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)

Median values and confidence intervals for hematology and serum and plasma chemistry parameters were established for 29 male and female healthy New Guinea snapping turtles (Elseya novaeguineae) held at 24.5 degrees C and 30.0 degrees C. Creatine kinase, albumin, potassium, and phosphorus values were significantly higher at 24.5 degrees C than at 30.0 degrees C. Glucose, alkaline phosphatase, aspartate transaminase, alanine aminotransferase, total carbon dioxide, and chloride values were significantly higher at 30.0 degrees C than at 24.5 degrees C. Cholesterol and calcium values were significantly higher in females than in males. Hemoglobin, packed cell volume, and bilirubin were significantly higher in males than in females, and bile acid values were significantly higher in serum than in plasma.
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PMID:Hematology and clinical chemistry reference ranges for clinically normal, captive New Guinea snapping turtle (Elseya novaeguineae) and the effects of temperature, sex, and sample type. 952 32

1. Groups of five male and five female CD-1 mice received a single intravenous injection of gadolinium chloride at dosages of 0 (saline control), 0.05, 0.1 and 0.2 mmol/ kg. All mice were necropsied 48 h post dose. 2. Plasma analysis showed increases in concentrations of lactate dehydrogenase (both sexes), aspartate aminotransferase and alanine aminotransferase (females only) in the 0.2 mmol/kg group. Cholesterol was elevated at all dosages in both sexes whilst globulin was raised in both sexes at 0.1 and 0.2 mmol/kg. 3. Histological lesions were present at all dosages and increased in severity in a dose-related fashion. The most common lesions were: mineral emboli in capillaries, accumulation of mineral in the mononuclear phagocytic system, hepatocellular necrosis, and lymphoid depletion, necrosis and mineralisation in the spleen. 4. Such observations are similar to those in rats given gadolinium chloride and should be assessed when evaluating the toxicological profile of gadolinium containing compounds being developed for nuclear magnetic resonance imaging.
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PMID:Gadolinium chloride toxicity in the mouse. 986 21

The relationship between ritonavir plasma concentration, efficacy, and tolerance was evaluated in 31 children with advanced HIV infection who were receiving a triple therapy with ritonavir as protease inhibitor. Median CD4+ lymphocyte count and median viral load before the initiation of ritonavir-containing combination therapy were 1320 cells/mL and 5 log10 copies/mL, respectively. Ritonavir was given at a dose ranging from 300 to 450 mg/m2 twice daily. The median follow-up of triple therapy was 19 months. Response was defined as a drop of viremia of more than 1 log. Plasma drug levels were determined twice during the observation period: after at least 4 weeks and after 3 months of combined treatment. Samples were collected before (residual) and 2 hours (T2) after drug intake. Cholesterol, triglycerides, alanine transaminase, aspartate transaminase, and gamma-glutamyl transpeptidase were assessed at the same time. The median values of ritonavir residual and T2 levels were 1.64 mg/L and 5.9 mg/L at observation 1 and 3.35 mg/L and 6.29 mg/L at observation 2, respectively. According to virologic response, median residual concentrations of ritonavir were 3.17, 2.52, and 1.04 mg/L for the complete, the partial, and the no-response groups. The authors observed a wide intersubject variability of ritonavir concentrations with an increase in residual levels between the two observation periods. Residual levels were correlated with virologic response whereas there was no direct association between T2 levels and long-term response. Patients with complete or partial response displayed statistically significantly higher residual concentrations than the no-response group. No correlation could be demonstrated between elevated plasma drug concentrations and abnormal cholesterol or triglycerides values. These results emphasize the importance of a sustained high ritonavir concentration to achieve optimal treatment efficacy. Furthermore, these results prove the clinical benefit of therapeutic drug monitoring and could potentially improve patient evaluation in terms of treatment efficacy, compliance, and viral resistance.
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PMID:Relationship between efficacy, tolerance, and plasma drug concentration of ritonavir in children with advanced HIV infection. 1094 79

Comprehensive hematologic and biochemical analyses were conducted on blood from 23 male and 31 female clinically stable captive mugger crocodiles (Crocodylus palustris). Erythrocyte mean corpuscular volume (MCV), potassium, cholesterol, and calcium concentrations were significantly greater in juvenile males than in juvenile females, but no significant differences were determined between parameters of subadult males and subadult females. The mean WBC count and mean heterophil count were significantly higher in adult males than in adult females. Mean uric acid concentration was significantly greater in adult females than in males. Mean erythrocyte count was significantly higher in adults than in juveniles. Adult mean WBC and lymphocyte counts were significantly lower than those of both juveniles and subadults. Subadults had significantly lower mean eosinophil counts than both adults and juveniles. Subadults had significantly lower mean alkaline phosphatase activities than juveniles, whereas the adults had significantly lower aspartate aminotransferase and alanine aminotransferase activities than other groups. Lactate dehydrogenase activities were significantly lower for subadults than for juveniles and adults. Cholesterol concentrations were significantly higher for subadults and juveniles compared with adults. Triglyceride concentration was significantly lower for subadults and highest for juveniles. Glucose concentrations were significantly higher for adults. Blood urea nitrogen was significantly lower for subadults than for both adults and juveniles. Uric acid concentrations were significantly higher for juveniles than for the subadults and adults. The subadult animals also had a significantly lower potassium concentration. The results obtained were then compared with known values for other crocodilian species.
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PMID:Hematology and blood biochemistry of captive mugger crocodiles (Crocodylus palustris). 1123 41

Male and female F-344 rats and B6C3F1 mice (10/sex/group) were exposed to N,N-dimethylformamide (DMF) by whole body inhalation exposure at 0, 50, 100, 200, 400, or 800 ppm, 6 h/day, 5 days/week, for 13 weeks. A concentration-dependent depression in body weight occurred in rats of both sexes at 400 (6-11%) and 800 ppm (20-22%). In contrast, all weight changes in both sexes of mice were within 10% of controls. No rats died, while 5 mice died from nonexposure-related causes. Relative liver weights were significantly increased at all DMF concentrations in both sexes and both species. Activities of serum sorbitol dehydrogenase (SDH) were statistically increased in male and female rats (200 to 800 ppm) on study days 4, 24, and 91 (13 weeks). Activities of alanine aminotransferase (ALT) and isocitrate dehydrogenase (ICD) were statistically increased in both sexes of rats exposed to 800 ppm DMF at all time points. Cholesterol (CHOL) levels were statistically increased in male and female rats (50-800 ppm) at all sampling time points. Levels of total bile acids (TBA) were statistically increased in both sexes of rats (400-800 ppm) on days 24 and 91. Centrilobular hepatocellular necrosis (minimal to moderate) was seen in rats of both sexes exposed at 400 and 800 ppm, with the lesions more severe in females. Centrilobular hepatocellular hypertrophy (minimal to mild) was found in all groups of DMF-exposed male mice, and in female mice exposed at 100-800 ppm. For male and female rats the no-observed-adverse-effect concentration (NOAEC) for microscopic liver injury was 200 ppm. The NOAEC was 50 ppm for female mice, but an NOAEC based upon the absence of microscopic liver injury was not determined in male mice.
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PMID:Thirteen-week inhalation toxicity of N,N-dimethylformamide in F344/N rats and B6C3F1 mice. 1265 34

The effects of chronic oral exposure (28 days) to aflatoxin B(1) (AFB(1)) and fumonisin B(1) (FB(1)) were studied in weaned piglets. Six experimental groups, each comprising two neutered males and two females, were fed ad libitum with rations containing: (A) 0 mg of FB(1) and 0 mg of AFB(1)/kg of feed (control); (B) 10 mg of FB(1)/kg of feed; (C) 30 mg of FB(1)/kg of feed; (D) 50 microg of AFB(1)/kg of feed; (E) 10 mg of FB(1) plus 50 microg of AFB(1)/kg of feed; (F) 30 mg of FB(1) plus 50 microg of AFB(1)/kg of feed. The animals were inspected twice daily and their body weight and feed consumption were recorded weekly and daily, respectively. Samples of feces and urine were collected 24 h after the start of the experiment, to check for fumonisin residues by HPLC analysis. Blood samples were drawn at the start of the experiment and after 28 days for quantification of hematological and biochemical parameters. Necropsies were performed after 28 days; at necropsy, the organs were weighed, inspected macroscopically and processed for histopathological and toxicological analyses. All piglets from groups C and F presented typical signs of pulmonary edema, with reduced feed consumption and body weight gain as well as pathological alterations. FB(1) was detected in feces and urine at 24 h of intoxication and in liver after 28 days of intoxication. Increases were detected regarding the following hematological and biochemical parameters in animals from treatments C and F: erythrocyte number; hematocrit; total bilirubin; total protein; activity of serum alkaline phosphatase, aspartate aminotransferase, and alanine aminotransferase. Cholesterol levels were significantly aumented only in animals from groups C and F, whereas albumin concentrations increased in groups C, F, B and E. The average organ/body weight ratio of piglets (hearth, liver and lung) were significantly greater in groups C and F. The only joint effects of FB(1) and AFB(1) detected (group F) were a decrease in feed consumption during the last week of intoxication and in feed conversion throughout the 28 days of intoxication. Chronic intoxication of piglets with AFB(1) and FB(1) leads to important losses of productivity.
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PMID:Toxicological effects of chronic low doses of aflatoxin B(1) and fumonisin B(1)-containing Fusarium moniliforme culture material in weaned piglets. 1290 68

The aim of this article is to examine the benefit-risk profile of rosuvastatin at doses of 10 to 40 mg. In dyslipidemic patients, rosuvastatin produced markedly greater reductions in low-density lipoprotein (LDL) cholesterol and equivalent or greater improvements in various lipid measures, including high-density lipoprotein (HDL) cholesterol, non-HDL cholesterol, and triglycerides when compared with atorvastatin, simvastatin, and pravastatin. In addition, rosuvastatin is more effective than these statins in allowing patients to reach National Cholesterol Education Program (NCEP) Adult Treatment Panel (ATP) III and Joint European Societies LDL cholesterol goals. The safety profile of rosuvastatin was reviewed (as of April 2003) in 12,569 patients, representing 14,231 patient-years of treatment at doses up to 80 mg. In controlled trials, rosuvastatin 10 to 40 mg demonstrated a similar adverse event profile to those for atorvastatin 10 to 80 mg, simvastatin 10 to 80 mg, and pravastatin 10 to 40 mg. Myopathy (defined as muscle symptoms plus serum creatine kinase levels >10 times the upper limit of normal) attributed to rosuvastatin occurred in < or = 0.03% of patients receiving rosuvastatin 10 to 40 mg. No cases of rhabdomyolysis occurred in patients receiving rosuvastatin 10 to 40 mg. Clinically significant alanine aminotransferase elevations occurred in 0.2% of patients receiving rosuvastatin and those receiving atorvastatin, simvastatin, and pravastatin. Compared with other widely used statins, the benefit-risk profile of rosuvastatin 10 to 40 mg appears to be very favorable.
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PMID:Benefit-risk assessment of Rosuvastatin 10 to 40 milligrams. 1294 73

The aim of this study was to determine the effect of opium on biochemical parameters in addicts with non-insulin-dependent diabetes mellitus (NIDDM). Twenty-three males and 26 females between 35 and 65 years of age, with NIDDM, addicted to opium, were selected as the case group. Twenty-three males and 26 females with NIDDM and no opium addiction served as controls. Fasting glucose, glycated haemoglobin (HbA1c), total cholesterol, high density lipoproteins-cholesterol (HDL-c), triglycerides (TGs), sodium (Na(+)), potassium (K(+)), calcium (Ca(2+)), iron (Fe(2+)), total iron binding capacity (TIBC), serum total protein, albumin, alanine aminotransferase (ALT), aspartate aminotransferase (AST), uric acid and urea were measured in the serum of the two groups. Serum protein electrophoresis was also carried out. Compared to the control group, in addicted males with NIDDM, HbA1c, K(+) and Fe(2+) were higher, and serum total protein, ALT and HDL-c were lower. No significant difference was observed between other factors. Albumin was lower in addicts, but no significant difference was observed between the albumin/globulin ratios. In addicted females with NIDDM, serum total protein, TIBC, ALT and AST were lower compared to non-addicts. Cholesterol tends to be lower in diabetic addicted males, HbA1c in addicted females and uric acid in addicted males was higher compared to non-addicted diabetics. Their differences, however, were not significant. According to our results, smoking opium increases serum glucose and decreases HDL-c, and thus adds to metabolic disorders in NIDDM patients. It also increases potassium and Fe(2) in males and decreases TIBC in females, and could therefore potentially interfere with water and iron metabolism.
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PMID:Effects of opium addiction on some serum factors in addicts with non-insulin-dependent diabetes mellitus. 1520 39

The present study was carried out to investigate the effects of copper (Cu) intake on lipid profile, oxidative stress and tissue damage in normal and in diabetic condition. Since diabetes mellitus is a situation of high-risk susceptibility to toxic compounds, we examined potential early markers of Cu excess in diabetic animals. Male Wistar rats, at 60-days-old were divided into six groups of eight rats each. The control(C) received saline from gastric tube, the no-diabetic(Cu-10), treated with 10 mg/kg of Cu(Cu(++)-CuSO4, gastric tube), no-diabetic with Cu-60 mg/kg(Cu-60), diabetic(D), diabetic low-Cu(DCu-10) and diabetic high-Cu(DCu-60). Diabetes was induced by an ip injection of streptozotocin (60 mg/kg). After 30 days of treatments, no changes were observed in serum lactate dehydrogenase, alanine transaminase and alkaline phosphatase, indicating no adverse effects on cardiac and hepatic tissues. D-rats had glucose intolerance and dyslipidemic profile. Cholesterol and LDL-cholesterol were higher in Cu-60 and DCu-60 than in C, Cu-10 and D and DCu-10 groups respectively. Cu-60 rats had higher lipid hydroperoxide (HP) and lower superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) serum activities than C and Cu-10 rats. LH was increased and GSH-Px was decreased, while no alterations were observed in SOD and catalase in serum of DCu-60 animals. DCu-60 rats had increased urinary glucose, creatinine and albumin. In conclusion, Cu intake at high concentration induced adverse effects on lipid profile, associated with oxidative stress and diminished activities of antioxidant enzymes. Diabetic animals were more susceptible to copper toxicity. High Cu intake induced dyslipidemic profile, oxidative stress and kidney dysfunction in diabetic condition. Copper renal toxicity was associated with oxidative stress and reduction at least, one of the antioxidant enzymes.
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PMID:Toxicity of copper intake: lipid profile, oxidative stress and susceptibility to renal dysfunction. 1550 Sep 42

Nonalcoholic fatty liver disease (NAFLD) is emerging as a component of the metabolic syndrome, although it is not known whether markers of NAFLD, including elevated concentrations of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALK), predict the development of metabolic syndrome. Our objective was to investigate the associations of elevated AST, ALT, and other liver markers, including C-reactive protein (CRP), with incident National Cholesterol Education Program-defined metabolic syndrome among 633 subjects in the Insulin Resistance Atherosclerosis Study who were free of metabolic syndrome at baseline. Insulin sensitivity (Si) and acute insulin response (AIR) were directly measured from the frequently sampled intravenous glucose tolerance test among African-American, Hispanic, and non-Hispanic white subjects aged 40-69 years. After 5.2 years, 127 individuals had developed metabolic syndrome. In separate logistic regression models adjusting for age, sex, ethnicity, clinic, and alcohol consumption, subjects in the upper quartiles of ALT, ALK, and CRP were at significantly increased risk of incident metabolic syndrome compared with those in the lowest quartile: ALT, odds ratio 2.50 (95% CI 1.38-4.51); ALK, 2.28 (1.24-4.20); and CRP, 1.33 (1.09-1.63). Subjects in the upper quartile of the AST-to-ALT ratio were at significantly reduced metabolic syndrome risk (0.40 [0.22-0.74]). After further adjustment for waist circumference, Si, AIR, and impaired glucose tolerance, the associations of ALT and the AST-to-ALT ratio with incident metabolic syndrome remained significant (ALT, 2.12 [1.10-4.09]; the AST-to-ALT ratio, 0.48 [0.25-0.95]). These associations were not modified by ethnicity or sex, and they remained significant after exclusion of former and heavy drinkers. In conclusion, NAFLD markers ALT and the AST-to-ALT ratio predict metabolic syndrome independently of potential confounding variables, including directly measured Si and AIR.
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PMID:Liver markers and development of the metabolic syndrome: the insulin resistance atherosclerosis study. 1624 37


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