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)

Humans are exposed to a number of toxic elements in the environment; however, most experiments with laboratory animals investigate only one toxic element. To determine if concomitant exposure to lead (Pb), cadmium (Cd), and/or arsenic (As) modified the changes produced by any one metal in various parameters of toxicity, 168 male, Sprague-Dawley, young adult rats were fed nutritionally adequate diets to which had been added 0 or 200 ppm Pb as Pb acetate, or 50 ppm Cd as Cd chloride, or 50 ppm As as sodium arsenate or arsanilic acid in a factorial design for a period of 10 weeks. At these concentrations, Cd and As reduced weight gain even when differences in food intake were taken into account; administration of both Cd and As depressed weight gain more than did either metal alone. Pb did not adversely affect food consumption or weight gain. Increased numbers of red blood cells (RBCs) were observed following administration of Pb, Cd, or As; usually more cells were observed when two or three metals were administered, compared to individual metals. Despite increasing numbers of circulating RBCs, hemoglobin and hematocrit were reduced, especially with the Pb-Cd combination and the Cd-arsanilic acid combination. Specific effects of Pb on heme synthesis were observed, including increased urinary excretion of delta-aminolevulinic acid; this increase was reduced by the presence of dietary cadmium. Analyses of blood showed values for the laboratory rat within normal ranges for blood urea nitrogen, creatinine, cholesterol, calcium, albumin, total protein, and bilirubin. Uric acid was increased by Pb, with little modification by dietary Cd or As content. Serum glutamate-oxalate transaminase activity was reduced by As. Serum alkaline phosphatase was greatly reduced by either As or Cd but not Pb. Combinations of As and Cd did not further reduce the activity of this enzyme. Kidney weight and kidney weight/body weight ratios were increased by Pb alone, with no effects of Cd or As alone or as interactions. Liver weight/body weight ratios were reduced in animals fed 50 ppm dietary Cd. Kidney histology shows predominantly Pb effects, namely, intranuclear inclusion bodies and cloudy swelling. Ultrastructural evaluation of kidneys from Pb-treated animals disclosed nuclear inclusion bodies of the usual morphology and mitochondrial swelling. Concurrent administration of Cd greatly minimized Pb effects on the kidney under conditions of this experiment. Liver histology suggests an increased rate of cell turnover with either As compound, but few specific changes.
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PMID:Effects of concurrent administration of lead, cadmium, and arsenic in the rat. 19 3

Toxicosis was induced in pregnant heifers by feeding 25,000 mg/head/day of FireMaster BP-6, a commercial blend of polybrominated biphenyls (PBB). The PBB feeding decreased dry matter intake approximately 50% by 4 days exposure. Emaciated animals became anorexic a few days prior to death at 33 to 66 days. Weight losses of heifers average 80 kg. Other clinical signs observed were dehydration, diarrhea, excessive salivation and lacrimation, fetal death, abortion, and general depression as evidenced by depressed heart and respiratory rates. Clinical signs were apparent after 10 days exposure and progressively intensified along with loss of condition until death. Clinicopathologic changes included significantly increased serum glutamic-oxaloacetic transaminase and decreased serum calcium by 30 days exposure. Lactate dehydrogenase, urea nitrogen, and bilirubin were elevated, and serum albumin decreased by 36 to 40 days. Principal urine changes were decreased specific gravity and moderate proteinuria. Pregnant heifers fed 0.25 or 250 mg/head/day for 60 days and nonpregnant heifers fed 250 mg/head/day for 180 days displayed neither clinical signs nor clinicopathologic changes indicating adverse effects from PBB exposure. Post-exposure, all heifers exposed to PBB for 60 days calved normally with zero calf mortality and were successfully rebred. Milk production was not different from control animals. Birth weights of calves from dams exposed to 250 mg PBB/head/day were significantly greater than calves of dams exposed to 0 mg or 0.25 mg/head/day. PBB exposure of dams produced no detrimental effects on calves as indicated by clinical signs, clinicopathologic changes, or performance.
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PMID:Effects of PBBs on cattle. I. Clinical evaluations and clinical chemistry. 21 5

The effect of N6,O2'-dibutyryl adenosine 3',5'-cyclic-monophosphate (dbcAMP) on the mobilization of calcium (Ca2+), inorganic phosphate (Pi) and lysosomal enzymes was studied in a bone culture system for 24 h using half calvaria from 6--7 day-old mice. DbcAMP inhibited spontaneous as well as parathyroid hormone-stimulated mineral mobilization. DbcAMP in a concentration of 5 x 10(-4)M also reduced the activities of beta-glucuronidase, beta-galactosidase and acid phosphatase found in the media while the activities of lactate dehydrogenase, aspartate aminotransferase and alanine aminotransferase were not affected. It is concluded that cAMP is not a stimulator but an inhibitor of bone resorption within the culture period studied (24 h) and that the cyclic nucleotide might interfere with release processes involved in bone resorption.
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PMID:Inhibitory effect of dibutyryl cyclic AMP on the release of calcium, inorganic phosphate and lysosomal enzymes from calvarial bones cultured for 24 hours. 22 6

Normal values for 13 chemical constituents of plasma were estimated from results for 837 presumably healthy children. Ninety microliters of specimen was analyzed for lactate dehydrogenase, aspartate aminotransferase, alkaline phosphatase, inorganic phosphorus, total calcium, total cholesterol, total proteins, albumin, uric acid, urea nitrogen, alanine aminotransferase, total bilirubin, and glucose. We used two Abbott ABA-100 Bichromatic Analyzers interfaced directly to the ABA Data Management System. For each test age- and sex-related variations were assessed and normal values were estimated for six different age groups.
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PMID:Microchemical analysis for 13 constituents of plasma from healthy children. 43 35

In order to verify the influence of sampling time on blood constituents, populations of supposedly healthy subjects were grouped according to age, sex, deviation from their ideal weight, state of fasting or nonfasting, and time of sampling. Each fasting subject in one group underwent two samplings during the course of a morning: the first at 08.00 and the second between 09.00 and 12.00. In the second group, the first was taken at 13.00, and the second between 14.00 and 16.00. Subjects in the second group had eaten a standard meal of 700 calories at 12.00. Differences between the paired samples from a given individual are discussed with respect to the time of sampling for plasma urea, creatinine, proteins, albumin, calcium, sodium, potassium, cholesterol, uric acid, chloride ions, phosphate, bilirubin, aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase, creatine phosphokinase, alkaline phosphatase, hemoglobin and erythrocyte and leukocyte counts. Variations due to the time of sampling were large for phosphorus, bilirubin, and leukocyte count.
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PMID:The effect of sex, deviation from ideal weight and sampling time on blood constituents in presumably healthy subjects. 43 75

Changes in concentration of a number of blood metabolites in 30 thoroughbred horses were recorded after an 1110 metre race. No significant changes occurred in blood urea or aspartate aminotransferase during the three hours after racing. Plasma sodium, potassium and calcium levels were increased immediately after racing but had returned to normal one hour after racing. Plasma phosphate showed a significant fall in concentration one hour after racing. Creatinine and lactic acid concentrations were elevated ten minutes after racing and although they subsequently decreased, the level of lactic acid was still significant one hour later. Uric acid levels were well above resting levels at ten minutes after racing but rose even more in the subsequent hour. Urinary uric acid levels were also elevated during this time. Three hours after racing some horses still had elevated plasma uric acid levels and all of them showed a significant rise in creatine phosphokinase. The possible physiological basis of these findings is discussed.
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PMID:Changes of blood metabolites in horses after racing, with particular reference to uric acid. 44 60

Jatropha curcas seed was fed to six calves at doses of 2.5, 1 and 0.25 g/kg once and to two other calves at 0.025 g/kg up to 14 days. The onset of toxic manifestations in the six calves was rapid and death occurred within 19 hours of administration. The two calves that received daily the lowest dose of J. curcas showed signs of poisoning and died within 10 to 14 days. The clinical signs of diarrhoea, dyspnoea, dehydration and loss of condition were well correlated with the pathological findings. There was an increase in aspartate aminotransferase, ammonia and potassium and a decrease in total protein and calcium in the serum of jatropha-poisoned calves.
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PMID:Effects of Jatropha curcas on calves. 45 22

The sequential development of the clinical signs and lesions in the organs of desert sheep and Nubian goats dosed with Jatropha curcas seeds at 0.05, 0.5 and 1 g/kg/day was studied. Diarrhoea, reduced water consumption, dehydration, sunken eyes, inappetence and loss in condition were the important signs of J curcas poisoning in sheep and goats. The main pathological changes were haemorrhage in the rumen, reticulum, lungs, kidneys and heart, catarrhal and/or haemorrhagic enteritis, hepatic fatty change, pulmonary congestion and oedema and straw-coloured fluid in serous cavities. An increase in the concentrations of AST, ammonia, potassium and sodium and a decrease in total protein and calcium were detected in the serum. Haematological changes were haemoconcentration and leucocytosis.
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PMID:Toxicity of Jatropha curcas in sheep and goats. 50 10

The 2-n-propyl (pr) and 2-n-butyl (bu) methylenedioxyindenes (MDIs) developed in our laboratories are intracellular calcium antagonists with coronary dilating and antiarrhythmic actions. Acute toxicity studies resulted, in mice, in an iv LD50 of 40 and 32 mg/kg for pr-MDI and bu-MDI, respectively, and an ip LD50 of 185 mg/kg for both MDIs. In rats, the ip LD50 was 175 and 240 mg/kg for pr-MDI and bu-MDI, respectively. An iv dose of 16 mg/kg decreased motor activity and prolonged barbiturate sleeping time in mice, but did not affect conditioned avoidance behavior or motor coordination tests. In sub-acute toxicity studies, rats received daily for 4 weeks 26.25 or 52.5 mg/kg ip of either MDIs, while mice received 23.13 or 46.25 mg/kg ip of either MDIs. No alterations were observed in serum alkaline phosphatase, glutamic-pyruvic transaminase, glutamic-oxalacetic transaminase, creatine phosphokinase, bilirubin, chloride, cholesterol, uric acid, prothrombin time, and bromsulphalein retention. Blood glucose was slightly lowered. Serum calcium was slightly lowered in male mice. The higher dose of pr-MDI elevated serum lactate dehydrogenase in rats. Both MDIs elevated serum isocitric dehydrogenase in male rats. Light microscopic examination of brain, kidney, liver, spleen, intestine, stomach, and myocardium showed no anomalies resulting from the 4-week MDI treatment, and electron microscopic examination of hepatocytes revealed no deleterious effects of either MDIs.
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PMID:Toxicological evaluation of new calcium antagonists: 2-substituted 3-dimethylamino-5,6-methylenedioxyindenes. 51 12

A study of cardiovascular risk factors in middle-aged twin men provided an opportunity to test for genetic variability in the SMA 12/60 (Technicon) battery of clinical chemistry tests. Classical twin methodology was used to analyze the variation of monozygotic and dizygotic twins. In addition, frequency of co-twin contact was used to control for effects of differences in shared environment. Genetic variability played a definite role in controlling four of the 11 reported tests: one-hour serum glucose, serum urea nitrogen, uric acid, and bilirubin. No genetic variation was found for lactate dehydrogenase, phosphorus, and alkaline phosphatase. Significantly higher means for calcium, total protein, albumin, and aspartate aminotransferase in monozygotic twins precluded any statement about heredity and environment for these tests.
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PMID:Genetic variability of clinical chemical values. 55 78


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