Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P17174 (aspartate aminotransferase)
 14,872 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Tri-ortho-cresyl phosphate (TOCP) was given orally or by subcutaneous (SC) injection to sheep and swine. Sheep given oral doses of 100, 200, or 400 mg of TOCP/kg of body weight developed an acute intoxication characterized by diarrhea dehydration, metabolic acidosis, and death within 6 days. Daily SC injections of TOCP in sheep caused either death or delayed neurotoxicosis depending upon the dosage. Increase of aspartate aminotransferase activity approximately 24 hours before the animal died and histopathologic changes confirmed that liver injury had occurred. Swine dosed with 100 to 1,600 mg of TOCP/kg had minimal signs of acute toxicosis, but developed severe delayed neurotoxicosis in approximately 15 days. Those given a 800 mg/kg dose by the oral route or SC injection had severely decreased serum acetylcholinesterase activity. In the swine which were euthanatized at 7 days after treatment, histopathologic examinations revealed no lesions (although the nervous system was not examined, because clinical neurologic signs were normal).
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PMID:Acute toxicity of tri-ortho-cresyl phosphate in sheep and swine. 718 Nov 94

Inoculation of 2 groups of dogs with 1 X 10(9) and 4 X 10(9) Leptospira interrogans serovar icterohaemorrhagiae produced disease varying from transient fever to uremia and death. Clinical signs of disease in the severely affected dogs were fever, dehydration, depression, and icterus. Laboratory changes in serum of infected dogs included increased urea nitrogen, creatinine, phosphorus, alkaline phosphatase, total bilirubin, aspartate aminotransferase, and alanine aminotransferase. Chloride concentration decreased in the serum of dogs with severe disease. The icterus in the infected dogs did not appear to be related to hemolytic anemia.
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PMID:Serum biochemical changes in dogs with experimental Leptospira interrogans serovar icterohaemorrhagiae infection. 727 Oct 27

Blood samples were collected from 16 Thoroughbred horses before, during and after the second day of a 3-day event. Plasma osmolality, concentrations of sodium, potassium, chloride, urea, creatinine, glucose, bilirubin, iron, total protein, albumin, alkaline phosphatase, aspartate aminotransferase, alanine aminotransferase, creatine kinase, calcium, inorganic phosphate, uric acid, cholesterol, triglycerides and non-esterified fatty acids were measured. Significant differences from pre-event values were found in all parameters with the greatest changes being found after the cross-country phase. Most parameters showed significant rises following exercise, except calcium and chloride, which decreased. It was deduced from the changes in biochemistry that dehydration, reduced glomerular filtration rate, increased glycogenolysis and increased lipid metabolism, were a result of this form of competitive exercise.
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PMID:Plasma biochemistry in the horse during 3-day event competition. 740 34

Megaesophagus was diagnosed in 9 adult ferrets. Clinical history of the ferrets included regurgitation, difficulty in swallowing, partial anorexia, and lethargy. Cachexia, dehydration, weakness, and ptyalism were observed on physical examination. Radiography revealed the esophagus of each ferret to be dilated in the thoracic and cervical regions. Of 4 ferrets that had lymphocytopenia, 2 had concurrent leukopenia. Serum biochemical analysis revealed high activity of alanine transaminase (4 ferrets) and aspartate transaminase (3), and hypoglycemia (4). Treatment included administration of fluid, antibiotics, and agents directed against possible primary causes of megaesophagus. Treatments were ineffective, and all of the ferrets died or were euthanatized. All 6 ferrets that were submitted for necropsy had bronchopneumonia, hepatic lipidosis, mild esophagitis, and gastritis. The etiopathogenesis of megaesophagus in the ferrets was not determined.
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PMID:Megaesophagus in nine ferrets. 796 Oct 71

An 11-month-old female Vietnamese pot-bellied pig was examined for severe dehydration and neurologic signs including disorientation, ataxia, blindness, and involuntary twitching of the muscles of the neck and head. Biochemical analyses of serum revealed hypernatremia, hyperchloremia, hyperkalemia, azotemia, hyperphosphatemia, hyperalbuminemia, and high activities of aspartate transaminase and creatine kinase. A diagnosis of salt toxicosis/water deprivation was made. Medical management consisted of intravenous administration of a high-sodium crystalloid solution, anti-inflammatory drugs, and other supportive care. Sodium concentration of fluids administered intravenously was adjusted to be slightly less than the pig's serum sodium concentration so that the serum sodium concentration was reduced gradually over 48 hours. Resolution of clinical signs was rapid and the pig was discharged after 8 days of hospitalization. Fourteen days after the initial examination, the pig appeared healthy except for visual deficits. Historically, prognosis with conventional treatment of salt toxicosis/water deprivation is poor; however, this alternative approach to treating this condition appears promising.
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PMID:High-sodium crystalloid solution for treatment of hypernatremia in a Vietnamese pot-bellied pig. 883 48

From 1984 through 1992, staff at The Marine Mammal Center (TMMC, Sausalito, California, USA) examined 207 northern elephant seals (Mirounga angustirostris) with a condition of unknown etiology called northern elephant seal skin disease (NESSD). The skin lesions were characterized by patchy to extensive alopecia and hyperpigmentation, punctate or coalescing epidermal ulceration, and occasionally, massive skin necrosis. Microscopic lesions included ulcerative dermatitis with hyperkeratosis, squamous metaplasia and atrophy of sebaceous glands. All diseased seals were less than 2 years of age and suffered from emaciation, depression, and dehydration. Mortality from septicemia increased significantly with severity of skin ulceration. Compared to 14 apparently unaffected seals, diseased seals had depressed levels of circulating thyroxine, triiodothyronine, retinol, serum iron, albumin, calcium, and cholesterol. Levels of alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase, gamma glutamyl transpeptidase, blood urea nitrogen, and uric acid were elevated. Morphometrically, diseased animals were approximately 15% smaller than normal seals of the same sage. Serum and blubber concentrations of 36 polychlorinated biphenyl congeners (sigma PCB) and dichloro-diphenyl-dichloroethylene (p,p'-DDE) were negatively correlated with body mass. Mean concentrations of sigma PCB and p,p'-DDE in serum in diseased seals were elevated as compared to apparently normal seals. Etiology of this syndrome remains unknown, but the possibility of PCB toxicosis cannot be ruled out.
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PMID:Clinical and pathological characterization of northern elephant seal skin disease. 924 88

The objective of this paper is to report 5 cases of rhabdomyolysis (RML) in patients with acute leukemia (AL). This occurred consecutively after the administration of chemotherapy, during the ensuing period of myelosuppression. Thirty-six patients with AL received, in a three-month period, 51 cycles of combined chemotherapy which included, in all of them, cytosine arabinoside (ARA-C); among them, along with myelosuppression, five experienced fever, infectious complications, gastrointestinal tract symptoms and severe myalgias. Serum creatine kinase (CK), liver function tests and a light microscopy muscle biopsy were performed on all of them. Ten-17 days after receiving chemotherapy, five patients (4 males and 1 female) with acute lymphoblastic leukemia developed incapacitating myalgias in neck, thighs and arms. CK and/or alanine aminotransferase and aspartate aminotransferase were increased 5-24 times above the normal range in four of these patients, and the muscle biopsy showed focal RML in all five. Myalgias were self-limited and lasted 4-10 days. In addition to the chemotherapy, other factors known to be capable of producing RML, such as sepsis, other medications, and dehydration were found. In conclusion, myalgias were due to focal RML produced probably by a combination of factors, particularly the chemotherapy along with dehydration due to gastrointestinal complications, infection, and the use of diverse antibiotics. The endemic nature of the finding in such a short period of time is outstanding.
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PMID:Rhabdomyolysis in patients with acute lymphoblastic leukemia. 929 34

Nitric oxide, a free radical inter- and intracellular messenger molecule, is important in exercise physiology. This study tested the hypothesis that serum nitric oxide concentrations change after strenuous exercise with severe generalized muscle cramps. The study group consisted of 77 professional football players in preseason training. All players' concentrations of serum nitrite and of other serum chemicals were determined during their preseason evaluations and compared with the concentrations in 40 serum samples taken from 25 of those same players who required intravenous rehydration for severe generalized muscle cramps after a training session. Player weight and percentage of body fat were significantly higher in players who received intravenous fluids than in players who did not. The serum of players requiring intravenous hydration showed evidence of skeletal muscle breakdown (increases in lactate dehydrogenase, creatinine phosphokinase, aspartate aminotransferase, and alanine aminotransferase) and of dehydration (elevations in protein, blood urea nitrogen, and cholesterol). The major finding, however, was a nearly 300% increase in serum nitrite concentrations in players requiring rehydration. There were no correlations between concentrations of nitrate and of any of the other serum chemicals. These data support the hypothesis that large amounts of nitric oxide are synthesized in professional football players after strenuous exercise with severe muscle cramps. The study design did not allow us to determine whether this increase in nitric oxide was due to exercise or muscle cramps or both, but it does provide a basis for evaluating these relationships.
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PMID:Postexercise increase in nitric oxide in football players with muscle cramps. 1049 91

Preparturient hypocalcemia was identified in 4 cats in a specific pathogen-free colony between 1995 and 1996. All cats had an acute onset of clinical signs, 3 to 17 days prior to parturition. Signs of depression, weakness, tachypnea, and mild muscle tremors were the most common clinical signs, following by vomiting and anorexia. Additional abnormalities included hypothermia, third eyelid prolapse, dehydration, pallor, lethargy, flaccid paralysis, and hyperexcitability. Hematologic abnormalities included leukocytosis with neutrophilia and lymphopenia. Hypocalcemia was documented in each queen. Common serum biochemical abnormalities included high aspartate aminotransferase and creatine kinase activities. All cats responded to IV or SC administration of 10% calcium gluconate. Queens were then given calcium orally prior to and following parturition. The queens did not have additional complications for the duration of the gestational or lactational periods.
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PMID:Preparturient hypocalcemia in four cats. 1053 Mar 27


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