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Query: UMLS:C0017638 (glioma)
 30,880 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clonal lines of murine neuroblastoma (NBP2) and rat glioma (C6) were used to investigate the effects of methylmercuric chloride (CH3HgCl). Glioma cells were more sensitive to CH3HgCl than NB cells on the criterion of growth inhibition, but these cells were equally sensitive to inorganic mercury (HgCl1), Tri-n-butyl lead acetate and acrylamide on the same criterion. Alpha-tocopherol, alpha-tocopheryl++ succinate and inhibitors of cAMP phosphodiesterase protected glioma cells against the growth-inhibitory effect of CH3HgCl, but they failed to protect NB cells in culture. Glioma factors, sodium ascorbate, non-inhibitory concentrations of prostaglandins E1 (PGE1), and glutamate enhanced the growth-inhibitory effect of CH3HgCl on both NB and glioma cells in culture. The levels of certain specific cAMP-dependent and -independent protein phosphorylations appear to be very sensitive to CH3HgCl, and can be altered in both cell types by concentrations of CH3HgCl which do not affect growth or morphology of these cells.
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PMID:New opportunities with neuronal cultures to study the mechanisms of neurotoxic injuries. 174 37

The effects of methylmercury (MeHg) on cytoplasmic microtubules in cultured neuroblastoma cells, glioma cells, and fibroblasts were compared. Neuroblastoma cells appeared to be more sensitive to disruption of microtubules by MeHg than the glioma cells or fibroblasts; cellular concentrations of mercury after MeHg were also higher in neuroblastoma cells. Recovery of microtubule structure was monitored in cells after removal of MeHg; addition of the chelating dimercaptosuccinic acid (DMSA) increased reassembly of microtubules. During MeHg treatment and early recovery, microtubule integrity was dependent on cellular mercury concentrations. However, after prolonged DMSA exposure, mercury appeared to reenter the cell, without causing dissociation of microtubules.
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PMID:Differential responses to methylmercury exposure and recovery in neuroblastoma and glioma cells and fibroblasts. 608 80

The effect of methyl mercury (MeHg) and triethyllead (Et3Pb) on the membrane bound SH-enzymes Na+K+ATPase and pyruvate dehydrogenase (PDH) was studied in relation to the effect on the galactosyl ceramide sulfotransferase (CST) and to morphological changes in glioma C6 cells. Two-day-old cultures were incubated for 1 or 20 hrs with 5-30 microgram MeHgC1 and 2-8 microgram Et3PbC1/mg cell protein. The results show that both compounds induced morphological changes and a reduction of CST activity at growth inhibitory concentrations. A less marked reduction of Na+K+ATPase was induced with increasing exposure time only in MeHgC1 treated cultures, and PDH activity was not affected by either of the compounds under the experimental conditions. Thus, an interference with Na+K+ATPase and PDH activities do not appear to be a primary effect of MeHg and Et3Pb intoxication.
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PMID:Effects of methyl mercury and triethyllead on Na+K+ATPase and pyruvate dehydrogenase activities in glioma C6 cells. 628 6

Two different -SH groups associated with the opiate receptors of the mouse neuroblastoma X rat glioma hybrid NG108-15 have been identified. Modification of these by N-ethylmaleimide (NEM) (presumed to be via alkylation) or by para-chloromercuribenzoic acid (presumed to be via formation of mercury adducts) decreases the binding of both opiate agonists and antagonists to these receptors. Agonist binding is more sensitive than antagonist binding to modification by NEM. Losses in antagonist binding are accounted for totally by decreases in the number of binding sites; there are no corresponding losses in antagonist affinity. Losses of antagonist binding exhibit a pseudo-first order rate constant; the modification of only one such group completely destroys the binding site. Both agonists and antagonists protect against modification of this group by NEM. Sodium and lithium, but not GTP, also protect this group, indicating that the action of these monovalent cations is directly on the receptor moiety. Losses in agonist binding stem not only from decreases in receptor number but also from selective losses in affinity. This -SH group appears to be different from the one at the binding site as sodium, GTP, and antagonist ligands do not protect against losses in agonist affinity. Agonist high affinity also is lost in a pseudo-first order fashion indicating that an alteration of only one -SH group per receptor complex is sufficient to produce this effect. The possible roles of two sulfhydryls in opiate receptor function are discussed.
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PMID:Protection of opiate receptors in NG108-15 against modification by N-ethylmaleimide. 629 30

Mercury compounds and some other metal ions were investigated with respect to their effect on in vitro tubulin polymerization and on cellular microtubules in mouse glioma. In vitro tubulin polymerization was completely inhibited by 2.5 X 10(-5) M Hg2+, 5 X 10(-5) M CH3Hg+, 2 X 10(-4) M Cr3+, 2.5 X 10(-4) M Cu2+, and 5 X 10(-4) M Cd2+. Zn2+ did not affect the polymerization up to 5 X 10(-4) M. Indirect immunofluorescence study with rabbit antiporcine tubulin antibody revealed that methylmercury disrupted the microtubule network at an early stage of growth inhibition. On the other hand, in the presence of Cd2+, Cu2+, and Cr3+ at their growth inhibitory concentrations, no effects on microtubule networks were observed for the first 1 hr. These results indicate that only methylmercury affects cellular microtubules, while other ions seem to interfere with other sites in the cells, although these ions showed the ability to depress in vitro tubulin polymerization.
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PMID:Effects of methylmercury and some metal ions on microtubule networks in mouse glioma cells and in vitro tubulin polymerization. 636 29

Methylmercury was taken up preferentially by mouse glioma and mouse neuroblastoma cells relative to inorganic mercury. Methylmercury uptake was depressed by lowering the cellular ATP level or the incubation temperature, while the uptake of inorganic mercury was not affected by these treatments. When the cells were treated with reagents such as cytochalasin B, colchicine and vinblastine which are known to affect membrane permeability, changes in permeability to methylmercury caused by these reagents were markedly different from those to inorganic mercury. Inorganic mercury above 2 x 10(-5)M caused the release of 2-deoxyglucose trapped in the cells and the amount of inorganic mercury taken up by the cells increased markedly at higher concentrations. Inorganic mercury thus appeared to move into the cells after disrupting the membrane barrier, while methylmercury can penetrate the cells without any noticeable damage to the barrier.
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PMID:Uptake of methylmercury and inorganic mercury by mouse glioma and mouse neuroblastoma cells. 689 18

Effects of methylmercury on the cell growth of mouse glioma in vitro were studied in relation to the microtubules as a possible target. The electron microscopic observation revealed that methylmercury added in culture medium specifically attacked microtubules in the cells at growth inhibitory concentration, while mercuric mercury injured microtubules to the same extent as other cell organelles. However the latter showed a little stronger depressing effect on tubulin polymerization in vitro than the former. Further, 3 other inorganic metal ions (Cd2+, Cu2+ and Cr3+), which were reported to suppress tubulin polymerization in vitro, did not disturb the microtubule networks even at their cell growth inhibitory concentrations. Therefore, of these metal compounds tested, when they were added in the culture medium, methylmercury seemed to specifically interact with microtubules and cause inhibition of cell growth.
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PMID:Mechanism of methylmercury cytotoxicity: by biochemical and morphological experiments using cultured cells. 721 10

Effects of Pb2+, Ni2+, Hg2+ and Se4+ on cultured human glioma U-343MG cells were investigated considering uptake, toxicity and, in combination with radiation, clonogenic cells survival. The cells were exposed to 0-100 microM of the metals for a week before the evaluation. The tests showed a tendency to toxicity with 10 microM nickel although not significant (P > 0.05). Selenium, lead and mercury exerted a significant toxicity (P < 0.05) at 2.5 microM, 10 microM and 1 microM, respectively. To challenge the clonogenic cell survival capacity, the cells were irradiated with 60Co photons after being exposed to the highest nontoxic concentration of the different metals. The clonogenic cell survival tests, after irradiation, showed no significant change if the cells were exposed to 5 microM nickel, 0.5 microM selenium or 5 microM lead compared with those not exposed. Mercury, 0.1 microM, gave a relative reduction in survival compared with only irradiated cells of 58 +/- 17%. Thus, only mercury affected the radiation-induced damage and/or repair. When exposed to the highest nontoxic concentrations of the different metals, the cultures did not display a significant uptake ratio (metal concentration ratio of exposed cells to control cells) of nickel (3.1 +/- 3.3), only a small uptake ratio of selenium (4.0 +/- 0.4), while there was a large uptake ratio of both lead (2.6 +/- 1.7) x 10(2) and mercury (1.5 +/- 0.2) x 10(1). The results indicated that nickel was neither especially toxic nor influenced the clonogenic cell survival after irradiation. Mercury was more toxic and also influenced the radiation sensitivity. Lead was taken up strongly but did not influence the radiation sensitivity. Selenium accumulated but gave no detectable effect on the radiation sensitivity.
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PMID:Effects of Pb2+, Ni2+, Hg2+ and Se4+ on cultured cells. Analysis of uptake, toxicity and influence on radiosensitivity. 935 73

Aquaporin-4 (AQP4), a mercury-insensitive water channel protein, is abundant in the central nervous system and is localized in astrocytes and ependymal cells. AQP4 is speculated to maintain the homeostasis of intracellular and extracellular water in the brain, but little is known about the mechanism of induction of its expression. To investigate the expressional regulation of AQP4, we analyzed changes in its expression during chemically induced differentiation of embryonal carcinoma cells (P19) to neuronal and astrocytic cells, and during the cell cycle of glioma cells. After exposure to retinoic acid for 4 days AQP4 mRNA expression started at the initiation of astrocytic differentiation of P19 cells at 6 days, and increased markedly by 21 days. AQP4 expression was parallel to that of GFAP, a marker intermediate filament of astrocytes. In glioma cell lines, AQP4 mRNA was not detected in the growing phase, but was induced when the cell cycle was arrested at G0/G1 by transient expression of p21. Although quiescent astrocytes in the G0/G1-phase cultured under the serum-free condition exhibited a high expression of AQP4, serum supplement moved them to the S-phase and markedly decreased the AQP expression. These results suggest that AQP4 expression may be induced not only at the initiation of astrocytic differentiation of neural stem cells, but also at the G0/G1-phase during the cell cycle of astrocytes.
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PMID:Regulation of aquaporin-4 expression in astrocytes. 1131 79

Organic mercury is a well-known neurotoxicant although its mechanism of action has not been fully clarified. In addition to a direct effect on neurons, much experimental evidence supports an involvement of the glial component. We assessed methylmercury hydroxide (MeHgOH) toxicity in a glial model, C6 glioma cells, exposed in the 10(-5)-10(-8) M range. The time course of the effects was studied by time-lapse confocal microscopy and supplemented with biochemical data. We have monitored cell viability and proliferation rate, reactive oxygen species (ROS), mitochondrial transmembrane potential, DNA oxidation, energetic metabolism and modalities of cell death. The earliest effect was a measurable ROS generation followed by oxidative DNA damage paralleled by a partial mitochondrial depolarization. The effect on cell viability was dose dependent. TUNEL, caspase activity and real-time morphological observation of calcein-loaded cells showed that apoptosis was the only detectable mode of cell death within this concentration range. N-acetyl-cysteine (NAC) or reduced glutathione (GSH) completely prevent the apoptotic effect of MeHgOH. The lowest effective MeHgOH concentration was 10(-7) M for ROS and DNA OH-adducts generation. The effect of submicromolar concentrations of MeHgOH on C6 cells could be relevant in the developmental neurotoxicity caused by low dose, long-term exposures, such as those of food origin. In addition, we have shown that the same concentrations are effective in the induction of DNA oxidative damage, with further potential pathogenetic implications.
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PMID:Time course assessment of methylmercury effects on C6 glioma cells: submicromolar concentrations induce oxidative DNA damage and apoptosis. 1242 38


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