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 endoinulinase produced by Chaetomium sp. C34 was purified to electrophoretic homogeneity, with recovery of 7.7% activity and purification factor of 30.8 fold by five steps including ammonium sulfate precipitation, DEAE-cellulose, Q-sepharose Fast Flow, Sephacryl S-200 and Pre-Packed Hydrophobic Column. Its subunit molecular weight was estimated to be about 66kD by SDS-PAGE. The optimum temperature and pH of the enzyme activity were 50 approximately 55 degrees C and 6.0 respectively. The K(m) and V(max) values for inulin were 0.199 mmol/L and 115 micromol/(mg x min) respectively. Cu2+ completely inhibited inulinase activity. An appreciable loss of activity was observed in presence of NBS, Mn2+, Zn2+, Fe2+ and EDTA. A ratio of inulinase activity to invertase activity (I/S) of 20 was found in purified inulinase. The endoinulinase hydrolyzed inulin and liberated inulooligosaccharides. But it lacked activity toward melezitose or raffinose.
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PMID:[Purification and properties of endoinulinase from Chaetomium sp]. 1611 Sep 61

Methanol extracts of domestic plants of Korea were evaluated as a potential inhibitor of neutral pH optimum and membrane-associated 60 kDa sphingomyelinase (N-SMase) activity. In this study, we partially purified N-SMase from bovine brain membranes using ammonium sulfate. It was purified approximately 163-fold by the sequential use of DE52, Butyl-Toyopearl, DEAE-Cellulose, and Phenyl-5PW column chromatographies. The purified N-SMase activity was assayed in the presence of the plant extracts of three hundreds species. Based on the in vitro assay, three plant extracts significantly inhibited the N-SMase activity in a time- and concentration-dependent manner. To further examine the inhibitory pattern, a Dixon plot was constructed for each of the plant extracts. The extracts of Abies nephrolepis, Acer tegmentosum, and Ginkgo biloba revealed a competitive inhibition with the inhibition constant (Ki) of 11.9 microg/ mL, 9.4 microg/mL, and 12.9 microg/mL, respectively. These extracts also inhibited in a dose-dependent manner the production of ceramide induced by serum deprivation in human neuroblastoma cell line SH-SY5Y.
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PMID:Identification of three competitive inhibitors for membrane-associated, Mg2+-dependent and neutral 60 kDa sphingomyelinase activity. 1617 18

Ferritin, a ubiquitously distributed iron storage protein, has been reported to interact with microtubules in vitro (Hasan et al., 2005, FEBS journal 272:822-831). Here, we demonstrate that ferritin binds with the microtubules in an oligomeric form and that the microtubule-bound ferritin contains more than two-fold amount of iron compared to the unbound ferritin fraction in vitro. Indirect immunofluorescence microscopy showed that a significant fraction of the ferritin molecules colocalized with the microtubules as oligomers in a wide variety of cell lines. These findings are consistent with the immediate oligomerization of rhodamine-labeled ferritin, microinjected in living human hepatoma cells. Ferritin oligomers were dynamic in the cytoplasm, and an anti-microtubule drug significantly inhibited their intracellular movement. Treatment of cells with an iron donor, ferric ammonium citrate, remarkably increased the number of cells containing ferritin oligomers. On the other hand, when the cells, such as mouse neuroblastoma cells, were deprived of iron, ferritin oligomers were localized in the microtubule dense, neurite shafts, but were disappeared from the microtubule deficient neurite tips. These data indicate that the microtubules provide a scaffold for the cytoplasmic distribution and transport of the iron-rich ferritin and implicate the role of microtubules in iron metabolism.
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PMID:Ferritin forms dynamic oligomers to associate with microtubules in vivo: implication for the role of microtubules in iron metabolism. 1660 54

A simple high performance liquid chromatographic technique has been developed to analyze urinary metabolites of catecholamines along with ultraviolet detection. The metabolites were extracted in ethyl acetate when a biospecimen was saturated with ammonium sulfate. Separation was effected on a column containing 5 microm of Diasphere C16 in the two-stage low-pressure gradient. The eluents were based on acetonitrile-isopropanol-0.02 M citric acid, added by potassium perchlorate, 5 g/l (3 and 10% of its organic phase). The complete chromatographic cycle was about 30 min. The extraction degree was 86-106%. The sensitivity (detection limit) of the technique at a signal/noise ratio of > 3 was 2 ng (vanilylmandelic acid), 3 ng (iso-vanilylmandelic acid) and 3,4-dioxyphenylacetic acid), 1 ng (5-hydroxyindoleacetic acid), and 5 ng (homovanillic acid). The linear dependence was in the range of 5 to 1,000 ng. The author presents his own findings and the data available in the literature on the content of metabolites of catecholamines and serotonin in healthy individuals and in patients with catecholamine-secreting tumors (pheochromocytoma and neuroblastoma).
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PMID:[HPLC analysis of urinary metabolites of catecholamines and serotonin for routine laboratory practice]. 1661 Jun 27

Nitrate as one of the two main nitrogen source compounds, acts also as a potent signal substance in plant growth and development. It is increasingly interesting to determine whether nitrate itself or the derived metabolites acts as a signal during the regulation. Rice seedlings were treated with different nitrogen forms (NO(-)(3) vs. NH(+)(4)) and total proteins extracted either from nitrate-fed or ammonium-fed leaves were separated by two-dimensional gel electrophoresis (2-DE), and then the differentially-expressed proteins were identified by MALDI-TOF-MS or ESI-Q-TOF-MS. Twenty-six proteins were up-regulated with NO(-)(3) as the nitrogen source while 6 were up-regulated with NH(+)(4) as the nitrogen source. MS analysis, in combination with database searching, allowed for only a total of 11 proteins identified with significant probability. Among them 7 nitrate-up-regulated proteins were identified, i.e., a PSII oxygen-evolving complex protein 1 (N1), a putative CC-NBS-LRR resistance protein MLA13 (N2), a 23-kD polypeptide of PSII (N3), a translation initiation factor eIF-5A (N5), a putative PSII oxygen-evolving complex protein 2 precursor (N8), an unknown protein (N17), and the ubiquitin carrier protein UBC7 (N18). Four ammonium-up-regulated proteins were identified as the ATP synthase beta subunit (A1), the putative aminotransferase (A3), a hypothetical protein (A5), and OSJNBb0032K15.22 (A6). These results give some new insights into both the biochemical adaptation of plant to different nitrogen forms (NO(-)(3)/NH(+)(4)) and the differences in responses signaled by NO(-)(3)/NH(+)(4) in rice.
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PMID:Differential expression of proteins in rice leaves cultivated with different forms of nitrogen nutrients. 1695 90

Classical hallmarks of Alzheimer's disease (AD) are a synaptic loss, cholinergic neuron death, and abnormal protein deposition, particularly of toxic amyloid-beta peptide (Abeta) that is derived from amyloid-beta protein precursor (AbetaPP) by the action of beta- and gamma-secretases. The trigger(s) initiating the biochemical cascades that underpin these hallmarks have yet to be fully elucidated. The typical forebrain cholinergic cell demise associated with AD brain results in a loss of presynaptic cholinergic markers and acetylcholine (ACh). Neurine (vinyl-trimethyl-ammonium hydroxide) is a breakdown product of ACh, consequent to autolysis and is an organic poison found in cadavre brain. The time- and concentration-dependent actions of neurine were assessed in human neuroblastoma (NB, SK-N-SH) cells in culture by quantifying cell viability by lactate dehydrogenase (LDH) and MTS assay, and AbetaPP and Abeta levels by Western blot and ELISA. NB cells displayed evidence of toxicity to neurine at > or = 3 mg/ml, as demonstrated by elevated LDH levels in the culture media and a reduced cell viability shown by the MTS assay. Using subtoxic concentrations of neurine, elevations in AbetaPP and Abeta1-40 peptide levels were detected in conditioned media samples.
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PMID:Neurine, an acetylcholine autolysis product, elevates secreted amyloid-beta protein precursor and amyloid-beta peptide levels, and lowers neuronal cell viability in culture: a role in Alzheimer's disease? 1698 75

Co-Administration of Cu(II) chelates are reported to decrease life threatening Cisplatin [Pt(II) (NH3)2(CL)2]-induced acute degenerative renal, gastrointestinal, thymic, and bone marrow states consistent with serious necrotizing and immune-mediated inflammatory disease. Initially it was found that copper sulfate treatment completely prevented lethality as well as gastric and nephrotoxicity without compromising Pt(II) (NH3)2(CL) 2 antineoplastic activity, which led to suggestions that prior Cu(II)-treatment be used clinically to prevent serious side effects of Pt(II) (NH3)2(CL)2-treatment. In the course of these studies it was discovered that Cu(II)-treatments alone inhibited neoplastic growth and increased survival of rat and mouse models of cancer. Subsequently it was discovered that a stable non-toxic and non-polar lipophilic chelate, Copper(II)2(3,5-diisopropylsalicylate)4, caused redifferentiation of cultured neuroblastoma and mouse muscle-implanted mammary adenocarcinoma without neoplastic cell killing. Another stable non-toxic and non-polar lipophilic chelate, Copper(II)2(3,5-ditertiarybutylsalicylate)4, was found to prevent Bax-initiated and caspases-3-activation mediated apoptosis. These remarkable observations are concluded to be due to enzyme-mimetic or modulating reactivities of Cu(II) chelates and/or facilitation of Cu(II or I)-dependent enzyme syntheses required to overcome inflammatory-neoplastic disease states. Further, approaches to treating neoplastic diseases by removal of Cu from tissues with ammonium tetrathiomolybdate in an anticopper approach to therapy are not well founded based upon existing scientific literature.
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PMID:Co-treatment with copper compounds dramatically decreases toxicities observed with cisplatin cancer therapy and the anticancer efficacy of some copper chelates supports the conclusion that copper chelate therapy may be markedly more effective and less toxic than cisplatin therapy. 1758 59

High blood levels of ammonium/ammonia (NH(4)(+)/NH(3)) are associated with severe neurotoxicity as observed in hepatic encephalopathy (HE). Astrocytes are the main targets of ammonium toxicity, while neuronal cells are less vulnerable. In the present study, an astrocytoma cell line 1321N1 and a neuroblastoma glioma hybrid cell line NG108-15 were used as model systems for astrocytes and neuronal cells, respectively. Ammonium salts evoked a transient increase in intracellular calcium concentrations ([Ca(2+)](i)) in astrocytoma (EC(50)=6.38 mM), but not in NG108-15 cells. The ammonium-induced increase in [Ca(2+)](i) was due to an intracellular effect of NH(4)(+)/NH(3) and was independent of extracellular calcium. Acetate completely inhibited the ammonium effect. Ammonium potently reduced calcium signaling by G(q) protein-coupled receptors (H(1) and M3) expressed on the cells. Ammonium (5 mM) also significantly inhibited the proliferation of 1321N1 astrocytoma cells. While mRNA for the mammalian ammonium transporters RhBG and RhCG could not be detected in 1321N1 astrocytoma cells, both transporters were expressed in NG108-15 cells. RhBG and RhBC in brain may promote the excretion of NH(3)/NH(4)(+) from neuronal cells. Cellular uptake of NH(4)(+)/NH(3) was mainly by passive diffusion of NH(3). Human 1321N1 astrocytoma cells appear to be an excellent, easily accessible human model for studying HE, which can substitute animal studies, while NG108-15 cells may be useful for investigating the role of the recently discovered Rhesus family type ammonium transporters in neuronal cells. Our findings may contribute to the understanding of pathologic ammonium effects in different brain cells, and to the treatment of hyperammonemia.
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PMID:Ammonium-induced calcium mobilization in 1321N1 astrocytoma cells. 1806 Dec 26

The determination of manganese in the presence of iron and chromium by differential pulse voltammetry and fundamental harmonic alternating current voltammetry was compared, including the case of very high element concentration ratios. The voltammetric measurements were carried out using a stationary mercury electrode in ammonia-ammonium chloride buffer (pH 9.6). The analytical procedure was verified by the analysis of the standard reference materials Portland Cement BCS 372, Spectrographic Zinc Spelter NBS-SRM 631, Stainless Steel (AISI 321) NBS-SRM 121d and Highly Alloyed Steel Eurostandard 281-1. Precision and accuracy, expressed as relative standard deviation and relative error respectively, were of the order of 3-5%, while the detection limit for each element was around 1 x 10(-9) M. The standard addition technique improved the resolution of the voltammetric methods, within a maximum experimental error of 5%, even in the case of very high concentration ratios, that is outside the non-interference concentration ratios 69:1 >c(Fe):c(Mn) > 1:74; 35:1 > c(Fe):c(Cr) > 1:30 and 63:1 > c(Fe):c(Mn) > 1:65; 32:1 > c(Fe):c(Cr) > 1:31 for the differential pulse and alternating current techniques respectively, extrapolating the linear section of the i(p) vs. concentration analytical calibration function for the element present at the lowest concentration. In contrast, the element with the greatest concentration was determined by the relevant calibration curve.
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PMID:Trace level voltammetric determination of manganese, iron and chromium in real samples in the presence of each other. 1896 61

The transient receptor potential vanilloid type 1 (TRPV1) has been reported as one of the key components in the pain pathway. Activation of the receptor causes a Ca(2+) influx in sensory C-fibres with secondary effects leading to neurogenic inflammation in the surrounding tissue. We have earlier reported specific activation of TRPV1 by surfactant-containing hygiene products. We have continued this project by investigating activation of the TRPV1 by shampoo and soap ingredients in low concentrations measured as intracellular Ca(2+) influxes in stably TRPV1-expressing neuroblastoma SH-SY5Y cells. As a TRPV1 specific control, the TRPV1 antagonist capsazepine was used. The response was quantified as the product induced Ca(2+) influx during 2 min in relation to the maximum response induced by the TRPV1 agonist capsaicin. The results show that anionic alkyl linear surfactant ingredients such as sodium lauryl sulphate, sodium laureth sulphate, ammonium lauryl sulphate, sodium C12-15 pareth sulphate and N-lauroylsarcosine concentration-dependently induced Ca(2+) influx that could be addressed to TRPV1. The cationic surfactants benzalkonium chloride and cetylpyridinium chloride induced a Ca(2+) influx that was not TRPV1 mediated as well as the zwitterionic surfactant cocamidopropyl betaine, the non-linear anionic surfactant sodium deoxycholate and the non-ionic surfactant Triton-X. These results reveal a new mechanistic pathway for surfactant-induced nociception.
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PMID:Anionic linear aliphatic surfactants activate TRPV1: a possible endpoint for estimation of detergent induced eye nociception? 1954 Mar 28


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