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)

Studies on aspartate aminotransferase (GOT) and L-alanine aminotransferase (GPT) of Paramphistomum explanatum have shown that GPT activity has more than twice the activity of GOT. The effect os some--SH reagents like cadmium, mercury, silver and iodoacetamide revealed that both enzymes were inhibited except that GOT was insensitive to cadmium ions. GPT was found to be much more sensitive to--SH reagents than GOT. There was unusual reaction to the two thiols used, cysteine and mercaptoethanol. Cysteine inhibited both the enzymes and mercaptoethanol activated GPT and inhibited GOT. Thiols in combination with iodoacetamide showed that the strong inhibitory effect of cysteine on both enzymes was reduced by iodoacetamide, but with mercaptoethanol the inhibitory effect on GOT was greater than when either of them was used alone, while GPT the effect of either counteracted each other. EDTA activated both enzymes and partially protected mercury inhibition of both enzymes and silver inhibition GOT only. It provided no protection against silver inhibition of GPT but complete protection of GPT against total inhibition by cadmium ions.
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PMID:Effect of some--SH and other reagents on aspartate aminotransferase and L-alanine aminotransferase of Paramphistomum explanatum Fischoeder, 1901. 41 89

Wild-trapped starlings (Sturnus vulgaris) were fed concentrations of Morsodren (2, 4, and 8 ppm), DDE or Aroclor 1254 (5, 25, and 100 ppm), or malathion (8, 35, and 160 ppm) that were found to be sublethal in pen-reared Coturnix quail fed these amounts for 12 weeks. Plasma enzymes had to be measured earlier than planned in starlings fed Morsodren (at three weeks) or the organochlorine compounds (at seven weeks) because of unexpected, subsequent mortality. Variations in enzyme response were greater in wild than in pen-reared birds, but not enough to mask the toxicant-induced changes in enzyme activity. Cholinesterase activities decreased in birds fed Morsodren or malathion, and increased in those fed the organochlorine compounds. Lactate dehydrogenase activities increased two-fold in starlings fed Morsodren and two- to four-fold in those fed the organochlorine compounds, but only 50% in those fed malathion. Further examination of enzyme profiles showed that creatine kinase and aspartate aminotransferase activities increased two- to four-fold in birds fed Morsodren or the organochlorine compounds but not at all in those fed malathion. Thus the classes of environmental contaminants fed to starlings could be easily distinguished by these enzymatic parameters. Evaluation of enzymatic profiles appears to be a potentially valuable technique to monitor the presence of toxicants in wild populations, especially if used to complement standard chemical residue analyses. Here the residue analyses showed, after three weeks feeding, that mercury in the carcasses reflected the concentrations fed daily, whereas accumulation in the livers was two- to four-fold greater. After seven weeks feeding, liver residues of either organochlorine compound were about three-fold higher than the concentrations fed daily. However, four times as much DDE as Aroclor 1254 had accumulated in the carcasses.
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PMID:Further studies on the use of enzyme profiles to monitor residue accumulation in wildlife: plasma enzymes in starlings fed graded concentrations of Morsodren, DDE, Aroclor 1254 and malathion. 80 76

Three hundred patients with acute pancreatitis have been studied. Pancreatitis was associated with alcoholism in 207, biliary tract disease in 51 and other conditions in 42. Twenty-two patients died, and an additional 34 patients required more than one week of treatment in the intensive care unit. Retrospective analysis of the first 100 patients identified 11 objective findings which correlated with the occurrence of serious illness or death. They were, on admission, age over 55 years, blood glucose level over 200 milligrams per cent, white blood count over 16,000 per cubic millimeter, serum lactic dehydrogenase level over 350 International units per liter and serum glutamic-oxalacetic transaminase level over 250 Sigma Frankel units per cent. During the initial 48 hours of therapy, the findings were hematocrit value decrease over 10 percentage points, serum calcium level below 8 milligrams per cent, base deficit over 4 milli-equivalents per liter, a blood urea nitrogen level increase over 5 milligrams per cent, estimated fluid sequestration over 6 liters and arterial oxygen tension less than 60 millimeters of mercury. Prospective application of these signs in the latter 200 patients permitted the accurate early identification of those with severe pancreatitis. Only one of 162 patients with fewer than three of these early features was seriously ill or died, while 24 of 38 patients with three or more early positive findings were seriously ill or died. The objective early identification of patients with severe pancreatitis permits more vigorous management of this group and also provides a basis for the selection of patients for the evaluation of proposed improved therapies. Percutaneous peritoneal dialysis in severe pancreatitis was evaluated in ten patients, with three or more positive early signs, who were randomly assigned to dialysis or continued conventional care. Morbidity was strikingly reduced in patients who underwent dialysis, and while death or more than nine days of intensive care occurred in two of five patients who did not receive dialysis, all five patients having dialysis recovered after fewer than nine days of intensive care treatment. Serious illness or death occurred in 31 of the first 100 patients but in only 26 of the more recent 200 patients. There has been a similar fall in mortality from 15.0 to 3.5 per cent. Factors which may contribute to this improvment include the objective early identification of patients with severe disease, the avoidance of early laparotomy whenever practical, the prolongation of nasogastric suction until all evidence of pancreatic inflammation has resolved, careful monitoring of respiratory function and early treatment of pulmonary complications and peritoneal dialysis in patients with severe disease.
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PMID:Prognostic signs and nonoperative peritoneal lavage in acute pancreatitis. 94 Oct 75

Changes in the protein metabolism of gill, kidney and intestine of freshwater fish, Cyprinus carpio exposed to 1, 15 and 30 days to sublethal concentration (0.1 mg/l) of mercury were studied. The total, soluble and structural protein contents recorded the depletion followed by progressive increase in accumulation of free aminoacids. Concurrently, the activity of protease in the tissues was also increased. A steady enhancement in the activities of aspartate aminotransferase and alanine aminotransferase paralleled the elevation of glutamate dehydrogenase activity in the organs studied. Levels of ammonia and urea have also reported elevation. All these changes clearly documented the induction of severe proteolysis. The magnitude of these changes increased overtime. These changes were more in the gill at the initial periods of exposure (1 and 15 days), but as the period of exposure increased, these changes were more pronounced in the kidney at 30 days of exposure to sublethal concentration of mercury.
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PMID:Shifts in protein metabolism in some organs of freshwater fish, Cyprinus carpio under mercury stress. 193 Feb 54

1. Rosy barb (Puntius conchonius) were exposed to 181 micrograms/l mercuric chloride for 48 h and the activity of acid and alkaline phosphatases (AcP and AIP), aspartate aminotransferase (AAT), alanine aminotransferase (AIAT), lactic dehydrogenase (LDH), and acetylcholinesterase (AchE) were measured in vivo in several organs. 2. The AcP activity was inhibited in the liver, gills, kidneys, and gut but stimulated in the gonads. With the exception of kidney, the AIP activity showed an increase in all the organs examined. The AAT and AIAT were generally inhibited in different organs. An increase in LDH activity occurred in the cardiac and skeletal muscles while the AchE activity was considerably lowered in the brain, gills, and liver. 3. In vitro exposure to mercury at concentrations ranging between 10(-10) and 10(-4) M, inhibited the AIP, AAT, AIAT, LDH, and AchE activities in the tissues examined. The AcP activity was also depressed in all the tissues except in the testes, in which a marginal increase was noted. 4. The in vivo and in vitro effects of Hg were not of similar quality implying sequestration of toxic cations in the intact animals.
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PMID:Use of the fish enzyme system in monitoring water quality: effects of mercury on tissue enzymes. 198 72

The effect of N-benzyl-D-glucamine dithiocarbamate (BGD) on the renal toxicity of inorganic mercury in rats was studied. Rats were injected i.v. with saline or HgCl2 (300 micrograms Hg/kg) and 30 min later they were injected i.p. with saline or BGD (2778 mumol/kg, a quarter of an LD50). Urinary excretion of gamma-glutamyl-transpeptidase (gamma-GTP), which is a brush border enzyme, in rats after mercury treatment significantly increased compared to that of the control in the 12-24 h urine specimen and reached a maximum value within 24 h after the treatment. Urinary excretion of N-acetyl-beta-D-glucosaminidase (NAG), which is a lysosomal enzyme, also significantly increased after mercury treatment compared to that of the control in the 12-24 h urine specimen and reached a maximum value within 48 h after the treatment. A change in urinary aspartate aminotransferase (AST) activity after mercury treatment followed a pattern similar to that observed with the urinary NAG. BGD treatment did not increase the urinary excretions of gamma-GTP, NAG, and AST. The uptake of p-aminohippuric acid (PAH) by renal cortical slices significantly decreased 24 h after mercury treatment. BGD injection after mercury treatment did not decrease the uptake of PAH by cortical slices. In addition, the microscopic examination of renal tissue from mercury-treated rats revealed necrosis of the proximal tubular cells. However, a photomicrograph of rat renal cortex after BGD treatment showed little abnormality. These results indicated that the mercury-induced renal damage was protected by the injection of BGD 30 min after mercury treatment.
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PMID:Effect of N-benzyl-D-glucamine dithiocarbamate on renal toxicity of inorganic mercury in rats. 239 73

The paper presents the results of a combined biochemical study of 111 patients suffering from recently diagnosed pulmonary tuberculosis combined with chronic opisthorchiasis (main group) and 36 tuberculosis patients without infestation (control group). It was established that the mixed abnormality was significantly more often accompanied by hypoproteinemia and hypoalbuminemia. The thymol and mercury-chloride sublimate tests produced positive results in 22.5 and 9.0% of the main group patients, respectively. Increased bilirubin content and alanine and aspartate aminotransferase activities were registered in both groups of patients only during medical treatment. Thus, the fact of altered protein forming function of liver in patients with tuberculosis combined with chronic opisthorchiasis has been established, which may be due both to tuberculosis infection and the Opisthorchis invasion. Insignificant hepatic protein-forming dysfunctions are not contraindications for long-term tuberculosis therapy.
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PMID:[Biochemical indices of the blood in patients with tuberculosis combined with chronic opisthorchiasis]. 261 4

The effects of three chelating agents, sodium N-benzyl-D-glucamine dithiocarbamate(NBG-DTC), 2,3-dimercaptopropanol(BAL), and D-penicillamine(D-PEN), on the distribution, excretion, and renal toxicity of inorganic mercury were compared in rats exposed to HgCl2. Rats were injected i.p. with 203HgCl2 (300 micrograms of Hg and 2 microCi of 203Hg/kg) and 30 min or 24 h later they were injected with a chelating agent (a quarter of an LD50). The injection of the chelating agents significantly enhanced the biliary and urinary excretions of mercury. BAL was the most effective for removal of mercury from the body at 30 min after mercury treatment. The extent of enhancing effect of the chelating agents for removal of mercury at 24 h after mercury was in the order NBG-DTC = BAL greater than D-PEN. The injection of BAL at 24 h after mercury treatment caused the redistribution of mercury to the heart and lung. NBG-DTC did not result in the redistribution of mercury to the heart, lung, and brain. Urinary excretion of protein and AST significantly increased 24-48 h after mercury treatment and decreased to the control values 72 h after mercury. The injection of the chelating agents at 30 min after mercury treatment significantly decreased the urinary excretion of protein and AST. In rats pretreated with mercury 24 h earlier, the chelating agents significantly decreased the urinary protein at 48 h after mercury treatment, but did not decrease the urinary AST. The results of this study indicate that the chelating agents are effective in removing mercury from the body, resulting in the protective effect against the mercury-induced renal damage.
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PMID:Comparative effects of chelating agents on distribution, excretion, and renal toxicity of inorganic mercury in rats. 278 Nov 44

The toxic effects of cadmium (Cd) and mercury (Hg), as chloride salts, were studied using an hepatic human fetal cell line (WRL-68 cells). From viability curves and the proliferative capacity of the cell in the presence of the metal, three different cell treatments were chosen, (1) 0.5 microM of the metal chloride for 24 h (acute low dose treatment), (2) 0.5 microM of the metal chloride for 7 days (chronic treatment), and (3) 5 microM of the metal chloride for 24 h (acute high dose treatment). WRL-68 cells grown in the presence of Cd exhibited the same proliferative curve as control cells, whereas in the case of Hg, the cells increased their proliferative capacity. Both metals produced ultrastructural alterations in different degrees, mainly observed as mitochondrial and RER structural changes, depending of the treatment and concentration of the metal used. Cytotoxicity was assessed by measuring the release of lactate dehydrogenase from the cells. Acutely high dose-treated cells showed the highest value for this parameter, and Cd-treated cells presented higher lactate dehydrogenase release than the Hg-treated ones. Cell damage was also measured by alanine aminotransferase (ALAT) and aspartate aminotransferase (ASAT) activities. Acute high dose Cd treatment caused the highest value of enzymatic release. Lipid peroxidation was significantly different with respect to control cells in chronic and acute high dose treatments with both metals. Metallothionein (MT) induction in response to Hg treatment was not detected. However, a dramatic induction of this protein occurred in Cd-treated cells. WRL-68 cells differentially respond to Cd and Hg making this hepatic fetal human cell line a useful tool in investigating the mechanism of toxicity of these heavy metals.
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PMID:Cadmium and mercury toxicity in a human fetal hepatic cell line (WRL-68 cells). 748 68

Problems with the assessment of organ damage caused by toxic substances in places of residence have recently appeared with increasing frequency. In spite of this there have been so far no uniform, objective research methods which could allow their accurate evaluation. This is why the attempt has been made to assess morphological and functional condition of the liver in patients chronically exposed to mercury compounds in the place of settlement. The research group consisted of 62 patients exposed to metallic mercury at a yearly rate exceeding 24 kg for average duration of 16 years. Patients with the liver or biliary tract diseases, symptoms of chronic circulatory insufficiency, Australia (HBs+) antigen carriers and alcoholics were excluded from the research group. The control group consisted of 29 males. AST and ALT activity, prothrombin level, bilirubin and protein concentration in blood serum were measured and scintigraphic and USG examinations of the liver were performed. Mercury concentrations were also established. Scintigraphic examination yielded an abnormal image of the liver in 52% of the exposed patients. The differences in frequency and intensity of scintigraphic changes in comparison with the control group were of statistical significance. No pathological changes were found in USG examination. Significantly higher ALT activity and bilirubin concentration and significantly lower total protein concentration were found in the exposed group. The correlation between the intensity of scintigraphic changes and mercury concentration were noted. Liver scintigraphic examination combined with biochemical analysis allows an assessment of the liver condition in chronic exposure to mercury compounds in the place of settlement.
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PMID:The assessment of the condition of the liver in patients chronically exposed to mercury compounds in the place of settlement. 764 91


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