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)

A method for determining serum catecholamine metabolites such as vanillylmandelic acid (VMA), 3-methoxy-4-hydroxyphenyl glycol (MHPG) and homovanillic acid (HVA) in neuroblastoma by using high performance liquid chromatography and electrochemical detector is described. The separation of catecholamine metabolites was performed on a reverse phase column with an eluting system containing citric acid-potassium hydrogen phosphate buffer and methanol as the organic modifier. The experimental results showed that VMA and HVA levels in the serum of neuroblastoma patients were 15-30 times higher than that of the normal control group. The same phenomenon also occurred in patients with stage II neuroblastoma. Serum VMA, MHPG and HVA levels reduced to normal in patients suffering from neuroblastoma after surgery. Serum catecholamine metabolites analysed by using HPLC/ECD is more simple, sensitive and reliable than that by usual urine assay and might be used for the diagnosis of neuroblastoma even in early stage.
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PMID:Determination of serum catecholamine metabolites in neuroblastoma by high performance liquid chromatography with electrochemical detection. 350 18

Due to a lack of L-Dopa-decarboxylase, the mouse neuroblastoma clone N 1 E-115 contains a high intracellular Dopa-content compared to a low noradrenaline- and dopamine-content. Because of this decarboxylase deficiency, the N 1 E-115 clone releases more than 95% of the produced Dopa into the culture medium. After renewal of the culture medium, Dopa production of the cells can be measured by the increase of Dopa in the medium. Dopa production was linear during 2 h and varied from 50-180 micrograms/mg prot-1 x h-1 between different subcultures. Dopa release into the medium was used as an indirect measure for the tyrosine-hydroxylase activity. Several dopaminergic agonist and antagonists were tested. Dopa production could be blocked dose-dependent by apomorphine (1 X 10(-7)-1 x 10(-6) M), but not by lisuride hydrogen maleate and bromocryptine. Several dopaminergic and adrenergic antagonists failed to reverse the apomorphine induced blockade of the tyrosine-hydroxylase activity.
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PMID:Dopa-release from mouse neuroblastoma clone N 1 E-115 into the culture medium. A test for tyrosine hydroxylase activity. 612 21

Proton NMR spectroscopy was used to study the effect of differentiation with prostaglandin E1 and theophylline on intact hybrid neuroblastoma X glioma cells. The standard proton NMR method showed more resolvable signals than the spin echo NMR spectra. The differentiated cells were found to contain significantly higher levels of glutamine than the undifferentiated precursors. Observations on cell extracts confirmed these results.
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PMID:Differences in metabolite levels upon differentiation of intact neuroblastoma X glioma cells observed by proton NMR spectroscopy. 631 24

5-S-Cysteinyldopa, a melanin precursor, has been shown to possess selective toxicity to tumour cells in vitro and in vivo. The mechanism of cytotoxicity of the catechol was studied in comparison with L-dopa and 5-S-cysteaminyldopamine. Growth inhibition of human neuroblastoma cell line of YT-nu by 5-S-cysteinyldopa was completely depressed by addition of catalase. Superoxide dismutase and five drugs thought to scavenge hydroxyl radicals or quench singlet oxygen had little effect on the cytotoxicity. Hydrogen peroxide itself was also cytotoxic at low concns. These results indicated that hydrogen peroxide was a mediator of the cytotoxicity of 5-S-cysteinyldopa. It is suggested that reaction of the catechol with cellular superoxide radicals contributes to the production of hydrogen peroxide in addition to autoxidation. Catalase reduced the cytotoxicity of L-dopa by half, while it had no inhibitory effect on the strong cytotoxicity of 5-S-cysteaminyldopamine.
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PMID:The mechanism of toxicity of 5-S-cysteinyldopa to tumour cells. Hydrogen peroxide as a mediator of cytotoxicity. 640 13

A dry ashing, flameless atomic absorption spectrometric method was evaluated to determine arsenic and selenium in foods. Samples were dry-ashed with Mg(NO3)2-MgO and dissolved in HCl. Selenate was reduced to selenite by boiling in 4N HCl. Selenate was reduced to selenite by boiling in 4N HCl, and arsenate to arsenite by treatment with KI. Hydrides of arsenic and selenium were generated by the addition of NaBH4 and were swept by nitrogen and hydrogen into a thermally heated silicate tube furnace. The detection limit was about 5 ppb for each element based on a 10 g sample. Analytical results obtained for several samples of NBS reference materials agreed with the certified values. The procedure was evaluated by another laboratory and results were satisfactory.
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PMID:Dry ashing, hydride generation atomic absorption spectrometric determination of arsenic and selenium in foods. 709 47

A hydrogen selenide (H2Se) evolution-electrothermal atomic absorption method is described for determining nanogram concentrations of total selenium (Se) in biological and environmental materials. A mixed acid digestion procedure is used to decompose organic material. Sodium borohydride, a redesigned hydride generator, and an electric-headed absorption tube are used for H2Se evolution and conversion to atomic Se. The method has a detection limit of 4 ng/mL and a sensitivity of 0.6 ng/mL, and is linear from 0 to 90 ng Se/mL. As determined on urine, water, and bovine liver, total and within-run precision had relative and standard deviation values of 5-17.2 and 5.5-12.6% respectively. Accuracy was established with 2 NBS and 3 EPA reference materials, and mean errors of 0 to +0.8 were obtained. Mean recoveries of 109 and 101% were obtained for 10 and 50 ng Se added to human urine.
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PMID:Hydrogen selenide evolution-electrothermal atomic absorption method for determining nanogram levels of total selenium. 722 21

In this paper, we show that human neuroectodermal cells exposed to 1-5 mM hydrogen peroxide or 10 nM-1 mM ascorbate die by programmed cell death induced by oxidative stress. The cell death by peroxide occurs within 4 h and involves approximately 80% of B-mel melanoma cells, while ascorbate causes cell death of approximately 86% of B-mel cells within 24 h. SK-N-BE(2) neuroblastoma cells are more resistant, 32% and 43% cell death for peroxide and ascorbate, respectively. In all cases, cell death causes hypodiploic DNA staining, evaluated by flow cytometry. Both cell lines can efficiently metabolise ascorbate due to significant levels of NADH-dependent semidehydroascorbate reductase and glutathione-dependent dehydroascorbate reductase. The cell death observed suggests a pro-oxidant, rather than anti-oxidant, role for ascorbic acid at physiological concentrations under these experimental conditions.
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PMID:Cell death by oxidative stress and ascorbic acid regeneration in human neuroectodermal cell lines. 757 46

A sensitive peroxidase-dependent luminol-enhanced chemiluminescence (ECL) assay for determination of hydrogen peroxide (H2O2) generation by tumour cells was established. This test system allows determination of H2O2 in concentrations as low as 25 pmol (50 nmol/L) and yields results which are comparable to those obtained using a less sensitive photometric method and a previously described scopoletin fluorescence assay. After 3 h incubation time 10(4) SK-N-SH neuroblastoma cells released 60 +/- 5 pmol H2O2 in the supernatant and this level was significantly (p < 0.025) increased by about 70% in the presence of 5 pmol (100 ng/mL) recombinant tumour necrosis factor alpha (TNF alpha). In contrast, H2O2 production was slightly reduced by TNF alpha at a very low concentration of 0.5 fmol (0.01 ng/mL).
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PMID:Measurement of endogenous and TNF alpha-mediated H2O2 production in supernatants of SK-N-SH neuroblastoma cells with an enhanced chemiluminescence assay. 798 27

The interactions of nitric oxide (NO) and ascorbate were explored on the control of growth of human brain tumor cells. Sodium nitroprusside, a NO-generating agent, inhibited the growth of SK-N-MC human neuroblastoma cells in a dose-dependent manner. The growth inhibitory effect of nitroprusside was potentiated by sodium ascorbate and inhibited by hemoglobin. Ascorbate-induced potentiation was also observed in U-373 MG human astrocytoma cells. In both tumor cell lines, this potentiation was blocked by catalase, suggesting that hydrogen peroxide may be involved in the potentiation mechanism. In astrocytoma cells, mannitol or deferoxamine also reversed ascorbate-induced potentiation, indicating involvement of hydroxyl radical. These results suggest that the combined treatment with nitroprusside and ascorbate may be a valuable therapeutic strategy for brain tumors.
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PMID:Potentiation of anti-proliferative effect of nitroprusside by ascorbate in human brain tumor cells. 818 Sep 63

The growth, interstitial fluid pressure (IFP) and interstitial fluid velocity (IFV) profiles of a human neuroblastoma propagated in the flank of an immune suppressed rat were characterized. IFP was measured in the tumor center as a function of size, while radial distributions of IFP and IFV were measured in 2-cm tumors. IFP and IFV were measured using the wick-in-needle and clearance of locally generated hydrogen techniques, respectively. These techniques have a high spatial resolution, permit repetitive measurements, and are minimally invasive. We observed that IFP in the neuroblastoma increased as the tumor grew. Furthermore, IFP increased and its IFV decreased from the periphery toward the center of the tumor. Measured IFP and IFV values were compared to theoretical expectations calculated from the Baxter and Jain mathematical model. The predictions were highly correlated to the measured IFP and IFV profiles with the transport impedence parameter alpha 2 = 24.4. From our measurement data and the Baxter-Jain equations, we computed the interstitium hydraulic conductivity for neuroblastoma to be 7.11 x 10(-6) cm2/mm Hg-sec.
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PMID:Characterization of neuroblastoma xenograft in rat flank. I. Growth, interstitial fluid pressure, and interstitial fluid velocity distribution profiles. 824 16


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