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)

Nutrient transport rates and cyclic AMP levels have been implicated in the regulation of cell proliferation. In the present study, however, changes in intracellular cyclic AMP level in several lines of cultured cells (normal 3T3 and SV40 and polyomavirus-transformed 3T3 cells; 3T6, C6 GLIOMA, MOUSE L, and Novikoff rat hepatoma cells) by treatment with papaverine, prostaglandine E1 or isoproterenol did not correlate with the inhibition of the uridine, hypoxanthine or deoxyglucose transport rates by these chemicals. Transport inhibitions by above chemicals or Persantin or Cytochalasin B occurred in most cell lines in the absence of any measurable change in intracellular cyclic AMP concentration. Furthermore, treatment of several cell lines with 1 mM dibutyryl cyclic AMP had no immediate effect on the transport of uridine, thymidine or deoxyglucose, although the transport capacity of the cells for uridine and thymidine, but not that for deoxyglucose, decreased progressively with time of treatment. We also observed that the uridine transport system of all cell lines derived from 3T3 cells and the hypoxanthine transport system of L cells exhibited high degrees of resistance to inhibition by the various chemicals. On the other hand, deoxyglucose transport was inhibited to about the same extent by these chemicals in all the cell lines investigated.
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PMID:Cyclic AMP, membrane transport and cell division. I. Effects of various chemicals on cyclic AMP levels and rate of transport of neucleosides, hypoxanthine and deoxyglucose in several lines of cultured cells. 16 72

Studies of glial cells in neural tissue culture systems suggest that glial cells subserve different functions during development and aging of the central nervous system and that they may help modulate the neuronal environment by virtue of their responsiveness to hormones and other intrinsic factors. There is a marked proliferation of glial cells during early stages of brain development, probably reflecting the involvement of glial cells in myelination and other growth processes. Studies in culture suggest that proliferation of glial cells can be induced by steroid hormones. The migration rate of glial cells from cerebellar explants of embryonic chick brain grown in organotypic culture was measured in control and hormone-treated explants. Treatment with cortisol, corticosterone, estradiol, and progesterone significantly elevated glial cell migration from the tissue explants. The influence of steroid hormones on glial cells may be mediated via a steroid intracellular mechanism. In C-6 glioma cells and in chick embryo dissociated brain cell cultures consisting predominantly of glial cells, 3H-corticosterone was shown to accumulate by a saturable but non-specific retention mechanism. In contrast, the accumulation of 3H-corticosterone by predominantly neuronal cultures was both saturable and specific. Glial cells in culture exhibit certain age-related changes, including changes in resting membrane potentials and in cellular responses to hormone treatment, as measured by changes in incorporation of 3H-leucine into protein and incorporation of 3H-uridine into RNA. The possibility that glial cells in vivo may likewise exhibit differential responses to hormones throughout the lifespan suggests that hormones may markedly influence cellular aging.
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PMID:Glial cells: modulators of neuronal environment. 37 65

Thymidine kinase activity in rat C6 glioma cells is inhibited by 50 to 70% after 4 hr incubation with 20 mM D-glucosamine. The inhibition is uncompetitive with respect to thymidine, reducing both the apparent Km and Vmax of the enzyme. The inhibition does not appear to be caused by the reversible combination of the enzyme with a cytoplasmic inhibitor, including D-glucosamine and its metabolites. The addition of D-glucosamine or its metabolites to cell-free thymidine kinase produced an inhibition which differed quantitatively and qualitatively from that which resulted from treatment of intact cells with D-glucosamine. The presence of a reversible cytoplasmic inhibitor of the enzyme was also excluded by mixing experiments. D-Glucosamine inhibited the incorporation of labeled uridine and amino acids into acid-precipitable material. The magnitude of inhibition of thymidine kinase activity and amino acid incorporation by D-glucosamine was comparable to that produced by cycloheximide, suggesting that the inhibition might arise from interference with enzyme synthesis. However, whereas the kinetics of recovery of amino acid incorporation from inhibition was rapid, thymidine kinase activity was depressed for at least 6 hr after drug washout. The results presented are best explained by assuming either that two forms of thymidine kinase are present in rat C6 cells and are differently affected by D-glucosamine or that D-glucosamine acts by two separate mechanisms to inhibit a single form of the enzyme.
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PMID:The inhibition of thymidine kinase in glial tumor cells by an amino sugar, D-glucosamine. 84 39

The amino sugar, D-glucosamine, inhibits the preformed route of thymidine metabolism in rat C6 glioma cells. This inhibition results from a concatenation of several distinct effects, including the inhibition of thymidine uptake, the reduction of thymidine phosphorylation, and an increased leakage of thymidine to the extracellular space. Each of these effects, while ostensibly small in magnitude, is significant and contributes to the observed inhibition of acid-precipitable thymidine incorporation by D-glucosamine. These effects of D-glucosamine, together with its known ability to reduce uridine nucleotide pools, may contribute to its toxicity toward certain experimental animal tumors.
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PMID:The inhibition of thymidine metabolism in tumor cells treated with D-glucosamine. 84 42

The following boron-containing nucleoside and glucose derivatives have been synthesized as potential boron delivery agents for boron neutron capture therapy (BNCT): 2'-O-(o-carboran-1-ylmethyl)uridine (4a), 3'-O-(o-carboran-1-ylmethyl)uridine (4b), sodium 7-(uridin-2'-ylmethyl)dodecahydro-7,8-dicarba-++ +nido-undecaborate (5), 5'-O-(o-carboran-1-ylmethyl)uridine (9), and 3'-O-(o-carboran-1-ylmethyl)-D-glucose (13). In vitro cellular uptake studies were performed with F98 rat glioma cells. Following 16 h incubation, cellular boron concentrations were determined by direct current plasma atomic emission spectroscopy (DCP-AES). Boron concentrations ranged from 65 to 103 micrograms/g of cells for the neutral closo structures compared with 1.5 micrograms/g of cells for the charged nido species. Cellular uptake of sodium mercaptoundecahydro-closo-dodecaborate (BSH), the compound currently being used in Japan for the treatment of malignant brain tumors by BNCT, was 2 micrograms/g of cells.
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PMID:Synthesis and in vitro evaluation of boronated uridine and glucose derivatives for boron neutron capture therapy. 157 91

The purpose of the present study was to examine the distribution pattern of electron-dense acridine orange (AO) chromatin interaction products in rat glioma C6 cells at different phases of the cell cycle. For synchronization in the early S-phase the cells in logarithmic growth were treated with 3 micrograms/ml aphidicolin, a specific inhibitor of DNA polymerase alpha and then cultured in normal medium. For synchronization in the M-phase the cells cultured with aphidicolin and then returned to normal medium were treated with 0.05 micrograms/ml colcemid. Histoautoradiographic analysis of the C6 cells using the pulse chase method demonstrated approximately 16 h of cell cycle time and about 6.5 h of S-phase. Ultracytochemically, AO chromatin interaction products were found in all phases of the cell cycle except for the mitotic phase, namely in G1, S, and G2. The highest percentage of AO chromatin interaction products was observed in the early S-phase and the lowest in the G2 phase. The mean number of AO chromatin interaction products per nuclear area increased in the course of S-phase parallel with an increase of 3H-uridine uptake during the S-phase. The results show a characteristic distribution pattern of AO label specific for each of the four stages of the cell cycle, however, the significance of the coincident RNA synthetic activity remains to be elucidated.
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PMID:Distribution pattern of acridine orange chromatin interaction products in rat glioma C6 cells at different phases of the cell cycle. 169 Apr 12

Isothermal (37 +/- 0.2 degrees C) exposure of glioma cells (LN71) for 2 h to 27 or 2450 MHz continuous-wave radiofrequency (RF) radiation in vitro modulated the rates of DNA and RNA synthesis 1, 3, and 5 days after exposure. The alterations indicate effects on cell proliferation and were not caused by RF-induced cell heating. The dose response for either frequency of the radiation was biphasic. Exposure to specific absorption rates (SARs) of 50 W/kg or less stimulated incorporation rates of tritiated thymidine (3H-TdR) and tritiated uridine (3H-UdR), whereas higher SARs suppressed DNA and RNA synthesis. Statistically significant time-dependent alterations were detected for up to 5 days postexposure, suggesting a kinetic cellular response to RF radiation and the possibility of cumulative effects on cell proliferation. General mechanisms of effects are discussed.
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PMID:Glioma proliferation modulated in vitro by isothermal radiofrequency radiation exposure. 230 Jun 67

Gap junctional intercellular communication (GJIC) as measured by metabolic cooperation was examined in a rat glioma cell line P98F47. X-ray induced mutants of P98F47 cells were grown in 6-thioguanine selective medium (6TG medium) to separate 6TG-resistant HGPRT- mutant cells (6TGr). By co-culturing 200 6TGr cells with varied high densities of the wild type 6TG-sensitive cells (6TGs), it was found that the recovery of 6TGr cells depended on the density of 6TGs cells. Higher densities of 6TGs cells reduced the recovery of 6TGr cells. These results demonstrate the ability of P98F47 cells to perform metabolic cooperation which is indicative of GJIC. When metabolic cooperation was inhibited, increased recovery of 6TGr cells was observed. Presented results also demonstrate metabolic cooperation between P98F47 glioma cells and normal rat glial cells. Effect of tumor promoting chemicals on metabolic cooperation of P98F47 cells was studied. 3H-uridine nucleotide autoradiography technique was used to confirm the above observations. The results suggest that these cells may provide the basis for an in vitro assay specially to study brain tumor promoters and neurotoxins.
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PMID:Gap junctional intercellular communication (GJIC) in rat glioma cells--characterizations to detect inhibitors of metabolic cooperation. 237 72

The existence of insulin receptors and biological responses to insulin on macromolecular synthesis have been studied in C6 glioma cells. Binding of 125I-insulin to C6 glioma cells was specific, time- and PH-dependent. Porcine insulin competed for 125I-insulin binding in a dose-dependent manner. Unlabeled polypeptides, including glucagon, bovine growth hormone, bovine prolactin did not compete for 125I-insulin binding. Scatchard analysis of the binding data gave a curvilinear plot which may indicate negative co-operativity or the existence of both high and low affinity (Ka = 7.55 x 10(10) - 4.25 x 10(9] sites. Incubation of cultures with insulin caused a time and dose-dependent stimulation of DNA, RNA and protein synthesis in C6 glioma cells (measured by 3H-thymidine, 3H-uridine or 3H-leucine incorporation into DNA, RNA, or protein respectively). The increase of macromolecular synthesis was admitted at more than 2 nM concentration of insulin. Maximal stimulation of DNA synthesis (142% of control) occurred 6 hours after incubation with 167 nM insulin. The same concentration of insulin caused a 45% increase in 1 hour on RNA synthesis, a 37% increase in 2 hour on protein synthesis. These results indicate that C6 glioma cells have specific insulin receptors capable of mediating effects of insulin on macromolecular synthesis. Insulin in the brain and even blood may be an important growth factor in the glioma cells of the patients with disrupted blood-brain-barrier.
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PMID:Insulin binds to specific receptors and stimulates macromolecular synthesis in C6 glioma cells. 304 34

This paper studies the influence of uridine on the effects exerted by D-glucosamine in rat C6 glioma cells. 2 mM uridine increased markedly both the cytotoxic effect of the aminosugar and the inhibition of thymidine incorporation into acid-insoluble fraction. Furthermore the complete resumption of the capacity to incorporate either 3H-thymidine or 3H-mannose which was observed after the removal of the aminosugar, was impeded when the cells were treated contemporaneously with D-glucosamine and uridine. An exposure for 4 hr to 20 mM glucosamine alone enhanced about 15-fold the cellular pool of UDP-N-acetylhexosamines; the addition of 2 mM uridine intensified the expansion of this pool, which became about 35-fold the control value. The findings suggest a connection between the accumulation of UDP-N-acetylhexosamines in the cells and the appearance of D-glucosamine cytotoxicity.
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PMID:Uridine enhances the cytotoxic effect of D-glucosamine in rat C6 glioma cells. 378 77


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