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)

In an attempt to elucidate the role of hepatic macrophages in liver injury, we investigated galactosamine-treated rats (500 mg per kg body weight). The rats received an i.v. injection of latex particles (2 x 10(9) particles per animal) prior to (latex-galactosamine) or 12 to 16 hr subsequent to the galactosamine treatment (galactosamine-latex). Effect of superoxide dismutase on hepatic injury induced by galactosamine or galactosamine-latex treatment was also examined. Oxygen-derived free radical-generating capacity of isolated hepatic macrophages was measured as chemiluminescence with the stimulation of phorbol myristate acetate or latex particles. As compared with normal rats, chemiluminescence of hepatic macrophages from galactosamine-treated rats was 5- to 10-fold enhanced 12 hr following galactosamine treatment and remained elevated for 48 hr. Chemiluminescence of the latex particle-pretreated macrophages in the liver was markedly suppressed even following the galactosamine treatment (p less than 0.01). Compared to galactosamine-treated rats, both lipid peroxide level in the liver tissue and AST and ALT concentration in serum were significantly decreased in the latex-galactosamine-treated rats (p less than 0.01) and increased in the galactosamine-latex-treated rats (p less than 0.01). Furthermore, superoxide dismutase supplementation protected against liver injury induced by the galactosamine-latex treatment. From these results, pretreatment with latex particles suppressed the free radical-generating capacity of hepatic macrophages and protected against hepatic injury induced by galactosamine. In contrast, injection of latex particles after galactosamine treatment aggravated hepatic injury, which was prevented by superoxide dismutase. These data suggest that liver injury induced by galactosamine is modulated by oxygen-derived free radicals from hepatic macrophages.
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PMID:Modulation of hepatotoxicity by macrophages in the liver. 283 5

Human polymorphonuclear neutrophils (PMN), when exposed to soluble or particulate stimuli, can destroy various types of cells. The purpose of the present work was to investigate the toxicity of phorbol myristate acetate (PMA)-stimulated PMN against hepatocytes. Neutrophils were incubated in basal conditions or after stimulation by 100 ng/ml PMA in the presence of rat hepatocytes isolated by collagenase digestion. Cytotoxicity was quantified by the percentage of alanine aminotransferase (ALAT) activity released by hepatocytes in the culture medium. Whereas unstimulated PMN had only minor effects, PMA-stimulated PMN induced, after a 16-hour incubation, a 29.5% ALAT activity release at a PMN/hepatocyte ratio of 20/1. At the same ratio, stimulated PMN induced a 1.5% and a 16.6% ALAT activity release at 1 and 4 hours, respectively. At 1 hour, electron microscopy showed intimate contacts between PMN and hepatocytes; hepatocytes appeared morphologically normal. Hepatocytic lesions were moderate at 4 hours and marked at 16 hours. Neutrophil-induced hepatocyte toxicity could not be explained by the production of reactive oxygen intermediates since: (a) hepatocyte toxicity was not prevented by either superoxide dismutase or by catalase; (b) PMN obtained from a subject with chronic granulomatous disease were as toxic as PMN obtained from a normal subject. By contrast, a proteinase-mediated mechanism could be implicated since: (a) the supernatant of stimulated PMN induced a 45.9% ALAT activity release, after 16 hours of incubation; (b) three neutral proteinase inhibitors (i.e., alpha 1-proteinase inhibitor, phenylmethylsulfonylfluoride, soybean trypsin inhibitor) as well as fetal calf serum decreased this toxic effect by 82, 86, 81 and 70%, respectively. These inhibitors had no or minor protective effect on the toxicity of stimulated PMN coincubated with hepatocytes. This could be explained by the existence of intimate contacts between PMN and hepatocytes impeding the action of antiproteinases. Our results suggest that PMA-stimulated PMN can damage hepatocytes through the release of proteinases and that the existence of close contacts between PMN and hepatocytes might play a major role in this toxic effect.
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PMID:Toxicity of phorbol myristate acetate-stimulated polymorphonuclear neutrophils against rat hepatocytes. Demonstration and mechanism. 284 80

The stability and storage characteristics were studied of 11 bovine enzymes of potential clinical significance, namely, aldolase, alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, acetylcholinesterase, creatine kinase, gamma glutamyltransferase, glutathione peroxidase (GSH-Px), alpha-hydroxybutyrate dehydrogenase, lactate dehydrogenase and superoxide dismutase (SOD). Enzyme activities in fresh serum were compared with those in plasma containing various anticoagulants including lithium heparin, EDTA and oxalate/fluoride. The same preservatives were assessed for their effects on the whole blood activities of GSH-Px and SOD. Stabilities of enzymes in plasma and serum stored at room (+20 degrees C), refrigerator (4 degrees C) or deep freeze (-20 degrees C) temperatures were also compared. In addition, SOD and GSH-Px activities in samples stored, at the same temperatures, as whole blood or aqueous lysates were monitored.
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PMID:Stability and storage characteristics of enzymes in cattle blood. 286 28

The stability and storage characteristics were studied of 11 ovine enzymes of potential clinical significance, namely, aldolase, alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, acetylcholinesterase, creatine kinase, gamma glutamyltransferase, glutathione peroxidase (GSH-Px), alpha-hydroxybutyrate dehydrogenase, lactate dehydrogenase and superoxide dismutase (SOD). Enzyme activities in fresh serum were compared with those in plasma containing various anticoagulants including lithium heparin, EDTA and oxalate/fluoride. The same preservatives were assessed for their effects on the whole blood activities of GSH-Px and SOD. Stabilities of enzymes in plasma and serum stored at room (+20 degrees C), refrigerator (4 degrees C) or deep freeze (-20 degrees C) temperatures were also compared. In addition, SOD and GSH-Px activities in samples stored, at the same temperatures, as whole blood or aqueous lysates were monitored. The results are discussed with particular reference to the differences between sheep and cattle.
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PMID:Stability and storage characteristics of enzymes in sheep blood. 286 29

A sample of 465 persons from Eastern Sicily was studied for 11 red-cell enzymes, namely GLO, GPT, EsD, PGP, PGD, Dia, AcP, PGM, SOD, CAI and CAII. The allele frequencies were compared with those of other Italian populations and showed that the island is homogeneous with the mainland for these systems. The rate of heterozygosity was studied as a function of interparental distance; although high (0.77) the correlation did not reach significance.
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PMID:Population structure of eastern Sicily. 302 78

Oxygen free radicals have been implicated in the pathogenesis of postischemic liver injury. High-dose superoxide dismutase (SOD), a radical scavenging enzyme, has been investigated in a rat model of liver ischemia reperfusion by biochemical monitoring. Blood vessels to the median and left lobe were clamped for 1 h and then reperfusion was allowed. The indices used were serial venous blood levels of AST, ALT, calcium, and ATP determination in liver tissue. In SOD-treated animals (7,5000 U i.v.) a significant attenuation of the rise in enzyme levels was observed as well as the absence of the decrease in calcium level in the early phase after reperfusion as compared with control rats, and furthermore ATP restoration was significantly increased.
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PMID:Effect of superoxide dismutase on liver ischemia-reperfusion injury in the rat: a biochemical monitoring. 322 31

The gene frequencies at eight loci in some European and Asian human populations have been subjected to spatial autocorrelation analysis, using Geary's c coefficient. Contrary to what is expected for markers affected only by gene flow and genetic drift, the spatial correlograms show distinct modes of gene frequency variation: there are significant clinal patterns (at the GLO and ESD loci), significant non-clinal patterns (AK, ADA, 6-PGD and GPT) and marginally significant patterns (PGP and SOD). Any hypothesis on the evolution of these polymorphisms should account for the observed heterogeneity of their geographical distributions.
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PMID:Diversity of some gene frequencies in European and Asian populations. III. Spatial correlogram analysis. 348 48

The role of vitamin E and selenium as protective agents against oxidative stress was evaluated by measuring liver chemiluminescence in situ. Weanling rats fed a vitamin E- and selenium-deficient diet showed liver chemiluminescence that was increased 60 and 100% over control values at 16 and 18 days respectively after weaning. At day 21, the double deficiency led to hepatic necrosis, as observed by optical and electron microscopy, and increased serum levels of lactate dehydrogenase and alanine aminotransferase. Single deficiencies, in either vitamin E or selenium, did not produce liver necrosis but increased liver chemiluminescence. Vitamin E deficiency led to a 23 and 50% increase in liver emission at days 18 and 20 respectively; selenium deficiency produced a 64% increase at day 16. The activity of liver selenium-glutathione peroxidase diminished to 13% of the control value in the rats fed doubly deficient and selenium-deficient diets. Activities of superoxide dismutase, catalase and non-selenium-glutathione peroxidase were not modified by the different diets. These results suggest that oxy-radical generation may play a major role in hepatic necrosis in vitamin E- and selenium-deficiency.
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PMID:Effect of vitamin E- and selenium-deficiency on rat liver chemiluminescence. 359 58

Allele frequencies are reported for 19 blood group, red cell enzyme, and serum protein loci (ABO, Rh, MN, Hb-A, LDH-A, LDH-B, SOD, PGM-1, PGM-2, 6PGD, GPT, ESD, ADA, ACP, PGK, MDH, Alb, Hp, and Tf) determined from 310 blood samples collected among the Gainj, a small population of tribal horticulturalists from highland Papua New Guniea. Fourteen of these loci display genetic variants, and ten of them are sufficiently polymorphic to permit a preliminary analysis of Gainj population structure. Patterns of variation among subdivisions of the population are analyzed using an approach analogous to a multivariate analysis of variance with unbalanced design, and weighted genetic distances are extracted from the results. The distance analysis indicates that patterns of genetic variation within this population reflect the geographical distribution of subdivisions, as well as subdivision size and movement among subdivisions. A parallel analysis of the Gainj and two other tribal groups from highland New Guinea, the Murapin Enga and the Simbai Valley Maring, suggests that the Gainj are both genetically divergent from neighboring populations and internally highly differentiated.
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PMID:The genetic demography of the Gainj of Papua New Guinea. I. Local differentiation of blood group, red cell enzyme, and serum protein allele frequencies. 713 24

1. Rainbow trout (Salmo gairdneri) of mean initial weight 15 g were given either a low-manganese or control diet containing 1.3 and 33 mg Mn/kg dry diet respectively. 2. Weight gains over a 24-week feeding period were the same for both groups of trout. 3. Hepatosomatic index, blood packed cell volume and haemoglobin concentration, plasma protein and the activities of aspartic aminotransferase (EC 2.6.1.1) and alanine aminotransferase (EC 2.6.1.2) were unaffected by dietary Mn intake. 4. Plasma potassium and iron levels were increased in the trout given the low-Mn diet. 5. The hepatic levels of magnesium, sodium, K, zinc, copper, Mn and phosphorus were significantly reduced in the fish given the low-Mn diet. 6. In those trout given the low-Mn diet the levels of Mn and calcium in the vertebral ash were significantly reduced. 7. The hepatic activity of Cu-Zu superoxide dismutase (EC 1.15.1.1; Cu-ZnSOD) and of Mn superoxide dismutase (EC1.15.1.1; MnSOD) in cardiac muscle and liver was reduced in the group of trout given the low-Mn diet. The fall in Cu-ZnSOD and MnSOD activities coincided with reduced tissue levels of their respective metal components.
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PMID:The effect of low dietary manganese intake on rainbow trout (Salmo gairdneri). 731 45


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