Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017638 (glioma)
 30,880 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Late passage C-6 glioma cells exhibit astrocytic properties as shown by a characteristic cell morphology and by high levels of the astrocytic cell maker glutamine synthetase (GS). In this study the effects of ethanol (0.2%-1.0% w/v) on the pattern of dibutyryl cyclic AMP (dBcAMP, 1 mM)-induced differentiation were examined using cell number and DNA content as indices for proliferation and cell morphology and GS activity to evaluate differentiation. Differences were observed in the susceptibility of cells to dBcAMP alone, ethanol alone, or simultaneous exposure to both drugs, when cultures were compared at logarithmic and postconfluent phases of growth. Exposure to dBcAMP decreased cell proliferation, induced a characteristic change in cell shape and increased GS activity. In logarithmic phase, simultaneous exposure of cells to ethanol and dBcAMP delayed the dBcAMP-induced change in cell shape and attenuated the mitosis-restricting properties of exposure to dBcAMP. Furthermore, GS activity was greater in dually treated cultures than in cultures treated with dBcAMP alone. We interpret this higher enzyme activity to be the consequence of increased cell-cell contact resulting from larger numbers of cells in the dually treated cultures, coupled with a subsequent dBcAMP-induction of this cytosolic enzyme. In postconfluent cultures, ethanol-exposure did not statistically alter DNA content; whereas GS activity was lower, suggesting that synthesis of GS may be impaired by cellular exposure to ethanol. Furthermore, enzyme activity was also lower in cultures treated with dBcAMP in concert with ethanol than in those treated with dBcAMP alone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Responses in astrocytic C6 glioma cells to ethanol and dibutyryl cyclic AMP. 286 87

The growth stimulating properties of bovine serum and colostrum were compared in rat hepatoma (HTC) and glioma (C6) cell cultures. A colostrum concentration of 2% was optimal for HTC cells, which then reached a terminal density 40% of that in serum-supplemented medium. The corresponding figures for C6 cells were 10 and 81%, respectively. After 4 d in culture, levels of lipid hydroperoxides were measured and compared. Highest levels of lipid hydroperoxides were found in HTC and C6 cells grown in unsupplemented medium. HTC and C6 cells grown in serum supplemented medium contained levels of 52 and 64%, respectively, of that in unsupplemented medium. The corresponding levels for cells grown in presence of colostrum were 40% for HTC and 44% for C6 cells. To obtain information on any functional alterations in the cells due to the presence of colostrum the induction of tyrosine aminotransferase (EC 2.6.1.5) and glutamine synthetase (EC 6.3.1.2) by dexamethasone was studied. Although colostrum seemed to increase the basal activities of the enzymes, no significant effects on the degree of induction could be detected.
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PMID:Lipid peroxidation and activities of tyrosine aminotransferase and glutamine synthetase in hepatoma and glioma cells grown in bovine colostrum-supplemented medium. 287 99

A comparative immunocytochemical study was carried out on intracerebral and extracranial gliomas of the rat produced by intracerebral injection of low (10th) and high (40th) in vitro passages of neoplastic glial cells. The cells injected were a neoplastic astrocytic clone-A15 A5-derived from a mixed glioma induced transplacentally by N-ethyl-N-nitrosourea (ENU) in a BD-IX rat. An inverse relationship was seen between the expression of the astrocytic markers glial fibrillary acidic protein (GFAP) and glutamine synthetase (GS) at low and high passage: GFAP decreased with increasing passage while GS increased. The distribution of vimentin, the major cytoskeletal component of immature glia, was constant, irrespective of passage--a feature consistent with previous in vitro findings. The expression of laminin by both reactive and neoplastic astrocytes increased with increasing passage, while high magnification examination revealed the presence of the glycoprotein fibronectin on the cell-surfaces of A15 A5-derived tumour cells. Both neoplastic and reactive astrocytes expressed S-100 protein with a higher proportion of positive cells in extracranial tumours. Occasional cells, probably actively phagocytizing populations of reactive astrocytes and macrophages, were positive for alpha-1-antitrypsin. None of the neoplastic cells expressed the oligodendrocyte marker carbonic anhydrase II. This immunocytochemical study supports previous morphological findings in differences in differentiation between the cells of tumours produced by high and low passage cells.
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PMID:Immunocytochemical characterization of the A15 A5 transplantable brain tumour model in vivo. 287 14

The four permanent human glioma-derived cell lines reported here are the first such lines for which the karyotypes have been followed from the original biopsies through the establishment of the lines in culture. Although ploidy changes were seen, each line retained either distinctive marker chromosomes or the overall original chromosomal distribution allowing the origin of each line to be established with certainty. D-263 MG expresses glial fibrillary acidic protein, all lines except D-245 MG are tumorigenic in athymic mice, and each line displays a unique pattern with respect to in vitro growth parameters and expression of biochemically defined markers, oncofetal antigens and lymphoid-associated markers. D-245 MG and D-259 MG are able to grow in the absence of supplemental glutamine; glutamine synthetase was detected in these cell lines both by immunocytochemistry and by direct assay. Thus, the four permanent human glioma-derived cell lines described here are representative of glioma lines in their general characteristics. D-259 MG retains numerous double minute chromosomes (DMs), D-263 MG contains two marker chromosomes with breaks in 9p, and D-247 MG and D-245 MG with stemlines containing 96 and 89 chromosomes contain eight and six normal copies (respectively) of chromosome No. 7. The retention in these four cell lines of the most common chromosomal abnormalities seen in biopsies of malignant human gliomas provides the opportunity to investigate the meaning of these specific chromosomal changes.
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PMID:Specific chromosomal abnormalities characterize four established cell lines derived from malignant human gliomas. 288 26

Lead has been demonstrated to induce precocious glial differentiation both in vitro and in vivo. Lead-treated rat glioma (C6) and cerebellar astrocytes exhibited cytoplasmic extensions and the presence of glial endfeet after a 3-day exposure to 10(-6) to 10(-4) M PbCl2. In similar experiments no effect was noted in neuroblastoma (Neuro-2a) or on neurite outgrowth from chick spinal cord explants. This prodifferentiative effect on glia was also seen in the cerebella of postnatal rats in which the developmental expression of glial-specific glutamine synthetase activity was significantly increased up to postnatal day 12 after chronic exposure to lead from time of birth via their dam's drinking water (400 mg PbCl2/l).
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PMID:Chronic low level lead exposure precociously induces rat glial development in vitro and in vivo. 289 24

Regulation of the biosynthesis of glutamine synthetase was studied in neuroblastoma cells (Neuro-2A) by use of a recently developed, sensitive radioisotopic assay. The removal of glutamine from the culture medium of these cells for 24 h resulted in a 10-fold increase in glutamine synthetase specific activity (15-fold after 2 weeks) compared with the basal level found in cells grown in the presence of 2 mM glutamine. Following the growth of these cells for 2 weeks in the presence of various concentrations of glutamine, a negative linear correlation was observed between the specific activity of glutamine synthetase (from 1.7 to 0.14 unit/mg) and the concentration of glutamine in the growth medium (from 0.5 to 2 mM). Cycloheximide or actinomycin D blocked the increase in glutamine synthetase activity observed in the absence of glutamine. These results suggest that the removal of glutamine led to the induction of glutamine synthetase by stimulating new enzyme synthesis. The enzyme was not degraded, but only diluted, by growth upon readdition of glutamine to the medium. The influence of glutamine depletion is also reported for C-6 glioma cells and glial cells in primary cultures.
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PMID:Derepression of the glutamine synthetase in neuroblastoma cells at low concentrations of glutamine. 612 53

Glutamine synthetase was found to be increased in C-6 glioma cells as a result of increasing culture passage and N-6,2'-O-dibutyryl cyclic AMP (dbcAMP) treatment. At low passage dbcAMP produced a 2.5-fold increase in glutamine synthetase activity per unit of cellular protein. At high passage control glutamine synthetase was approximately double that seen at low passage, but dbcAMP produced an additional 65% increase. Lactate dehydrogenase activity was also increased by dbcAMP treatment at both low and high passage, but culture passage produced no change in the lactate dehydrogenase. With increasing culture passage, the ratio of cellular protein to DNA doubled. Therefore, expression of data per unit of protein tended to minimize the apparent changes in activity. The maximum increase in glutamine synthetase activity produced by both dbcAMP and increasing culture passage and expressed on a DNA basis was 5.6-fold. The increase in glutamine synthetase activity was generally linear during the first 20 h of drug treatment, after which enzyme activity remained nearly constant up to 72 h. Ninety percent or more of the dbcAMP remained in the medium at the end of 48-h exposure of cells to dbcAMP. 8-br-Cyclic AMP also increased glutamine synthetase activity of C-6-cels, but n-butyrate did not. Isoproterenol, which increases cyclic AMP in C-6-cells, increased glutamine synthetase activity. The effect of isoproterenol on glutamine synthetase was inhibited by the beta-adrenergic blocking agent sotalol. Cycloheximide (10 micrograms/ml) inhibited the dbcAMP effect on glutamine synthetase activity and also decreased the control enzyme activity by 60%.
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PMID:Induction of glutamine synthetase by dibutyryl cyclic AMP in C-6 glioma cells. 612 56

Cytotoxic effects of L-glutamate and related compounds were investigated on rat glioma C6 cells in vitro. Within 12-24 h, addition of glutamate to the culture medium, resulted in degeneration of the C6 cells. The ED50 for glutamate-induced damage was about 4 mM. Seventeen structural analogues of glutamate, including agonists and antagonists for glutamate receptors as well as glutamate-uptake inhibitor, were examined concerning their toxicity on C6 cells. Among them, L-aminoadipic acid, DL-aminopimelic acid, DL-homocysteic acid, L-cysteic acid, quisqualic acid, L-glutamic acid diethyl ester and 2-amino-4-phosphonobutyric acid elicited similar degeneration at comparable concentrations. The D-isomer of glutamate was not cytotoxic. Following differentiation of C6 cells with 1 mM dibutyryl cyclic AMP or 3 mM sodium butyrate, they were no longer susceptible to L-glutamate and L-aminoadipate. C6 cells treated with 10 microM hydrocortisone, which is known to induce glutamine synthetase activity, were also resistant to L-glutamate, but not to L-aminoadipate. The decomposition of cellular DNA in glutamate-treated cultures was confirmed by flow cytometer analysis. The results demonstrate that the sensitivity of C6 cells to glutamate-induced cytotoxicity was modified by cellular metabolic conditions. This indicates that cultured glioma C6 cells are a useful model system to investigate the molecular mechanism of glutamate gliotoxicity in vitro.
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PMID:Sensitive and insensitive states of cultured glioma cells to glutamate damage. 614 80

The phenotypic expression of cells derived from human anaplastic astrocytomas, rat glioma, normal human adult and foetal brain tissue have been examined for differentiated and malignancy-associated properties. Glial fibrillary acidic protein (GFAP), high affinity glutamate and gamma-amino butyric acid (GABA) uptake and glutamine synthetase were used as indicators of astroglial differentiation. Plasminogen activator and tumour angiogenesis factor were the malignancy-associated markers. The normal adult brain-derived lines showed some differentiated astroglial features and expressed low levels of the malignancy-associated properties. The foetal cultures contained highly differentiated astroglia while the glioma lines showed considerable phenotypic heterogeneity from highly differentiated to undifferentiated. The least differentiated glioma cells exhibited the highest plasminogen activator activities. The density-dependent control of phenotypic expression was also investigated. High affinity GABA uptake, and GFAP in rat C6 glioma cultures, increased with increasing monolayer cell density, events probably mediated by an increase in the formation of cell-cell contacts at confluence. Plasminogen activator activity decreased with increasing cell density.
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PMID:Interrelationship between differentiation and malignancy-associated properties in glioma. 620 Jan 30

A study was made of the effect of opioid peptides, (Leu)-enkephalin and its synthetic analog dalargin, on the maturation speed (differentiation) and proliferation activity of glioma C-6 cells. This effect on phenotypes of glioma C-6 cells was determined using some biochemical parameters: changes in the activity of glutamine synthetase (astrocytic marker) and cyclic nucleotide phosphorohydrolase (oligodendrocytic marker) in the culture of glioma C-6 cells in the early and late passages. The biochemical analysis was made at the Laboratory in Denver, USA, and we thank Prof. A. Vernadakis for the possibility to carry out a part of this work that helped us to find the growth activity of opioid peptides on the C-6 cells. Proliferation was examined in cultivation conditions approximately conforming the conditions of cultivation for the primary glial cell cultures. The control proliferation level was high in this case. It is demonstrated that opioid peptides accelerate (or strengthen) the expression of phenotypic signs in C-6 glioma cells in early and late passages changing specific activity of the marker enzymes, i.e. operating as a growth factor. Opioid peptides show glial growth factor characteristics on the glioma C-6 glial cell model as well, for glioma C-6 is known to be a perfect model to analyse the action of different substances on the glia.
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PMID:[The effect of opioid peptides on a decreased proliferation and on an increased maturation rate of glioma C-6 cells manifested by enhanced marker enzyme activity]. 770 17


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