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:2.6.1.2 (alanine aminotransferase)
26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

1,1,1,3,3-Pentafluoropropane (HFC 245fa) is a volatile, low boiling liquid. It was inactive in a reverse mutation (Ames) assay using five strains of Salmonella typhimurium and one strain of Escherichia coli. It was also inactive in an in vivo mouse micronucleus assay with exposures of 101,000 ppm. In a chromosome aberration study with human lymphocytes, some activity was seen when cell cultures were exposed to atmospheres of 30% v/v or higher for 24 h without metabolic activation. No activity was seen in assays using less than 30% v/v or exposure times of less than 24 h. No activity was seen in the presence of metabolic activation even with exposures of 70%. It was not toxic by the dermal route. There was no mortality or significant signs of toxicity when rats and mice were given 4- h exposures to levels of 203,000 ppm or 101,000 ppm of HFC 245fa, respectively. In a cardiac sensitization study with dogs involving intravenous administration of epinephrine, the no observed effect level (NOEL) was 34,000 ppm and the threshold for a response was 44,000 ppm. In a rat inhalation, developmental toxicity study, a slight reduction in pup weight was seen at 50,000 ppm, but not at 10,000 ppm. There were no developmental effects at any level. A series of three inhalation toxicity studies were conducted. All involved daily 6-h exposures up to 50,000 ppm. The first study involved 14 consecutive snout-only exposures. There were no treatment-related effects on body weight, survival, or histologic parameters. BUN, GPT, and GOT levels frequently were elevated compared to controls , whereas cholesterol levels tended to be lower. The second study involved 28 consecutive whole-body exposures. Again, there were no treatment related effects on body weight, survival, or histological parameters. Urine volume was increased. Increases were also seen in several red blood cell parameters. These may be related to partial dehydration. Increases were seen in BUN levels and alkaline phosphatase (AP), GPT, GOT and CPK activities, primarily in rats exposed at 10,000 and 50,000 ppm. Urinary fluoride levels were also elevated in an exposure- related pattern. In the third study, whole-body exposures were conducted 5 days per week for 13 weeks. There were no treatment-related effects on survival, clinical observations, body weight gain, or food consumption. Urine volumes were increased, urinary fluoride levels were elevated, and increases were seen in red blood cell counts, and related parameters and increases were seen in AP, GOT, GPT and CPK activities. These effects were seen in the 10,000 and 50,000 ppm exposure level groups. Histopathologic examination did not show any effects on the kidney, liver, or lungs. There was an increased incidence of myocarditis in all animals exposed at 50,000 ppm and the majority exposed at 10,000 ppm. It was described as mild. Based on these findings, 2000 ppm appears to be a no observed adverse effect level.
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PMID:The acute, genetic, developmental, and inhalation toxicology of 1,1,1,3,3-pentafluoropropane (HFC 245fa). 1063 May 82

Sodium selenate and sodium selenite are used as supplements to poultry and livestock feed to promote growth and prevent selenium deficiency diseases. Both compounds have been found in chemical waste sites. Thirteen-week toxicity studies were conducted by administering the chemicals to groups of male and female F344/N rats and B6C3F1 mice in drinking water. Animals were evaluated for hematology, clinical chemistry, urinalysis (rats only), histopathology, and reproductive system effects. In the studies of sodium selenate, groups of 10 male and 10 female rats and mice received 0, 3.75, 7.5, 15, 30, or 60 ppm sodium selenate for 13 weeks. These concentrations were estimated to deliver 0, 0.1, 0.2, 0.4, 0.6, 1.1 (males), or 0.8 (females) mg selenium/kg body weight for rats and 0, 0.3, 0.5, 0.8, 1.5, or 2.6 mg/kg selenium for mice. All male and female rats exposed to 60 ppm died. The final mean body weights of rats exposed to 30 ppm sodium selenate and of mice exposed to 30 or 60 ppm were 13% to 29% lower than those of the controls. Water consumption by rats and mice exposed to 15 ppm or greater was decreased. Decreases in urine volume and increases in erythrocyte counts, hematocrit, hemoglobin concentrations, alanine aminotransferase activities, urea nitrogen, and urine specific gravity were considered related to dehydration, as indicated by the decreased water consumption and mean body weights in groups showing these differences. Administration of 7.5 ppm sodium selenate or greater was associated with increased incidences of renal papillary degeneration in rats. Dehydration may have been a contributing factor. No lesions related to sodium selenate administration occurred in mice. In the studies of sodium selenite, groups of 10 male and 10 female rats and mice received 0, 2, 4, 8, 16, or 32 ppm sodium selenite for 13 weeks. These concentrations were estimated to deliver 0, 0.08, 0.13, 0.2, 0.4, 0.8 (males), or 0.9 (females) mg/kg selenium for rats and 0, 0.14, 0.3, 0.5, 0.9, or 1.6 mg/kg selenium for mice. Two female rats exposed to 32 ppm died during the study. The final mean body weights of rats and mice exposed to 32 ppm were 17% to 54% lower than those of the controls. Water consumption by exposed rats and mice decreased with increasing exposure concentration. Changes in hematology, clinical chemistry, and urinalysis parameters similar to those observed in rats exposed to sodium selenate were observed in rats exposed to sodium selenite. These effects were also considered related to dehydration, as indicated by the decreased water consumption and mean body weights in exposed groups. Sodium selenite administration was associated with increased incidences of renal papillary regeneration in rats. Dehydration may have been a contributing factor. No lesions related to sodium selenite administration occurred in mice. Based on mortality in rats, body weight depression, and renal lesions, sodium selenate and sodium selenite were more toxic to rats than to mice. These chemicals caused increases in estrous cycle length in rats; sodium selenite also caused an increase in estrous cycle length in mice. Based on mortality, body weight depression, decreased water consumption, and renal papillary lesions, the estimated no-observed-adverse-effect level (NOAEL) in rats was 0.4 mg selenium/kg body weight for sodium selenate and for sodium selenite. Based on body weight depression and decreased water consumption, the estimated NOAEL in mice was 0.8 mg selenium/kg body weight for sodium selenate and 0.9 mg selenium/kg body weight for sodium selenite. NOTE: These studies were supported in part by funds from the Comprehensive Environmental Response, Compensation, and Liability Act trust fund (Superfund) by an interagency agreement with the Agency for Toxic Substances and Disease Registry, U.S. Public Health Service.
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PMID:NTP Toxicity Studies of Sodium Selenate and Sodium Selenite (CAS Nos. 13410-01-0 and 10102-18-8) Administered in Drinking Water to F344/N Rats and B6C3F1 Mice. 1196 37

Forty-six cats with clinical haemobartonellosis were studied; 75 per cent of the cats of known age were two-and-a-half years old or younger, 50 per cent were intact males and 19.5 per cent were castrated males. The predominant signs of the disease were tachypnoea, lethargy, depression, anorexia, infestation with fleas, pale mucous membranes, icterus, emaciation, dehydration, splenomegaly, anaemia, leucocytosis, increased activities of alanine aminotransferase and aspartate aminotransferase, and azotaemia. Thirty-eight per cent of the cats that were tested for feline leukaemia virus (FeLV) antigen were positive, and 22 per cent of those tested for feline immunodeficiency virus (FIV) antibodies were positive. The prevalence of both FeLV and FIV was much higher than in the general Israeli cat population. The cats infected with both Haemobartonella felis and FeLV had a significantly lower body temperature, were more anaemic and the mean cell volume of their erythrocytes was greater than in the cats with haemobartonellosis alone.
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PMID:Retrospective study of 46 cases of feline haemobartonellosis in Israel and their relationships with FeLV and FIV infections. 1216 25

Birds have evolved alternate physiologic strategies to contend with dehydration, starvation, malnutrition, and reproduction. Basic anatomic and functional differences between birds and mammals impact clinical chemistry values and their evaluation. Interpretation of the results of standard biochemical analyses, including BUN, alanine aminotransferase, aspartate aminotransferase, creatine kinase, gamma glutamyltransferase, bilirubin, ammonia, alkaline phosphatase, cholesterol, bile acids, glucose, albumin, globulins, calcium, phosphorus, prealbumin (transthyretin), fibrinogen, iron, and ferritin, is reviewed and discussed in relation to these physiological differences. The use and interpretation of alternative analytes appropriate for avian species, such as uric acid, biliverdin, glutamate dehydrogenase, and galactose clearance, also are reviewed. Normal avian urine and appropriate use of urinalysis, an integral part of laboratory diagnosis in mammalian species that frequently is omitted from avian diagnostic protocols, is discussed.
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PMID:Clinical chemistry of companion avian species: a review. 1218 2

Cupric sulfate is an inorganic salt which is widely used in industry, agriculture, and veterinary medicine. Its applications include use as an algicide in potable waters and as a feed additive and therapeutic agent in swine, sheep, and cattle. Because copper salts are found in human water supplies, toxicity studies of cupric sulfate pentahydrate were conducted in male and female F344/N rats and B6C3F1 mice by the drinking water (2-week studies only) and dosed feed routes (2-week and 13-week studies). Animals were evaluated for hematology, clinical chemistry, urinalysis, reproductive toxicity, tissue metal accumulation, and histopathology. In the 2-week drinking water studies, groups of five rats and five mice per sex received cupric sulfate at concentrations of 300 to 30,000 ppm for 15 days. One female rat, one male mouse, and three female mice in the 3000 ppm groups and all rats and mice in the 10,000 and 30,000 ppm groups died before the end of the studies. The remaining mice and rats in the 3000 ppm groups gained little or lost weight. Water consumption in the three highest dose groups of both species was reduced by more than 65%. Clinical signs observed in these groups were typical of those seen in moribund animals and were attributed to dehydration. The only gross or microscopic change specifically related to cupric sulfate toxicity was an increase in the size and number of cytoplasmic protein droplets in the epithelium of the renal proximal convoluted tubule in male rats from the 300 and 1000-ppm groups. In the 2-week feed studies, groups of five rats and five mice per sex were fed diets containing 1000 to 16,000 ppm cupric sulfate. No chemical-related deaths occurred in any dose group. Compared to the controls, rats and mice in the two highest dose groups had reduced body weight gains which were attributed to decreased feed consumption. Hyperplasia with hyperkeratosis of the squamous epithelium on the limiting ridge of the forestomach was seen in rats and mice of each sex; this lesion was more severe in rats than in mice. Inflammation of the liver, periportal to midzonal in distribution, occurred in rats in the 8000 and 16,000 ppm groups. Depletion of hematopoietic cells was evident in rats of each sex in the bone marrow (8000 and 16,000 ppm) and spleen (16,000 ppm). Kidneys of male and female rats in the 4000, 8000, and 16,000 ppm groups had an increased number and size of protein droplets in the epithelia of the renal cortical tubules. In the 13-week feed studies, groups of 10 rats per sex received diets containing 500 to 8000 ppm cupric sulfate, and groups of 10 mice per sex received diets containing 1000 to 16,000 ppm cupric sulfate for 92 days; estimates of cupric sulfate consumption ranged from 32 to 551 mg/kg per day for rats and 173 to 4157 mg/kg per day for mice. There were no chemical-related deaths in rats or mice, and no clinical signs of cupric sulfate toxicity were recorded. Final mean body weights were lower than those of the controls for animals of both species receiving doses of 4000 ppm cupric sulfate and greater. In mice in the 13-week studies, there was a dose-related decrease in liver weights. Hematologic, clinical chemistry, and urinalysis evaluations of rats in the 13-week study revealed variable chemical-related changes that were, for the most part, restricted to the 4000 and 8000 ppm groups. Increases in serum alanine aminotransferase and sorbitol dehydrogenase activities in both sexes were indicative of hepatocellular damage, as were increases in 5'-nucleotidase and bile salts in males. Decreases in mean cell volume, hematocrit, and hemoglobin indicated the development of a microcytic anemia, while increases in reticulocyte numbers at the same time points suggested a compensatory response to the anemia by the bone marrow. Increases in urinary glucose and N-acetyl-beta-D-glucosaminidase (a lysosomal enzyme) and aspartate aminotransferase (alpha-cytosolic enzyme) were suggestive of renal tubule epithelial damage. Dose-related increases in copper occurred in all male rat tissues examined (lissues examined (liver, kidney, plasma, and testis). These increases were accompanied by increases in zinc in the liver and kidney. Plasma calcium was significantly reduced in the 4000 and 8000 ppm groups, and there was a trend toward reductions in calcium in the kidney and testis as well. In the 8000 ppm group, plasma magnesium was significantly increased relative to the controls. Rats in the three highest dose groups had hyperplasia and hyperkeratosis of the forestomach, inflammation of the liver, and increases in the number and size of protein droplets in the epithelial cytoplasm and the lumina of the proximal convoluted tubules. These effects were similar to those seen in the 2-week feed study, and the incidence and severity of these lesions were dose related. Many of the droplets in male rat kidneys were large and had irregular crystalline shapes. These droplets stained strongly positive for protein but were negative by iron, PAS, and acid-fast (lipofuscin) staining methods. α-2-Microglobulin was present in the droplets of male rats, but there was no dose- related, qualitative difference in the content of this protein. In the 4000 and 8000 ppm groups, copper was distributed in a periportal to midzonal pattern in the liver and was restricted to the cytoplasm of the proximal convoluted tubule epithelium in the kidney. Copper was present in some, but not all, of the protein droplets. Transmission electron microscopy of the livers of rats of each sex revealed increases in the number of secondary lysosomes in hepatocytes in the periportal area. In mice of each sex receiving 4000 ppm cupric sulfate and higher in the 13-week study, there was a dose-related increase in hyperplasia with hyperkeratosis of the squamous mucosa on the limiting ridge of the forestomach. Minimal positive staining for copper was present in the liver and was limited to high-dose (16,000 ppm) male and female mice. Cupric sulfate produced no adverse effects on any of the reproductive parameters measured in rats or mice of either sex. In summary, administration of cupric sulfate to rats in feed or drinking water resulted in significant gastric changes and hepatic and renal damage. The primary lesion in rats was an increase in the size and number of proteinaceous droplets in the epithelial cytoplasm and lumen of the proximal convoluted tubule. For rats in the 13-week study, the no-observed-adverse-effect level (NOAEL) for evidence of histologic injury to the kidney was 1000 ppm for males and 500 ppm for females, while the NOAEL for liver inflammation was 1000 ppm for males and 2000 ppm for females. Hyperplasia with hyperkeratosis of the epithelium on the limiting ridge separating the forestomach from the glandular stomach was also seen in rats of each sex, and the NOAEL for this change was 1000-ppm cupric sulfate in the feed. Additionally, clinical pathology alterations noted in the 13-week study, along with histologic changes in bone marrow noted in the 2-week feed study, were indicative of a microcytic anemia with a compensatory bone marrow response. Mice appeared to be much more resistant to the toxic effects of cupric sulfate than rats. The primary target tissue in mice was the epithelium of the limiting ridge of the forestomach. The NOAEL for the hyperplasia and hyperkeratosis seen at this site in mice was 2000-ppm cupric sulfate in the feed. Synonyms: Chalcanthite; Copper sulfate; cupric sulfate pentahydrate; bluestone; blue vitriol; Roman vitriol; Salzburg vitriol. (NOTE: These studies were supported in part by funds from the Comprehensive Environmental Response, Compensation, and Liability Act trust fund (Superfund) by an interagency agreement with the Agency for Toxic Substances and Disease Registry, U.S. Public Health Service.)
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PMID:NTP technical report on the toxicity studies of Cupric Sulfate (CAS No. 7758-99-8) Administered in Drinking Water and Feed to F344/N Rats and B6C3F1 Mice. 1220 95

We report a case of a 26-year-old White woman with a history of anorexia nervosa who developed severe liver damage and multiorgan dysfunction. At admission to our medical unit, her body mass index (BMI) was 10.8. Biochemical evaluation showed a marked increase in serum levels of aspartate aminotransferases (AST = 9,980 IU/L), alanine aminotransferase (ALT = 3,930 IU/L), amylase (1,002 IU/L), lipase (1,437 IU/L), creatine phosphokinase (CPK; 783 IU/L), and lactate dehydrogenase (LDH = 6,830 IU/L). Glomerular filtration rate was reduced (35 ml/min), reflecting dehydration and prerenal azotemia. No other cause of acute liver damage except malnutrition was evidenced. Hydration and nutritional support were the unique medical treatment. A rapid recovery occurred in few days and all laboratory data were normal at discharge after a 37-day hospitalization.
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PMID:Acute liver damage in anorexia nervosa. 1518 81

A 4.5-year-old female degu (Octodon degus) was minimally responsive with a poor body condition, a rough haircoat, and moderate dehydration. Blood was present around its urethral orifice and on the cage bedding. Laboratory analyses revealed leukocytosis with neutrophilia and anemia; hypoproteinemia and hypoalbuminemia; hyperglycemia, hyperphosphatemia, and elevated alanine aminotransferase, blood urea nitrogen, and creatinine; and hematuria and pyuria with occasional squamous and transitional epithelial cells. A urine culture was positive for coagulase-negative Staphylococcus sp. On gross necropsy, the right kidney was enlarged, cystic, and greenish-brown, with a 10-mm, hemorrhagic, granular mass extending from the renal pelvis into the cranial cortex. Only a small amount of renal cortex appeared normal. The urinary bladder had focal areas of hemorrhage and contained frank blood. Histologically, the papillary mass in the right renal pelvis comprised basophilic, moderately anaplastic, clustered epithelial transition cells consistent with a transitional cell carcinoma. Internally, the tumor showed squamous metaplasia and moderate multifocal interstitial fibrosis. The right kidney cortex contained a choristoma comprising trabecular bone, mature adipocytes, and cellular infiltrates suggestive of osteocytes, lymphocytes, and plasma cells. The urinary bladder had mild to moderate, focal, hemorrhage with neutrophilic inflammation and contained focal areas of mild transitional cell epithelial hyperplasia; these changes may have been secondary to irritation by hemorrhage in the renal pelvis. There was no evidence of metastasis. Renal transitional cell tumors are rare in rodents. This is the first report of both a renal transitional cell carcinoma and a renal choristoma in a degu.
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PMID:Renal transitional cell carcinoma and choristoma in a degu (Octodon degus). 1593 23


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