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)

Several aspects of the regulation of the pentose phosphate pathway were examined in cultured normal human cortical astrocytes and gliomas of pathological grades I-IV. The generation of radiolabeled CO2 from [1-14C]glucose by the oxidative arm of the pentose phosphate pathway is a saturable process and has a maximum flux rate of 8-9 nmol/hr/mg cell protein. The flux can be blocked by the glycolytic inhibitor iodoacetamide but is unaffected by agents which inhibit oxidative phosphorylation. The magnitude of the pentose phosphate flux is directly related to the glioma grade. Grade IV gliomas (glioblastoma) show a pentose phosphate flux rate of approximately 4% of the total glucose flux. The flux rate can be increased by pharmacological agents which decrease the NADPH/NADP+ ratio. Both the activity and the regulation of glioma glucose-6-phosphate dehydrogenase (G6PDH) are altered in high-grade gliomas. While the affinity constants for cofactors in whole homogenates were not significantly different in glioma or normal astrocyte homogenates, normal astrocytes have a lower Km for glucose-6-phosphate and a G6PDH activity which is 10-fold greater than that of gliomas. NADPH is a powerful regulator of G6PDH activity in the normal astrocytes and in gliomas. At a NADPH/NADP+ ratio of 7:1 the normal astrocyte G6PDH is entirely inhibited, while the glioma enzyme is only 70% inhibited even at a ratio of 20:1. Increased metabolic flux through the oxidative arm of the pentose phosphate pathway is apparently due to an altered form of G6PDH.
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PMID:Regulation of the pentose phosphate pathway in human astrocytes and gliomas. 350 33

S-100 protein is a highly acidic protein unique to the nervous system and exists predominantly in the cytoplasm of glial cells in a water-soluble form. The exact biological function is still unknown in spite of its well-known biochemical properties. Some investigators have reported that the amount of S-100 protein in developing brains increased in proportion to the brain's development and differentiation. In order to clarify the relationship between S-100 protein and differentiation of glial cells the changes of DNA synthesis and the amount of the water-soluble S-100 protein were investigated on cultured rat glioma (C-6) cells in the course of the morphological differentiation induced by dibutyryl cyclic AMP (dbc-AMP). C-6 cells were cultured in Eagle's minimum essential medium supplemented with 10% fetal calf serum and incubated in a humidified atmosphere of 5% CO2-95% room air at 37 degrees C. Dbc-AMP was added to the media at the concentration of 1 mM, and the media were changed every 48 hrs. A flow cytometric analysis of DNA histogram patterns was performed to investigate the changes of DNA synthesis using a Cytofluorograf FC 4800 A-50 (Bio/Physics). The changes of the amount of S-100 protein were examined by micro-complement fixation assay as described by Levine using rabbit antisera against bovine S-100 protein. Dbc-AMP inhibited the growth of C-6 cells remarkably and induced morphological changes resembling normal astrocytes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Changes of the DNA synthesis and the amount of S-100 protein associated with the morphological differentiation of cultured glioma cells]. 632 50

In 27 pentobarbital-anesthetized cats cerebral blood flow and regulation of cerebral blood flow was measured one to 3 weeks following stereotactical xenotransplantation of a rat glioma clone into the internal capsula. Tumor growth was accompanied by severe vasogenic peritumoral edema in the white matter of the tumor-bearing hemisphere. White matter water content in the vicinity of the tumor increased from 69.1 +/- 0.9 to 0.5 +/- 0.7 ml/100 g wet weight (means +/- SE) which corresponds to an increase in tissue volume of about 60%. Intracranial pressure after 3 weeks was 12 +/- 2.6 mm Hg. Blood flow in the peritumoral white matter decreased from 32.2 +/- 5.6 to 18.6 +/- 1.9 ml/100/g/min but it did not change in the peritumoral grey matter or the opposite hemisphere. The decrease in blood flow was due to the volume expansion of the swollen edematous tissue and not to a compression of the microcirculation because neither flow nor vascular resistance changed when referred to dry rather than to wet weight of the edematous tissue. Flow regulation in the peritumoral edematous white matter was disturbed. CO2 reactivity of blood flow was 5.4% mm Hg change in aPCO2 (non-edematous contralateral white matter 6.4%/mm Hg), and the autoregulatory capacity between 40 and 170 mm Hg was 0.7%/mm Hg (non-edematous white matter 1.0% mm Hg). It is concluded that in the absence of significant intracranial hypertension, even severe degrees of vasogenic peritumoral edema do not interfere with blood flow and flow regulation. This is in contrast to the cytotoxic type of edema, and indicates that microcirculatory compression by edema, when present, is the consequence of pericapillary glial hydrops and not of an accumulation of extravasated edema fluid.
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PMID:Blood flow and regulation of blood flow in experimental peritumoral edema. 723 66

Some reports have demonstrated that selenium can inhibit tumorigenesis in some tissues of animal. However, little is known about the inhibitory effect on malignant tumor cells of brain. The purpose of our study was to determine the biological effect of selenium on growth of rat glioma and human glioblastoma cell lines. Cell lines C6 and A172 were obtained from Japanese Cancer Research Resources Bank, Tokyo, Japan (JCRB). Cells were cultured in Dulbecco's Modified Eagle's Medium (DMEM) supplemented with 10% fetal calf serum at 37 degrees C in a humidified atmosphere of air and 5% CO2. Antiproliferative effects of selenium were evaluated using growth rate assay quantifying cell number by MTT assay. An antiproliferative effect of selenium was found in two cell lines, which was more effective on human A172 glioblastoma and less effective on rat C6 glioma.
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PMID:Effect of selenium on malignant tumor cells of brain. 757 18

We used the pH-sensitive fluorescent dye BCECF to study intracellular pH (pHi) regulation in primary cultures of rat astrocytes and C6 glioma cells. Both cell types contain three pH-regulating transporters: 1) alkalinizing Na+/H+ exchange; 2) alkalinizing Na+ + HCO3-/Cl- exchange; and 3) acidifying Cl-/HCO3- exchange. Na+/H+ exchange was most evident in the absence of CO2; recovery from acidification was Na+ dependent and amiloride sensitive. Exposure to CO2 caused a cell alkalinization that was inhibited by DIDS, dependent on external Na+, and inhibited 75% in the absence of Cl- (thus mediated by Na+ + HCO3-/Cl- exchange). When pHi was increased above the normal steady-state pHi, a DIDS-inhibitable and Na(+)-independent acidifying recovery was evident, indicating the presence of Cl-/HCO3- exchange. Astrocytes, but not C6 cells, contain a fourth pH-regulating transporter, Na(+)-HCO3- cotransport; in the presence of CO2, depolarization caused an alkalinization of 0.12 +/- 0.01 (n = 8) and increased the rate of CO2-induced alkalinization from 0.23 +/- 0.02 to 0.42 +/- 0.03 pH unit/min. Since C6 cells lack the Na(+)-HCO3- cotransporter, they are an inferior model of pHi regulation in glia. Our results differ from previous observations in glia in that: 1) Na+/H+ exchange was entirely inhibited by amiloride; 2) Na+ + HCO3-/Cl- exchange was present and largely responsible for CO2-induced alkalinization; 3) Cl-/HCO3- exchange was only active at pHi values above steady state; and 4) depolarization-induced alkalinization of astrocytes was seen only in the presence of CO2.
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PMID:Intracellular pH regulation in primary rat astrocytes and C6 glioma cells. 785 88

The isotopically substituted molecule (6-13C, 1, 6, 6-2H3)glucose was evaluated to determine whether metabolic 2H loss would prevent its use in quantitating pentose phosphate pathway (PPP) activity. PPP activity causes the C1 of glucose to be lost as CO2, while C6 can appear in lactate. 2H NMR analysis of the lactate produced from this glucose can distinguish (3-2H)-lactate (from C1 of glucose) from (3-13C, 3, 3-2H2)lactate (from C6 of glucose). 2H NMR spectroscopic analysis of medium containing (6-13C, 1, 6, 6-2H3)glucose after incubation with cultured rat 9L glioma cells suggested a 30.8 +/- 2.1% PPP activity as compared with 6.0 +/- 0.8% from separate, parallel incubations with (1-13C)glucose and (6-13C)glucose. Subsequent experiments with other isotopically labeled glucose molecules suggest that this discrepancy is due to selective loss of 2H from the C1 position of glucose, catalyzed by phosphomannose isomerase. Failure to consider 2H exchange from the C1 and C6 positions of glucose can lead to incorrect conclusions in metabolic studies utilizing this and other deuterated or tritiated glucose molecules.
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PMID:Metabolic loss of deuterium from isotopically labeled glucose. 798 74

Recently, interest has grown in the area of low-power laser effects upon tissues. We used a 51Cr cell labeling technique with glioma tissue to better understand these effects. Canine 2C5 gliosarcoma cells with intracellular 51Cr were exposed to CO2 laser in the range of 0.2 to 3.0 J/cm2. Correlative analysis of the data indicated that there is a strong direct relationship between laser fluence and the percent of total intracellular 51Cr released from the glioma cells with a coefficient of correlation (r) of +0.93. The calculated standard error of the correlation coefficient was +/- 0.06 and the coefficient of determination (r2) was 0.86. These results indicate that the 51Cr cell labeling technique is a useful method for quantifying the low-power laser effects on the integrity of the cell membrane of gliosarcoma cells in vitro. However, further investigation is needed to clarify the specific mechanisms by which the CO2 laser induces changes upon these cells.
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PMID:Low-level CO2 laser-induced release of 51chromium from canine 2C5 gliosarcoma cells. 826 21

The feline infusion model of brain edema was used to evaluate the pathophysiological effects of 0.6 ml infusions of autologous serum protein (66%), human serum protein (66%), human glioma cyst fluid and a tissue culture medium (TCM) on the structure and function of the forebrain white matter. These infusions increased local white matter water content by between 10.8 and 12.5 ml/100 g brain and were associated with moderate increases in ICP and CSF outflow resistance and a significant decrease in lumped craniospinal compliance. Cortical somatosensory potentials, motor evoked potentials, EEG and local cerebral blood flow (rCBF) at normocapnia were generally unchanged by the various infusions. All infusates except the 66% autologous serum protein infusion impaired rCBF CO2 reactivity. Histologically all infusates caused marked extracellular edema. The autologous serum protein infusion caused no additional histological changes whereas the glioma cyst infusates caused profound endothelial and astrocytic swelling, focal endothelial necrosis, basement membrane disruption, perivascular microglial reaction and pavementation and perivascular migration of polymorphonuclear leukocytes. Similar but less marked changes were seen after infusion of human serum protein whilst the TCM produced only minimal changes. The intensity and extent of Evans Blue extravasation into the forebrain white matter was greatest with glioma cyst infusates and with all infusions reflected the extent to microvascular changes. These studies show that products derived from gliomas cause additional damage to the blood-brain-barrier than that caused by non-autologous serum proteins. These results add further support for the existence of glioma derived permeability factors (GDPF), but suggest neither serum proteins nor glioma derived compounds in the white matter interstitium significantly influence local electrophysiological function. Some limitations of the infusion edema model when using non-autologous infusions and difficulties quantitating brain dysfunction are emphasised.
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PMID:Neuropathological and neurophysiological effects of interstitial white matter autologous and non-autologous protein containing solutions: further evidence for a glioma derived permeability factor. 846 May 70

We have tested the hypothesis that modulated radiofrequency (RF) fields may act as a tumor-promoting agent by altering DNA synthesis, leading to increased cell proliferation. In vitro tissue cultures of transformed and normal rat glial cells were exposed to an 836.55 MHz, packet-modulated RF field at three power densities: 0.09, 0.9, and 9 mW/cm2, resulting in specific absorption rates (SARs) ranging from 0.15 to 59 muW/g. TEM-mode transmission-line cells were powered by a prototype time-domain multiple-access (TDMA) transmitter that conforms to the North American digital cellular telephone standard. One sham and one energized TEM cell were placed in standard incubators maintained at 37 degrees C and 5% CO2. DNA synthesis experiments at 0.59-59 muW/g SAR were performed on log-phase and serum-starved semiquiescent cultures after 24 h exposure. Cell growth at 0.15-15 muW/g SAR was determined by cell counts of log-phase cultures on days 0, 1, 5, 7, 9, 12, and 14 of a 2 week protocol. Results from the DNA synthesis assays differed for the two cell types. Sham-exposed and RF-exposed cultures of primary rat glial cells showed no significant differences for either log-phase or serum-starved condition. C6 glioma cells exposed to RF at 5.9 muW/g SAR (0.9 mW/cm2) exhibited small (20-40%) significant increases in 38% of [3H]thymidine incorporation experiments. Growth curves of sham and RF-exposed cultures showed no differences in either normal or transformed glial cells at any of the power densities tested. Cell doubling times of C6 glioma cells [sham (21.9 +/- 1.4 h) vs. field (22.7 +/- 3.2 h)] also demonstrated no significant differences that could be attributed to altered DNA synthesis rates. Under these conditions, this modulated RF field did not increase cell proliferation of normal or transformed cultures of glial origin.
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PMID:DNA synthesis and cell proliferation in C6 glioma and primary glial cells exposed to a 836.55 MHz modulated radiofrequency field. 909 41

The present work was undertaken to study the metabolic response of C6 glioma cells to physiologically relevant doses of delta9-tetrahydrocannabinol (THC), the major active component of marijuana. At those concentrations (i.e. nanomolar range), THC produced a dose-dependent increase in the rates of glucose oxidation to CO2 and glucose incorporation into phospholipids and glycogen. The THC-induced stimulation of glucose utilization was (i) dose-dependent up to 100 nM THC, (ii) mimicked by the synthetic cannabinoid HU-210, and (iii) prevented by pertussis toxin and the CB1 receptor antagonist SR141716A. In contrast to THC, forskolin markedly depressed CO2 production, phospholipid synthesis and glycogen synthesis from glucose. The forskolin-induced inhibition of glucose utilization was (i) mimicked by dibutyryl-cAMP, and (ii) prevented by THC, HU-210 and H-7, an inhibitor of the cAMP-dependent protein kinase. Likewise, THC was able to antagonize in part the forskolin-induced elevation of intracellular cAMP concentration, and this antagonistic effect was prevented by SR141716A. However, THC per se did not affect basal cAMP concentration. Results thus indicate that physiologically relevant doses of THC stimulate glucose metabolism in C6 glioma cells through a cannabinoid receptor-mediated process. Although cannabinoid receptors may be coupled to inhibition of adenylyl cyclase in C6 glioma cells, this does not seem to be the mechanism involved in the THC-induced stimulation of glucose metabolism.
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PMID:Delta9-tetrahydrocannabinol stimulates glucose utilization in C6 glioma cells. 936 16


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