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)

Cyclopiazonic acid (CPA) was given daily to groups of guinea pigs at doses of 0.00625, 0.0125, 0.025, 0.05, 0.1, 0.2, 0.4, 0.8, 1.6, and 1.95 mg/day for 30 days. All guinea pigs were sensitized and survivors were skin tested twenty-five days later with Mycobacterium tuberculosis. Mortalities occurred only in the two greatest dose groups. Signs of disease included anorexia, roughened hair coat, diarrhea and incoordination. The major histopathologic changes occurring in these two groups included hepatocellular vacuolar degeneration and necrosis of the gastric mucosa with infiltration of neutrophils in the deep gastric mucosa. CPA did not affect cutaneous hypersensitivity to M. tuberculosis, complement activity, serum glycocholic acid concentrations or weight gains. There were increases in aspartate aminotransferase, alanine aminotransferase, and sorbitol dehydrogenase concentrations in the serum of guinea pigs in the two greater dose groups, but no changes were found in serum concentrations of SAP. There was a slight increase in the serum bilirubin concentrations in the greater dose groups.
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PMID:Effect of cyclopiazonic acid on delayed hypersensitivity to Mycobacterium tuberculosis, complement activity, serum enzymes, and bilirubin in guinea pigs. 309 99

Clinically normal Nubian goats were given the antiprotozoal drug imidocarb at single intramuscular doses of 6, 12, 18 and 24 mg/kg, and the various clinical, biochemical and pathological manifestations were recorded. At a dose of 6 mg/kg the drug produced no change in any of the parameters studied. At higher doses, the drug produced dose dependent changes which included increased heart and respiratory rates, increased defaecation, urination, depression, incoordination of movement, weakness of the hindlegs, recumbency, and finally death. Just prior to death, there was a significant decrease in the number of erythrocytes, and in packed cell volume, and haemoglobin concentration. In plasma there was an increase in the activity of aspartate transaminase, urea and creatinine concentrations and inhibition of cholinesterase activity. The main histopathological changes were associated with hepatic and renal damage. Three goats were pre-treated with atropine sulphate (1 mg/animal) and after one hour given imidocarb intramuscularly at a dose of 12 mg/kg. The changes were similar but much less severe when compared with those in animals given imidocarb alone at the same dose.
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PMID:Some effects of imidocarb in goats. 408 55

We describe a strain of BALB/c mice, designated NCTR-BALB/c, carrying a new genetic disorder characterized by excessive tissue deposition of cholesterol and phospholipid. The mice exhibit progressive incoordination, grow less rapidly, and die 80-120 days after birth. In comparison with control animals of the same age, organ weights in the affected animals are lower in absolute value but higher relative to body weight, except for the thymus, which is atrophied, and for the lung and testes, whose absolute weights are not changed. Vacuolated cells are found in many tissues, and large foam cells are present in reticuloendothelial system (RES)-rich organs. Compared with those of BALB/c controls, serum lipoproteins migrate more slowly on electrophoresis; the amount of beta-lipoproteins is increased, while alpha-lipoprotein content is decreased. Serum total cholesterol remains normal. The serum activities of aspartate aminotransferase, creatine phosphokinase, and N-acetyl-beta-glucosaminidase are elevated. Free cholesterol levels are increased 8-10-fold in liver, spleen, and thymus, and about 2-fold in other tissues; but esterified cholesterol levels are normal. The phospholipid content of several tissues is increased 50-100%, largely as a result of an increase in sphingomyelin content. Significant increases in phosphatidylcholine occur also in spleen and lung. The disorder is inherited, affecting both sexes equally, and appears to be transmitted as an autosomal recessive mutation.
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PMID:Lysosome lipid storage disorder in NCTR-BALB/c mice. I. Description of the disease and genetics. 676 31

Six out of 15 Nubian goats kids were given single oral doses of metolachlor (Dual 720 EC) at 2,000 or 500 mg/kg liveweight and died within 1 h of the dosing. Other 6 goats were given daily oral doses at 200 or 25 mg/kg and died or were slaughtered between days 8 and 25. In goats receiving single doses, the signs of poisoning were convulsive episodes, incoordination of movement, tremors, severe muscular spasms, stiffness, profuse salivation, respiratory distress, abnormal posture and recumbency. In goats receiving metolachlor at daily doses, the signs were similar, but developed slowly. Increases in the activities of serum AST and GGT and in the concentration of urea, and decreases in total protein concentration were correlated with clinical changes and lesions.
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PMID:Experimental metolachlor toxicosis in Nubian goats in the Sudan. 770 34

The acute toxicity of 2,4-dichlorophenoxyacetic acid (2,4-D), a herbicide, was studied in chicks dosed with 100, 300, 500, or 600 mg 2,4-D/kg BW, by the oral route. Clinical, laboratory, and histopathological methods were used as indicators of toxicity. After acute exposure, the herbicide decreased motor activity and induced muscular weakness and motor incoordination; decreased weight gain; increased serum creatine kinase (CK) and alkaline phosphatase (AP) activities and serum uric acid (UA), creatinine (CR), and total proteins (TP) levels; and did not change serum aspartate aminotransferase (AST) or alanine aminotransferase (ALT) activities. These changes were time- and dose-dependent and reversible. The LD50 (lethal dose 50%) calculated for oral 2,4-D in chicks was 420 mg/kg BW (385 to 483). Chromatographic analysis of the serum of the intoxicated chicks showed the presence of the herbicide; the amount found was dose- and time-dependent, increasing from 2 to 8 h after exposure and decreasing afterwards. Histopathological post-mortem studies conducted on intoxicated chicks showed hepatic (vacuolar degeneration of the hepatocytes), renal (tubular nephrosis), and intestinal (hemorrhagic) lesions. Taken together, the observed alterations mainly reflected kidney and muscle tissue damage, although hepatic toxicity may also have occurred after acute 2,4-D intoxication.
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PMID:Acute 2,4-dichlorophenoxyacetic acid intoxication in broiler chicks. 956 31

The comparative effects of diazinon and malathion on Najdi sheep were described in sheep allotted as untreated controls, diazinon-treated at 25 mg/kg/d or 50 mg/kg/d, and malathion-treated at 25 mg/kg/d or 50 mg/kg/d. Although serum cholinesterase (ChE) activity was reduced, neither significant clinical signs nor severe pathological changes were produced in sheep dosed orally with 25 or 50 mg diazinon/kg/d for 21 d. Both oral dose levels of malathion were lethal to sheep between 1 and 6 d and caused, prior to death, hyperexcitability, tremors, clonic convulsions, salivation, nasal discharge, incoordination of movement, paresis of the limbs and recumbency. Lesions were widespread congestion and hemorrhage, patchy pulmonary cyanosis, gastroenteritis and hepatonephropathy. These changes were accompanied by increases in the activities of serum SDH and AST, in the concentrations of urea, triglyceride and cholesterol, and decreases in ChE activity and in RBC, PCV and Hb values.
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PMID:Comparative effects of diazinon and malathion in Najdi sheep. 1050 28

Three-mo-old male Wistar rats were sprayed with 250, 500, 1000 and 2000 ppm amitraz 2 w apart or given single doses of 50, 100, or 250 mg/kg p.o, i.m. or i.p. No effects were observed in the amitraz-sprayed rats. Single doses of amitraz p.o, i.m. or i.p. was non-toxic at 50 mg/kg, toxic at 100 mg/kg and lethal at 250 mg/kg within 24 h of dosing. Survivors were killed 48 h post-dosing. Features of toxicity were depression, incoordination of movement, paresis of the limbs, hepatonephrotoxicity, muscular hemorrhage at site of injection and peritonitis following i.p. injection. These changes, accompanied by leucopenia, were correlated with alterations in serum AST and concentrations of serum constituents. Amitraz did not inhibit serum ChE activity.
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PMID:Effects of amitraz given by different routes on rats. 1059 39

Changes in hematological and serum biochemistry parameters in female zinc (Zn)-dosed farm-raised mallards (Anas platyrhynchos) fed four different diets were examined. Sixty ducks received an average dose of 0.97 g of Zn in the form of eight, 3.30-mm diameter shot pellets containing 98% Zn and 2% tin, and another 60 ducks were sham-dosed as controls. Fifteen ducks from each of the two dosing groups were assigned to one of four dietary treatments: corn only, corn with soil, commercial duck ration only, or commercial duck ration with soil. Shot-pellet dissolution rates ranged from 7 mg/Zn/day to 27 mg/Zn/day. Regardless of diet, the Zn dose resulted in mortality; incoordination; paralysis and anorexia; decreased body, liver, pancreas, gonad, and gizzard weight; increased kidney weight; and macroscopic lesions. Zn-dosed ducks had a lower mean erythrocyte packed cell volume (PCV), higher mean reticulocyte count, and a greater number of individuals with immature and/or abnormal erythrocytes, than did control mallards. Mean total leucocyte counts were higher in Zn-dosed ducks than in controls. Zn-dosed ducks that had soil available had higher leucocyte counts than those without soil. Zn-dosed ducks were characterized by a marked heterophilia and relative lymphopenia. In Zn-dosed ducks, the mean lymphocyte count was highest in those provided a commercial duck ration, and lowest in those fed corn. In control ducks, the mean lymphocyte count was highest in ducks fed corn, and lowest in those provided soil along with a commercial duck ration. Zn-dosed mallards had higher serum aspartate aminotransferase and amylase levels, and lower alkaline phosphatase activities than control ducks. Serum phosphorus and uric acid concentrations were higher, and calcium, glucose, and total protein levels lower, in Zn-dosed ducks than in control ducks. Diet did affect serum calcium, phosphorus, total protein, and uric acid concentrations. Differences in erythrocyte and leucocyte parameters, serum enzyme activities, and metabolite concentrations were associated with dose and diet effects. Diets high in protein and other organic matter and calcium and phosphorus did not prevent or substantially alleviate Zn toxicosis in farm-raised mallard ducks.
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PMID:Influence of diet on the hematology and serum biochemistry of zinc-intoxicated mallards. 1068 52

The acute toxicity of dried Nerium oleander leaves to Najdi sheep is described in 12 sheep assigned as untreated controls, N. oleander-treated once at 1 and 0.25 g/kg body weight and N. oleander-treated daily at 0.06 g/kg body weight by drench. Single oral doses of 1 or 0.25 g of dried N. oleander leaves/kg body weight caused restlessness, chewing movements of the jaws, dyspnea, ruminal bloat, incoordination of movements, limb paresis, recumbency and death 4-24 hr after dosing. Lesions were widespread congestion or hemorrhage, pulmonary cyanosis and emphysema, hepatorenal fatty change and catarrhal abomasitis and enteritis. The daily oral doses of 0.06 g dried N. oleander leaves/kg body weight caused less severe signs and death occurred between days 3 and 14. In these animals, the main lesions were hepatonephropathy and gelatinization of the renal pelvis and mesentry and were accompanied by significant increases in serum AST and LDH activities, in bilirubin, cholesterol and urea concentrations and significant decreases in total protein and albumin levels, anemia and leucopenia.
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PMID:Acute toxicity of various oral doses of dried Nerium oleander leaves in sheep. 1178 96

Melia azedarach fruits were administered at single doses ranging from 5 to 30 g/kg bw to 10 calves. The animals dosed with 25 g/kg bw and 30 g/ kg bw died, as well as 1/2 cattle that received 15 g/kg bw. Clinical signs were depression, ruminal stasis, anorexia, diarrhea, incoordination, muscle tremors, difficulty to stand, sternal recumbence, hypothermia and dyspnea. Serum AST and CPK were increased. Signs appeared 4 to 24 h after dosing and the clinical manifestations continued for 20 to 72 h. Macroscopic findings included congestion of the intestine, focal or diffuseyellow discoloration of the liver, and brain congestion. LiQuid content was in rumen, reticulum and intestines. The liver had swollen and vacuolated hepatocytes, and necrotic hepatocytes were scattered throughout the parenchyma or concentrated in the periacinar zone. Degenerative and necrotic changes were in the epithelium of the forestomachs. There was also necrosis of lymphoid tissue. Skeletal muscles had hyaline degeneration and fiber necrosis.
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PMID:Intoxication of cattle by the fruits of Melia azedarach. 1204 65


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