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)

The chronic toxicity of potassium clavulanate (CVA-K) and BRL28500 were evaluated using dogs in 26-week intravenous administration studies followed by a 5-week off-dose period. The doses for CVA-K and BRL28500 were 10, 20, 50 and 100 mg/kg (p.f.a.), and 80, 160, 320 and 800 mg/kg (p.f.a.) respectively. There were no deaths in either of the groups. For general condition, dogs dosed with CVA-K at 100 mg/kg showed reddening of the skin and mucous membranes, shaking of the head, facial oedema, a decrease in food intake and a reduction in body weight. Also some dogs of the same group showed decreased spontaneous activity, emaciation and signs of dehydration. In the BRL28500 treatment groups, there was reddening of the skin and mucous membranes, vomiting and salivation at 800 mg/kg. Urinalysis of dogs dosed with CVA-K showed occasional dark yellow coloration of the urine. There was also a very weak and equivocal response or positive reaction for protein, occult blood, and urine sugar in some animals at 100 mg/kg. Some dogs dosed with BRL28500 also showed either a very weak and equivocal response or slight positive reaction for occult blood at 320 mg/kg and above, and dark yellow coloration of the urine at 800 mg/kg. Haematological examination of the CVA-K groups showed increases in leukocyte count and platelet count at the highest dose of 100 mg/kg. No haematological abnormalities were noted in any of the BRL28500 groups. Serum biochemical studies of dogs dosed with CVA-K revealed a decrease in total protein at 50 mg/kg and above, and increases in Al-P, total bilirubin, GPT, BUN and creatinine at 100 mg/kg. In the BRL28500 treatment groups, there were increases in total cholesterol and triglyceride at 160 mg/kg and above. In dogs dosed with CVA-K there was an increase in liver weight at 100 mg/kg. Histopathological examination showed a ground glass-like appearance of the hepatocyte cytoplasm and also altered distribution of PAS positive material at 50 mg/kg and above. In the BRL28500 groups, there was an increase in liver weight at 320 mg/kg and above. There were the same ground glass-like appearance in hepatocytes and altered distribution of PAS positive material at 800 mg/kg. In view of the above results, the maximum non-effect dose levels in the present studies were considered to be 20 mg/kg for CVA-K and 80 mg/kg for BRL28500.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Chronic intravenous toxicity studies of potassium clavulanate and BRL28500 in dogs]. 382 May 67

Sixteen athletes (11 men, 5 women), averaging 21 years of age, were studied before and after four weeks of daily exhaustive exercise (six days/week) during an endurance training course. In comparing blood chemistries before and after training, concentrations of blood glucose, total serum lipids, serum triglycerides, and serum cholesterol were significantly reduced; serum free fatty acid ( SFFA ) level was significantly increased; and serum protein and serum phospholipid concentrations remained unchanged. It was concluded that exhaustive training produces reduced blood glucose (but not clinically significant hypoglycemia) with increased fat utilization as a result of depletion of carbohydrate storage and that such training reduces the resting levels of serum cholesterol and serum triglycerides. The increased hematocrit, serum Na+, and serum K+ concentrations observed were presumably due to plasma water loss from excessive perspiration. Concentrations of blood urea nitrogen (BUN) and serum glutamic-oxaloacetic transaminase (SGOT) were increased significantly; serum glutamic-pyruvic transaminase (SGPT) and serum creatinine showed no significant changes. None of the athletes showed evidences of water-electrolyte deficiency syndrome, renal dysfunction, or liver cell damage, despite a persistent mild degree of dehydration and catabolic state noted after training.
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PMID:Metabolic effects of exhaustive training of athletes. 674 92

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

Cytauxzoonosis is a rapidly and highly fatal disease in cats that is caused by the protozoan Cytauxzoon felis, which may be transmitted by Ixodid ticks (Dermacentor variabilis) from parasitemic bobcats (Lynx rufus). During an 8-year period, cytauxzoonosis was diagnosed in 8 cats, 7 cats within 14 months. Risk factors for these cats were warm weather, access to a wooded environment, and exposure to ticks. The most consistent clinical signs were acute lethargy, anorexia, decreased response to external stimuli (depression), icterus, dehydration, and capillary refill time > 2 seconds. Pertinent clinicopathologic findings were normocytic normochromic anemia, leukopenia, and thrombocytopenia; high serum concentrations of total bilirubin and glucose, low serum concentrations of albumin and potassium, high serum alanine transaminase activity; and, bilirubinuria. Confirmation of cytauxzoonosis was made by cytologic or histologic identification of the C felis organism. Splenic, lymph node, and bone marrow aspirates can provide an antemortem diagnosis when the number of parasitized erythrocytes is low on blood smears. Supportive treatment of 6 cats was temporarily palliative in some, but all 8 cats either died (3) or were euthanatized (5) when they became moribund. Survival time from observed onset of illness to death was < 5 days. Necropsy of 4 cats revealed predominately pulmonary involvement with venous congestion. Histologic examination revealed venous occlusion by parasitized mononuclear phagocytes in all tissue specimens, but only minimal inflammatory infiltrates.
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PMID:Cytauxzoonosis in cats: eight cases (1985-1992). 796 Oct 73

The physical, clinicopathologic, and survival rates of 77 cats with severe spontaneous hepatic lipidosis are detailed in this report. Cats were subdivided into groups designated as idiopathic lipidosis if no other disease process was recognized, or secondary lipidosis if another disease process was diagnosed. Cats were also subdivided into groups designated as survivors or nonsurvivors on the basis of successful recuperation at 4 months after initial diagnosis. Differences between disease and survival groups were evaluated for significance. Overall, more female cats and middle-aged cats were affected. Presenting complaints of vomiting, anorexia, weakness, and weight loss were common. Physical assessment of most cats showed obvious hepatomegaly, jaundice, dehydration, and a weight loss > or = 25% of usual body weight. Neurobehavioral signs indicative of hepatic encephalopathy, other than ptyalism and depression, were rare. Clinicopathologic features are characterized by hyperbilirubinemia and increased activities of serum ALT, AST, and ALP, with only small if any increase in gamma GT activity. Clinical features distinguishing cats with hepatic lipidosis from those with other serious cholestatic disorders include absence of hyperglobulinemia and low gamma GT activity relative to ALP activity. Although coagulation tests were abnormal in 45% of cats tested (n = 44), few cats showed clinical bleeding tendencies. Most cats received prophylactic vitamin K1 therapy. Forty two cats received aggressive nutritional and supportive care and of these 55% survived. Cats with idiopathic disease were significantly younger, had significantly higher ALP activity and bilirubin concentration, and had a slightly better survival rate than cats with secondary lipidosis. Low PCV, hypokalemia, and an older age were significantly related to nonsurvival. Because of the variety of diets and food supplements used in case management, the influence of nutritional factors on survival could not be evaluated.
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PMID:A retrospective study of 77 cats with severe hepatic lipidosis: 1975-1990. 811 31

Medical records and histologic sections of 40 cats with acute pancreatitis were reviewed. Two distinct groups of cats with pancreatitis were established by histologic analysis of tissue. Group 1 (32 cats) had acute pancreatic necrosis (APN). Group 2 (8 cats) had suppurative pancreatitis. Ages of affected cats ranged from 3 weeks to 16 years. The majority consisted of indoor cats of the Domestic Short-Haired breed but Siamese cats were over-represented relative to the general population (P < 0.05). Twenty-two percent of cats were obese and 57% were underweight. Thirty-eight percent of cats had acute disease. In the other cats, two stages in the progression of the disease were evident: (1) anorexia, weight loss, and lethargy, followed by (2) acute deterioration, development of shock, and a moribund state, despite fluid therapy. The most common clinical signs were severe lethargy (100%), reduced appetite (97%), dehydration (92%), and hypothermia (68%). The initial hemogram occasionally showed a neutrophilia (30%) and anemia (26%) but packed cell volume (PCV) decreased markedly to the extent that 55% of cats were anemic terminally. Serum biochemical abnormalities included increased activities of ALT (68%) and ALP (50%), and increased concentrations of bilirubin (64%) and cholesterol (64%). Cats with APN were hyperglycemic (64%), glycosuric (60%) and ketonuric (20%), whereas cats with suppurative pancreatitis tended to be hypoglycemic (75%). Renal failure and electrolyte abnormalities were mild or infrequent except for hypokalemia (56%). This study characterizes a severe necrotizing pancreatitis in the cat similar to that reported in other species, and a histologically distinct suppurative pancreatitis.
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PMID:Acute necrotizing pancreatitis and acute suppurative pancreatitis in the cat. A retrospective study of 40 cases (1976-1989). 1146 88

Pathologic water loss from sickle erythrocytes concentrates the abnormal hemoglobin and promotes sickling. The Ca2+-activated K+ channel (Gardos channel) contributes to this deleterious dehydration in vitro, and blockade of K+ and water loss via this channel could be a potential therapy in vivo. We treated five subjects who have sickle cell anemia with oral clotrimazole, a specific Gardos channel inhibitor. Patients were started on a dose of 10 mg clotrimazole/kg/d for one week. Protocol design allowed the daily dose to be escalated by 10 mg/kg each week until significant changes in erythrocyte density and K+ transport were achieved. Blood was sampled three times a week for hematological and chemical assays, erythrocyte density, cation content, and K+ transport. At dosages of 20 mg clotrimazole/kg/d, all subjects showed Gardos channel inhibition, reduced erythrocyte dehydration, increased cell K+ content, and somewhat increased hemoglobin levels. Adverse effects were limited to mild/moderate dysuria in all subjects, and a reversible increase in plasma alanine transaminase and aspartic transaminase levels in two subjects treated with 30 mg clotrimazole/kg/d. This is the first in vivo evidence that the Gardos channel causes dehydration of sickle erythrocytes, and that its pharmacologic inhibition provides a realistic antisickling strategy.
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PMID:Therapy with oral clotrimazole induces inhibition of the Gardos channel and reduction of erythrocyte dehydration in patients with sickle cell disease. 863 22

Many dogs competing in long distance sled dog races do not complete the race. In this study the plasma biochemical variables of dogs that completed a long distance sled race were compared with those of dogs that did not complete the race. Blood samples were collected from dogs completing the race and from retired dogs, within six hours of their finishing or retiring. The plasma concentrations of magnesium, phosphate and triglyceride and the plasma activities of alkaline phosphatase and alanine aminotransferase were significantly (P < 0.003) greater in the dogs that retired than in the dogs that completed the race. Dogs that finished had significantly higher (P < 0.003) plasma urea nitrogen and uric acid concentrations and gamma-glutamyl transpeptidase activity than dogs that retired. These differences were judged not to be clinically significant. The dogs that retired showed no evidence of dehydration, significant plasma electrolyte abnormalities, or myopathy.
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PMID:Performance failure in Alaskan sled dogs: biochemical correlates. 893 61


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