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

A spectrum of quantitative and qualitative methods was adapted to the RA-1000/RA-XT selective analyser for the purpose of excluding or detecting common types of intoxication in the emergency laboratory of our primary care community hospital. Ethanol and salicylates (measured photometrically) and acetaminophen (measured immunologically by EMIT tox) were quantitatively analysed in serum. immunological group tests (EMIT tox) for barbiturates, benzodiazepines, tricyclic antidepressants and related compounds were used for qualitative analysis. Well established clinical chemical methods (aspartarte aminotransferase, alanine aminotransferase, creatine kinase, pseudocholinesterase, glucose and lactate) were applied to the serum samples using the same selective analyser. Within and between run precision, accuracy, recovery and detection ranges (linearity) fulfilled the recommendations of forefield toxicological analysis for all methods. Ethanol (g/l), measured photometrically with the RA-1000 analyser, agreed with the reference method (headspace gas-chromatography) with a correlation coefficient greater than 0.99 (y = 0.06 + 0.98x). Acetaminophen and salicylates showed correlation coefficients greater than 0.94 and greater than 0.99, when compared with manual colorimetric procedures (acetaminophen (mg/l): y = -3.22 + 0.896x; salicylates (mg/l): y = -2.1 + 1x). Qualitative group tests for barbiturates, benzodiazepines and tricyclic antidepressants measured with the RA-1000 analyser were in good agreement with the EMIT single test procedure. The ranges of the quantitative methods allowed quantification of analytes from therapeutic (non-toxic) to very high levels in undiluted samples (ethanol 0.05 up to 4 g/l; salicylates 32 up to 1200 mg/l and acetaminophen 1.9 up to 200 mg/l). The low detection limits of the qualitative tests allowed the recognition of compounds in plasma that were present in low concentrations and/or displayed only minor reactivity with the antibodies provided by the EMIT tox test kits. As a consequence, decision limits for all three group tests in serum were lowered to near the detection limit: (table: see text) For quantitative tests the lower limits of quantification were: (table: see text) The working reagents were stable for at least 14 days at 4-8 degrees C. Calibration curves were stable over the expiration period of reconstituted original reagents (6-12 weeks), also when working reagents were prepared in aliquots from stored reconstituted reagents. Application of the newly adapted programme to serum samples of nearly two hundred patients showed it to be suitable for screening patients in which intoxication is suspected or needs to be excluded.
 ...
PMID:Mechanized toxicological serum tests in screening hospitalized patients. 168 24

In vitro models have shown that metabolites of ethanol (acetaldehyde and lactate) stimulate collagen synthesis, thereby, suggesting that they may be important as fibrogenic mediators. The relevance of these findings for fibrogenesis in the human liver in vivo, however, has not as yet been demonstrated. Serum markers for collagen (PIIINP, using radioimmunoassays employing polyclonal antibodies and Fab-fragments (PIIINP-Fab), respectively) and basement membrane (laminin) metabolism were therefore investigated in 25 alcoholic cirrhotics (Pugh-Score: 6.7 +/- 1.9 S.D.) and in 19 comparable nonalcoholic cirrhotics (Pugh-Score: 6.3 +/- 1.5, n.s.) with only slight evidence for inflammation: GOT 28 +/- 22 vs. 24 +/- 21 U/l; GPT 24 +/- 23 vs. 31 +/- 28 U/l; gamma-globulins 24 +/- 8 vs. 22 +/- 5%, respectively (all n.s.). Severity of the disease was assessed by quantitative liver function tests. Levels of PIIINP, PIIINP-Fab and laminin measured by RIA were 21 +/- 19 micrograms/l, 90 +/- 42 micrograms/l and 2.5 +/- 0.8 U/ml in alcoholic cirrhosis and 10 +/- 6 micrograms/l, 61 +/- 10 micrograms/l and 1.9 +/- 0.4 U/ml in nonalcoholic cirrhosis, respectively (all p less than 0.01). Differences on PIIINP and PIIINP-Fab remained significant even after accurate matching for galactose elimination capacity, aminopyrine breath test and hepatic sorbitol clearance. Laminin levels were higher in alcoholic cirrhosis only after matching for the hepatic sorbitol clearance (p less than 0.01). The higher levels of serum markers for collagen and basement membrane metabolism in alcoholic vs. nonalcoholic patients with cirrhosis at equal severity of the disease and with only minimal signs of inflammation may be the clinical reflection of a specific fibrogenic effect of ethanol metabolites.
 ...
PMID:Higher levels of serum aminoterminal type III procollagen peptide, and laminin in alcoholic than in nonalcoholic cirrhosis of equal severity. 173 19

The inability of the 'ethanol/high vitamin A Lieber-DeCarli diet' to induce liver fibrosis in two different rat strains was further evaluated by determining changes in parameters of liver cell damage and of retinoid and lipid metabolism. In the ethanol/vitamin A-treated group, slight but constant hepatic cell damage, as indicated by elevated alanine aminotransferase, aspartate aminotransferase and glutamate dehydrogenase activities in blood, was already observed at 6 months and maintained until the time of death at 16 months. Serum gamma-glutamyl transaminase activities were not raised. Moderate parenchymal liver cell damage was not accompanied by fibrosis. Hypertriglyceridemia or hypercholesterolemia were observed at 6-16 months of chronic alcohol administration. This response was strain dependent. In ethanol-treated rats of both strains, total liver retinoids and serum retinol concentrations were not altered. Therefore, the hypothesis that interaction between alcohol and retinoids is a major factor in the pathogenesis of alcoholic liver disease, needs to be reconsidered.
 ...
PMID:Chronic administration of ethanol with high vitamin A supplementation in a liquid diet to rats does not cause liver fibrosis. 2. Biochemical observations. 174 28

31P Nuclear magnetic resonance (NMR) spectroscopy and 1H NMR imaging were used to examine the effect of short-term ethanol feeding on the rat testis. Weanling rats were pair-fed for 10 weeks either on ethanol containing liquid diet (36% ethanol of total calories) or a diet in which dextrimaltose was isocalorically substituted for the ethanol of the alcohol-containing diet. In vivo 31P NMR of the testes was used to determine the intratesticular pH and the relative concentrations of various phosphorus-containing metabolites. The integrity of the blood-testes barrier was evaluated using 1H NMR imaging following a gadolinium diethylene tetramine pentaacetic acid derivative (Gd-DTPA) administration as a vascular contrast agent. After the completion of NMR studies, the testis and the liver were freeze-clamped to allow for the assay of their adenosine-5'-triphosphate (ATP) contents. Serum was assayed for its content of aspartate aminotransferase (AST), alanine aminotransferase (ALT), alcohol and testosterone. Ethanol feeding resulted in the following: (a) a reduction in the body weight (p less than 0.05), (b) a reduction in the testicular phosphodiesters (PDE) PDE/ATP ratio (p less than 0.05), (c) an increased change in the testis image intensity difference between pre- and post-iv Gd-DTPA images, (c) a reduction in the testicular and hepatic content of ATP, and (d) increased serum levels of AST and ALT.(ABSTRACT TRUNCATED AT 250 WORDS)
Alcohol Clin Exp Res 1991 Dec
PMID:Effect of short-term ethanol feeding on rat testes as assessed by 31P NMR spectroscopy, 1H NMR imaging, and biochemical methods. 178 76

We examined total cholesterolemia, triglyceridemia, high density lipoproteins- (HDL) cholesterolemia, apolipoproteins A1 and B, body mass index, albuminemia and alanine aminotransferase in 60 heroin addicts. After comparing 23 control subjects with the heroin addicts the result was that the latter have significantly lower mean values of total cholesterolemia and of HDL-cholesterolemia and higher values of triglyceridemia. They also have significantly higher prevalences of cases of hypocholesterolemia and of hypo-HDL-cholesterolemia. Within the addict group there is no linear correlation between total cholesterolemia and body mass index; there is, however, an inverse linear correlation between total cholesterolemia and alanine aminotransferase. Therefore, the alterations found in the lipid pattern of heroin addicts are not due to malnutrition but hypothetically to liver diseases which are frequent in these patients.
Drug Alcohol Depend 1991 Dec 31
PMID:Plasma cholesterol and triglycerides in heroin addicts. 179 28

A study was carried out on 65 male workers heavily exposed to lead in the ceramic tile manufacturing industry in order to assess the effects of alcohol on the biological indicators of lead (PbB, ALA-D, ALA-U, ZPP). All subjects selected for the study had PbB levels greater than or equal to 60 micrograms/dl, normal levels of serum iron and no haemoglobin disorders. The subjects were divided into three groups according to alcohol intake checked by anamnestic investigation, mean corpuscular volume (MCV) values and liver function parameters, as follows: Group A--27 subjects, controls, with daily alcohol intake less than 80 ml, MCV less than or equal to 95 mu 3, normal GGT, AST and ALT levels; Group B--20 subjects, heavy drinkers, with daily alcohol intake greater than or equal to 80 ml, MCV greater than 95 mu 3, occasionally high GGT, but normal AST and ALT values; Group C--18 subjects, heavy drinkers, with daily alcohol intake greater than or equal to 80 ml, MCV greater than 95 mu 3, abnormal GGT, AST and ALT levels. The length of lead exposure did not significantly differ in the three groups. The well-known effects of ethanol intake on PbB, ALA-D and ALA-U values were confirmed, with the following mean values in the three groups: Group A: PbB = 66.0 (micrograms/dl), ALA-D = 10.3 (mU/ml r.c.), ALA-U = 8.4 (mg/l); Group B: PbB = 68.3 (micrograms/dl), ALA-D = 6.7 (mU/ml r.c.), ALA-U = 9.1 (mg/l); Group C: PbB = 71.5 (micrograms/dl), ALA-D = 4.6 (mU/ml r.c.), ALA-U = 12.7 (mg/l).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Influence of alcohol on the behavior of dose and effect indicators in workers exposed to inorganic lead: unexpected behavior of ZPP]. 180 15

Mice consume high levels of alcohol for a short period of time resulting in increased toxicity and lethality. The effects of lower doses that could be consumed without death for prolonged periods were studied. The effects of moderate doses of ethanol on indices of lipid peroxidation (LP), liver lipid accumulation and hepatotoxicity were studied in C57BL/6 mice. Three groups of mice were fed diets in which ethanol provided 0, 25 or 30% of the total calories for 3, 7, 10 and 13 weeks. Increased hepatic cholesterol, phospholipid and triglycerides, indicative of changes in liver lipid metabolism; and increased levels of hepatic malondialdehyde, conjugated dienes, lipid fluorescence, serum alanine aminotransferase and minimal changes in liver architecture indicative of LP and liver damages, were observed in mice fed the alcoholic diets. Such increases were time and dose dependent. These results suggest that continuous ingestion of lower levels of dietary ethanol in mice produces biochemical and hepatotoxic responses which are indicative of the health risk often associated with high alcohol intake.
Alcohol Alcohol 1991
PMID:Effects of prolonged ethanol consumption on hepatic lipids and hepatotoxicity in C57BL/6 female mice. 180 38

Effects of chronic ethanol consumption and one day food deprivation on the hepatotoxicity of low dose carbon tetrachloride (CCl4; 0 to 100 ppm inhalation for eight hours) in rats were investigated by using biochemical and histopathological methods. Liver malondialdehyde (MDA) contents were significantly increased by exposure to 5 ppm to 50 ppm CCl4 in ethanol treated rats or by exposure to 25 ppm to 50 ppm CCl4 in food deprived rats but not in rats without ethanol or food deprivation. The MDA concentrations reached a maximum at 10 ppm and 50 ppm CCl4 in ethanol treated and food deprived rats, respectively, and decreased to the non-exposed concentration at 100 ppm CCl4. At greater than or equal to 50 ppm CCl4 plasma MDA contents increased significantly only in ethanol treated rats. None of the exposure concentrations influenced plasma glutamic-oxaloacetic transamidase (GOT) and glutamic-pyruvic transaminase (GPT) activities in rats that were only exposed to CCl4 whereas exposure to 10 ppm or higher concentrations combined with ethanol increased both activities. To a lesser extent food deprivation combined with exposure to greater than or equal to 25 ppm CCl4 had the same effect. No histopathological changes were found in the liver of rats exposed to less than or equal to 10 ppm CCl4, and only a few ballooned hepatocytes were seen in centrilobular areas when exposure was 25 ppm or higher. The presence of ballooned and hepatocytes became a regular feature of mid-zonal areas in ethanol treated rats and in the centrilobular areas of food deprived rats after exposure to </= 10 and </=25 ppm CC1(4) respectively. Necrotic hepatocytes were seen in centrilobular areas in liver from ethanol treated and food deprived rats when exposure CC1(4) was >/=25 ppm and >/=50 ppm respectively. These results indicate that consumption of ethanol and food deprivation potentiate CCl(4) induced hepatic damage even at low concentrations of CCl(4) by promoting lipid peroxidation. Thus heavy drinking may be a risk factor for CCl(4) induced hepatic damage even though the CCl(4) concentration is as low as the threshold limit value.
 ...
PMID:Ethanol and food deprivation induced enhancement of hepatotoxicity in rats given carbon tetrachloride at low concentration. 191 7

One hundred and three patients presenting to the Mt. Sinai Medical Center emergency department (ED), who appeared on clinical grounds to be acutely intoxicated, were studied to determine the rate of clearance of ethanol from blood. The mean presenting serum ethanol level was 299 mg/dL. The rate of clearance was found to be 20.43 mg/dL/h with a standard deviation of 6.86 mg/dL/h. No correlation was found between rate of ethanol clearance and serum levels of amylase, alkaline phosphatase, glutamate-oxaloacetate or glutamate-pyruvate transaminase, lactic dehydrogenase, or total bilirubin. Similarly, no correlation was found between rate of clearance and race, sex, age, or time of day. We conclude that although the average patient presenting to the emergency department will clear ethanol at about 20 mg/dL/h, a standard deviation of 6 mg/dL/h means that only 83% of these patients will have clearance rates between 8 and 32 mg/dL/h, and that if accurate estimates are necessary, serial determinations of two or more levels are needed.
 ...
PMID:Rate of clearance of ethanol from the blood of intoxicated patients in the emergency department. 143 Sep 89

An electro-neuro-physiological, biochemical and hematological study was carried out in 3 groups of non-symptomatic drinkers: those in group A had a daily alcohol intake of less than 40 grams of alcohol; group B had a daily intake of between 40 and 80 grams of alcohol and those in group C had an intake greater than 80 grams of alcohol per day. The aim of this study was to demonstrate that all the parameters evaluated show quicker alterations when the intake of ethanol is chronic. Electroneuro-physiological parameters were less sensitive than the following indexes: VCM, GGT, GOT, GPT. However, in 50.9% of the patients there were changes in conduction speed, which is an important point to take into account when making a therapeutic decision.
 ...
PMID:[Hematological, biochemical and electroneurophysiological changes in asymptomatic drinkers: a sensitivity study]. 195 76


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>