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Query: UMLS:C0027819 (neuroblastoma)
 27,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

As indicated by immunofluorescence with neurofilament antiserum and by electron microscopy two neuroblastoma clones in suspension culture contained a pool of neurofilament subunits which could be induced to assemble into filaments following exposure to vinblastine and colchicine. Under the same culture conditions neuroblastoma cells treated with aluminum extended thick processes with many filaments. The processes were much smaller in nontreated cells but still contained bundles of filaments. These filaments persisted after inhibition of protein synthesis by cycloheximide. In the long neurites formed by cells attached to plastic immunofluorescence with neurofilament antiserum was particularly intense at the growth cone.
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PMID:Neurofilament protein in clonal lines of mouse neuroblastoma. 38 76

Instrumental neutron activation analysis by the monostandard method has been applied to the analyses of biological NBS standard reference materials; 1571 Orchard Leaves and 1577 Bovine Liver. Aluminum foils containing 0.100% gold or 2.00% cobalt were used as the monostandards. The gamma-ray spectral data were recorded on punched paper tape and were analyzed by a computer assisted data processing. The following 25 elements were determined: Al, Ca, Cl Cu, Mg, Mn, V (by short period irradiation), As, Ba, Br, Co, Cr, Cs, Eu, Fe, Hg, K, La, Na, Rb, Sb, Sc, Se, Sm and Zn (by long period irradiation). The results were compared with the certified values by NBS and the reported values in literatures to prove the reliability and accuracy of the monostandard method.
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PMID:Neutron activation analysis of biological materials by the monostandard method. 54 35

The neurotoxic effects of the commercial organic solvents n-hexane and methyl n-butyl ketone (MBK), recently discovered to cause profound peripheral neuropathy in man, were studied in neuronal-like cells in tissue culture. These agents are known to induce marked proliferation of 10nm neurofilaments in peripheral and central axons of both humans and rats. In a murine neuroblastoma cell line, previously reported to show filamentous hyperplasia when exposed to aluminum ions, both MBK and n-hexane induced a highly reproducible series of cytotoxic effects at the light and electron microscopic levels and caused dose-dependent inhibition of cellular proliferation. In contrast, two closely related but clinically non-toxic solvents, methyl isobutyl ketone and methyl ethyl ketone, caused little or no cytopathological or growth inhibiting effects. MBK and its major water soluble derivative, 2,5-hexane dione (HD), produced identical cytotoxic changes in vitro, supporting the postulate that HD is the toxically active agent in victims exposed to MBK. Although MBKlthought MBK and n-hexand adversely affected the extension of maintenance of neuritic processes, electron microscopy and immunofluorescent reaction failed to reveal any proliferation of 10 nm cytoplasmic filaments in the intoxicated cells. Also, these agents had no deleterious effect on in vitro brain microtubule polymerization. In contrast, aluminum ions produced a doserelated inhibition of neurotubule assembly, similar to that seen with the filament-inducing agents colchicine and vinblastine. The results suggest that the fibrous cytoskeleton may not be the primary or essential target of MBK n-hexane and related human neurotoxins.
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PMID:Effects of neurotoxic industrial solvents on cultured neuroblastoma cells: methyl n-butyl ketone, n-hexane and derivatives. 73 76

Patients with aluminum-induced encephalopathy syndromes have been shown to have a high level of aluminum concentration in the brain. In the present study, the effects of aluminum were studied in mouse neuroblastoma cells (N-2A) grown in medium supplemented with aluminum (100 microM). It was found that aluminum enhanced neurite growth within 2 days of exposure. The mean total length of neurites in the control after 14 days in culture was 29.8 +/- 4.7 microns, whereas the neurite length of cells pre-exposed to aluminum for 2 days and then maintained in normal media for an additional 12 days was 56.4 +/- 8.9 microns. Further, the duration of exposure did not significantly promote a greater neurite response. The neurite length of cells exposed to aluminum for 14 days (60.7 +/- 9.6 microns) was not statistically different from that of cells exposed to aluminum for 2 days. Using morin stain, intracellular aluminum was detected within 24 h of exposure in the majority of aluminum-exposed cells. Intracellular aluminum did not disappear from those cells even after they were grown for 12 days in control medium. Our finding suggests that a brief exposure (2 days) to low level aluminum (100 microM) is sufficient to cause long-lasting effects on the morphology of neuroblastoma cells in culture. Such neurite behavior associated with aluminum exposure may suggest a morphological basis for the dementia seen in aluminum encephalopathy.
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PMID:Enhanced neurite growth in cultured neuroblastoma cells exposed to aluminum. 128 Jul 92

We have been investigating the use of three culture types for both screening and mechanistic neurotoxicology in vitro. These are the neuroblastoma cell lines (IMR32 - human; C-1300 - mouse), primary mixed monolayer cultures of the rat and chick embryonic midbrain ('micromass' systems) and organotypic whole rat brain reaggregate cultures. The performance of these models for neurotoxicity resting has been investigated with ethylcholine mustard aziridinium (ECMA), vincristine, aluminium, glutamate receptor antagonists, MPTP, and 'hypothyroidism'. From a 'screening' viewpoint, in vitro exposure through a tiered testing system (ranging from simple cytotoxicological parameters in the neural cell lines to neurotransmitter measurements in the organotypic cultures) may permit detection of CNS neurotoxicity and delineation of possible mechanisms. The type of developmental neurotoxicological information gained is highlighted in the cases of aluminum and the glutamate receptor antagonists. High concentrations of aluminum caused significant neural cell death in differentiated neuroblastoma cell lines after approximately two weeks exposure in vitro. In contrast, cell death was detected in the developing midbrain cultures as early as 24 - 48 hr. Studies in whole brain reaggregates suggest that cholinotoxicity may occur in a similar time-frame and is consistent with some of aluminium's effects in vivo. Preliminary experiments have shown that exposure of immature developing midbrain rat primary cultured neurones to the glutamate receptor antagonists, AP3 and MK-801 induces neural cell death which may relate to control of NGF by glutamate cells. Developing neural culture systems may prove useful for testing agents which cause neurotoxicity through disturbances of neurotrophic function.
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PMID:Models for the in vitro assessment of neurotoxicity in the nervous system in relation to xenobiotic and neurotrophic factor-mediated events. 150 34

The presence of the trivalent metallic cations, aluminum and boron, in the culture medium of differentiated human LAN-5 neuroblastoma cells results in increased amounts of specific isomers of microtubule-associated tau proteins. The cells were differentiated to a neuronal phenotype by the addition of retinoic acid. Six-day exposures of the differentiated cells to a 1-mM dose of aluminum or boron yielded increases in tau protein immunoreactivity to the monoclonal antibodies Tau-1 and Alz-50. Significant increases in immunoreactivity were seen at treatment levels of aluminum down to 100 microM. The increases in tau proteins were independent from increases in levels of total cell protein. Control cultures treated with the divalent cations zinc and iron showed no increases in levels of tau proteins.
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PMID:Effects of aluminum on tau proteins in human neuroblastoma cells. 195 63

The recently reported presence of alumino-silicates in the core of Alzheimer's senile plaques raises a number of questions concerning the little studied area of interactions between solid particles and neuronal tissue. In this preliminary study we report that contact between crystalline alumino-silicates and cultured neuroblastoma cells selectively caused a rapid increase in membrane electrical conductance and loss of excitable activity. Severe morphological deterioration was subsequently evident within 30 min of exposure. Similar effects were induced by a magnesium silicate mineral but not by aluminum hydroxides or by silicon in the form of quartz. Homogeneously charged synthetic particles did not induce changes in electrical function of the cells. These results suggest that a layout incorporating both negative and positive charges, as can be found on the broken edges of platy clay metallo-silicates, and the non-isodiametrical geometry of the particles may be necessary for the acute neurotoxic interaction observed.
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PMID:Toxic effects of alumino-silicates on nerve cells. 208 76

Aluminum uptake studies in viable neuroblastoma cells were performed. Aluminum uptake was largely dependent on the pH of the suspension medium. At physiological pH values, cells were apparently unable to incorporate detectable amounts of aluminum in the absence of proper mediators. Aluminum uptake was enhanced as the pH decreased, attaining a plateau at about pH 6.0. In experiments with 2 x 10(6) cells/ml, pH 6.0, and 25 microM aluminum in the medium, aluminum incorporation reached saturation at 5 nmol of aluminum/mg of cellular protein, accounting for 60-70% of aluminum added. At pH 6.0, cells showed a large capacity for accumulating aluminum; about 70% of intracellular aluminum was associated with the postmitochondrial fraction. At neutral pH, application of apotransferrin seemed to facilitate aluminum translocation into cells via membrane receptors. Fatty acids were also capable of mediating aluminum uptake at neutral pH, probably by forming aluminum-fatty acid complexes. Low molecular weight aluminum chelators, e.g., citrate, inhibited aluminum uptake. Treatment of cells with energy metabolism blockers had virtually no influence on aluminum uptake, indicative of passive mechanisms. The results suggest that aluminum uptake occurs via different modes dependent on growth conditions, such as medium pH.
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PMID:Aluminum uptake by neuroblastoma cells. 211 72

The effects of the neurotoxin aluminum on markers of synaptic neurotransmission, adenosine 3',5'-monophosphate, and neurofilaments have been evaluated in a neuroblastoma x glioma hybridoma (NG108-15). Cells were exposed for 4 days to 2 mM aluminum lactate, a concentration that did not suppress growth. Compared to controls, the activity of choline acetyltransferase was significantly increased by 37% associated with an up-regulation in enzyme activity (Vmax). Muscarinic receptors, measured by [3H]QNB binding, were reduced by 41%. In contrast, the activities of acetylcholinesterase and glutamate decarboxylase were not significantly changed. Aluminum raised the level of cyclic AMP by 20%, although adenylate cyclase activity was unchanged. Small amounts of both phosphorylated and non-phosphorylated neurofilaments were detected in NG108-15 cells. Aluminum intoxication, however, did not alter the quantity, ultrastructure, or immunoreactivity of neurofilaments. Our results demonstrate the capability of aluminum to produce selected changes in cholinergic markers and levels of cyclic AMP in a rapidly dividing cell line.
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PMID:The effect of aluminum on markers for synaptic neurotransmission, cyclic AMP, and neurofilaments in a neuroblastoma x glioma hybridoma (NG108-15). 217 66

NB2a/dl neuroblastoma cells were exposed to aluminum chloride or aluminum lactate (0.1-1 mM) for 3 and 6 days. Additional cultures were exposed to aluminum salts as the cells were stimulated to elaborate axonal neurites by dibutyryl cyclic AMP. By phase-contrast microscopy, aluminum salts had no effect on the morphology of undifferentiated (NB2a(-] or differentiated (NB2a(+] cells, or on neuritic elaboration and maintenance. Silver straining by the Bielschowsky method, however, demonstrated argyrophilic accumulations in perikarya of many NB2a(-) and NB2a(+) cells treated with aluminum salts. At the ultrastructural level, whorls of intermediate filaments were the most prominent abnormalities in neuronal perikarya. Although phosphorylated high-molecular weight neurofilament subunits (NF-H) are normally detected by immunocytochemical analyses only within axonal neurites of NB2a/dl cells, aluminum salt treatment caused the detection of phosphorylated epitopes of NF-H within perikaryal of NB2a(-) and NB2a(+) cytoskeletons, suggesting that the argyrophilic filamentous accumulations are composed at least partly of phosphorylated NF-H.
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PMID:Aluminum salts induce the accumulation of neurofilaments in perikarya of NB2a/dl neuroblastoma. 275 11


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