Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.6.1.1 (aspartate aminotransferase)
21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This report is the first in a series about a large multidisciplinary study designed to determine whether chronic marijuana (MJ) smoke exposure results in residual behavioral and/or neuropathological alterations in the rhesus monkey. Prior to the initiation of a year of chronic MJ smoke exposure, 64 periadolescent male rhesus monkeys were trained for 1 year to perform five operant behavioral tasks and then divided, according to their performance in these tasks, into four exposure groups (n = 15-16/group): (1) a high dose (HI) group, exposed 7 days/week to the smoke of one standard MJ cigarette; (2) a low dose (LO) group, exposed on weekend days only to the smoke of a standard MJ cigarette; (3) an extracted MJ cigarette (EX) group, exposed 7 days/week to the smoke of one ethanol-extracted MJ cigarette; and (4) a sham group (SH), exposed 7 days/week to sham exposure conditions. Daily exposures for 1 year were accomplished using a mask that covered the subjects' nose and mouth. Average body weights (initially 3.7 +/- 0.5 kg, mean +/- SD) and rates of weight gain (approximately 0.1 kg/month) were the same for all groups throughout the entire experiment. During the first week of exposure, plasma concentrations of delta-9-tetrahydrocannabinol and 11-nor-9-carboxy-THC in the HI group were 59 +/- 7 (mean +/- SE) and 5.5 +/- 1.5 ng/ml, respectively, 45 min after MJ smoke administration and did not change significantly at similar times after exposure throughout the remainder of the year. Whole blood carboxyhemoglobin levels increased to approximately 13% 1 min after exposure to smoke in either the MJ or the EX groups. Comparison of blood chemistry and hematology values before, during, and after exposure indicated no differences for most parameters. During exposure, lymphocytes, alkaline phosphatase and gamma-glutamyl transferase were depressed in the HI group compared to in the SH group. During exposure, aspartate aminotransferase was elevated for both the HI and EX groups, suggesting a general effect of smoke exposure. Because these effects were transient and remained within the range of reported normal values, these data indicate that long-term, experimental exposure to MJ smoke is feasible and does not compromise the general health of the rhesus monkey.
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PMID:Chronic marijuana smoke exposure in the rhesus monkey. I. Plasma cannabinoid and blood carboxyhemoglobin concentrations and clinical chemistry parameters. 168 42

(1) Liver cirrhosis was induced in male rats by treatment with carbon tetrachloride and phenobarbitone for 130-142 days. Detailed histological examination showed all livers from rats treated with carbon tetrachloride had annular fibrosis, necrosis, loss of normal hepatic architecture and other features that were consistent with an established micronodular cirrhosis. (2) Plasma biochemical analysis showed a significant reduction in total protein concentration (13%), which was due entirely to a reduction in plasma albumin (29%). There were also large increases in the plasma activities of alkaline phosphatase (110%) and aspartate aminotransferase (159%), when compared to phenobarbitone-treated controls. Plasma cholesterol was also increased (67%), but other plasma analytes were not significantly altered. (3) The soleus (Type I), plantaris (Type II) and gastrocnemius (Types I and II) muscles were dissected and examined for possible differential effects. There were minor reductions in all three muscle weights, but these changes did not reach statistical significance. The protein, RNA and DNA concentrations, total muscle content and content relative to body weight in cirrhotic rats were also not significantly altered in any of the muscles. Cirrhosis did not cause any perturbations in derived parameters, i.e. amount of synthetic apparatus per cell, RNA/DNA ratio, apparent cell size, protein/DNA ratio and the capacity for protein synthesis or RNA/protein ratio. (4) The gastrocnemius was fractionated into soluble, stromal and myofibrillar proteins. The concentrations and contents of all three proteins were unaltered in cirrhotic animals, compared to controls. (5) It is concluded that in this experimental model of cirrhosis there were no effects on those skeletal muscle variables which are strikingly altered by chronic alcohol feeding.(ABSTRACT TRUNCATED AT 250 WORDS)
Alcohol Alcohol 1990
PMID:Liver histology, blood biochemistry and RNA, DNA and subcellular protein composition of various skeletal muscles of rats with experimental cirrhosis: implications for alcoholic muscle disease. 170 23

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.
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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

Homogeneous aspartate aminotransferase (purity--99%, yield--70%) has been prepared from chicken heart cytosol. The purification procedure included fractionation with ammonium sulfate and ethanol and crystallization. Crystals (0.3 x 0.5 x 2 mm) of the free enzyme were prepared from ammonium sulfate solution and studied by X-ray analysis at 2.5 A resolution.
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PMID:[Crystallization of free aspartate aminotransferase from chicken heart cytosol]. 178 67

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

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)
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PMID:[Influence of alcohol on the behavior of dose and effect indicators in workers exposed to inorganic lead: unexpected behavior of ZPP]. 180 15

Serum beta-hexosaminidase (Hex) isoenzymes analyzed by enzyme immunoassay were investigated in a group of alcoholics (n = 38) hospitalized for detoxication, in another group of alcoholics (n = 22) abstinent between 6 days and 10 years and in a reference group (n = 20). Hex "B" isoenzyme was elevated in all 38 patients hospitalized for detoxication but only 35 of these had total Hex values above the upper limit of the reference group. The Hex A isoenzyme, gamma-glutamyltransferase, and aspartate aminotransferase showed considerable overlap between these patients and the reference group. In the group of 22 abstinent patients only one had an increased level of Hex A, Hex "B," and total Hex, whereas 10 had gamma-glutamyltransferase values above the upper limit of the reference group. It is concluded that Hex "B" is a useful marker for alcohol abuse.
Alcohol Clin Exp Res 1991 Jun
PMID:Serum beta-hexosaminidase isoenzyme: a sensitive marker for alcohol abuse. 183 3

To study the effects of ethanol on the hepatotoxicity of N-nitrosodimethylamine (NDMA), 5 mg NDMA/kg body weight was injected intraperitoneally 3 times a week for 6 weeks into rats pair-fed liquid diets containing 36% of energy either as ethanol or as additional carbohydrates. Another group of rats was pair-fed with the same diets but injected with saline instead of NDMA. Co-administration of ethanol and NDMA produced much higher elevations of serum alanine and aspartate aminotransferase and glutamic dehydrogenase activities than the administration of either agent alone. The combined treatment also slightly increased focal necrosis, whereas other liver lesions (steatosis and fibrosis) and the functional impairment of mitochondrial respiration were not affected significantly. Microsomal low Km NDMA demethylation, as well as NDMA denitrosation, were inhibited markedly by incubation with an antibody against P450IIE1, suggesting the involvement of this alcohol-inducible P450 in both NDMA bioactivation reactions. The addition of ethanol inhibited P450-dependent demethylation and denitrosation of NDMA in liver microsomes, whereas both activities were enhanced markedly by chronic ethanol administration. At ethanol concentrations similar to those prevailing in the blood of alcohol-fed animals at the time of NDMA administration, hepatic microsomal demethylation and denitrosation remained significantly higher in ethanol-fed rats given NDMA than in controls. Our results suggest that bioactivation plays a critical role in the hepatotoxicity of NDMA and its aggravation by chronic alcohol consumption.
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PMID:Effects of ethanol consumption on bioactivation and hepatotoxicity of N-nitrosodimethylamine in rats. 185 64

The effects of moderate alcohol intake on serum (SHEX)- and urinary beta-hexosaminidase (UHEX) were studied in ten healthy volunteers, who ingested 60 g of 100% ethanol daily for 10 days. The drinking period was preceded and followed by an abstinence period. Moderate drinking and abstinence were rapidly and significantly reflected on SHEX, while UHEX levels did not change significantly during the study. Gramma-glutamyl transpeptidase (GGT), aspartate aminotransferase (ASAT) and alanine aminotransferase (ALAT) decreased during the first abstinence period (P less than 0.05), but stayed thereafter at a constant level. It is concluded that SHEX may better reflect recent alcohol consumption than UHEX, GGT, ASAT or ALAT.
Drug Alcohol Depend 1990 Feb
PMID:The effects of moderate drinking and abstinence on serum and urinary beta-hexosaminidase levels. 196 91

We report here the use of the biochemical marker desialylated transferrin to aid in the diagnosis of nonalcoholic steatohepatitis. Conventional biochemical tests used for the detection of chronic alcohol consumption fail to differentiate nonalcoholic steatohepatitis patients from alcoholic subjects. In addition, even in those alcoholic subjects with alcoholic liver disease in whom biopsy has been performed, it is impossible to differentiate these two disease states on the basis of morphological examination alone. In this study we have examined two new markers of excessive alcohol intake, desialylated transferrin and mitochondrial AST in subjects with nonalcoholic steatohepatitis and in patients consuming excessive amounts of alcohol. All nonalcoholic steatohepatitis patients consumed minimal or no alcohol and were diagnosed by morphological criteria based on liver biopsy specimens. Alcoholic subjects were consuming in excess of 80 gm/day ethanol, often with clinical evidence of overt alcoholism. Control subjects included both healthy controls and patient controls with liver diseases unrelated to alcohol. The ratio of desialylated transferrin/total transferrin was elevated only in patients who consumed excessive amounts of alcohol, whereas the ratio of mitochondrial AST to total AST (mitochondrial AST/total AST) was not significantly different between alcoholic subjects and patients with nonalcoholic steatohepatitis. The sensitivity and specificity for the ratio desialylated transferrin/total transferrin was 81% and 98%, respectively, whereas the sensitivity for the mitochondrial AST/total AST ratio was 92%; the specificity was only 50%, indicating that there were a large number of false-positives. All the conventional markers were less sensitive and less specific than the ratio desialylated transferrin/total transferrin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Markers of chronic alcohol ingestion in patients with nonalcoholic steatohepatitis: an aid to diagnosis. 199 16


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