats. 112 69

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

Five groups of five weanling rats were each fed a Torula yeast-based diet either unsupplemented or supplemented with 30 mg beta-carotene/kg, 30 IU vitamin E/kg, 1 mg selenium/kg or 30 mg coenzyme Q10/kg. Elevated levels of plasma aspartate aminotransferase and alanine aminotransferase are sensitive indicators of liver damage. The former enzyme was lower (P less than 0.01) in the vitamin E-, selenium- and beta-carotene-supplemented groups than in the unsupplemented control group, and the latter enzyme was lower in the vitamin E- and selenium-supplemented groups, suggesting a relatively equal effectiveness of these three antioxidants against liver damage. Erythrocytes were tested for protection against uninduced oxidative damage or that induced by 1 mmol/L bromotrichloromethane (BrCl3C) by measuring thiobarbituric acid-reactive substances (TBARS), hemoglobin, hemolysis, protein precipitation, alanine release and several enzyme activities. In untreated erythrocytes, selenium, beta-carotene and coenzyme Q10 exhibited protection by lowering (P less than 0.05) TBARS and alanine release, but only vitamin E protected against hemolysis. In BrCl3C-treated erythrocytes, vitamin E, selenium and beta-carotene protected by decreasing (P less than 0.05) protein precipitation, whereas selenium and beta-carotene decreased alanine release. The results of this study suggested that, in a manner analogous to vitamin E and selenium, beta-carotene and coenzyme Q10 function as antioxygenic nutrients.
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PMID:Comparative antioxidant effectiveness of dietary beta-carotene, vitamin E, selenium and coenzyme Q10 in rat erythrocytes and plasma. 199 57

Rats were fed for 23 d diets adequate or deficient in vitamin B-6 and containing selenium as either sodium selenite, selenocysteine (SeCys) or selenomethionine (SeMet). They were then injected with 75Se of the same chemical form and killed 2 d later. Tissue deposition of stable and radiotracer selenium and the activity of glutathione peroxidase (GSHPx) were used to assess selenium utilization. Erythrocyte levels of selenium and GSHPx were lower in vitamin B-6--deficient animals for all forms of selenium; however, 75Se deposition in erythrocytes was not affected by vitamin B-6 status. The activities of cystathionine lyase, aspartate aminotransferase and selenocysteine lyase were lower in livers of vitamin B-6--deficient rats than in vitamin B-6--supplemented rats. The proportion of liver and kidney 75Se soluble in 5% trichloroacetic acid and 0.1 M 2-mercaptoethanol was consistently lower in vitamin B-6--deficient animals, but cation-exchange chromatography of tissue extracts did not identify a specific low-molecular-weight species. Tissue retention of 75Se provided as SeMet was increased in vitamin B-6--deficient animals, but the proportion of 75Se retained in muscle and liver as SeCys was significantly reduced. These findings suggest that the conversion of SeMet to a form available for GSHPx synthesis is reduced by vitamin B-6 deficiency.
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PMID:Effects of vitamin B-6 deficiency on selenium metabolism in the rat. 262 89

Biochemical studies were conducted in experimentally induced selenium toxicity in recently weaned guinea pigs. A significant drop in blood glucose level, in comparison to controls, was observed in animals fed selenium-enriched barley (organic form) as well as those fed ordinary barley mixed with sodium selenite (inorganic form). Estimation of total serum proteins also revealed a significant drop in both these groups. SGOT (EC 2.6.1.1) activity was comparatively lower but no significant alteration was noticed in SGPT (EC 2.6.1.2). The erythrocytic glutathione peroxidase activity was significantly increased in inorganic selenosis followed by that in organic one, in comparison to controls. All these alterations were of mild degree in guinea pigs which were given sodium arsenite (10 ppm) along with sodium selenite (30 ppm) in the feed.
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PMID:Experimental selenium toxicity in guinea pigs: biochemical studies. 274 31


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