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)

An analytical method is presented for determining cadmium, copper, and lead by differential pulse anodic stripping voltammetry and zinc by cathodic scan differential pulse voltammetry. Food samples are dry ashed using a sulfuric acid ashing aid, dissolved in dilute nitric acid, buffered at pH approximately 4.3 with an acetate buffer, and quantitatively analyzed using the technique of standard additions at a hanging mercury drop electrode. The quantitation limits (5 times the estimated detection limits) are approximately 5 ng/g for Cd, Cu, and Pb, and 50 ng/g for Zn. Accuracy of the method is established by (a) analysis of NBS Standard Reference Material No. 1577 Bovine Liver, (b) comparison of results obtained by the method described with those obtained by independent analytical methods, and (c) quantitative recovery of analyte metals from fortified, noncanned food samples. Results from an interlaboratory method trial indicate that the method is suitable for the analysis of a variety of food types.
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PMID:Dry ash-voltammetric determination of cadmium, cooper, lead, and zinc in foods. 89 6

A method using electronically excited oxygen for destruction of organic matter and atomic absorption spectrophotometry for the determination of beryllium, cadmium and tellurium in animal tissues is presented. Samples are solubilized in dilute aqua regia after being subjected to an oxygen plasma, low-temperature (less than 190 degrees C) ashing system for 20 to 30 hours. Recovery data from spiked NBS freeze-dried bovine liver indicate a quantitative determination for the three elements. Limits of detection in micrograms of element per milliliter of solubilized sample solution are: beryllium, 0.05; cadmium 0.05; and tellurium, 0.50. Beryllium, cadmium, and tellurium assay data are reported for the fresh tissues of albino rats exposed to inorganic chemicals by oral or intraperitoneal routes. The tissues analyzed include: adrenal, brain, femur, heart, kidney, liver, lung, mesenteric lymph node, pancreas, prostate, seminal vesicle, spleen, testicle, and tracheal-bronchial lymph node.
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PMID:Determination of beryllium, cadmium, and tellurium in animal tissues using electronically excited oxygen and atomic absorption spectrophotometry. 111 Dec 68

A synthetic antisense oligodeoxyribonucleotide with sequence complementary to the messenger RNA (mRNA) coding for human metallothionein (MT) II was prepared and tested for its ability to inhibit both constitutive- and cadmium-induced MT protein synthesis in neuroblastoma-IMR and Chang liver cells in culture. The sense oligonucleotide was also prepared and tested as a control for its sequence-specific effects. Oligonucleotide entry into cells was enhanced through the use of a polybrene carrier so that nearly 30% of a 10 microM dose of oligonucleotide was shown to be associated with cells. The antisense oligonucleotide inhibition of MT protein synthesis rendered both cell types more sensitive to cadmium toxicity. However, the sense oligonucleotide had no effects on either MT protein synthesis or sensitivity to cadmium toxicity.
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PMID:Antisense oligonucleotide-mediated inhibition of metallothionein protein synthesis in neuroblastoma IMR 32 and Chang liver cells in culture. 130 15

We have used single cell imaging of [Ca2+]i and single channel cell-attached patch clamp recording to characterise the Ca2+ channels present on the plasma membrane of retinoic acid-differentiated human neuroblastoma (SH-SY5Y) cells. Exposure to raised K+ (45 or 60 mM) for 1 min resulted in a transient rise in [Ca2+]i which was abolished by cadmium (100 microM). The amplitude of the evoked rise varied from cell to cell. Both omega-Conus toxin (500 nM) and nifedipine (10 microM) reduced, but did not abolish, the rise in [Ca2+]i whereas Bay K 8644 (3 microM) potentiated it. In single channel records both L- and N-type Ca2+ channel openings were observed during membrane depolarisations from a holding potential of -90 mV. L-type channel openings (unitary conductance 22.5 pS) were prolonged by S(+)-PN 202-791 (500 nM) and could still be evoked from a depolarised holding potential (-40 mV). N-type channel openings (unitary conductance 12.5 pS) were unaffected by the dihydropyridine agonist but were inactivated at a holding potential of -40 mV. These results indicate that, in contrast to previous observations using whole cell recording, retinoic acid-differentiated SH-SY5Y cells express both L- and N-type Ca2+ channels.
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PMID:Characterisation of the L- and N-type calcium channels in differentiated SH-SY5Y neuroblastoma cells: calcium imaging and single channel recording. 137 5

1. Pharmacological and kinetic properties of high-voltage-activated (HVA) Ca2+ channel currents were studied using the whole-cell and perforated patch-clamp methods in a mouse neuroblastoma and rat glioma hybrid cell line, NG108-15, differentiated by dibutyryl cyclic AMP or by prostaglandin E1 and theophylline. 2. The HVA currents were separated into two components by use of two organic Ca2+ channel antagonists, omega-conotoxin GVIA (omega CgTX) and a dihydropyridine (DHP) compound, nifedipine. One current component, IDHP, was blocked by nifedipine (Kd = 8.2 nM) and was resistant to omega CgTX. Conversely, the other component, I omega CgTX, was irreversibly blocked by omega CgTX and was resistant to DHPs. Thus, IDHP could be studied in isolation by a short application of omega CgTX, while I omega CgTX could be studied in the presence of nifedipine. 3. The voltage for half-activation of IDHP was smaller than that of I omega CgTX by 13 mV. IDHP was activated at potentials that were subthreshold for voltage-dependent K+ currents of the cell, whereas I omega CgTX was not. 4. Time courses of activation and deactivation of IDHP were faster than those of I omega CgTX. 5. Voltage-dependent inactivation was small for both IDHP and I omega CgTX at any potential. 6. Ca(2+)-dependent inactivation of IDHP was faster and more prominent than that of I omega CgTX. The time course of the Ca(2+)-dependent inactivation of IDHP, but not I omega CgTX, was slowed as the membrane potential was made more positive between -20 and 30 mV, although amplitude of the current was increased. 7. Alkaline earth metal ions carried the two components of IHVA in the same order: Ba2+ greater than Sr2+ greater than Ca2+. 8. Metal ions blocked the two components of IHVA in the same order of potency: Gd3+ greater than La3+ greater than Cd2+ greater than Cu2+ greater than Mn2+ greater than Ni2+. 9. An alkylating agent, N-ethylmaleimide (NEM, 0.1 mM), selectively augmented IDHP by 30%. 10. During the course of cellular differentiation induced by dibutyryl cyclic AMP, IDHP appeared earlier than I omega CgTX. 11. These results indicate that two classes of Ca2+ channels contribute to the HVA currents of this cell line. The DHP-sensitive channel is more apt to generate Ca2+ spikes and Ca2+ plateau potentials than the omega CgTX-sensitive channel.
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PMID:Dihydropyridine-sensitive and omega-conotoxin-sensitive calcium channels in a mammalian neuroblastoma-glioma cell line. 137 34

1. The M-like current IK(M,ng) in differentiated NG108-15 mouse neuroblastoma x rat glioma hybrid cells has been studied using tight-seal, whole-cell patch-clamp recording. 2. When calculated from steady-state current-voltage curves, the conductance underlying IK(M,ng) showed a Boltzmann dependence on voltage with half-activation voltage Vo = -44 mV (in 3 mM [K+]) and slope factor (a) = 8.1 mV/e-fold increase in conductance. In 12 mM [K+] Vo = -38 mV and a = 6.9 mV. The deactivation reciprocal time constant accelerated with hyperpolarization with slope factor 17 mV/e-fold voltage change. 3. The reversal potential for deactivation tail currents varied with external [K+] as if PNa/PK were 0.005. 4. Steady-state current was increased on removing external Ca2+. In the presence of external Ca2+, reactivation of IK(M, ng) after a hyperpolarizing step was delayed. This delay was preceded by an inward Ca2+ current, and coincided with an increase in intracellular [Ca2+] as measured with Indo-1 fluorescence. Elevation of intracellular [Ca2+] with caffeine also reduced IK(M, ng). 5. IK(M, ng) was inhibited by external divalent cations in decreasing order of potency (mM IC50 in parentheses): Zn2+ (0.011) greater than Cu2+ (0.018) greater than Cd2+ (0.070) greater than Ni2+ (0.44) greater than Ba2+ (0.47) greater than Fe2+ (0.69) greater than Mn2+ (0.86) greater than Co2+ (0.92) greater than Ca2+ (5.6) greater than Mg2+ (16) greater than Sr2+ (33). This was not secondary to inhibition of ICa since: (i) inhibition persisted in Ca(2+)-free solution; (ii) La3+ did not inhibit IK(M, ng) at concentrations which inhibited ICa; and (iii) organic Ca2+ channel blockers were ineffective. Inhibition comprised both depression of the maximum conductance and a positive shift of the activation curve. Addition of Ca2+ (10 microM free [Ca2+]) or Ba2+ (1 mM total [Ba2+]) to the pipette solution did not significantly change IK(M, ng). 6. IK(M, ng) was reduced by 9-amino-1,2,3,4-tetrahydroacridine (IC50 8 microM) and quinine (30 microM) but was insensitive to tetraethylammonium (IC50 greater than 30 mM), 4-aminopyridine (greater than 10 mM), apamin (greater than 3 microM) or dendrotoxin (greater than 100 nM). 7. IK(M, ng) was inhibited by bradykinin (1-10 microM) or angiotensin II (1-10 microM), but not by the following other receptor agonists: acetylcholine (10 mM), muscarine (10 microM), noradrenaline (100 microM), adrenaline (100 microM), dopamine (100 microM), histamine (100 microM), 5-hydroxytryptamine (10 microM), Met-enkephalin (1 microM), glycine (100 microM), gamma-aminobutyric acid (100 microM) or baclofen (500 microM).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Kinetic and pharmacological properties of the M-current in rodent neuroblastoma x glioma hybrid cells. 140 9

Effects of Cd2+, Co2+, Fe2+ and Mg2+ (1 microM and 100 microM) and Pb2+ (1 microM and 90 microM) on single-channel properties of the small-conductance (SK) and large-conductance (BK) Ca(2+)-activated K+ channels were investigated in inside-out patches of N1E-115 mouse neuroblastoma cells. Cd2+, Co2+ and Pb2+, but not Fe2+ and Mg2+, cause SK channel opening. The potency of the metals in enhancing the SK channel-open probability follows the sequence Cd2+ approximately Pb2+ > Ca2+ > Co2+ >> Mg2+, Fe2+. The four metals that cause SK channel opening are equipotent in enhancing the opening frequency of SK channels. The BK channel is activated by Pb2+ and Co2+, whereas Cd2+, Fe2+ and Mg2+ are ineffective. The potency of the metals in enhancing BK channel-open probability, open time and opening frequency follows the sequence Pb2+ > Ca2+ > Co2+ >> Cd2+, Mg2+, Fe2+. The results show that SK channels are much more sensitive to Cd2+ than BK channels and indicate that Cd2+ is a selective agonist of SK channels. It is concluded that the various metal ions bind to the same regulatory site(s) at which Ca2+ activates the SK and BK channels under physiological conditions. The different potency sequences of metal ions with respect to BK and SK channel activation indicate that the regulatory sites of these Ca(2+)-activated K+ channels have distinct chemical and physical properties.
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PMID:Divalent cations activate small- (SK) and large-conductance (BK) channels in mouse neuroblastoma cells: selective activation of SK channels by cadmium. 148 79

The whole-cell patch-clamp technique was used to record outward K+ currents in the human neuroblastoma cell line SH-SY5Y. These K+ currents were inhibited by tetraethylammonium (20 mM) and by 4-aminopyridine (2 mM). The Ca2+ channel blocker Cd2+ (0.2 mM) also inhibited K+ currents, indicating that a component was Ca(2+)-activated. Glibenclamide, a presumed selective inhibitor of ATP-sensitive K+ channels, caused reversible inhibitions of the K+ currents and appeared to accelerate their inactivation. These effects were not significantly affected by intracellular ATP (ATPi), and were observed in the presence of 0.2 mM Cd2+. It is concluded that glibenclamide inhibits a voltage-gated, Ca(2+)- and ATPi-independent K+ current in SH-SY5Y cells.
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PMID:Glibenclamide inhibits a voltage-gated K+ current in the human neuroblastoma cell line SH-SY5Y. 154 35

Superfusion with Pb2+ induces a slow, noninactivating and reversible inward current in voltage-clamped N1E-115 neuroblastoma cells. The amplitude of this inward current increases in the range of 1-200 microM Pb/+. Single-channel patch-clamp experiments have revealed that this inward current is mediated by discrete ion channels. Reversal potentials from linear I-V relationships are close to 0 mV for whole-cell and single-channel currents and the single-channel conductance amounts to 24 pS. The Pb2(+)-induced membrane current is not mediated by various known types of ion channels, since it is not blocked by external tetrodotoxin, tetraethylammonium, D-tubocurarine, atropine, ICS 205-930 and by internal EGTA. In Na(+)-free solutions superfusion with Pb2+ neither evokes a whole-cell inward current, nor single-channel openings. At -80 mV the open-time distribution of the single channels activated by 1 microM Pb2+ is dual exponential with time constants of 17 and 194 msec. When the Pb2+ concentration is increased from 1 to 20 microM these time constants decrease to 2 and 13 msec, but the amplitude of single-channel currents remains -1.9 nA. Cd2+ and Al3+ induce inward currents and single-channel openings similar to Pb2+. Time constants fitted to the open-time distribution of single channels are 14 and 135 msec in the presence of 1 microM Cd2+ and 15 and 99 msec in the presence of 50 microM Al3+. Conversely, Cu2+ induces an irreversible inward current in neuroblastoma cells. Single-channel openings are undetected in the presence of Cu2+ and in Na(+)-free solutions Cu2+ is still able to induce an inward current. It is concluded that Pb2+, Cd2+ and possibly Al3+ activate a novel type of metal ion-activated (MIA) channel in N1E-115 cells.
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PMID:Novel type of ion channel activated by Pb2+, Cd2+, and Al3+ in cultured mouse neuroblastoma cells. 169 42

Expression of myc-box genes can be reduced by Interferon (c-myc in Daudi cells) or Retinoic acid (N-myc in neuroblastoma cells). Interferon did not reduce N-myc expression in neuroblastoma cells. However, after transfection of the human neuroblastoma cell line LS with a vector, providing the Cadmium inducible expression of an antisense N-myc transcript, drastic reduction of N-myc RNA was achieved in these cells by incubation with Cadmium and Interferon. Treatment with Cadmium alone resulted in a comparably small reduction of N-myc transcripts in these cells. Interferon alone did not appreciably affect N-myc expression. Reduction of N-myc was accompanied with reduced cell proliferation and morphological differentiation. It is assumed that most of the inhibitory effects observed are mediated by the Interferon inducible 2-5A system.
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PMID:Reduction of N-myc expression by antisense RNA is amplified by interferon: possible involvement of the 2-5A system. 169 69


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