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)

The frequency of thyroid antibodies was investigated in 1314 healthy blood donors. Twenty-three of 870 males (2.6%) were positive for thyroglobulin antibody (TA), 34 (3.9%) for thyroid microsomal antibody (MA) and 19 (2.2%) for both TA and MA. Thirty-four of 484 females (6.2%) were positive for TA, 46 (9.5%) for MA and 29 (6.0%) for both TA and MA. Eighty-six of 1314 blood donors were positive for TA and/or MA. There was no difference in liver function tests between AAT and controls. In females, the incidence of thyroid antibodies tended to increase with age. However, the subjects aged under 19 showed another peak of incidence of thyroid antibodies. The values of total T4, T3 and free T4 were not different between 86 subjects with positive thyroid antibodies (asymptomatic autoimmune thyroiditis, AAT) and 86 sex- and age-matched controls without thyroid antibodies, whereas serum TSH of AAT was significantly higher than that of controls. Nine of 86 (10.5%) subjects with AAT had apparently increased basal TSH level.
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PMID:Thyroid antibodies in healthy blood donors. 653 99

Hyperbaric oxygen (HPO) was administered to rats (100% O2 at 2.8 atm for 90 min) immediately or 1 hr after severe carbon tetrachloride (CCl4) intoxication in order to study the mechanisms of protection against hepatocellular injury by hyperoxia. Slight to moderate hepatocellular injury was observed, particularly by morphologic criteria, 4 hr after CCl4 intoxication. Little cell death was observed; 24 hr after CCl4, 20% of the untreated animals died. In the survivors, the following typical changes occurred in the liver: extensive hepatocellular swelling, vacuolization and necrosis; severe ultrastructural alterations; binding of CCl4 to microsomal lipids; elevation of lipid peroxidation products (conjugated dienes); little decrease in cytochrome b5 and severe decrease in cytochrome P-450 levels. Serum transaminase (alanine aminotransferase and aspartate aminotransferase) levels were elevated. Immediate treatment with HPO prevented the mortality and markedly decreased the hepatocellular necrosis 24 hr after intoxication. Immediate HPO treatment did not lower the levels of free CCl4 in the liver. However, the rise in lipid peroxidation products caused by CCl4 intoxication at 4 hr was reduced. Delayed treatment with HPO (1 hr after CCl4) prevented the mortality but was less effective in preventing necrosis. Some hepatocellular protection was still demonstrable. In particular, the rise in lipid peroxidation products was reduced. Hyperoxia protects hepatocytes against CCl4 toxicity. The rapid decline in protective effect within 60 min of intoxication suggests that hyperoxia inhibits CCl4 activation and/or damage from molecular intermediates. Hyperoxia has little effect on the progression of sublethal injury to cell death in the livers of CCl4-intoxicated rats.
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PMID:Protection of hepatocytes with hyperoxia against carbon tetrachloride-induced injury. 653 53

When exposing rats to drinking water containing 100 p.p.m. fluoride for 8 weeks, no effect could be detected in biochemical parameters of the liver, such as the concentrations of the polyamines putrescine, spermidine and spermine; the levels of microsomal protein and cytochrome P-450; or the activities of two associated monooxygenases, aryl hydrocarbon hydroxylase and ethylmorphine N-demethylase. Neither was there any increase in plasma glutamic-oxalacetic transaminase indicative of liver damage.
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PMID:No effect of prolonged fluoride exposure on cytochrome P-450 and associated monooxygenases or on the level of polyamines in the rat. 663 14

The toxic effects of paraquat administered to rats in drinking water for a period of 30 days were studied. Paraquat had no effect on the body weight gain or on organ weights of rats. However, microsomal NADPH-cytochrome c reductase activity and cytochrome P-450 content were increased in rats given paraquat in drinking water. The obtained differences were statistically significant. Serum alkaline phosphatase activity was not significantly changed with respect to control animals but a statistically changed, with respect to control animals, statistically significant decrease was established in serum glutamic-oxaloacetic transaminase and serum glutamic-pyruvic transaminase activity of test animals compared to values obtained for control groups. Hematological data showed that paraquat caused a decrease in hemoglobin concentration and total red blood cell number, while the total white blood cell number was significantly increased compared to values obtained for control animals.
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PMID:Subacute toxicity of paraquat in rats--biochemical effects. 664 84

The effects of allyl alcohol, galactosamine, bromobenzene, and corn oil administration were evaluated in male Fischer 344 rats at 4 to 5, 14 to 15, and 24 to 25 months of age to determine if susceptibility to hepatotoxic injury is modified as a consequence of aging. Parameters measured were (1) severity of hepatocellular necrosis as judged by light microscopy of liver sections, (2) activity of alanine aminotransferase and aspartate aminotransferase in serum, and (3) hepatic microsomal cytochrome P-450 content and NADPH-cytochrome P-450 reductase activity. Allyl alcohol toxicity was more severe in middle-aged and old rats than in young-adult rats. In contrast, galactosamine and bromobenzene toxicities were slightly decreased or unchanged in old rats. The results demonstrate that aging has effects on some types of chemically induced hepatotoxicity.
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PMID:Influence of aging on the susceptibility of rats to hepatotoxic injury. 671 May 24

Groups of four 6- to 12-month-old male goats were injected intraruminally with a lethal dose (3 mg/kg of body weight) of aflatoxin B1 (AFB1). Drugs were administered parenterally before (pretreatment) or beginning 8 hours after goats were doses with AFB1. These drugs were phenobarbital (PB), phenylbutazone (PBZ), piperonyl butoxide (PRO), benzoflavones, water, and 5% glucose solution (D5W). Most groups given the drugs after AFB1 was administered also were given intraperitoneal injections of methionine-sodium thiosulfate (MET-TS) solution. Clinical signs of toxicosis, serum aspartate aminotransferase activities, serum bilirubin concentrations, duration of illness, mortality, and gross and microscopic pathologic findings taken together indicated that toxicosis was increased with MET-TS + PB therapy, PBZ pretreatment, PBZ therapy, benzoflavone pretreatment, benzoflavone therapy, MET-TS + benzoflavone therapy, and MET-tS + water therapy. Toxicosis was not altered appreciably by MET-TS + PBO therapy. Beneficial effects (less severe toxicosis) were produced by PB pretreatment; these effects were prolonged maintenance of strength, vigor, and appetite and (in 1 goat that recovered) absence of pathologic changes or serum bilirubin increase. Therapy with MET-TS + D5W (but not MET-TS alone) also lengthened maintenance of strength, vigor, and appetite, but did not prevent pathologic changes. The beneficial effect of MET-TS therapy reported in a previous study (AFB2 dosage of 4 mg/kg) was not observed with the 3 mg/kg lethal dose. In conclusion, therapy for acute aflatoxicosis with inducers of hepatic microsomal enzymes is ineffective (PBO) or contraindicated (PB, PBZ, benzoflavones). Therapy with D5W may be a useful adjunct to other therapeutic drugs, but multiple intraperitoneal injections of D5W may decrease survival time because of stress.
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PMID:Effect of some enzyme inducers, fluids, and methionine-thiosulfate on induced acute aflatoxicosis in goats. 680 46

Male New Zealand White rabbits were treated with microsomal enzyme inducers, inhibitors of hemoprotein synthesis or action, and glutathione precursor and depletor before they were orally given the median lethal dose (LD50) of aflatoxin B1 (AFB1; 0.4 mg/kg) at the start of a 7-day experimental period. The drugs administered, mean duration of illness (hours), and survival percentage were as follows: controls (saline solution)-85, 50%; phenobarbital (PB)-100, 100%; phenylbutazone-115, 67%; benzoflavone-39, 17%; stanozolol-67, 67%; cobaltous chloride (CoCl2)-46, 67%; piperonyl butoxide (PBO)-88, 100% cysteine (CYS)-68, 100%; ethyl maleate-71, 83%. Signs of toxicosis included decreased feed and water consumption, weight loss, dehydration, lethargy, and emaciation; some rabbits died or were euthanatized. Clinico-pathologic changes included increased serum aspartate aminotransferase (AST) activity by 24 hours and bilirubin concentration by 48 to 72 hours after AFB1 was given. Grossly, livers were pale or tan and friable, with prominent lobular architecture. Kidneys of affected rabbits were pale to dark red. Microscopically, livers were normal or had lesions as great as extensive necrosis, hemorrhage, mineralization, and bile duct proliferation. Treatment of rabbits with PB, CoCl2, PBO, and CYS protected against AFB1 hepatic pathology, and PB, PBO, and CYS also had protective effect against lethality. Ethyl maleate provided some protection against lethality and increased serum AST activity and bilirubin concentration. Toxicosis was enhanced by benzoflavone; phenylbutazone and stanozolol had litte influence.
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PMID:Effect of enzyme inducers and inhibitors and glutathione precursor and depleter on induced acute aflatoxicosis in rabbits. 680 67

The influence of Zn on the acute hepatotoxicity of pyrrolizidine alkaloids (PAs) was determined in male rats. Zinc, 72 mumol/kg as ZnCl2, was administered ip for 3 consecutive days, followed 16 h after the last dose by a single ip injection of purified mixed PAs (80, 120, or 160 mg/kg) obtained from tansy ragwort (Senecio jacobaea). Hepatotoxicity of the PAs was assessed by measuring the activities of plasma glutamic-oxaloacetic transaminase (GOT) and glutamic-pyruvic transaminase (GPT) and by histological examination of the liver. There was a dose-dependent increase in plasma GOT and GTP 24 h after PA administration, whereas no significant increase of these enzymes was seen after administering Zn alone. The 7-fold increase in plasma GOT and 12-fold increase in GPT after PA (120 mg/kg) were reduced to 2.4- and 2.1-fold, respectively, by Zn pretreatment. The PA-induced liver necrosis was either reduced in severity or abolished by Zn when the PA dose was 80 or 120 mg/kg. These results suggest a protective effect of Zn against PA hepatotoxicity. The protective effect was associated with a marked increase in liver metallothionein and a significant decrease in hepatic cytochrome P-450 content, aminopyrine N-demethylase activity, and in vitro microsomal conversion of the PAs to pyrroles. Liver nonprotein sulfhydryls were unchanged. The possible role of metallothionein in the sequestration of pyrrole metabolites merits further investigation.
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PMID:Protective action of zinc against pyrrolizidine alkaloid-induced hepatotoxicity in rats. 709 90

Administration of a single high dose of styrene (878 mg/kg ip in corn oil) to young male rats produced significant elevations in the activities of serum transaminases: 230, 209, and 71% increases in the activity of serum glutamic-oxaloacetic transaminase (SGOT) and 163, 437, and 227% in that of serum glutamic-pyruvic transaminase (SGPT) at 2, 6, and 24 h, respectively, after the dose. These results demonstrated that styrene could produce acute hepatic injury in young rats. Urinary nonprotein sulfhydryl contents and mandelic, phenylglyoxylic, and hippuric acids were all increased. Pretreatment of rats with phenobarbital and 3-methylcholanthrene did not further enhance the activities of SGOT and SGPT after styrene, but produced changes in other biochemical parameters, for example, an increase in liver weight, decrease in serum albumin and globulin concentrations, increase in serum alkaline phosphatase activity at 2 and 6 h, and increase in urinary urobilinogen concentrations. In addition, such pretreatments further increased the nonprotein sulfhydryl contents at 2 and 6 h after styrene injection. Pretreatment of rats with the microsomal enzyme inhibitor SKF 525-A failed to prevent the hepatotoxicity induced by styrene and did not modify the overall urinary excretion profiles of styrene metabolites. This study suggests that the mechanism of the activation/deactivation process leading to the metabolism and hepatotoxicity of styrene is complex and that alternative pathways not dependent on cytochrome P-450 might also be involved.
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PMID:Effects of microsomal induction and inhibition on styrene-induced acute hepatotoxicity in rats. 733 32

Our previous studies showed that polybrominated biphenyl (PBB) induced hepatic microsomal cytochrome P-450 in dairy cattle but did not elevate hepatic cytosolic ornithine decarboxylase or serum isocitrate dehydrogenase. These enzymes would be expected to increase during hepatotoxic injury and regeneration. Thus, PBB appeared to be a hepatotoxin in rats but not in cattle. In order to identify and confirm the response capability of bovine liver to hepatotoxins, we administered thioacetamide, a hepatotoxin known to induce hepatonecrosis, to a dairy calf. A progression of clinical signs of toxicosis was evident until the animal was moribund by 23 hr postdosing. Histolopathologic alterations in the liver included centrilobular necrosis with congestion and subcapsular microhemmorrhage. Marked changes in serum protein profiles were not noted. However, distinct increases in serum Fe and bilirubin occurred with progressing toxicosis, as did sharp declines in glucose and triglycerides. Serum lactic dehydrogenase, alkaline phosphatase, glutamic-oxaloacetic transaminase, isocitrate dehydrogenase and glutamic-pyruvate transaminase were elevated. Elevation of ornithine decarboxylase was dramatic when compared to the level in normal fetal bovine liver. From studies of its kinetic properties, bovine liver ornithine decarboxylase appears to have an apparent Km for ornithine decarboxylase of .45 mM. Liver homogenates from PBB-treated animals did not form inhibitors to ornithine decarboxylase. Compared with the thioacetamide-treated calf, the normal adult bovine, pregnant adult and 6-month fetus had relative activities of .2 .4 and 5.8%, respectively. These studies show that ornithine decarboxylase is low in liver of normal cattle, but is elevated markedly by agents that cause hepatonecrosis.
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PMID:Ornithine decarboxylase, serum isocitrate dehydrogenase and clinical chemistry changes during thioacetamide-induced hepatotoxicity in a calf. 734 23


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