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)

Total serum protein, serum albumin, total urine protein excretion, and the serum activity of several enzymes--aldolase (ALS), cholinesterase (CHS), leucine aminopeptidase (LAP), isocitrate dehydrogenase (ICD), aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), alpha-hydroxybutyrate dehydrogenase (HBD), creatine kinase (CK), alkaline phosphatase (ALP), and gamma-glutamyl transferase (GGT)--were estimated in rats with nephrotic syndrome (NS) at 2, 4, 6, 8, 10, 12, 16, 20, and 30 days after a single injection of puromycin aminonucleoside (PAN). It was found that: (a) total serum protein and serum albumin diminished on day 4 and returned to control values on days 20 and 30, respectively; (b) total urine protein excretion rose on day 4, reached a peak value on day 8, and then fell substantially but still remained higher than control values on day 30; (c) ALS and CHS activities increased; (d) LAP, ICD, and AST activities showed a biphasic pattern, first increasing and then decreasing; (e) ALT, LDH, HBD, CK, and ALP activities decreased; and (f) GGT activity remained unchanged. The differences in the profiles of the enzyme activities suggest their independent regulation in experimental NS induced by PAN.
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PMID:Activity of serum enzymes in puromycin aminonucleoside-induced nephrotic syndrome. 146 3

The sickle cell trait (HbAS) does not seem to affect exercise performance. It remains unclear, however, whether the capability to sustain repeated brief maximal effort and recovery by HbAS subjects, is also preserved. To study this, nine HbAS and nine matched controls underwent on two different occasions, a series of four, approximately 2-min duration, maximal cycle exercise tests separated by 20-min recovery periods of either absolute rest (P) or light pedaling (A) as well as an incremental test to exhaustion. In all tests, work performed, heart rate, blood hematocrit, lactate, and serum creatine kinase (CK), lactate dehydrogenase (LDH), and aspartate aminotransferase (GOT) were measured. Performances were similar in HbAS and HbAA subjects in both the predominantly anaerobic and aerobic exercise series. There were no observable differences in work, power, or heart rate in the two groups both during peak exercise or recovery periods. A significant hemoconcentration was observed during P, with hematocrit increasing in HbAS from 46.4 +/- 0.7% to 48.3 +/- 0.4% at the end of the last recovery period. Similar changes were seen in HbAA. Significantly greater fluid losses were found during A (1.3 +/- 0.2 l in A and 0.6 +/- 0.1 l in P for HbAS; P < 0.001), but fluid losses were similar in each type of recovery in the two groups. Despite similar performance, significantly lower blood lactate concentrations were consistently found in HbAS in each of the three exercise series (P < 0.001). Lower lactate levels in HbAS were observed only at exercise loads above the lactate threshold during the incremental test (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of different modalities of exercise and recovery on exercise performance in subjects with sickle cell trait. 147 14

Sex- and age-related nephrotoxicity due to 1,2-dichloropropane was studied in vitro by means of renal cortical slices obtained from Wistar rats. Reduced glutathione content, organic anion accumulation (p-aminohippurate), and release of malondialdehyde (to measure the extent of lipid peroxidation), aspartate aminotransferase, gamma-glutamyltransferase and lactate dehydrogenase into the incubation medium were determined. Sex differences in naive rats parameters were slight, but male were more susceptible to toxic effects of 1,2-dichloropropane than female rats; glutathione depletion, lipid peroxidation, and loss of organic anion accumulation were higher in male than in female slices. During senescence, naive male rats showed a progressive decrease of glutathione content (statistically significant from 7-9 months of age), increase of spontaneous lipid peroxidation from the same age, and increase of signs of cytotoxicity (release of aspartate aminotransferase and lactate dehydrogenase into the incubation medium) from 3-4 months of age. A loss of organic anion accumulation started from 7-9 months of age. Slices from rats of 3-4 months old showed the apparently highest susceptibility to 1,2-dichloropropane but depletion of glutathione content and loss of organic anion accumulation were at the same level in the oldest rats. The age decrease of control values caused the differences in the percentage ratio and then, apparently, a lower DCP effect. On the contrary, the increase of aspartate aminotransferase released in the incubation medium by DCP-treated slices corresponded to the age-related increase in cytotoxicity.
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PMID:Sex- and age-related nephrotoxicity due to 1,2-dichloropropane in vitro. 148 87

The abilities of potential chemoprotectants to inhibit cytotoxicity of ricin have been determined in vitro, using the macrophage cell line J744A.1. Six compounds were tested: alpha- and beta-galactopyranosylamine; N-bromoacetyl-alpha-D-galactopyranosylamine; N-bromoacetyl-beta-D-galactopyranosylamine; N-bromoacetylglucopyranosylamine; and N-bromoacetylmannopyranosylamine. Of the six compounds which were tested, only N-bromoacetyl-alpha-D-galactopyranosylamine and N-bromoacetyl-beta-D-galactopyranosylamine exhibited significant activity against ricin toxicity, as indicated by the release of lactate dehydrogenase (LDH) and aspartate aminotransferase (AST). The alpha-isomer provided greater protection against ricin toxicity and also exhibited less inherent cytotoxicity in the absence of ricin, as compared to the beta-isomer. Neither the alpha- and beta-galactopyranosylamines nor the glucose and mannose analogs were promising as potential chemoprotectants.
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PMID:An assessment of potential chemoprotectant activity against ricin toxicity by mechanism based glycosidase inhibitors in macrophage J744A.1 cell cultures. 148 63

Oak poisoning occurred in crossbred cattle due to eating immature tender oak (Quercus incana) leaves. Mortality was 70%. The animals exhibited anorexia, severe constipation and brisket edema. The feces were hard, pelleted and coated with blood and mucous. Significant reductions in blood hemoglobin and mean corpuscular hemoglobin, and significant elevations in serum bilirubin were observed. Serum urea nitrogen and creatinine were greatly increased. There was bilirubinuria, proteinuria, hypoproteinemia and hypocalcemia, and greatly increased activities of serum aspartate aminotransferase, lactate dehydrogenase and alkaline phosphatase. The levels of tannins and condensed tannins were 97.7 mg tannic acid equivalent and 5.8 mg catechin equivalent/g of dry leaves. There was extensive nephro- and hepatotoxicity in the affected cattle due to hydrolysable tannins and simple phenols in the oak leaves.
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PMID:Oak (Quercus incana) leaf poisoning in cattle. 150 80

The aim of this study was to determine whether some muscular pathology existed in fighting bulls, in relation or not to the weakness shown in these animals during the bullfight (corrida for males and tienta for females). Creatinine kinase (CK), lactate dehydrogenase (LDH) and aspartate transaminase (AST) serum enzyme activities were increased after the corrida or the tienta. Most of the fighting bulls (78%) had some histological lesions in the skeletal or cardiac muscle, with predominance of chronic lesions. Clinical signs of these chronic lesions could only be seen after some trigger-effect, such as physical, exercise or stress, as shown after the corrida or tienta.
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PMID:[Muscular lesions and enzymatic activities in fighting bulls]. 151 Mar 39

Dried, milled Cestrum laevigatum plant material was drenched to 6 ewes at doses ranging from 2,5 to 10 g/kg/day for 1 to 47 days. The most noticeable clinical signs were depression, anorexia and ruminal stasis. These signs were accompanied by clinical pathological changes indicative of liver involvement such as increases in the serum activities of aspartate transaminase, lactate dehydrogenase and gamma-glutamyltransferase. Hepatosis characterized by accentuated lobulation, and centrilobular to midzonal coagulative necrosis, haemorrhage and congestion occurred in 2 of the 3 ewes given high doses of plant material. Liver lesions in the other animals included disappearance of hepatocytes and collapse of the reticulin stroma in the centrilobular areas. Spongy changes in the cerebral white matter were evident in the ewes of the high-dose group. Ultrastructural changes in the liver comprised degeneration and necrosis of hepatocytes and occasionally endothelial cells, and disruption of sinusoidal walls.
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PMID:Experimentally-induced Cestrum laevigatum (Schlechtd.) poisoning in sheep. 151 94

The histogram has long been used in the clinical laboratory for the depiction and manipulation of frequency data. We present recent results of refinements to the usual histogram procedures along with modern alternative methods of estimating frequency distributions, including the kernel and discrete maximum penalized likelihood estimation (DMPLE) approaches. We compared these nonparametric methods on 15 different types of simulated distributions, and on several sets (greater than 1000 subjects/set) of real data, including alanine aminotransferase, aspartate aminotransferase, and lactate dehydrogenase levels. Each frequency curve estimation technique was evaluated by measuring the integrated mean square error between each technique's prediction and the true underlying distribution, using Monte Carlo techniques on sample sets with size 49 and 119. The kernel method was the clear method of choice, both in performance (best in 22/36 cases) and in practical usage.
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PMID:Nonparametric probability density estimation: improvements to the histogram for laboratory data. 154 24

The hepatotoxic effects of hyperthermia have been proposed to be related to lipid peroxidation as a consequence of oxidative stress. This can result from exposure of the cell to "radical oxygen" species such as the superoxide and hydrogen peroxide generated by the activity of the oxidase form (type O) of xanthine oxidase (XO), which is converted to that form by perfusion of the liver at hyperthermic temperatures. These radical species are not reactive enough in themselves to cause cell damage but require the presence of a catalyst such as low molecular weight chelated iron. In these studies, ferritin was shown to be a source of iron for the oxidative stress of hyperthermia. (a) Iron was released from ferritin in vitro by the activity of rat liver XO. The rate of iron release from ferritin in this incubation system was a function of the amount of type O XO present and the temperature. Inclusion of allopurinol or superoxide dismutase in the incubation resulted in significantly lower rates of iron release. (b) Livers from Sprague-Dawley rats were perfused at 42.5 degrees and 37 degrees C for 1 h. During the recirculating perfusion, loss of iron from the liver into the perfusate was significantly greater (P less than 0.05) at 42.5 degrees C than at 37 degrees C. Also, there was a pronounced increase in the lactate dehydrogenase and aspartate aminotransferase enzymes in the perfusate during perfusion at 42.5 degrees C. Furthermore, intrahepatic levels of low molecular weight chelated iron were significantly (P less than 0.05) increased following perfusion at 42.5 degrees C. All these responses were abrogated by the inclusion of allopurinol in the perfusate. (c) Oxidative stress, assessed by the efflux of glutathione and oxided glutathione from the liver at 42.5 degrees and 37 degrees C, was significantly (P less than 0.05) increased at the hyperthermic temperature. This oxidative stress was inhibited by iron chelation and allopurinol. These results demonstrate that there is a causal relationship between the generation of superoxide by type O XO produced by hyperthermic perfusion and mobilization of iron from ferritin to form a pool of low molecular weight chelated iron. This iron pool in combination with active oxygen species leads to oxidative stress and lipid peroxidation.
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PMID:Involvement of xanthine oxidase in oxidative stress and iron release during hyperthermic rat liver perfusion. 155 Oct 99

The effect of the pyoverdin Pf (an iron chelating agent isolated and purified from Pseudomonas fluorescens CCM 2798) was studied on iron overloaded rat hepatocyte cultures. Iron overload was obtained by addition of 5-80 microM ferric nitrilotriacetate to the culture medium. Twenty-four hours after iron treatment, a significant increase in aspartate aminotransferase and lactate dehydrogenase in the culture medium was observed. This corresponded to intracellular decrease in the activity of these two enzymes and correlated with a decrease in albumin secretion and an increase in total free malondialdehyde production. The iron toxicity was inhibited by desferrioxamine B. Pyoverdin Pf added to the hepatocyte cultures served as an effective agent to prevent iron toxicity induced in overload. The observed effect of the pyoverdin Pf was as potent as that of desferrioxamine B.
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PMID:Inhibition of iron overload toxicity in rat hepatocyte cultures by pyoverdin Pf, the siderophore of Pseudomonas fluorescens. 156 81


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