Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.6.1.1 (aspartate aminotransferase)
 21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of pretreatment with cyclosporine, allopurinol, or methylprednisolone on ischemia-reperfusion injury of the liver were investigated. A total of 32 adult mongrel dogs that received one of the pretreatments were divided into four groups and were subjected to 90 min liver ischemia. Serum activities of aspartate aminotransferase (s-AST) and lactate dehydrogenase, (s-LDH) as well as animal survivals were used as indicators of liver injury. The elevation of both s-AST and s-LDH was significantly suppressed by pretreatment with cyclosporine as much as by allopurinol. However a significant improvement in animal survival was obtained only in the cyclosporine-pretreated group. Pretreatment with methylprednisolone did not affect either the activities of s-AST and s-LDH or animal survivals when compared with the control group. These data suggest that cyclosporine is a potent protector against ischemic liver injury--as effective as allopurinol or methylprednisolone. Although the precise mechanism of the effect of cyclosporine on liver ischemia still remains unknown, these observations may be of use in liver transplantation.
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PMID:Attenuation of ischemia-reperfusion injury of the liver in dogs by cyclosporine. A comparative study with allopurinol and methylprednisolone. 185 50

Seventeen serum markers (including 9 enzyme activities) for eventual tissue damage were studied after ESWL in 40 patients with unilateral kidney calculosis. No changes were established in the 8 non-enzymic parameters and the activities of amylase, lipase, AST (GOT), ALT (GPT) and CK-MB. A statistically significant increase was found in LDH, alpha-HBDH, CK (twice) and glutamate dehydrogenase (3 times). The slight elevation of LDH and alpha-HBDH could be due to haemolysis caused by the shock waves. Increased activity of CK suggested myolysis and that of GlDH a hepatocellular damage.
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PMID:Acute changes of serum markers for tissue damage after ESWL of kidney stones. 188 66

The distribution of LDH and CK isoenzymes in blood plasma of ten clinically sound Thoroughbreds with reasonable performance and without elevated clinico-chemical blood variables (reference group) was compared with 57 Thoroughbreds, which had histories of mild locomotor disturbances and/or poor performance and had elevated CK, LDH and/or AST activities (trial group). The trial group was subdivided according to the number of altered blood variables and in the groups with two as well as three altered blood variables also according to the extent of alteration of the total CK activity. The pattern of LDH and CK isoenzyme distribution in the blood plasma of the reference group was the following: 22% LDH1, 36% LDH2, 34% LDH3, 6% LDH4 and 2% LDH5 as well as 75% CK1 and 15% CK2. The remaining 10% of the plasma electropherogram could not be alloted to any one of the two CK bands. All trial groups built showed a similar pattern of changes in their isoenzyme distribution independent on kind and combination of altered enzyme activities. The shares of CK1, LDH4 and LDH5 were significantly increased whilst the shares of CK2, LDH1 and LDH2 decreased. A multiple analysis of variance demonstrated that only increased total CK activities had a pronounced effect on distribution of LDH and CK isoenzyme patterns in the trial group (p less than 0.01 for LDH2, LDH3, LDH4, CK1 and p less than 0.05 for CK2). The conclusion of the study was that the altered distribution pattern of LDH and CK isoenzymes of the trial group signalized an increased skeletal muscle membrane leakage.
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PMID:[LDH and CK isoenzyme patterns in the blood plasma of horses with elevated CK, LDH and AST activities]. 191 50

Beginning the day after hatching, American kestrel (Falco sparverius) nestlings were orally dosed for 10 consecutive days with 5 microliters/g of corn oil (controls) or one of the diphenyl ether herbicides (nitrofen, bifenox, or oxyfluorfen) at concentrations of 10, 50, 250, or 500 mg/kg in corn oil. At 500 mg/kg, nitrofen resulted in complete nestling mortality, bifenox in high (66%) mortality, and oxyfluorfen in no mortality. Nitrofen at 250 mg/kg reduced nestling growth as reflected by decreased body weight, crown-rump length, and bone lengths including humerus, radius-ulna, femur, and tibiotarsus. Bifenox at 250 mg/kg had less effect on growth than nitrofen, but crown-rump, humerus, radius-ulna, and femur were significantly shorter than controls. Liver weight as a percent of body weight increased with 50 and 250 mg/kg nitrofen. Other manifestations of impending hepatotoxicity following nitrofen ingestion included increased hepatic GSH peroxidase activity in all nitrofen-treated groups, and increased plasma enzyme activities for ALT, AST, and LDH-L in the 250-mg/kg group. Bifenox ingestion resulted in increased hepatic GSH peroxidase activity in the 50- and 250-mg/kg groups. Nitrofen exposure also resulted in an increase in total plasma thyroxine (T4) concentration. These findings suggest that altricial nestlings are more sensitive to diphenyl ether herbicides than young or adult birds of precocial species.
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PMID:Developmental toxicity of diphenyl ether herbicides in nestling American kestrels. 194 22

The effect of temperature and duration of storage on clinico-chemical variables was investigated in Na heparinized plasma and plasma or serum of Na heparinized whole blood and whole blood of horses, respectively. The values of AST, Gamma-GT, AP, bilirubin, cholesterol, urea, total protein, albumin, Ca, Mg and Na varied in all the sample substrates investigated at 20-22 degrees C and 4 degrees C less than +/- 10% during the observation period of up to four days. In the Na heparinized plasma samples kept at 20-22 degrees C and 4 degrees C also LDH, CK, inorganic P and K did not differ significantly from its initial values during the four days. However, in the plasma of sampled stored at 20-22 degrees C as Na heparinized whole blood, the increases of LDH, CK, P and K until the fourth day of storage reached 56%, 49% and 69% and in the serum of samples kept as whole blood 90%, 165%, 147% and 48% respectively. While at 4 degrees C in the plasma of samples stored as Na heparinized whole blood until the fourth storage day only K increased significantly (by 28%), the LDH, CK and K values in the serum of samples stored as whole blood rose to 118%, 136% and 141% respectively. In the Na heparinized plasma samples kept at -18 degrees C all the measured variables did not differ significantly from the initial values during the storage time of 10 weeks.
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PMID:[The effect of storage time, temperature and initial test material on clinico-chemical blood variables]. 195 Feb 33

Alterations in the rat brain carbohydrate and related metabolisms were studied during acute and chronic acephate toxicity. The rats were divided into three batches of eight in each batch. The first batch was treated with chronic (50 mg.Kg-1.day-1 for 7 weeks) and second batch was treated with acute (600 mg.Kg-1.day-1 for one day) doses of acephate, third group was served as control which received vehicle only. The representative enzymes like SDH, MDH, LDH, GDH, AAT and AlAT activities were decreased significantly during chronic treatment. Whereas MDH, LDH, AAT and AlAT activities showed significant increase during acute treatment. The glycogen and pyruvate levels showed nonsignificant elevation and lactate and total carbohydrate levels were depleted in the brains of chronic acephate treated rats. Reverse trend was observed with regard to lactate and pyruvate during acute toxicity whereas the total carbohydrates and glycogen levels were significantly elevated. The decreased oxidative potential and reduced flux of ketoacids into TCA cycle through transamination reactions indicate that acephate caused energy crisis in the brain during chronic treatment. During acute treatment the inhibited succinate oxidation was compensated by the ketoacid contributions through transamination reactions. The neuro transmitter balance with particular reference to glutamate during toxic stress was reflected through the GDH levels in both the treatments.
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PMID:Alterations in glycolytic and oxidative potentials of rat brain during acute and chronic acephate treatments. 195 6

Clinically healthy silver foxes obtained from a closed colony were investigated for the purpose of establishing base-line data for this species. The anthropometry (body weight; body length; length and width of the head; width, depth, and circumference of the chest; length of the tail), anatomical measurements (weight; longitudinal and transverse length; thickness of the main organs) and serum biochemical assays (AST, ALT, ALP, LDH, CK, lipase, GGT, T-Cho, beta-Lipo, TG, Phos-Lip, Tp, T-Bil, UA, BUN, Crea, Glu, Ca, IP, Mg, Fe, Na, K, Cl, LDH and CK isoenzymes) were carried out. The data were presented as mean values with standard deviations, and compared with those of the dog. The coefficient of variation (CV) for each of the anthropometric parameters was low, except for that of female body weight for which the CV was 17%. The body size of the male was larger than the female, and the weights of the main organs, corresponding to body size, were greater than the female. The results were equivalent to those for a Beagle dog aged between 3 and 5 months. Significant differences between the sexes were detected in the following parameters: concentrations of BUN, beta-Lipo and T-Bil (p less than 0.01); concentration of Mg and Glu (p less than 0.05); activity of LDH and lipase (p less than 0.05). The biochemical data ware uniform with some exceptions. These were AST (142 IU/l) and ALP (122 IU/l) in a 5-year-old male fox, Glu (over 200 mg/dl) in four 2-year-old female foxes, CK (629 IU/l) in a 2-year-old female fox, and finally CK (366 IU/l) and lipase (428 IU/l) in an 8-year-old female fox, all of which were elevated. These data were similar to the reference values for the dog previously reported. The reference values presented in this report for the silver fox will be valuable as a guide for clinical diagnosis and research.
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PMID:Reference data on the anatomy and serum biochemistry of the silver fox. 195 49

Studies were conducted on male adult rabbits to find out the changes in blood glucocorticoid levels along with the changes in aspartate aminotransferase activity in blood and the role of pyridoxine on the glucose tolerance pattern under hypoxic stress. Hypoxic stress was produced by exposing the animals to a simulated altitude of 7,000 m for 6 h. In the first set of experiments 10 rabbits were used. Blood haemoglobin level, plasma and erythrocyte glucocorticoid levels and erythrocyte GOT activity were measured just before and after the exposure to hypoxia. Erythrocyte GOT activity was measured both without and with 50 mg of pyridoxal phosphate addition to the incubation mixture. Glucocorticoid levels in plasma increased by 11% whereas in erythrocytes the increase was 55% after hypoxia. Percent stimulation of erythrocyte GOT activity with pyridoxal phosphate before exposure to hypoxia was 180% but increased to 321% after exposure. In the second set of experiments another 10 rabbits were used. First they were exposed to hypoxia without pyridoxine hydrochloride feeding and then after 7 days with 3 mg of pyridoxine hydrochloride feeding. For glucose tolerance tests the animals were fed with 1 g of glucose immediately after the hypoxic exposures. Plasma reduced glutathione (GSH), LDH and ICDH activities increased and GOT activity was depressed after hypoxic stress, but when the animals were fed pyridoxine hydrochloride prior to the exposure the enzyme activities remained unaltered after hypoxic stress. Pyridoxine hydrochloride did not alter the pattern of glucose tolerance after hypoxic stress.
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PMID:Effects of pyridoxine supplementation on blood glucocorticoids level, aspartate aminotransferase activity and glucose tolerance pattern under acute hypoxic stress. 204 60

Verapamil, a calcium channel blocker, improves myocardial preservation during cold cardioplegia and protects against renal damage during periods of warm and cold ischemia. To determine if verapamil could prevent ischemic damage to livers during and after cold storage, harvested rat livers were flushed with either University of Wisconsin (UW) solution or UW solution with 25 mg/liter verapamil. Twenty rats were used in each group. After 24 hr of storage at 4 degrees C, livers were perfused with oxygenated blood through the portal veins for 2 hr at 37 degrees C and pH 7.4. Liver enzymes, electrolytes, and perfusate flow rate were determined at 30-min intervals. At 90 min of perfusion, the verapamil group of livers had less elevation of AST (110 +/- 17 IU/liter vs 172 +/- 25 IU/liter, P less than 0.05), ALT (115 +/- 21 IU/liter vs 210 +/- 34 IU/liter, P less than 0.05), and LDH (962 +/- 170 IU/liter vs 1452 +/- 253 IU/liter, NS). Verapamil livers produced more bile than controls (6.9 +/- 1.9 microliters/g vs 2.3 +/- 1.7 microliter/g, P less than 0.05) and maintained a higher portal flow rate throughout the perfusion. Both groups showed similar reduction in liver weights after storage (3.9 +/- 0.9% vs 2.8 +/- 0.7%) and required the same amount of bicarbonate for correction of acidosis during perfusion (2.6 +/- 0.2 mM vs 2.8 +/- 0.2 mM). Light microscopic exam after perfusion showed hepatocyte damage in 30% of control livers, but 0% of verapamil livers. We conclude that verapamil-treated rat livers showed less damage and better function upon reperfusion after 24 hr of cold storage. This agent may be clinically useful as an additive to the UW preservation solution for livers.
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PMID:Verapamil improves rat hepatic preservation with UW solution. 205 66

Serum activities of alanine-aminotransferase (ALAT, EC 2.6.1.2), aspartate-aminotransferase (ASAT, EC 2.6.1.1), lactate dehydrogenase (LDH, EC 1.1.1.27), and alkaline phosphatase (AP, EC 3.1.3.1) were increased significantly after a dose of 0.16 g/kg/b. w. (ip.) carbon tetrachloride (tetrachloromethane) in rats pretreated with 10% (v/v) ethanol for one and 10 weeks in comparison with water/carbon tetrachloride-treated animals. At the end of 30 and 52 weeks of ethanol consumption these levels were very slightly increased or not detectable. Ethanol treatment alone did not cause an increase in serum enzyme activities or histological liver damage, but caused a diminished intake of fluid and food and in some cases also a reduction of weight gain in the animal body. Significant decrease in body weight after carbon tetrachloride was more evident in rats pretreated with ethanol (1 week greater than 10 greater than or equal to 52 weeks) than in water drinking animals, the lethality caused by carbon tetrachloride was also higher after one and 10 weeks than after 30 to 52 weeks of ethanol pretreatment. The results indicate a decrease of carbon tetrachloride toxicity with increased duration of ethanol pretreatment. This phenomenon could be attributed to reduced sensibility to those alcohol effects which are responsible for increase of carbon tetrachloride toxicity.
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PMID:Influence of ethanol pretreatment of differing duration on toxic effects of carbon tetrachloride in rats. 208 Sep 8


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