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)

Fatty acid ethyl esters (FAEE), esterification products of ethanol and fatty acids, have been implicated as mediators of ethanol-induced organ damage. Because cytosolic enzymes such as aspartate aminotransferase, lipase, and amylase appear in the blood after liver or pancreatic damage, we hypothesized that FAEE synthase, which is both cytosolic and membrane bound, is also released into the blood of patients with liver or pancreatic disease. We used a method involving thin-layer chromatography coupled with gas chromatography-mass spectrometry to reliably identify and quantify FAEE. In this study, we demonstrated that patients with liver or pancreatic disease release FAEE synthase into their plasma in amounts proportional to the amount of aspartate aminotransferase (r = 0.78), amylase (r = 0.65), and lipase (r = 0.63). These data indicate that liver and pancreatic damage results in release of FAEE synthase into the blood. The presence of FAEE synthase in plasma permits nonoxidative ethanol metabolism in the plasma.
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PMID:Fatty acid ethyl ester synthase, an enzyme for nonoxidative ethanol metabolism, is present in serum after liver and pancreatic injury. 856 27

Using lithium heparin plasma and serum, we compared the values of 27 biochemical analyses performed with a Kodak Ektachem 500 analyzer. For 16 of the 27 tests, we observed statistical differences between the mean results obtained from the analysis of heparinized plasma and those obtained from the analysis of serum (Student t-test; P < .001). However, none of these differences were medically significant. When the concentration of lithium heparin was increased to three and five times normal (reflecting incomplete Vacutainer tube filling), alanine aminotransferase, amylase, aspartate aminotransferase, lipase, and potassium all exhibited some changes compared with serum. Therefore, heparin may be used to shorten the turnaround time in the routine biochemistry laboratory, but the anticoagulant tubes should be completely filled to prevent spurious intraindividual variations in serial specimen analysis.
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PMID:Is heparinized plasma suitable for use in routine biochemistry? 859 42

A 51-year-old man developed a large retroperitoneal tumor with liver and lymph node metastases; there was no radiological evidence of pancreatic involvement. Despite the progression of disease, results of laboratory tests, notably serum amylase, were normal except for minor increases in aspartate aminotransferase and gamma-glutamyltransferase and a marked increase in lipase. The increased lipase was not attributable to formation of macroenzyme. To determine the source of the lipase, we fractionated serum and a tumor biopsy homogenate, using electrophoresis. The lipase pattern obtained from the patient's serum differed from that seen in serum from a patient with acute pancreatitis. Additionally, the lipase pattern obtained from a homogenate of biopsy sample from the retroperitoneal tumor did not match the pattern observed for normal pancreas. Apparently, the source of this increased serum lipase activity was the nonpancreatic tumor.
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PMID:Chronic increased serum lipase without evidence of pancreatitis: tumor-derived lipase? 859 14

There is strong evidence that genetic factors contribute to the development of obesity in humans as well as laboratory animals. Another important factor leading to obesity is an increase in energy intake. However, it is difficult to make normal rats obese by controlling daily food intake. There is no report of normal adult male Wistar rats becoming obese and diabetic on a high-fat diet. The aim of the present study was, therefore, to make normal adult Wistar rats obese by infusing high fat and hypercaloric diet through the cannula without disturbing the free movement and to investigate the influence of an increase in the caloric intake on body weight and glucose metabolism. High-fat hypercaloric diet (360 kcal/kg body wt./day; H group) or control diet (180 kcal/kg body wt./day; C group) was continuously infused into the stomach of normal adult male Wistar rats weighing approximately 300 g through gastric cannulas for 27 days. On day 28 after a 24-h fasting, serum concentrations of aspartate aminotransferase, alanine aminotransferase, total cholesterol, triglyceride, phospholipid, and free fatty acids (FFA) were determined, and intragastric glucose loading test (2 g/kg body wt.) was performed. The average weekly body weight gain in the H group was twice as much as that of the C group (40.0 +/- 2.4 vs. 19.4 +/- 1.9 g/week, P < 0.001). Serum levels of triglyceride, phospholipid, total cholesterol, and FFA were significantly elevated in the H group compared to those in the C group. Liver weight in the H group was significantly higher than that in the C group and showed steatosis. Pancreas weight (-13%) as well as protein (-12%), amylase (-53%) and trypsin content (-26%) were all reduced, whereas pancreatic DNA content was significantly increased in the H group compared to those in the C group. Serum glucose and insulin concentrations before and after glucose loading in the H group were significantly higher than those in the C group. Moreover, the insulin response relative to glucose response in the H group was significantly high compared to that in the C group, indicating the presence of insulin resistance. These results indicate that feeding of high-fat hypercaloric diet makes normal Wistar male adult rat obese associated with hyperlipidemia, hyperinsulinemia, and glucose intolerance.
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PMID:High-fat hypercaloric diet induces obesity, glucose intolerance and hyperlipidemia in normal adult male Wistar rat. 879 99

The acute, subchronic and chronic toxicities of 2,4-dichlorophenoxyacetic acid (2,4-D) were studied ir rats. Animals were exposed acutely (600 mg/kg), subchronically (200 ppm for 30 d) and chronically (200 ppm for 180 d) to 2,4-D by the oral route. Clinical, laboratory and histopathological methods were used as indicators of toxicity. After acute exposure, the herbicide decreased locomotor activity and induced ataxia, sedation, muscular weakness (mainly of the hind quarters) and gasping for breath; increased aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), alkaline phosphatase (AP), amylase activities and creatinine levels; decreased total protein (TP) and glucose levels; and increased hematocrit values. Subchronic and chronic 2,4-D exposures did not induce overt clinical signs or symptoms of intoxication. However, subchronic herbicide exposure increased AST activity and albumin and hematocrit values, and chronic exposure increased AST, AP and LDH activities, decreased amylase and glucose levels, but did not change hematocrit values. Chromatographic analysis of the serum of chronically exposed rats showed the presence of the herbicide; the amount found (3.76 +/- 1.16 micrograms/ml) suggested the absence of 2,4-D accumulation within the body. Although macroscopic or histopathological lesions were not observed in acutely, subchronically or chronically 2,4-D exposed rats, the laboratory data obtained suggest tissue injuries after dosing, since the results are considered early indicators of primarily hepatic and muscle tissue damage.
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PMID:Acute, subchronic and chronic 2,4-dichlorophenoxyacetic acid (2,4-D) intoxication in rats. 888 38

Five of 8 patients with rhabdomyolysis treated at our hospital following the Great Hanshin Earthquake were diagnosed with crush syndrome. One patient with crush syndrome and 3 patients with rhabdomyolysis and no renal dysfunction recovered with conservative therapy, while 1 crush syndrome patient recovered with peritoneal dialysis (PD). Of the 3 patients who died, 2 had undergone continuous arterio-venous hemofiltration (CAVH). We examined the laboratory data to identify any factors that may be prognostic for crush syndrome. The serum amylase levels were significantly higher and the levels of aspartate transaminase (AST) and lactic dehydrogenase (LDH) tended to be higher from the patients who died. Examination of the serum amylase, AST and LDH levels may be useful for assessing the prognosis in patients with crush syndrome.
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PMID:Treatment of crush syndrome patients following the great Hanshin earthquake. 917 97

Intravenous injection into the rat of sublethal doses of Tityus serrulatus scorpion venom (100 micrograms protein/kg) or its major neurotoxin tityustoxin-I (TsTX-I, 20 micrograms/kg) caused, 30-180 min after injection, statistically significant increases in the serum levels of aspartate aminotransferase, amylase, creatine kinase and lactate dehydrogenase, as well as hyperglycemia, a high level of plasma free fatty acids and a low level of liver glycogen. The in vitro serum levels of the above enzymes did not change. For alanine aminotransferase, gamma-glutamyl transferase and alkaline phosphatase, neither in vitro nor in vivo alterations were observed. The whole venom and TsTX-I caused hepatic congestion with hemolysis and hydropic degeneration. Other histological lesions included edema and congestion with subpleural hemorrhage in the lungs, hypertrophy of fibers with degeneration areas in the heart, and congestion and hemorrhage in the kidneys. In the salivary glands, alterations to the acini and ductules were visible. In the adrenal glands no morphological alterations could be detected at the studied doses. The results suggest that the in vivo enzymatic and histopathological alterations are due to tissue lesions evoked by the whole venom and TsTX-I. An indirect effect, however, induced by stimulation of acetylcholine and catecholamine release in the postganglionic nerve terminals, cannot be excluded.
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PMID:Biochemical and histopathological alterations induced in rats by Tityus serrulatus scorpion venom and its major neurotoxin tityustoxin-I. 924 4

Plasma chemistry and haematological studies were conducted on chickens with coccidiosis. Male White Leghorn chickens, of two weeks old, were inoculated with 5 x 10(4) Eimeria tenella sporulated oocysts or with 1 x 10(6) E acervulina sporulated oocysts. Blood samples were taken four, seven and 11 days after inoculation. A wet chemistry system was applied to measure the plasma activities of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, gamma glutamyltransferase, creatine kinase, amylase and lactate dehydrogenase and the concentrations of creatine, total bilirubin, urate, total cholesterol, total protein, albumin, glucose and triglycerides. A dry chemistry system was applied to measure sodium, potassium, chloride and calcium. The number of red blood cells and packed cell volume were determined by a micro cell counter and blood pH was measured with a blood gas analyser. The erythrocyte count, packed cell volume, sodium and chloride levels in the chickens infected with E tenella were significantly (P < 0.05) lower than those of the uninfected controls. The significant decrease in blood pH of the chickens infected with E acervulina suggests malabsorption associated with duodenal lesions induced by the infection.
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PMID:Evaluation of plasma chemistry and haematological studies on chickens infected with Eimeria tenella and E acervulina. 925 31

The increasing availability and use of automatic analysers in clinical chemistry have revealed a number of endogenous interferences. We evaluated the effect of bilirubin, haemolysis and lipaemia on the Falcor-600 analytical system (Menarini Diagnostics) and the Dax-48 (Bayer Diagnostic). We studied the potential endogenous interferences in the measurement of serum glucose, urea, creatinine, cholesterol, triacylglycerols, total bilirubin, total protein, aspartate aminotransferase, alanine aminotransferase and gamma-glutamyltransferase on both analysers; and albumin, direct bilirubin, uric acid, inorganic phosphorus, iron, calcium, magnesium, chloride, sodium, potassium, alkaline phosphatase, amylase, lactate dehydrogenase and creatine kinase on the Dax-48. We followed the guidelines of the Spanish Society of Clinical Biochemistry and Molecular Pathology. Bilirubin samples were prepared using bovine bilirubin, and studied in the concentration range of 20 to 400 mumol/l. For haemolysis, the pool was spiked with a diluted haemolysate of human red cells to achieve a concentration range of 10 to 120 mumol/l of haemoglobin. Lipaemia was studied using samples spiked with Intralipid, a fat emulsion, at concentrations from 1 g/l to 6 g/l (3 to 18 mumol/l of triacylglycerols).
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PMID:Potential interfering substances on Falcor-600 and Dax-48 analytical systems. 936 98

Death from ferric chloride poisoning has never been reported in Taiwan. We report a fatality from the suicidal ingestion of ferric chloride solution used as an etching agent for printed circuitry. A 25-y-old woman presented with vomiting after ingestion of 200 ml ferric chloride solution (pH 1.0). She had hypoxemia and severe metabolic acidosis with respiratory alkalosis initially. Three hours after her ingestion she presented with drowsy consciousness, tachycardia, tachypnea and protracted vomiting. Laboratory studies showed leukocytosis, elevated glucose, aspartate aminotransferase, amylase, lactate dehydrogenase, and total bilirubin, coagulation defect and hemolysis. Aspiration pneumonia and vision loss were also noted. Four hours after ingestion cardiopulmonary arrest suddenly occurred after severe vomiting and she expired. Toxicological studies showed marked elevation of serum iron (2440 micrograms/dl); the estimated oral dose of ferric chloride was equivalent to 11.52 g (230 mg/kg) of elemental iron. This patient did not receive deferoxamine due to rapid deterioration and a late diagnosis. Deferoxamine should be given in any symptomatic patient or in the presence of anion gap metabolic acidosis with a history of ferric chloride ingestion.
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PMID:A fatal case of acute ferric chloride poisoning. 946 7


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