Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027819 (neuroblastoma)
 27,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mg2+ATPase and (Na+ + K+)ATPase activities were measured in clonal line NN hamster astroblasts and in clonal lines M1 and N1E-115 mouse neuroblastoma cells after the cells had been subjected to the acute and chronic actions of 100 mM ethanol. Exposure of the astroblasts to ethanol for periods as long as 68 days produced an increase in total cellular Mg2+ ATPase activity, as measured in cell homogenates; however, activity reverted to control levels upon withdrawal of ethanol. Chronic exposure of clonal line N1E-115 neuroblastoma cells to ethanol produced an increase in Mg2+ATPase and (Na+ +K+)ATPase activities. In contrast, the activities of both ATPases of clonal line M1 neuroblasts were unaffected by chronic exposure to ethanol. Acute exposure of cell homogenates to 100 mM ethanol inhibited Mg2+ ATPase and (Na+ + K+)ATPase of astroblasts but not that of neublastoma cells. These findings suggest that neural cells in culture may serve as useful models for studying the effects of ethanol on specific cell types.
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PMID:The chronic and acute effects of ethanol on adenosine triphosphatase activity in cultured astroblast and neuroblastoma cells. 13 50

Administration of ethanol induces the synthesis of hepatic metallothionein and metallothionein mRNA in the liver but not in the brain. Furthermore, ethyl alcohol, methyl alcohol and isopropyl alcohol enhance the synthesis of metallothionein in Chang cells but not in neuroblastoma IMR-32 cells in culture. The results of this study are interpreted to suggest that the mechanisms of synthesis of metallothionein and the utilization of essential metal nutrients in the brain and peripheral tissues are not identical.
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PMID:Differential stimulation of hepatic and brain metallothioneins by ethanol. 130 38

The effect of nifedipine dissolved in different solvents on the two types of calcium channel currents in neuroblastoma cells was investigated using the whole cell version of the patch clamp technique. Nifedipine dissolved in dimethylsulfoxide (nifedipine/DMSO) decreased the transient calcium channel (T channel) current by 50% at a concentration of 10 microM. This inhibitory effect was concentration-dependent and reversible. In contrast, T channel currents were not inhibited by nifedipine at a similar concentration dissolved in acetone or ethanol. Further experiments were carried out with dried nifedipine/DMSO. Dried nifedipine/DMSO powder re-dissolved in acetone or ethanol at a concentration of 10 microM decreased the T channel current by 32% and 37%, respectively. In addition, within the concentration range of 10 nM to 100 microM nifedipine/DMSO inhibited the long-lasting calcium channel (L channel) current more effectively than did nifedipine dissolved in acetone. The concentration of solvent (DMSO, ethanol, acetone) in the bath was fixed at 0.3% to reach different final concentrations of nifedipine. Solvents alone at a final concentration of 0.3% did not show any effect on T or L channel currents. UV absorbance measurements indicated that the combination of nifedipine, solvent and bath solution did not result in precipitation of the dihydropyridine during the experimental protocol. It is concluded that when DMSO is used as the solvent, nifedipine is not only a more effective L channel antagonist but also a T channel antagonist in neuroblastoma cells.
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PMID:Modification by solvents of the action of nifedipine on calcium channel currents in neuroblastoma cells. 132 Feb 11

Many Indian Ayurvedic (science of life) agents have been introduced into the U.S.A. as food supplements. Two of them, Maharishi Amrit Kalash-Ambrosia (MAK-A) and Maharishi Amrit Kalash-Nectar (MAK-N) are under investigation. This study shows that an ethanol extract of MAK-A induced morphological (neurite formation) and biochemical (increase of activity of tyrosine hydroxylase by about 15-fold) differentiation in murine neuroblastoma (NBP2) cells in culture, whereas an aqueous extract of MAK-A increased only the activity of tyrosine hydroxylase but to a much lesser extent. The treatment time of 3 days was needed for the expression of maximum differentiation. Ethanol extracts of MAK-A and aqueous extracts of MAK-A increased the intracellular level of adenosine 3',5'-cyclic monophosphate (cAMP) by about 4-fold in 3 days but they did not do so in 15 min. Ethanol extracts of MAK-A also induced neurite formation in neuroblastoma cells grown in serum free medium but the concentration requirement was about a fifth of that needed in serum. The treatment time of 24 hr was sufficient to induce optimal differentiation in neuroblastoma cells grown in serum free medium. The differentiating agents in ethanol-MAK-A were resistant to heat and light and could not be removed by treatment with activated charcoal. Neither ethanol-MAK-N nor aqueous-MAK-N induced differentiation in neuroblastoma cells, suggesting that the differentiating agents were present only in MAK-A.
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PMID:Ayurvedic (science of life) agents induce differentiation in murine neuroblastoma cells in culture. 135 73

This report describes the effect of Bay K-8644 dissolved in various solvents on two types of calcium channel currents in neuroblastoma cells. Transient calcium channel (T channel) currents were not affected by Bay K-8644 dissolved in ethanol (EtOH) or polyethylene glycol (PEG). However, at the same concentration of 0.6 microM, Bay K-8644 dissolved in dimethylsulfoxide (DMSO) (Bay K-8644/DMSO) decreased the T channel current by 50%. The concentration of all three solvents in the bath was fixed at 0.3% to reach different final concentrations of Bay K-8644. At this fixed solvent concentration, the inhibitory effect of Bay K-8644/DMSO on T channel currents was dose-dependent; the solvents alone did not have any effect on T channel currents; and DMSO pretreatment of cells did not render the T channel current sensitive to Bay K-8644 dissolved in EtOH or PEG. Bay K-8644/DMSO was dried using a flash evaporator and redissolved in EtOH or PEG. Dried Bay K-8644 that was redissolved in EtOH or PEG to achieve a final concentration of 0.6 microM inhibited T channel currents by 39 or 35%, respectively. Furthermore, Bay K-8644 (10 nM) increased L channel currents by 80% with DMSO, but only 30% with EtOH as the solvent. These results show that in neuroblastoma cells Bay K-8644/DMSO, within the concentration range examined, is a T channel antagonist and more effective L channel agonist than Bay K-8644 dissolved in the two other solvents.
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PMID:Bay K-8644 in different solvents acts as a transient calcium channel antagonist and a long-lasting calcium channel agonist. 137 52

The present study reports on the development of a model for maintaining constant ethanol concentrations over time in cell culture media. When neuroblastoma x glioma cells (NG 108-15) were grown in ethanol containing media under standard cultivation conditions in the incubator at 37 degrees C, a 90% evaporation was observed after 24 hr. To counteract evaporation, the cell culture dishes were placed inside polystyrene boxes together with an open dish containing an appropriate amount of ethanol. By using such procedure, the decrease in ethanol concentration in the culture media was completely avoided. Cultivating cells in ethanol-free media inside sealed plastic boxes did not change their viability, growth rate, protein and phospholipid composition of the cells or the pH of the media, compared to cultures grown outside the boxes.
Alcohol Alcohol 1992 May
PMID:A method for maintaining constant ethanol concentrations in cell culture media. 144 66

We have studied the molecular mechanisms underlying neuronal adaptation to chronic ethanol exposure. NG108-15 neuroblastoma cells were used to perform a detailed analysis of ethanol-induced changes in neuronal gene expression. High resolution, quantitative two-dimensional (2-D) gel electrophoresis of in vitro translation products showed both dose-dependent increases and decreases in specific mRNA abundance following treatment with ethanol at concentrations seen in actively drinking alcoholics (50-200 mM). Dose response curves for representative members of the increasing or decreasing response groups had very similar profiles, suggesting that similar mechanisms may regulate members of a response group. Some mRNAs that increased with ethanol treatment appeared identical to species induced by heat shock while other mRNAs were only induced by ethanol. We conclude that chronic ethanol exposure can produce specific coordinate changes in expression of neuronal mRNAs, including some members of the stress protein response. However, the overall pattern of ethanol-responsive gene expression is distinct from the classical heat shock subgroup of stress proteins response. Changes in gene expression and specifically, mechanisms regulating a subset of stress protein expression, could be an important aspect of neuronal adaptation to chronic ethanol seen in alcoholics.
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PMID:Ethanol-responsive gene expression in neural cell cultures. 156 14

Alcohol metabolism in the human brain has been characterized as essentially nonoxidative in nature, with the esterification of ethanol with fatty acids via fatty acid ethyl ester synthase. This pathway of ethanol metabolism is related to end organ damage in the brain but the neural cell type expressing FAEES has not been identified. In this study human and rodent neuroblastoma and glioma cell lines are assayed for fatty acid ethyl ester synthase activity. Cells with neuronal properties demonstrated higher activity than glioma cell lines. We confirmed the presence of the mRNA for one type of synthase, fatty acid ethyl ester synthase-III in three neuronal cell lines--N1E115 cells, PC12 cells, and SK-N-MC cells. These results support the hypothesis that FAEES activity is expressed chiefly in cells with neuronal properties and suggest that non-oxidative ethanol metabolism is potentially related to the toxic effect of ethanol on the human brain.
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PMID:Nonoxidative ethanol metabolism: expression of fatty acid ethyl ester synthase-III in cultured neural cells. 162 45

The effect of acute ethanol (EtOH) exposure on 5-HT3 receptor-mediated ion current was examined in whole-cell patch-clamp recordings from NCB-20 neuroblastoma cells. The physiologic and pharmacologic properties of 5-HT-activated ion current in NCB-20 cells indicated that it was mediated by 5-HT3 receptors. EtOH potentiated 5-HT3 receptor-mediated current in a concentration-dependent manner at concentrations (25-100 mM) which are achieved during EtOH intoxication in vivo.
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PMID:Ethanol potentiation of 5-HT3 receptor-mediated ion current in NCB-20 neuroblastoma cells. 171 59

Recent studies indicate that ethanol (EtOH) potentiates ion current through the channel associated with the 5-hydroxytryptamine3 (5-HT3)-type serotonin receptor. The present study was designed to determine 1) whether such potentiation occurs in adult mammalian neurons expressing 5-HT3 receptors; 2) whether potentiation is selective for the 5-HT3 receptor, relative to other ligand-gated ion channels; and 3) possible mechanisms by which EtOH potentiates this response. EtOH potentiated 5-HT3 receptor-mediated ion current in freshly isolated nodose ganglion neurons at concentrations similar to those previously reported to be effective in neuroblastoma cells (25-100 mM). Current was blocked by the selective 5-HT3 antagonist ICS 205-930 even in the presence of EtOH, and current activated by a 5-HT3 agonist (2-methyl-5-HT) was potentiated by EtOH. Thus, EtOH appears to produce potentiation via an alteration in the function of 5-HT3 receptors and not through an independent effect. gamma-Aminobutyric acidA receptor-mediated Cl- current was not potentiated by EtOH in neurons in which potentiation of responses to 5-HT was observed. Methanol potentiated 5-HT3 receptor-mediated current with a potency lower than that of EtOH. Potentiation by EtOH decreased with increasing 5-HT concentration. In addition, EtOH increased the decay rate of current. EtOH did not alter the reversal potential of the 5-HT3 receptor-mediated current. These observations indicate that intoxicating concentrations of EtOH selectively potentiate 5-HT3 receptor-mediated responses by increasing the apparent potency of 5-HT for activating ion current.
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PMID:Ethanol potentiation of 5-hydroxytryptamine3 receptor-mediated ion current in neuroblastoma cells and isolated adult mammalian neurons. 171 16


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