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)

Growth studies were done on a cultured rat liver cell line (RLC-GAI) grown in a chemically defined medium in the presence of lead nitrate. Lead reversibly inhibited the growth of these cells even after 6 d of exposure to the heavy metal. To compare lead sensitivity in various cell lines, GI50 and LD50 values were determined in the RLC-GAI cells as well as two glioma cell lines (B82 and C(6)) and a neuroblastoma cell line (N18). The LD50 values paralleled but were consistently lower than the GI50 values. Since lead is known to affect heme synthesis, hemin was added to test the possibilty of preventing the growth-inhibitory effect of the lead. The growth capacity of lead-treated cells did not change with the addition of hemin. It is thought that differentiated cultured cell lines such as these could be useful in examining the molecular mechanism of lead toxicity.
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PMID:Cellular and molecular toxicology of lead. I. Effect of lead on cultured cell proliferation. 56 52

The high-affinity transport system for glycine in plasma membrane vesicles from C6 glioma cells is dependent on Na+ and also on the presence of Cl- in the incubation medium. This anion requirement is relatively specific for Cl-, since other anions are also capable of stimulating the glycine transport in the following order of decreasing efficacy: Cl- greater than Br- greater than SCN- congruent to I- greater than NO3- greater than F-. Chloride ions raise the Vmax for transport and, to a lesser extent, act on the Km. The data provided by direct measurements of the coupling of sodium and chloride to the transport of glycine by using a kinetic approach suggest a stoichiometry for the translocation cycle catalyzed by the glycine transporter of two sodium ions and one chloride ion per glycine zwitterion.
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PMID:The role of chloride ions on the transport of glycine in plasma membrane vesicles from glial cells. 292 73

In a population-based case-control study of 416 incident gliomas in adults carried out in Melbourne, Australia, between 1987 and 1991, 409 age-sex-matched case-control pairs (243 male and 166 female) had adequate data available to examine associations between the dietary intake of N-nitroso compounds, N-nitroso precursors, other nutrients including N-nitroso inhibitors, and the risk of glioma. Dietary intakes were based on the reported frequency of consumption of 59 food items. Increased odds ratio (OR) were observed in males who consumed high levels of bacon, corned meats, apples, melons and oil. OR less than unity were observed in men consuming cabbage and cola drinks, and in women who consumed wholegrain bread, pasta, corned meat, bananas, cauliflower, brocoli, cola drinks and nuts. Generally, N-nitroso associations were greater in men and micronutrient associations were greater in women. Elevated OR in men, but not women, were associated with the intake of N-nitroso dimethylamine (NDMA), retinol and vitamin E. The intake of nitrate (largely of vegetable origin) was protective in women but not in men. When analyzed using multiple logistic regression, the association with NDMA intake in males was not modified by dietary micronutrient intakes. In females, beta carotene alone, though not directly associated with risk, modified the effect of NDMA. On balance, this study added only limited support to the N-nitroso hypothesis of glial carcinogenesis.
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PMID:Dietary factors and the risk of glioma in adults: results of a case-control study in Melbourne, Australia. 792 41

The aim of this work was to examine the effects of changes in external K+ concentration (Ko) around its physiological value, of various K+ channels blockers, including internal Cs+, of vacuolar H(+)-ATPase inhibitors and of the protonophore CCCP on the resting potential and the voltage-dependent K+ current of differentiated neuroblastoma x glioma hybrid NG108-15 cells using the whole-cell patch-clamp technique. The results are as follows: (i) under standard conditions (Ko = 5 mM) the membrane potential was -60 +/- 1 mV. It was unchanged when Ko was decreased to 1 mM and was depolarized by 4 +/- 1 mV when Ko was increased to 10 mM. (ii) Internal Cs+ depolarized the membrane by 21 +/- 3 mV. (iii) The internal application of the vacuolar H(+)-ATPase inhibitors N-ethylmaleimide (NEM), NO3- and bafilomycin A1 (BFA) depolarized the membrane by 15 +/- 2, 18 +/- 2 and 16 +/- 2 mV, respectively. (iv) When NEM or BFA were added to the internal medium containing Cs+, the membrane was depolarized by 45 +/- 1 and 42 +/- 2 mV, respectively. (v) The external application of CCCP induced a transient depolarization followed by a prolonged hyperpolarization. This hyperpolarization was absent in BFA-treated cells. The voltage-dependent K+ current was increased at negative voltages and decreased at positive voltages by NEM, BFA and CCCP. Taken together, these results suggest that under physiological conditions, the resting potential of NG108-15 neuroblastoma cells is maintained at negative values by both voltage-dependent K+ channels and an electrogenic vacuolar type H(+)-ATPase.
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PMID:Contribution of a H+ pump in determining the resting potential of neuroblastoma cells. 800 50

A population-based case-control study was performed in South-West Germany in 1987/88 with 115 histological confirmed glioma and 81 meningioma cases and 418 randomly selected controls. On the basis of information from a food-frequency questionnaire and questions on food preparation and food supply, the role of dietary carcinogens, in particular N-nitroso compounds or their precursors, on risk for glioma and meningioma were analyzed by multiple logistic regression. Eleven food groups were investigated. The intake of processed meat was significantly associated with an increased risk of glioma. The intake of any food group was not significantly related to meningioma risk. Among single meat products, a significantly higher risk of glioma was found for cooked ham, processed pork meat and fried bacon. For the consumption of 3 N-nitrosamines, assessed from the intake of processed meat and cheese, significant positive relations to glioma risk were found. These N-nitrosamines were also related to meningioma risk, although to a less pronounced extent. The risk for occurrence of glioma was significantly increased for those using vegetable fat frequently for deep frying, as compared with non-users. For the dietary intake of nitrate, nitrite, vitamin C, specific alcoholic beverages, total alcohol, and water from a non-central supply, no elevated risk was found in this study.
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PMID:Dietary carcinogens and the risk for glioma and meningioma in Germany. 843 29

Glial cells are thought to protect neurons from heavy-metal toxicity. To gain a better understanding of mechanisms of protection against lead compounds, a number of lead-resistant C6 rat glioma cell sublines have been isolated. After 8 mo of growth in the absence of lead nitrate, three sublines still maintain their lead-resistant phenotype. None of the lead-resistant sublines are cross-resistant to Cd(II) or Ni(II), but all are cross-resistant (in varying degrees) to Hg(II), As(III), Sb(III), and Sn(II), and one is resistant to trimethyl tin. No inducible lead resistance is seen in any glioma line. One subline has been used to create cell-cell hybrids with wild-type cells. The hybrids exhibit dominance of the lead-resistant phenotype. To identify and analyze altered gene expression at the mRNA level in the lead-resistant sublines, the differential display technique was used. Numerous differences are seen between amplified fragments from wild-type and lead-resistant cells. Candidate clones are now being analyzed to confirm the differential expression and to isolate cDNAs that confer lead resistance.
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PMID:Isolation and properties of lead-resistant variants of rat glioma cells. 987 35

The production of superoxide and nitric oxide induced in U87 glioma treated with lipopolysaccharide (LPS) and interferon-gamma (IFN-gamma) was examined by electron spin resonance (ESR) spectroscopy using a newly designed flow-type quartz cuvette without detaching cells from the culture plate. ESR spectra of 2,2,6, 6-tetramethyl-4-hydroxy-1-piperidinyloxy (TEMPOL) with U87 cells on a quartz culture plate were measured at 15 min intervals. The signal intensity of TEMPOL decreased in the presence of U87 cells at the pseudo-first order rate. The signal decay was accelerated in the U87 cells treated with LPS/IFN-gamma for 24 h, and was suppressed in the presence of superoxide dismutase and catalase. By the spin-trapping method, nitric oxide from U87 cells pretreated with LPS/IFN-gamma for 24 h was measured by the ESR, but only a weak signal of nitric oxide adducts was detected. Further, the nitrite and nitrate levels in the medium did not increase for 24 h. By the ESR measurement of cells on culture plates without detachment stress, it was found that the production of superoxide was induced by LPS/IFN-gamma, but that of nitric oxide was not, in U87 glioma cells.
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PMID:Induction of superoxide in glioma cell line U87 stimulated with lipopolysaccharide and interferon-gamma: ESR using a new flow-type quartz cell. 1076 20

Nitric oxide (NO) is thought to be a mediator in many of the processes of malignant brain tumor progression. We examined NO production in the brain of normal conscious, freely moving rats with or without implanted C6 glioma. Both nitrite (NO(2)(-)) and nitrate (NO(3)(-)) in the dialysates of the two groups were measured using an in vivo microdialysis technique. The mean concentration of NO(2)(-) in the glioma group was two-times higher than that in the control group (P<0.01). Concentrations of both NO(2)(-) and NO(3)(-) in the glioma and control groups decreased following intraperitoneal injection of N(G)-nitro-L-arginine methyl ester (L-NAME), a non-selective inhibitor of NO synthase (NOS). NO production was also significantly suppressed in the glioma group, but not the control group, by intraperitoneal injection of 2-amino-5,6-dihydro-6-methyl-4H-1,3-thiazine (AMT), a selective inhibitor of inducible NOS (iNOS). On immunohistochemical examination, diffuse iNOS-positive cells were located within glioma tissue. ED1-positive cells (microglia/macrophages) were intermingled between glioma cells on double immunostaining. These results indicate that the basal level of NO production in the glioma group is higher than that in the control group and that the increased NO production was continuously induced by iNOS-expressing cells in glioma.
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PMID:Pathodynamics of nitric oxide production within implanted glioma studied with an in vivo microdialysis technique and immunohistochemistry. 1268 26

Capsaicin induces apoptosis in some types of cells, but its mechanism remains obscure. In this study, peroxynitrite, a powerful oxidant generated from the reaction of superoxide and nitric oxide (NO) in biological system, was demonstrated to be responsible for capsaicin-mediated apoptosis in C6 glioma cells. Capsaicin-induced apoptosis was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assay, and also identified by Annexin V staining and comet assay. Capsazepine and ruthenium red, the vanilloid receptor 1 (VR1/TPRV1) antagonists, did not inhibit capsaicin-induced apoptosis. Exposure to capsaicin not only promoted the generation of superoxide and iNOS, but also markedly suppressed the expression of SODs. Nitrite and nitrate, the NO metabolites accumulated in the medium, and the nitrotyrosine was also increased in proteins of C6 glioma cells exposed to capsaicin. Pretreatment of cells with 4 microM ebselen (a peroxynitrite scavenger) showed effective inhibitory effect on the capsaicin-induced apoptosis. These results suggest that peroxynitrite can act as a potential mediator in the capsaicin-induced apoptosis in C6 glioma cells.
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PMID:Involvement of peroxynitrite in capsaicin-induced apoptosis of C6 glioma cells. 1568 Oct 35

Astrocytes in the CNS produce inflammatory mediators in response to several stimuli and cytokines. Here we investigated the in vitro effect of leptin on inducible nitric oxide synthase (iNOS) expression in a glioma cell line (C6). After hormone stimulation, culture media were analysed for accumulated stable oxidation products of NO (NO2(-) and NO3(-), designated as NO(x)), cellular RNA was extracted to determine iNOS mRNA level by RT-PCR and cellular lysates were prepared for protein expression. Leptin induced a concentration-dependent increase of NO release, related to iNOS induction. This effect was potentiated by IFN-gamma, or TNF-alpha, or IFN-gamma plus IL-1beta. Pyrrolidine dithiocarbamate (PDTC) and N-alpha-tosyl-L-lysine chloromethyl ketone (TLCK), two inhibitors of NF-kappaB activation, as well as the specific proteasome inhibitor MG132, blocked leptin-induced iNOS. The role of NF-kappaB was also confirmed by time course studies on degradation of IkappaB-alpha, which began to degrade 5 min after treatment with leptin and returned to basal level after 30-60 min. Pre-incubation of cells with MG132 inhibited leptin-induced IkappaB-alpha degradation. These results confirm the pro-inflammatory role of leptin and identify it as a potential up-regulator of cytokine-induced inflammatory response in the CNS.
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PMID:Leptin induces nitric oxide synthase type II in C6 glioma cells. Role for nuclear factor-kappaB in hormone effect. 1634 70


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