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

Groups of 8 male crossbreed domestic goats were given 3 dosage levels of aflatoxin B1 [(AFB1) mg/kg of body weight/day] orally: 0.1 for 34 days; 0.2 for 18 days; or 0.4 for 10 days. Clinical condition, feed consumption, and selected blood values were determined. Clinical signs of toxicosis included decreased feed consumption, slight-to-moderate loss of body weight, mucopurulent nasal discharge, dyspnea, coughing, lethargy, icterus, diarrhea (4 goats), and subnormal body temperature 24 to 48 hours before death. Clinicopathologic changes included increases in total RBC count, PCV, hemoglobin concentration, serum bilirubin concentration, and serum activities of aspartate aminotransferase, isocitric dehydrogenase, and ornithine carbamyl transferase. Goats given the 2 smaller dosage levels of AFB1 had slight increases of serum total protein (TP) concentration compared with control goats, but goats given the larger dosage levels of AFB1 initially had a slight decrease in TP. Aflatoxin had little effect on total WBC count. Serum alanine aminotransferase (ALT) activities in goats given the 2 larger dosage levels of AFB1 were similar to those of control goats, but goats given the smallest dosage level of AFB1 had increased serum ALT activities. Aflatoxin did not produce consistent dose-related changes in serum alkaline phosphatase activities. Seemingly, goats are susceptible to aflatoxin. Onset of clinical signs was dose-related. Onset and magnitude of increases in PCV, hemoglobin concentration, serum bilirubin concentration, and activities of serum aspartate aminotransferase, ornithine carbamyl transferase, and isocitric dehydrogenase were dose-related. Changes in TP and activities of serum ALT and alkaline phosphatase were neither dose-related nor were they potentially useful indicators of toxicosis.
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PMID:Caprine aflatoxicosis: experimental disease and clinical pathologic changes. 643 Jan 34

The clinical and clinicopathologic effects of excess oral pyridoxine hydrochloride (150 mg/kg body weight/day) and clioquinol (200 mg/kg body weight/day) alone and in combination were evaluated in adult Beagle dogs over an experimental period of approximately 100 days. Anorexia and loss of body weight occurred in the first weeks of the trial period in each treatment group, but was most severe in dogs given both compounds. Dogs in each treatment group (10 of 10 pyridoxine-treated dogs, 6 of 13 clioquinol-treated dogs and 12 of 13 pyridoxine plus clioquinol-treated dogs) developed neurologic disease, manifested principally by ataxia. Pyridoxine-treated dogs had proprioceptive loss involving both fore- and hindquarters, characterized by stiff, spastic, dysmetric leg movements. In clioquinol-treated dogs, dysmetric leg movements were accompanied by failure to support body weight in the hindquarters, but similar forelimb involvement occurred in severely affected dogs. The neurologic disease in dogs given both compounds varied; signs in some dogs resembled those of affected dogs of the pyridoxine-treated group, and in others, those in clioquinol-treated group. Erythrocyte counts, hemoglobin concentrations and packed cell volumes were reduced in dogs in each treatment group and were lowest in dogs given both compounds. Plasma protein was mildly reduced in dogs given pyridoxine or pyridoxine plus clioquinol. Few or no differences were present in the leukocyte counts, blood urea nitrogen concentrations, in activities of serum alanine aminotransferase and aspartate aminotransferase, and in concentrations of sodium, chloride or potassium in treated dogs as compared to control dogs.
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PMID:The subacute neurotoxicity of excess pyridoxine HCl and clioquinol (5-chloro-7-iodo-8-hydroxyquinoline) in beagle dogs. I. Clinical disease. 645 37

Complex laboratory investigations were carried out to 280 workers from a plant, exposed to vinylchloride and dichlorethane. Some hematological indices were followed up (hemoglobin, erythrocytes, leukocytes and platelets) and liver function (GGTP, GOT, GPT, AP, OCP and blood glutathione). Again GGTP and blood platelets significance was confirmed as a diagnostic sign of VCh disease. The inhibitory effect of VCh upon the OCP in the workers exposed is confirmed for the first time. OCP is proposed to be included in Instruction 099. A new case of VCh disease was diagnosed, where the combined effect of VCh and dichlorethane is admitted.
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PMID:[Changes in the biochemical indices of workers exposed to vinyl chloride and dichloroethane]. 648 28

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.
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PMID:Metabolic effects of histidine-deficient diets fed to growing rats by gastric tube. 649 66

Investigations were carried out with a total of 276 high-producing and clinically healthy cows that had freshly calved on 11 farms, being divided into groups according to the extent to which ketonuria was present if al all. Whole blood and blood serum were sampled to determine the ketone bodies, blood sugar, erythrocyte and leukocyte counts, hemoglobin, inorganic phosphorus, Ca, Mg, total protein, carotene, and activity of the GOT and GPT enzymes as well as the activity of lactic acid dehydrogenase, alkaline phosphatase, aldolase, and leucine aminopeptidase. Studied were the body temperature, the pulse rate, and the respiration rate. It was found that on farms with ketosis in cows ketonuria was manifested most often after the ketone bodies in the blood rose to 10-12 mg%. At the same time the blood sugar level was lowered and as a rule it showed reverse correlation with the levels of ketonemia and ketonuria. In such cows there was a lowering trend with the Ca and carotene contents and the erythrocyte count, and the respiration rate was higher. There were no changes in the body temperature, pulse rate, leukocyte count, Ca, Mg, hemoglobin, protein, and the activity of aldolase. The activity of the other enzymes mentioned was higher, and it correlated positively with the rise of ketonemia and ketonuria. With diseased cows the activity of alkaline phosphatase only was shown to be lower, negatively correlating with ketonuria.
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PMID:[Changes in the serum enzymes and clinical and clinico-biochemical indices of cows with subclinical ketosis]. 653 57

A total of 96 crossbred pigs received various levels of sodium selenite to determine the effect of dietary selenium (Se) on growing swine fed corn-soybean meal diets. Levels of supplemental Se were 0, 4, 8, 12, 16 and 20 micrograms/g. There were linear decreases (P less than .01) in both gain and feed intake with increasing levels of dietary Se. Feed/gain increased numerically as dietary Se increased. Hair Se increased quadratically (P less than .01) and blood Se increased linearly (P less than .01) with increasing level of dietary Se. Cell volume and hemoglobin were not affected by dietary treatment. Increasing dietary Se significantly increased glutathione peroxidase (GSH-Px), glutamic-oxalacetic transaminase (GOT). and glutamic-pyruvic transaminase (GPT). External signs of selenosis were noted in some pigs fed 12 or 20 micrograms/g of Se. The toxic level of Se in a corn-soybean meal diet for crossbred pigs appears to be between 4 and 8 micrograms/g. Of variables studied, growth rate was the most sensitive indicator of chronic selenosis in swine.
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PMID:Toxic effects of selenium on growing swine fed corn-soybean meal diets. 654 46

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

Nineteen hundred sixteen agricultural workers who have been living in a rural area in central Japan were studied. Their age, blood pressure, Broca index, hemoglobin content, serum total cholesterol, and activity of serum cholinesterase and transaminase (GOT and GPT) were determined. The relation between the cholinesterase activity and certain physiochemical factors of the subjects was studied. Cholinesterase activity (ChE) is related to certain factors such as age, hemoglobin content (Hb), serum total cholesterol (TCh), transaminase activity (GPT), and Broca index (BI). A multiple regression equation exists between the cholinesterase activity and these factors: ln ChE = a (age) + b (Hb2) + c X ln GPT + d X ln TCh + e BI + f, where a, b, c, d, e, and f are constants. The estimated value of cholinesterase activity agrees with its measured activity. The partial correlation coefficients of the equation can be classified into the following three classes: (1) The partial correlation coefficients of total cholesterol and Broca index are nearly constant without distinction of sex and season. (2) The coefficient of hemoglobin content has a small seasonal and sexual difference. (3) The coefficients of age and GPT have a great seasonal and sexual difference. Using the equation, the most probable value of cholinesterase activity can be estimated. Therefore, the significant changes of its activity may be attributed to the toxic effects of insecticides or the abnormality of liver function.
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PMID:Multiple regression analysis of the cholinesterase activity with certain physiochemical factors. 669 17

4-Fluoro-3-nitroaniline (4-F-3-NA), an intermediate used in the production of commercial hair dyes, was administered daily for 90 days via po intubation to Charles River CD rats at doses of 40, 120, or 360 mg/kg to determine its subchronic toxicology. All animals receiving 360 mg/kg died prior to termination of the study. The principal effect to rats of 4-F-3-NA exposure was alteration of the hematopoietic system characteristic of hemolytic anemia. Hematocrit, hemoglobin concentration, and erythrocyte count were decreased and reticulocytes increased in a dose-related pattern in both male and female animals. Histopathological change consistent with hemolytic anemia was observed in the bone marrow (erythroid hyperplasia), kidneys (deposition of biliverdin and pigment-laden macrophages in the tubules), liver (pigmented Kupffer cells), and spleen (increased hematopoiesis) in males and females. Heinz bodies and an increase in methemoglobinemia were not observed in this study. In the testes, aspermia and testicular degeneration were seen in isolated tubules, but these changes were significant only at the high dose. Additional pathologic changes noted at the high dose included colloid depletion and follicular cell hypertrophy of the thyroid gland, hypertrophy of the zone fasciculata in the adrenal glands, and lymphoid cell depletion in mesenteric lymph nodes. The calcification of the myocardium and coronary arteries was considered metastatic in nature, secondary to kidney damage. Serum ALT and BUN were elevated in males and AP was elevated in females from the high dose group. Glycosuria, bilirubinuria, and urobilinogenuria were also increased in both sexes at this dose.
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PMID:Subchronic oral toxicology of 4-fluoro-3-nitroaniline in the rat. 671 Apr 91

Twenty-one male rabbits were divided into three groups: rabbits of two groups were given pelleted food containing cadmium chloride at a dose level of 300 micrograms Cd/g over periods of 44 or 19 weeks. Rabbits of the last group were given ordinary commercial pelleted food and served as controls. Cadmium increased urinary protein and amino acid by week 19 and increased it to a remarkably high level by week 44. After cessation of cadmium exposure, rabbits of the first group (44 weeks exposure group) showed only little recovery from cadmium health effects: proteinuria and aminoaciduria were slightly improved. Depressed hepatic functions were also slightly improved, but did not return to the control level in 24 weeks. Fat and bone metabolism also remained depressed below the control level. Anemia did not also readily recover. On the other hand, rabbits of the second group (19 weeks exposure) recovered from the effects of cadmium: proteinuria and aminoaciduria in most animals disappeared soon after the end of cadmium exposure, plasma GPT fell after 1 week, and hemoglobin and hematocrit returned to normal in 6-11 weeks. The above results show that after cessation of cadmium exposure, mild cadmium-induced health effects were reversible in a short period, while more severe effects were not readily reversible. High performance liquid chromatographic (HPLC) profiles of renal and hepatic cadmium-thionein (Cd-MT) during and after exposure to cadmium showed no correlation to the degree of cadmium health effects, and therefore, did not help to elucidate mechanisms of the recovery from cadmium-induced health effects, probably because cadmium not bound with metallothionein (non-MT-Cd) is responsible for inducing renal effects.
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PMID:Reversibility of cadmium-induced health effects in rabbits. 673 56


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