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)

Pretreatment of syngeneic strain A mice with aldehyde-fixed neuroblastoma cells (clone NB6R) almost completely protected the mice against challenge with viable NB6R cells. In contrast, tumor growth was enhanced in mice treated with fixed cells after challenge with viable cells.
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PMID:Modification of growth of neuroblastoma cells in syngeneic mice by aldehyde-treated neuroblastoma cells. 126 64

We have developed a new assay method for phospholipase A2 (EC 3.1.1.4.), towards ethanolamine plasmalogen using pyrenesulfonyl-labeled plasmenylethanolamine as the substrate. This procedure is sensitive to about 3 pmol/ml per min and is absolutely specific for plasmalogen. In this method, the product of phospholipase A2, pyrenesulfonyl-labeled lysoplasmalogen, is hydrolyzed to aldehyde and labeled glycerophosphoethanolamine with hydrochloric acid exposure, and after TLC separation, the pyrenesulfonyl-glycerophosphoethanolamine is quantitated spectrofluorometrically. The excitation and emission wave lengths were 340 and 376 nm, respectively. The activity of bovine brain homogenate was 44.1 +/- 6.47 pmol/min per mg protein (n = 3). Among bovine brain subcellular fractions, the distribution and specific activity of the enzymes were highest in cytosol (38.7 +/- 1.58% and 102.6 +/- 16.2 pmol/min per mg protein, n = 3). The activities of neural tumor cells, PC12 pheochromocytoma, Neuro2A and SKNSH neuroblastoma and U1242MG glioblastoma, were 34.4 +/- 6.83 (n = 5), 7.05 +/- 0.97 (n = 4), 5.25 +/- 1.69 (n = 5), and 9.68 +/- 1.35 (n = 4), pmol/min per mg protein (M +/- S.E.M.), respectively.
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PMID:Phospholipase A2 activities with a plasmalogen substrate in brain and in neural tumor cells: a sensitive and specific assay using pyrenesulfonyl-labeled plasmenylethanolamine. 217 64

The cytochemical properties of intracellular membrane systems which are likely to be subcellular sites of glycoprotein oligosaccharide synthesis and trafficking have been compared in cultured neuroblastoma cells (as a potential model system) and in Purkinje neurons of rat cerebellum. In aldehyde-fixed N18 cells, permeabilized with Triton X-100, concanavalin A (Con A) binding sites were found in the somata, neurites, and growth cones. Con A binding sites in growth cones appeared as a fine, membranous network. Wheat germ agglutinin (WGA) binding sites were restricted to the perinuclear region of the soma and to the distal tips of growing neurites. As shown previously, Purkinje cell somata and presynaptic terminals also contain Con A binding sites. In this study, WGA and succinylated WGA binding sites were observed in the presynaptic terminals of Purkinje cells. Neuraminidase enzyme digestion prior to lectin labeling removed or greatly reduced WGA binding in the neuropil of the deep nucleus but not in presynaptic terminals of Purkinje cells. Succinylated WGA binding sites were not affected by neuraminidase digestion. Neuraminidase digestion also exposed Ricinis communis agglutinin I binding sites in the neuropil and in synaptic terminals of Purkinje cells. These results in combination with previous studies of intracellular lectin cytochemistry of neurons in the central nervous system demonstrate the similarity of these cells to neuroblastoma cells in their intracellular lectin binding characteristics. Results of the lectin cytochemical studies after neuraminidase digestion of presynaptic terminals support the possibility that neurons may use a post- or extra-Golgi system for the addition of peripheral sugars to the oligosaccharides of certain glycoproteins destined for the cell surface.
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PMID:A comparative study of the intracellular lectin binding sites of neurons in culture with neurons in situ. 241 90

The presence of 1% ethanol in culture medium during heat treatment (40 degrees C for 8 hours and 43 degrees C for 15 minutes) was sufficient to enhance the effect of hyperthermia on murine neuroblastoma cells (NBP2) in culture, on the criteria of growth (number of viable cells per dish) and survival (colony formation). However, the metabolites of ethanol, acetaldehyde, and sodium acetate at concentrations of 0.003% and 0.125% in culture medium, respectively, under the same experimental conditions did not modify the effect of heat (40 degrees C) on these cells. The presence of same concentration of ethanol, acetaldehyde, or sodium acetate for 15 minutes or 8 hours at 37 degrees C did not affect the growth or the survival of NB cells in culture. These results suggest that ethanol itself rather than its metabolites is responsible for the enhancement of heat effect on NB cells. When ethanol and its metabolites were allowed to remain in the culture medium for the entire periods of heat treatment and observation, they also enhanced the effects of heat on NB cells; however, acetaldehyde was more effective.
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PMID:Ethanol. A heat sensitizer on neuroblastoma cells in culture. 394 38

Neuroblastoma tumors, as well as cultured cells of neuroblastoma, contain high monoamine oxidase activity. The major deaminated metabolite of tyramine-H(3) in the incubation mixtures with the tumors or with the cultured cells is p-hydroxyphenylacetaldehyde. Upon addition of reduced nicotinamide-adenine dinucleotide phosphate, the aldehyde was further metabolized by the reductive pathway to p-hydroxyphenylethanol, whereas upon addition of nicotinamide-adenine dinucleotide phosphate the aldehyde was only metabolized to a minor extent by the oxidative pathway to p-hydroxyphenylacetic acid. Aldehyde dehydrogenase activity is very low in the neuroblastoma tumors and in the cultured neuroblastoma cells. The generation of aldehydes and alcohols by the action of monoamine oxidase suggests that the deaminated metabolites of biogenic amines might exhibit some toxic effects in neuroblastoma patients.
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PMID:Tyramine-H3: deaminated metabolites in neuroblastoma tumors and in continuous cell line of a neuroblastoma. 438 60

In murine C1300 neuroblastoma cells, clone Neuro 2A, the major fraction of the necessary increase in cell surface area during the cell cycle occurs within a short period around mitosis. During this period cell cycle-related modulations in a number of structural, dynamic and transport properties are most prominent. In this study we have examined the mechanism of rapid plasma membrane growth during mitosis, and the resulting changes in the ultrastructural features of the plasma membrane, by scanning and freeze-fracture electron microscopy as well as by electron microscopy of ultrathin sections. Our observations show that plasma membrane growth occurs by the fusion with and the incorporation into the plasma membrane of cytoplasmic multilamellar, lipidic membrane vesicles. Such vesicles are not observed at other times in the cell cycle. As a consequence, IMP-free domains appear transiently in the mitotic and early post-mitotic plasma membrane. Comparison of replicas prepared from glutaraldehyde-fixed cells and unfixed, ultrarapidly frozen cells showed that aldehyde fixation artefactually induces a bleb-like appearance of these domains. The IMP-free domains disappear in the G1-phase as a result of the mobilization and lateral redistribution of membrane components. It is argued that mitotic membrane growth by preferential incorporation of membrane lipids not only serves to accomodate for the necessary increase in cell surface area, but also provides a mechanism for plasma membrane-mediated regulation of the cell cycle.
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PMID:Ultrastructural aspects of rapid plasma membrane growth in mitotic neuroblastoma cells. 666 97

A new method was developed to follow the translocation of gangliosides from their site of synthesis within the cell to the plasma membrane. Cultured mouse neuroblastoma N18 and rat glioma C6 cells were labeled for increasing times with D- [1-3H]galactose and then subjected to mild oxidation with NaIO4. Under the conditions chosen, oxidation was essentially restricted to cell-surface sialic acid residues, which were converted to derivatives with an aldehyde function. The labeled gangliosides were isolated from the cells and reacted with dinitrophenylhydrazine to form dinitrophenyl (DNP) derivatives of the oxidized gangliosides. The DNP-gangliosides then were separated from their unmodified counterparts by thin-layer chromatography. Thus, the rate of labeling of surface gangliosides was distinguished from the rate of labeling of total gangliosides. Our results indicated that the transfer of gangliosides from the site of synthesis to the cell surface required approximately 20 min and that newly synthesized gangliosides appeared to be transported to the plasma membrane at a constant rate. No essential differences were found in the rates of translocation of different ganglioside species by N18 cells or between gangliosides of N18 and C6 cells.
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PMID:Translocation of newly synthesized gangliosides to the cell surface. 711 67

Antiserum was produced in rabbits against the polyamine spermidine (Spd) conjugated to bovine serum albumin (BSA). The reactivity of the serum to Spd and a variety of structurally related compounds was quantified by a new immunocytochemical model system incorporating an enzyme-linked immunosorbent assay (ELISA) binding test. This is based on the principle of coupling these compounds to the wells of microtiter plate activated with poly-L-lysine and glutaraldehyde and incubating the wells by the indirect immunoperoxidase method. The antiserum showed a 25% cross reaction with spermine (Spm), putrescine (Put), and cadaverine (Cad), and a 1% cross reaction with 1,3-diaminopropane (Dap), but no cross reaction with monoacetyl polyamines and amino acids. The antibody binding was inhibited most effectively by absorption of the antiserum with N1-acetylspermidine and Spd in the ELISA inhibition test. Also, immunoblot analysis of the antiserum with nitrocellulose paper gave completely identical results to the ELISA binding tests. Spd-like immunoreactivities in human melanoma BD and neuroblastoma IMR 32 cell lines are presented as examples of the staining pattern obtained with the antiserum. Absorption of the serum with N1-acetylspermidine and Spd was demonstrated to abolish the immunostaining reaction. The immunohistochemical model is simple: amines and amino acids are bound in the same way as in aldehyde-fixed tissues and, in comparison to immunoblot analysis, the immunoreactivity can be more easily and accurately quantified by assay with the antibody. The model should prove useful in assessing the specificity of other antisera.
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PMID:A new enzyme-linked immunosorbent assay (ELISA) for studying immunocytochemical procedures using an antiserum produced against spermidine as a model. 840 72

We examined the effects of 2-methoxyestradiol, a metabolite of estradiol, on cell death in retinoic acid (RA)-differentiated neuroblastoma SH-SY5Y cell cultures. Cell death was induced by 2-methoxyestradiol in a concentration-dependent manner. Estradiol and 2-methoxyestradiol failed to induce cell death. The cell death response to 2-methoxyestradiol was sensitive to the protein synthesis inhibitor cycloheximide and the apopain inhibitor Ac-Asp-Glu-Val-Asp-H(aldehyde). 2-Methoxyestradiol also induced internucleosomal for and endogenous neuroactive steroid metabolite in the etiology of some neurodegenerative diseases.
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PMID:The endogenous estrogen metabolite 2-methoxyestradiol induces apoptotic neuronal cell death in vitro. 862 72

An endogenous neurotoxin, N-methyl(R)salsolinol, has been proved to be involved in the pathogenesis of Parkinson's disease. Increased level of N-methyl(R)salsolinol in the cerebrospinal fluid and high activity of its synthesizing (R)salsolinol N-methyltransferase in lymphocytes were confirmed in the majority of parkinsonian patients. Recently this neurotoxin was found to induce apoptosis in human dopaminergic neuroblastoma SH-SY5Y cells. In this study, we tried to elucidate the intracellular mechanism of apoptosis induced by N-methyl(R)salsolinol, and proved activation of caspase 3 after incubation with this toxin by Western blot analysis. Further, a caspase 3 inhibitor, acetyl-L-aspartyl-L-glutamyl-L-valyl-L-aspartic aldehyde, prevented the nucleosomal DNA fragmentation completely. These results demonstrate that caspase 3 mediates apoptosis induced by an endogenous neurotoxin, N-methyl(R)salsolinol, which may cause apoptotic cell death of dopamine neurons in Parkinson's disease.
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PMID:Apoptosis induced by an endogenous neurotoxin, N-methyl(R)salsolinol, is mediated by activation of caspase 3. 1038 Sep 99


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