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)

The plasma electrolytes, Na+, K+, Ca2+, Cl- and osmolarities had high values in capture-stressed big gamefish. Blood metabolites measured after stress showed glucose and lactate elevations. The activity of the plasma enzymes alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, creatine kinase and lactate dehydrogenase suggested tissue disruptions following severe capture stress. Haematocrit values and methaemoglobin were high in capture-stressed gamefish. The plasma chemistry of resting and capture-stressed snapper (Chrysophrys auratus) was studied for comparison. Specific differences in plasma biochemistry appeared to be the result of different strategies of fish behaviour during capture.
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PMID:Physiological stress responses in big gamefish after capture: observations on plasma chemistry and blood factors. 287 36

The average biological intra-individual CV in 20 patients with chronic liver diseases (CLD), estimated for 14 analytes during a stationary phase, significantly exceeded that for a normal group in the cases of Na+, K+, Cl-, total protein, albumin, cholinesterase, hemoglobin, and alpha-amylase; it did not differ significantly from the normal group for cholesterol, alkaline phosphatase, aspartate aminotransferase, and alanine aminopeptidase; and it was significantly lower than in the normal group for alanine aminotransferase and gamma-glutamyltransferase. There were no significant sex-related differences in mean intra-individual variation in CLD patients. Individual values were gaussian-distributed for all analytes, including enzymes. The estimated biological component of intra-individual variation and the analytical variation as determined for each laboratory can be used to derive decision-making criteria in monitoring CLD.
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PMID:Intra-individual variation of analytes in serum from patients with chronic liver diseases. 288 11

The administration of sodium N-methyl-N-dithiocarboxy-D-glucamine (NaG) at 500 mg/kg, i.p., or sodium calcium diethylenetriaminepentaacetic acid (DTPA) at 632.5 mg/kg, i.p., reduces the serum enzyme levels characteristic of hepatic damage following the intravenous administration of cadmium chloride (3.5 mg CdCl2.2.5H2O/kg). Some effect on serum enzyme levels was found even when the interval between administration of cadmium chloride and that of the antagonist was as great as 4 h. The enzymes examined included aspartate aminotransferase (AST), gamma-glutamyl transpeptidase (GGT), alanine aminotransferase (SGPT), and alkaline phosphatase (AP). A histopathological examination of the livers of such animals also reveals the presence of a significant protective action.
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PMID:Chelating-agent suppression of cadmium-induced hepatotoxicity. 289 Jul 68

Experiments were undertaken to examine the ability of selenium to protect against acetaminophen-induced hepatotoxicity and to examine possible mechanisms for this protective effect. Pretreatment of male, Sprague-Dawley rats with sodium selenite (12.5 mumol Se/kg, ip) 24 hr prior to acetaminophen administration produced a significant protection against the hepatotoxic effects of acetaminophen as assessed by a decrease in the plasma appearance of alanine aminotransferase and aspartate aminotransferase activities following acetaminophen. This was accompanied by an increase in the hepatic glutathione levels in selenium-treated animals and an inhibition in the decrease in hepatic glutathione content observed in animals receiving hepatotoxic doses of acetaminophen. Selenium pretreatment decreased the in vivo covalent binding of acetaminophen metabolites to hepatic protein, but did not alter hepatic microsomal cytochrome P-450 content or NADPH cytochrome c reductase activity, suggesting that selenium does not significantly alter the metabolism of acetaminophen to reactive electrophilic metabolites by the cytochrome P-450-dependent mixed-function oxidase enzyme system. Selenium produced an increase in the activity of gamma-glutamylcysteine synthetase which may account for the increased glutathione availability in selenium-treated animals and increased the activities of glutathione S-transferase and glucose-6-phosphate dehydrogenase. Examination of the urinary metabolite profile in selenium-treated animals revealed that the urinary excretion of acetaminophen and its metabolites was significantly increased over a 72-hr period. The increase occurred in the AAP-glucuronide metabolite while parent AAP and AAP-sulfate were actually decreased in selenium-treated rats. No change in recovery was observed in the AAP-glutathione or AAP-mercapturate urinary metabolites. While the glutathione conjugating system is enhanced by selenium treatment, amelioration of acetaminophen toxicity is most likely the result of enhanced glucuronidation which effectively diverts the amount of acetaminophen to be converted by the cytochrome P-450 system to the toxic metabolite.
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PMID:Protective effects of selenium on acetaminophen-induced hepatotoxicity in the rat. 290 Nov 47

Patients with proximal stomas or high fistulas and defunctionalized intestine who are receiving total parenteral nutrition (TPN) often develop hepatic enzyme abnormalities and hyperbilirubinemia. A technique was developed to collect intestinal secretions from proximal stoma and to reinfuse these secretions into the distal part of the intestine. This technique was applied in eight patients with a disrupted intestinal tract. A significant decrease (p less than 0.05) in elevated serum bilirubin, alkaline phosphatase and gamma-glutamyl transpeptidase levels was observed. Alanine aminotransferase and aspartate aminotransferase levels did not change significantly. The plasma sodium levels, slightly subnormal before reinfusion (131.0 +/- 4.6 millimolar per liter), despite enormous supplementation, normalized during reinfusion (137.0 +/- 4.0 millimolar per liter). TPN was continued during this infusion. This suggests that TPN by itself does not cause intrahepatic cholestasis. Neither could it be explained by an effect of secondary bile acids because these were most likely not produced as bile did not reach the distal defunctionalized intestine. Three possible mechanisms are suggested. Restoration of passage in the distal intestine may diminish bacterial overgrowth, endotoxin production and absorption. Enlargement of the bile acid pool may diminish the susceptibility of the liver to the deleterious effects of endotoxins. We advocate this reinfusion technique to overcome the metabolic disturbances occurring in those patients with high-output stomas or fistulas arising from the proximal parts of the small intestine.
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PMID:Reinfusion of secretions from high-output proximal stomas or fistulas. 290 95

The effect of oral administration of vanadate, in normalizing blood glucose levels of streptozotocin-treated rats (ST-rats), is further characterized and its mode of action is determined. We have examined the effects of two orally administered doses of sodium metavanadate. High concentrations of orally administered vanadate (0.8 mg/ml in drinking water) reduced blood glucose levels within 2-4 days of application and led to the appearance of hypoglycemia in test animals. Lower concentrations of vanadate (0.2 mg/ml in drinking water) also lowered blood glucose levels within 4 days, but did not lead to hypoglycemia for at least 3 weeks. These effects of vanadate were found to be reversible; hyperglycemia recurred within 2 days after removal of vanadate from the drinking water. In streptozotocin-treated rats receiving low vanadate treatment, circulating levels of vanadate were about 0.8 microgram/ml after 3 weeks of treatment. These rats became anabolic, while rats receiving high vanadate treatment remained catabolic. Subsequent to vanadate treatment, adipocytes derived from ST-rats responded to lower insulin concentrations. In addition, vanadate treatment lowered the increased insulin binding capacity of liver plasma membranes derived from ST-rats. Insulin binding capacity under these conditions approached that of control non-ST-rats. Basal rates of hexose uptake in muscle and liver tissues were doubled in vanadate-treated ST-rats. It is concluded that the oral administration of vanadate leads to normoglycemia by stimulating glucose uptake. Treatment with "low vanadate" leads to the formation of a stable anabolic and normoglycemic state in ST-rats and appears to restore insulin responsiveness of target tissues, without apparent signs of toxicity. Vanadate treatment did not impair either kidney or liver function, as assayed by the measurement of serum urea, creatinine, and glutamic-oxaloacetic transaminase.
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PMID:Oral administration of vanadate normalizes blood glucose levels in streptozotocin-treated rats. Characterization and mode of action. 295 56

A 3-year-old mare repeatedly had clinical signs of rhabdomyolysis on mild exertion. Serum creatine kinase and aspartate transaminase activities were high at rest. Responses to dietary sodium bicarbonate were tested through 7 alternating periods of supplementation of a basal ration of timothy hay and oats. Physical signs; venous blood pH and gases; blood glucose and lactate; serum electrolytes, enzymes, and creatinine; and urine pH were monitored before and after exercise. Dietary sodium bicarbonate raised resting venous blood pH and bicarbonate slightly and significantly increased urine pH from pH 7.46 to 8.2 (P less than 0.001). An exercise test included 5 minutes at the walk followed by 20 minutes at the trot. The exercise induced gait stiffness, muscle fasciculations, and muscle induration when the diet was not supplemented, but not when it was supplemented with sodium bicarbonate. Myoglobin was present in 16 of 21 urine samples after exercise during nonsupplemented periods, but only in 3 of 28 urine samples during supplemented periods (P less than 0.0001). Bicarbonate supplementation significantly decreased the responses of blood lactic acid, serum creatine kinase, and aspartate transaminase to exercise. Supplementation of the diet was associated with higher venous blood pH and bicarbonate ion concentrations throughout exercise. Dietary sodium bicarbonate apparently mitigated or prevented physical, chemical, and enzymatic characteristics of exertional rhabdomyolysis in this mare, possibly through its enhancement of buffering capacity in muscle tissue fluids.
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PMID:Dietary sodium bicarbonate as a treatment for exertional rhabdomyolysis in a horse. 300 12

Tonsillectomy in adults and older children is typically accompanied by 7 to 14 days of pain. On the basis of clinical observations of patients treated perioperatively with dantrolene sodium for malignant hyperthermia, we hypothesized that pharyngeal muscle spasms are a major factor in tonsillectomy pain. We entered 113 patients, 11 years of age and older, into a double-blind, placebo-controlled study to evaluate the effectiveness of dantrolene sodium in reduction of tonsillectomy pain. Patients were randomly assigned either dantrolene (1.5 mg/kg per day) or placebo orally four times a day for 5 days postoperatively. On a standardized questionnaire, the patient recorded pain, diet, activity level, analgesics, and side effects, daily for 2 weeks. Also, alkaline phosphatase (alk phos) and serum aspartate aminotransferase (SGOT) levels were determined before the operation and 2 weeks after. Patients who received dantrolene had no significant differences in subjective pain, diet, or activity level scores from those of patients who received placebo. Dantrolene patients did, however, require significantly less analgesic use than placebo patients (p = 0.034, 0.015, and 0.005 for postoperative days 2, 3, and 4, respectively). There was no significant difference in side effects or changes in liver enzyme between the dantrolene and placebo groups. We conclude that dantrolene sodium, given in the dosage noted, is effective in reduction of analgesic requirements after tonsillectomy.
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PMID:Oral dantrolene sodium for tonsillectomy pain: a double-blind study. 312 47

Conditions for reductive methylation of amine groups in proteins using formaldehyde and cyanoborohydride can be chosen to modify selectively the active site lysyl residue of aspartate aminotransferase among the 19 lysyl residues in each subunit of this protein. Apoenzyme must be treated, under mildly acidic conditions (pH = 6), at a relatively low molar ratio of formaldehyde to protein (40:1); and, upon reduction with sodium cyanoborohydride, 85% of the formaldehyde is incorporated at Lysine 258 and 15% at the amino-terminal alanyl residue. The modified protein, characterized after tryptic hydrolysis, separation of the peptides by high performance liquid chromatography procedures and subsequent amino acid analysis, shows that lysine 258 is preferentially modified as a dimethylated derivative. Modified apoenzyme can accept and tightly bind added coenzyme pyridoxal phosphate, as measured by circular dichroism procedures. The methylated enzyme is essentially catalytically inactive when measured by standard enzymatic assays. On the other hand, addition of the substrate, glutamate, produces the characteristic absorption spectral shifts for conversion of the active site-bound pyridoxal form of the coenzyme (absorbance at 400 nm) to its pyridoxamine form (absorbance at 330 nm). Such a half-transamination-like process occurs as in native enzyme, albeit at several orders of magnitude lower rate. This event takes place even though the characteristic internal holoenzyme Schiff's base between Lys-258 and aldehyde of bound pyridoxal phosphate does not exist in methylated, reconstituted holoenzyme. It is concluded that this chemically transformed enzyme can undergo a half-transamination reaction with conversion of active site-bound coenzyme from a pyridoxal to a pyridoxamine form, even when overall catalytic turnover transamination cannot be detected.
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PMID:Site-specific methylation of a strategic lysyl residue in aspartate aminotransferase. 313 Mar 80

Primary cultured rat hepatocytes were used to study the cytotoxicity of sodium valproate (VPA). Cytotoxicity was monitored by measurement of leakage of intracellular enzymes into the culture medium: lactate dehydrogenase (LDH), glutamate oxaloacetate transaminase (GOT), glutamate pyruvate transaminase (GPT). The effects of D,L-carnitine and albumin administration on the cytotoxicity were evaluated. LDH leakage rose with an increasing dose of VPA. Administrations of D,L-carnitine and albumin reduced VPA hepatotoxicity. Our data suggest that VPA-induced hepatotoxicity is dose-related and may be modulated by serum carnitine and albumin levels.
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PMID:Evaluation of the cytotoxicity of sodium valproate on primary cultured rat hepatocytes. 314 9


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