Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.6.1.2 (alanine aminotransferase)
 26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tetrahymena pyriformis Wh 14 was grown in Erlenmeyer flasks under continuous stirring at 30 degrees C for three days . After the culture had produced dry matter of about 100 mg HCB was added in acetone at a dose level of 0, 0.001, 0.1 and 1.0 ppm to the culture and incubated for another 7 days. At a dose level of 0.001 ppm the activity of delta-aminolevulinate dehydratase, hexokinase, and pyruvate kinase remained unaffected but was increased for glutamic-oxaloacetic transaminase, glutamic dehydrogenase, isocitrate dehydrogenase, and malate dehydrogenase while 0.1 ppm HCB increased the activity of all enzymes studied, the only exception being glutamic-pyruvic transaminase, the activity of which was depressed by HCB exposure. A concentration of 1.0 ppm HCB depressed the activity of most of the enzymes below control values with the exception of the two mitochondrial enzymes, MDH and ICDH, studied here.
 ...
PMID:Effect of hexachlorobenzene (HCB) on the activity of some enzymes from Tetrahymena pyriformis. 10 53

Effects of histidine deficiency on muscle carnosine and anserine levels and on activities of enzymes associated with histidine catabolism and protoporphyrin synthesis were investigated. Male Sprague-Dawley (150 g) rats were tube-fed isonitrogenous, isocaloric, defined diets containing 0%, low (0.013%) or adequate (0.45%) histidine for 8-13 days. While histidine-deficient animals maintained body weight, muscle and plasma histidine and carnosine concentrations decreased rapidly and remained low following a 3-day histidine repletion period. Hepatic histidine ammonia-lyase and histidine-pyruvate transaminase activities were decreased in histidine-deficient animals, whereas formiminotransferase activity was unchanged. Hematocrit levels and hemoglobin concentrations declined progressively during histidine depletion and the activity of erythrocyte and hepatic delta-aminolevulinic acid dehydratase also decreased relative to controls. Evidence is presented indicating that decreased histidine catabolism combined with carnosine and hemoglobin degradation can provide sufficient histidine to explain the slow onset of negative nitrogen balance associated with histidine deficiency and that impaired protoporphyrin synthesis may partially explain the anemia observed in the absence of dietary histidine.
 ...
PMID:Metabolic effects of histidine-deficient diets fed to growing rats by gastric tube. 649 66

Linkage data on aminolevulinate dehydratase (ALADH, E.C. 4.2.1.24) and a series of other human genetic markers are presented. One hundred and two families (25 of them being informative) from southwestern Germany were tested. Close linkage (theta = 0.05) between ALADH and the following markers could be excluded: Rh, PGM1, Fy, ACP1, MNSs, HLA, Bf, GLO, PGM3, Jk, Pi, PGP, K, GPT. There is some evidence of possible linkage with HPA.
 ...
PMID:Aminolevulinate dehydratase (E.C. 4.2.1.24): linkage analysis. 695 72

Two main equal groups of clinically healthy, non pregnant rabbits were classified into 4 subgroups (5 rabbits each). The 1st and 2nd subgroups were treated with sulphaquinoxaline or sulphadiazine in a single oral dose of 100 mg/kg b. wt., while the 3rd and 4th subgroups received a repeated oral dose of 100 mg/kg b. wt., daily for 5 successive days, respectively. The second main group received lead acetate in a dose of 4.2 mg/kg b. wt. per day for 2 months, then was classified as in case of the 1st main group and administered the respective sulphonamides in their recommended doses. The experimental lead intoxication was found to decrease the free delta-aminolevulinic acid dehydratase (delta-ALA-D) activity in blood of lead intoxicated rabbits after 4 and 8 weeks. Also, the ratio of free and with glutathione reactivated delta-ALA-D was increased 2.9 and 2.2 after 4 and 8 weeks, respectively as compared with before lead administration (1.19), indicating toxicity. The sulphonamide/creatinine ratio was increased after administration of both sulphonamides but higher in lead intoxicated rabbits as compared with healthy ones. The AST/ALT ratio was decreased 4 and 8 weeks after lead exposure. The AST, ALT and AST/ALT ratio, alkaline phosphatase, urea and creatinine were not altered in healthy rabbits. Repeated oral administration of sulphadiazine caused a significant increase in serum AST, ALT, alkaline phosphatase and creatinine level in healthy and lead intoxicated rabbits. On the other hand, AST/ALT ratio in both healthy and lead intoxicated rabbits was found to decrease 1 h after the last dose as compared with before treatment.
 ...
PMID:Interaction between lead toxicity and some sulphonamides in rabbits: effect on certain blood constituents and serum enzymes. 801 95

The effects of meso 2, 3-dimercaptosuccinic acid (DMSA), sodium 2, 3-dimercaptopropane 1-sulfonate (DMPS) and S-adenosyl L-methionine (SAM) on the enzymatic activities of mice were studied. The mice were given intraperitoneal (i.p.) injections of these chelating agents (1 mmol/kg) and 3 h later the activity of delta-aminolevulinic acid dehydratase (ALAD) in the blood, and aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamyltranspeptidase (gamma-GT), alkaline phosphatase (ALP) in the liver and kidney were determined. The activity of blood ALAD was significantly increased by the administration of DMSA and SAM while DMPS had only a moderate effect. The activities of other hepatic enzymes changed little when the mice were treated with these chelating agents, except for a significant reduction in hepatic ALP activity following DMPS administration. Arsenic (III) administration markedly increased the activities of ALT and ALP in the liver and kidneys. The changes in the enzymatic activities by treatment with arsenic were prevented by injection of DMSA, DMPS and SAM, DMSA being the most effective. These results indicate that DMSA, DMPS and SAM were not toxic to the liver or kidneys of mice and that treatment with DMSA is more effective than DMPS or SAM in protecting mice from acute hepatic or renal toxicity caused by arsenic.
 ...
PMID:Effects of some thiol chelators on enzymatic activities in blood, liver and kidneys of acute arsenic (III) exposed mice. 955 1

Many authors in different studies have reported the antagonism between Mg and Pb. Our previous results suggested that oral Mg treatment have better effect on investigation biochemical parameters (protoporphyrins, aminolevulinic acid--ALA and d-aminolevulinic dehydratase ALA-D) used in evaluating Pb intoxication, then CaNa2EDTA, chelation agents, currently used in therapy of Pb intoxication. The toxic effect of Pb induced considerably modifies the activity of many other enzymes. In this work we have examined the influence of Mg (as alternative therapy of Pb poisoning) on enzymes activity--biochemical markers for general health conditions--aspartate aminotransferase (AST), alanine aminotransferase (ALT) and alkaline phosphatase (ALP) in condition of lead intoxication. Many studies showed disturbances of activity ALT, AST and ALP. The aim of this study was to confirm positive effects of Mg intake in condition of such intoxication at the level on activity of investigated enzymes. The experiment was performed on 45 male Wister rats, divided in three groups. I--control group; II--group treated daily for 30 days with 100 mg Pb, per kg body weight and next 60 without Pb treatment (spontaneous detoxication); III group--the same treatment as II group for the first 30 days, but next 60 days rats were treated orally with 40 mg Mg/kg body weight. Activity of AST and ALT was significant increased in condition of Pb poisoning, but ALP activity was significant reduced. Influence of excessive oral Mg treatment was positive: decrease of AST activity and ALT activity, which was probably in correlation with significant elimination of Pb from liver and increase of ALT enzyme activity at the normal level.
 ...
PMID:The influence of magnesium on the activity of some enzymes (AST, ALT, ALP) and lead content in some tissues. 1263 69

Most ecotoxicological risk assessments of wildlife emphasize contaminant exposure through ingestion of food and water. However, the role of incidental ingestion of sediment-bound contaminants has not been adequately appreciated in these assessments. This study evaluates the toxicological consequences of contamination of sediments with metals from hard-rock mining and smelting activities. Lead-contaminated sediments collected from the Coeur d'Alene River Basin in Idaho were combined with either a commercial avian maintenance diet or ground rice and fed to captive mute swans (Cygnus olor) for 6 weeks. Experimental treatments consisted of maintenance or rice diets containing 0, 12 (no rice group), or 24% highly contaminated (3,950 microg/g lead) sediment or 24% reference (9.7 microg/g lead) sediment. Although none of the swans died, the group fed a rice diet containing 24% lead-contaminated sediment were the most severely affected, experiencing a 24% decrease in mean body weight, including three birds that became emaciated. All birds in this treatment group had nephrosis; abnormally dark, viscous bile; and significant (p <or= 0.05) reductions in hematocrit and hemoglobin concentrations compared to their pretreatment levels. This group also had the greatest mean concentrations of lead in blood (3.2 microg/g), brain (2.2 microg/g), and liver (8.5 microg/g). These birds had significant (alpha = 0.05) increases in mean plasma alanine aminotransferase activity, cholesterol, and uric acid concentrations and decreased plasma triglyceride concentrations compared to all other treatment groups. After 14 days of exposure, mean protoporphyrin concentrations increased substantially, and mean delta-aminolevulinic acid dehydratase activity decreased by more than 95% in all groups fed diets containing highly contaminated sediments. All swans fed diets that contained 24% lead-contaminated sediment had renal acid-fast intranuclear inclusion bodies, which are diagnostic of lead poisoning in waterfowl. Body weight and hematocrit and hemoglobin concentrations in swans on control (no sediment) and reference (uncontaminated) sediment diets remained unchanged. These data provide evidence that mute swans consuming environmentally relevant concentrations of Coeur d'Alene River Basin sediment developed severe sublethal lead poisoning. Furthermore, toxic effects were more pronounced when the birds were fed lead-contaminated sediment combined with rice, which closely resembles the diet of swans in the wild.
 ...
PMID:Toxicity of lead-contaminated sediment to mute swans. 1271 82

The concept that selenium-containing molecules may be better antioxidants than classical antioxidants, has led to the design of synthetic organoselenium compounds. In the present investigation subchronic deleterious effects of cadmium-intoxication in mice and a possible protective effect of diphenyl diselenide (PhSe)2 (5 micromol/kg) were studied. Male adult Swiss albino mice (25-35 g) received CdCl2 (10 micromol/kg, subcutaneously), five times/week, for 4 weeks. A number of toxicological parameters in blood, liver, kidney, spleen and brain of mice were examined including delta-aminolevulinic acid dehydratase (delta-ALA-D) activity, lipid peroxidation and ascorbic acid content, the parameters that indicate tissue damage such as plasma alanine aminotransferase (ALT), aspartate aminotransferase (AST), urea, creatinine and lactate dehydrogenase (LDH) were also determined. The results demonstrated that cadmium caused inhibition of delta-ALA-D activity in liver (24%), kidney (33%) and spleen (73%) and (PhSe)2 therapy was effective in restoring enzyme activity in all tissues. A reduction in ascorbic acid content was observed in kidney (11%) and spleen (10.7%) of cadmium-treated mice and (PhSe)2 was only effective in improving this reduction in kidney. An increase of lipid peroxidation induced by cadmium was noted in liver (29%) and brain (28%) tissues and (PhSe)2 therapy was effective in restoring TBARS levels in both tissues. We also observed an increase on plasma LDH (1.99-times), AST (1.93-times) and ALT (4.24-times) activities. (PhSe)2 therapy was effective in restoring AST activity at control level. (PhSe)2 did not present toxic effects when plasma parameters were evaluated. The results suggest that the administration of an antioxidant (PhSe)2, during cadmium intoxication may provide beneficial effects by reducing oxidative stress in tissues.
 ...
PMID:Diphenyl diselenide reverses cadmium-induced oxidative damage on mice tissues. 1573 37

Concomitant oral supplementation of Aloe vera, (1, 2 or 5% w[sol ]v in drinking water) during arsenic exposure (0.2 mg[sol ]kg, intraperitoneally, once daily for 3 weeks) was investigated in rats for its protective value. Animals exposed to arsenic (III) showed a significant inhibition of delta-aminolevulinic acid dehydratase (ALAD) activity, a marginal decrease in glutathione (GSH) and an increase in zinc protoporphyrin (ZPP) level in blood. White blood corpuscles (WBC) level decreased while most of the other clinical blood parameters like red blood cells count, haemoglobin, MCV, MCH, MCHC ratio and platelet number, etc. remained unaltered on arsenic exposure. Hepatic reduced GSH, oxidized glutathione (GSSG) level remained unaltered, thiobarbituric acid reactive substance (TBARS) level increased significantly while the activity of alkaline phosphatase (ALP), aspartate aminotransferase (AST), alanine aminotransferase (ALT) and catalase decreased on arsenic exposure. Renal GSH contents decreased while superoxide dismutase (SOD) activity decreased significantly on arsenic exposure. Concomitant administration of Aloe vera had remarkable protective action on inhibited blood ALAD activity and restored blood GSH level while most of the other blood biochemical parameters remained unchanged on Aloe vera supplementation. Interestingly, most of hepatic biochemical variables indicative of oxidative stress showed protection; no effect of Aloe vera on blood and liver arsenic concentration was noted. Also, no effect of Aloe vera on most of the altered renal biochemical parameters were noticed. The results thus lead us to conclude that simultaneous supplementation of Aloe vera protects against arsenic induced oxidative stress but does not influence the arsenic concentration in these organs.
 ...
PMID:Protective value of Aloe vera against some toxic effects of arsenic in rats. 1579 4

The deleterious effect of acute cadmium-intoxication in mice testes was evaluated. Animals received a single dose of CdCl2 (2.5 or 5 mg/kg, intraperitoneally) and a number of toxicological parameters in mice testes were examined, such as delta-aminolevulinic acid dehydratase (delta-ALA-D) activity, lipid peroxidation, hemoglobin and ascorbic acid contents. Furthermore, the parameters that indicate tissue damage such as plasma alanine aminotransferase (ALT), aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) were also determined. Thus, a possible protective effect of 2,3-dimercapto-1-propane-sulfonic acid (DMPS) and diphenyl diselenide (PhSe)2 were studied. The results demonstrated an inhibition of delta-ALA-D activity, a reduction of ascorbic acid and an increase of lipid peroxidation induced by cadmium, indicating testes damage. Furthermore, we observed an increase of plasma LDH, AST and ALT activities. DMPS (400 mol/kg) and (PhSe)2 (100 micromol/kg) partially protected from the inhibitory effect of 2.5 mg/kg CdCl2 on delta-ALA-D and from the increase of TBARS (thiobarbituric acid reactive species) levels. (PhSe)2 therapy was effective in ameliorate ascorbic acid content when the cadmium dose was 2.5 mg/kg. Treatment with DMPS and (PhSe)2, individually or combined, was inefficient in reducing cadmium-induced plasma LDH and ALT activity increase. The use of combined therapy (DMPS plus (PhSe)2) proved to be efficient in decreasing cadmium levels in testes and in ameliorating plasma AST activity from animals that received the highest dose of cadmium.
 ...
PMID:Efficacy of 2,3-dimercapto-1-propanesulfonic acid (DMPS) and diphenyl diselenide on cadmium induced testicular damage in mice. 1600 Feb 34


1 2 3 4 Next >>