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:2.6.1.1 (aspartate aminotransferase)
21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The hepatocyte and haematopoietic cell contents of the liver of the foetal guinea pig were measured over the latter half of gestation. Hepatocytes represented about 30% of liver volume at mid-gestation and this increased to 70-80% by term; cell volume remained fairly constant until 5-7 days before term, then more than doubled. Haematopoietic cells represented about 5% of liver volume at mid-gestation and this progressively fell to <1% by term. At 75% of gestation hepatocytes and haematopoietic cells were prepared from perfused foetal livers by collagenase digestion. Enzyme activity of the hepatocyte was, without exception, similar to that of the whole liver. In general, enzyme activity in the haematopoietic cells was similar to that in erythrocytes, with relatively low values for aldolase, glycerol 3-phosphate dehydrogenase, phosphoglycerate mutase, enolase, lactate dehydrogenase, phosphoenolpyruvate carboxykinase, fructose 1,6-bisphosphatase, isocitrate dehydrogenase, ;malic' enzyme, glutamate dehydrogenase and aspartate aminotransferase. The haematopoietic cell contribution to total enzyme activity in the foetal liver was usually much less than 10% and could thus not account for the major changes in hepatic enzyme activity over the latter half of gestation. Hepatocytes contained hexokinase isoenzymes I and III, aldolase isoenzymes A and B and pyruvate kinase isoenzymes 1, 2 and 4. The haematopoietic cells contained hexokinase isoenzyme I and two additional bands of activity with slightly greater mobility, aldolase isoenzyme A and pyruvate kinase isoenzymes 2 and 4.
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PMID:The distribution of enzyme and isoenzyme activities between parenchymal and haematopoietic cells in the liver of the foetal guinea pig. 43 88

Traditional clinical variables of periodontal pathology have only limited value as indicators for future disease progression in patients with adult periodontitis. Consequently, other aspects of the periodontal lesion are being examined for their diagnostic utility. Analysis of the host response in gingival crevicular fluid (GCF) is among the most intensely studied of these new diagnostic approaches. Specific indicators of the humoral immune response, cellular immune response, and acute inflammatory response have been identified in GCF. The relationship of indicators of the humoral immune response to active periodontal disease is equivocal. Specific indicators of the cellular immune response in GCF may ultimately prove to be important diagnostically, but the relationship of any specific marker to active periodontal disease has not been reported. In contrast, the acute inflammatory response in GCF has been extensively studied and a number of factors appear to be associated with an increased risk for future disease progression. Indicators of enhanced polymorphonuclear leukocyte activity, (lysosomal beta-glucuronidase, lysosomal collagenase), prostaglandin E2, and an indicator of acute tissue destruction (the cytoplasmic enzymes aspartate aminotransferase) have been associated with the occurrence of clinical attachment loss. An example of the application of a GCF marker in a periodontitis clinical trial is provided by describing the relationship of lysosomal beta-glucuronidase in GCF at baseline and 2 weeks following root planing and scaling to the occurrence of disease activity during the following 6 months. Persistently elevated levels of this enzyme were related to clinical attachment loss. The positive, negative, and total predictive values for beta-glucuronidase as an identifier of clinical attachment loss were 86%, 71%, and 76%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The host response in gingival crevicular fluid: potential applications in periodontitis clinical trials. 147 31

A study was conducted to investigate morphologic as well as metabolic characteristics of microcarrier-attached hepatocytes in culture, and also to evaluate the effect of intraperitoneal transplantation of the microcarrier-attached hepatocytes on acute hepatic failure in rats induced by D-galactosamine (GalN). Rat hepatocytes were isolated by collagenase perfusion, and cultured on collagen-coated microcarriers. Protein synthesis estimated by [14C] leucine incorporation was four-fold higher in microcarrier culture than in cell suspension. The rates of albumin, transthyretin and bile acid syntheses in hepatocytes cultured on microcarriers were similar to those in monolayer culture. When microcarrier-attached hepatocytes were intraperitoneally transplanted into rats with Galn-induced acute liver failure, a marked improvement in survival rate was observed as compared with control rats which received injections of microcarriers alone (80% vs 0% beyond 6 days of transplantation). Mean serum glutamate oxaloacetate transaminase (SGOT), serum glutamate pyruvate transaminase (SGPT), methionine and glucose levels were similar in both groups, while serum bilirubin and ammonia levels were lower (P less than 0.1, P less than 0.05) in rats transplanted with the microcarrier-attached hepatocytes. Immunohistochemical examinations revealed that the transplanted hepatocytes around microcarriers had albumin synthesis activity, whereas almost no albumin synthesis was demonstrated in recipient liver. In conclusion, intraperitoneal transplantation of the microcarrier-attached hepatocytes will provide sufficient metabolic support, representing detoxication of ammonia (and presumably bilirubin) and synthesis of albumin, to allow GalN-damaged liver function to restore. Microcarrier culture of isolated hepatocytes seems to be one of the most appropriate tools for an artificial liver support.
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PMID:Effects of intraperitoneal transplantation of microcarrier-attached hepatocytes on D-galactosamine-induced acute liver failure in rats. 168 85

During the past few years, a considerable number of studies have examined different aspects of the host response in gingival crevicular fluid (GCF), including the relationship of specific markers to the active phases of periodontal disease. Various indicators of the acute inflammatory response (the lysosomal enzymes beta-glucuronidase and collagenase, the cytoplasmic enzyme aspartate aminotransferase, and the arachidonic acid metabolite PGE2) have been shown to be associated with clinical attachment loss in chronic adult periodontitis in man and experimental periodontitis in animal models. In contrast, the relationship of indicators of the humoral immune response in GCF to active periodontal disease is equivocal. Furthermore, a number of indicators of the cellular immune response have been identified recently in GCF (i.e., Interleukin-1 alpha, IL-1 beta, tumor necrosis factor-alpha), but their relationship to active phases of periodontal disease have not been studied. The polymorphonuclear leukocyte (PMN) is the cellular hallmark of acute inflammation. Evidence from the GCF studies suggests that hyperreactivity of these cells plays a critical role in the active phases of some forms of periodontal disease. Metabolic activation of PMN can be associated with a number of potentially destructive reactions. The major effector mechanism for tissue destruction that can be specifically identified with the PMN is the synergistic effect of the release of PMN proteases and the generation of reactive oxygen metabolites by these cells. Priming of the PMN, where the PMN response is enhanced by agents that do not initiate the response, may be an important mechanism for PMN activation in the crevicular environment; for example, cytokines such as IL-1 beta and TNF-alpha, and lipopolysaccharides released from subgingival Gram-negative bacteria, can serve this function. The hypothesis proposed here argues that in addition to the severe forms of periodontal disease that have been associated with qualitative or quantitative PMN defects, tissue destruction in the periodontum can be observed with hyperreactivity of these cells. These differing conclusions do not create a dilemma, but may represent opposite ends of a balance that is no longer in equilibrium.
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PMID:Host mediators in gingival crevicular fluid: implications for the pathogenesis of periodontal disease. 173 70

Recent studies have shown that Cd-induced testicular interstitial cell (TIC) tumors can be prevented by low-dose Cd pretreatment. However, the mechanism by which low-dose Cd induces such tolerance is unclear. Thus, in this study we assessed the effects of in vivo Cd pretreatment (3 mumol/kg) on Cd uptake, cytotoxicity, metal content (Zn, K, and Ca), and low molecular weight testicular Cd-binding proteins (low Mr TC-BPs) of isolated TICs exposed to Cd in vitro. TICs were isolated by collagenase dispersion of Wistar (WF/NCr) rat testes and incubated with Cd (1.0 mM) for 15 to 60 min. In vivo Cd pretreatment decreased in vitro Cd uptake by 24% after 1 hr of incubation with Cd. In vivo Cd pretreatment also resulted in a marked reduction of in vitro Cd-induced cytotoxicity, as reflected by reduced loss of cellular K, glutamic-oxaloacetic transaminase, as well as reduced lipid peroxidation and decreased Cd-induced Ca influx into TICs in vitro. These cytotoxic effects were not attributed solely to cell death as TIC viability remained high even after 1 hr of in vitro Cd exposure. Cd-induced inhibition of intercellular enzymes, as assessed by cellular lactate dehydrogenase activity, was also reduced by low-dose Cd pretreatment. Cd pretreatment did not alter basal levels of Zn, Ca, or K. Neither low-dose in vivo Cd pretreatment nor in vitro Cd exposure appeared to greatly alter levels of the low Mr TCBPs as assessed by electrophoresis. In vivo Zn pretreatment, which also effectively inhibits Cd-induced testicular tumors, results in a similar reduction in Cd-induced cytotoxicity in TICs. This indicates that treatments which result in reduced Cd-induced TIC tumors are consistently capable of reducing Cd-induced cytotoxicity in isolated TICs in vitro.
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PMID:Effect of in vivo low-dose cadmium pretreatment on the in vitro interactions of cadmium with isolated interstitial cells of the rat testes. 208 10

Primary human hepatocytes were used to study bile salt hepatotoxicity and the hepatoprotective potential of ursodeoxycholate in vitro. Hepatocytes were obtained by collagenase perfusion of healthy human liver tissue and were treated with glycochenodeoxycholate for 24 hr 1 day after plating. Clear signs of cytotoxicity were observed at concentrations of about 100 mumol/L glycochenodeoxycholate. Toxicity was determined by release of alkaline phosphatase, gamma-glutamyl transferase, AST, ALT or lactate dehydrogenase into the culture medium, by measuring DNA synthesis of the cultured liver cells and by testing the viability of the hepatocytes using trypan-blue dye exclusion. Addition of ursodeoxycholate, which by itself proved to be of little toxicity, significantly reduced the hepatotoxic effects of glycochenodeoxycholate: 72% +/- 6% of the cells survived treatment with 500 mumol/L glycochenodeoxycholate alone, but addition of 100 mumol/L ursodeoxycholate increased the survival rate to 87% +/- 4% (p less than 0.05). Moreover, all enzymes tested were secreted at a significantly lower level when ursodeoxycholate was present. Similarly, the cellular DNA synthesis was maintained at significantly higher levels as a result of ursodeoxycholate treatment. We conclude that (a) primary human hepatocytes are a suitable model for studying hepatotoxicity of bile salts in vitro, (b) ursodeoxycholate reduces hepatotoxicity of other bile salts and (c) ursodeoxycholate can act hepatoprotectively by itself (i.e., alteration of the metabolism of other bile salts is not necessarily required).
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PMID:Ursodeoxycholate reduces hepatotoxicity of bile salts in primary human hepatocytes. 240 54

A simple yet effective method (iso-density percoll centrifugation) has been developed for consistently preparing isolated rat liver parenchymal cells with over 98% initial viability. The method has been applied to cells isolated by a variety of collagenase digestion techniques. This procedure involves the low-speed centrifugation (50 X g) of the initial cell suspension through a percoll medium having a density of 1.06 g/ml and results in the separation of single and viable parenchymal cells from cell aggregates, debris, and nonparenchymal cells. The enriched parenchymal cells have been shown to be superior to untreated cells by a number of criteria including: preparation homogeneity, cell morphology, maintenance of cytochrome P-450, hormonal responsiveness (measured by the induction of tyrosine aminotransferase after treatment with glucagon or dexamethasone, or both), plasma membrane integrity (determined by both trypan blue exclusion and leakage of glutamic-oxaloacetic transaminase), and the DNA repair capability after treatment with benzo[a]pyrene or 2-acetylaminofluorene.
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PMID:Use of a low-speed, iso-density percoll centrifugation method to increase the viability of isolated rat hepatocyte preparations. 287 Oct 8

We recently described a preferential reduction of the secretory response to nutrient secretagogues (glucose; leucine plus glutamine) in islets maintained in culture after in vitro exposure to streptozotocin (SZ). The present study is an attempt to further clarify the biochemical mechanisms behind this defective insulin response. Mouse pancreatic islets were collagenase isolated and, after 4-5 days in culture, exposed during 30 min at 37 C to 1.8 mM SZ or vehicle alone (controls). The islets were subsequently cultured for 7 days in medium RPMI 1640 plus 10% calf serum, before the enzymatic and metabolic studies were performed. The activities of the glycolytic enzymes, hexokinase, glucokinase, and glyceraldehyde 3-phosphate dehydrogenase, were similar in the control and SZ-exposed islets. The relative amount of cytosolic and mitochondria-bound hexokinase was also unaffected by SZ. However, there was a 30-40% decrease in the activity of NAD+- and NADP+-dependent glutamate dehydrogenase and glutamate-aspartate transaminase in the SZ-treated islets. This coincided with a 40% decrease in L-[U-14C]glutamine oxidation in the SZ-treated islets. The D-glucose catabolism was further examined in the presence of D-[5-3H] and D-[6-14C] glucose. There was no difference between control and SZ islets in terms of glucose utilization at either 1.7 or 16.7 mM glucose. The oxidation of D-[6-14C]glucose was nevertheless decreased by more than 50% in SZ islets incubated at 16.7 mM (but not 1.7 mM) glucose. Altogether, these converging observations suggest a perturbation of distal regulatory processes, apparently at the mitochondrial level, in the D-glucose and L-glutamine catabolism of SZ-exposed islets. Whether this reflects a primary action of SZ on the islet mitochondria, or an inhibitory effect of SZ on the synthesis of mitochondrial enzymes, as a result of nuclear DNA damage, remains to be elucidated.
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PMID:Defective catabolism of D-glucose and L-glutamine in mouse pancreatic islets maintained in culture after streptozotocin exposure. 296 23

Benzyl chloride (BCl) is used in the manufacture of basic and acidic dyes, pharmaceutical products, resins, and synthetic tannins. BCl is known to have caused liver malfunctions in some workers exposed to 2 ppm BCl vapors. This study was conducted to investigate the effect of BCl on isolated male rat hepatocytes using several toxicity parameters. The hepatocytes were isolated by a collagenase perfusion technique and were incubated in airtight tubes with 1.8 and 3.6 mM BCl in a shaking water bath at 37 degrees C for 10, 30, 60, and 120 min. Throughout the incubation period the cell viability was determined by trypan blue exclusion and leakage of cytosolic enzymes such as lactate dehydrogenase (LDH), aspartate transaminase (AST), and alanine transaminase (ALT). Exposure to BCl resulted in a significant decrease in cell viability as assessed by trypan blue and significant increase in leakage of these enzymes compared to the controls.
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PMID:Effect of benzyl chloride on rat hepatocytes. 319 58

It is becoming increasingly apparent that the traditional clinical criteria are inadequate for: determining active disease sites in periodontitis, monitoring quantitatively the response to therapy or measuring the degree of susceptibility to future breakdown. In an attempt to develop objective measures, a wide variety of studies have been undertaken using saliva, blood, plaque and gingival crevicular fluid (GCF) as the specimen source. Examination has included: specific bacteria and their products; host cells and their products (enzymatic and antibacterial, both immunologic and non-immunologic); products of tissue injury derived from local epithelial and connective tissues and bone. Although most of the work to date has failed to provide reliable aids to the clinician, refinements in techniques for sampling and the availability of more sophisticated analytic techniques give cause for optimism. Methods proposed for detection of disease-associated bacteria in subgingival plaque vary in their sensitivity and specificity. Dark field microscopy shows some correlation with existing disease; however, the limited specificity of this method imposes severe restrictions on its usefulness. Highly specific polyclonal and monoclonal antisera to suspected pathogens Bacteroides gingivalis and Actinobacillus actinomycetemcomitans have been developed and improved methods of identification of these microbes in plaque by ELISA immunofluorescence and flow cytometry are under development. With respect to the host response, a strong correlation between antibody patterns to specific bacteria and periodontal disease categories appears to be emerging. Although most studies have focused on serum antibody derived from peripheral blood, a shift to detection of local antibody response appears to be likely. Techniques of measurement that are exquisitely sensitive have been developed for detection of major immune recognition proteins such as antibody and complement in crevicular fluid. Research efforts attempting to correlate local antibody response to local disease activity are underway. Measurement of GCF flow rate, endotoxin, H2S, butyrate and a variety of enzymes (e.g., collagenase, arylsulfatase, B-glucuronidase) show good correlation with levels of gingivitis. In periodontitis, the most promising markers of tissue breakdown are prostaglandins of the E series, the enzymes collagenase and aspartate aminotransferase, sulfated glycosaminoglycans, osteoclastic activating factor and bone resorptive capacity of crevicular cells. Assay of the migration of crevicular leucocytes in vivo can serve as an indicator of a defect in host resistance.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Indicators of periodontal disease activity: an evaluation. 352 56


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