Topic
Sodium cyanide
About: Sodium cyanide is a research topic. Over the lifetime, 1144 publications have been published within this topic receiving 17972 citations. The topic is also known as: sodium salt of hydrocyanic acid.
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TL;DR: The methods were tested with samples from central and peripheral nervous tissues and purified enzymes and the values of choline acetyltransferase activity obtained in the presence of sodium cyanide or EDTA and synthetic acetyl-CoA were similar to those obtained with acetyl -CoA synthesized in situ.
Abstract: 1. The methods for the assay of choline acetyltransferase were based on the reaction between labelled acetyl-CoA and unlabelled choline to give labelled acetylcholine. 2. Both synthetic acetyl-CoA and acetyl-CoA formed from sodium [1-(14)C]acetate or sodium [(3)H]acetate by incubation with CoA, ATP, Mg(2+) and extract from acetone-dried pigeon liver were used. 3. [1-(14)C]Acetylcholine was isolated by extraction with ketonic sodium tetraphenylboron. 4. [(3)H]Acetylcholine was precipitated with sodium tetraphenylboron to remove a ketone-soluble contaminant in sodium [(3)H]acetate and then extracted with ketonic sodium tetraphenylboron. 5. The values of choline acetyltransferase activity obtained in the presence of sodium cyanide or EDTA and synthetic acetyl-CoA were similar to those obtained with acetyl-CoA synthesized in situ. 6. The assay of acetylcholinesterase was based on the formation of labelled acetate from labelled acetylcholine. The labelled acetylcholine could be quantitatively removed from the acetate by extraction with ketonic sodium tetraphenylboron. 7. The methods were tested with samples from central and peripheral nervous tissues and purified enzymes. 8. The blank values for choline acetyltransferase and acetylcholinesterase corresponded to the activities in 20ng. and 5ng. of brain tissue respectively.
1,033 citations
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TL;DR: Observations suggest that damage in hypoxic neurons is mediated by synaptic activity, and cell death could be prevented by treatment with magnesium, which eliminates synaptic activity.
Abstract: Cultured hippocampal neurons, when exposed to cyanide or an anoxic atmosphere in the early stages of differentiation, were not visibly affected. However, neurons in the mature cultures died when exposed to cyanide or anoxia. Cell death could be prevented by treatment with magnesium, which eliminates synaptic activity. These observations suggest that damage in hypoxic neurons is mediated by synaptic activity.
439 citations
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TL;DR: RuCl3-catalyzed oxidative cyanation of tertiary amines with sodium cyanide under molecular oxygen (1 atm) at 60 degrees C gives the corresponding alpha-aminonitriles, which are versatile synthetic intermediates of various compounds such as amino acids and unsymmetrical 1,2-diamines in excellent yields.
Abstract: RuCl3-catalyzed oxidative cyanation of tertiary amines with sodium cyanide under molecular oxygen (1 atm) at 60 °C gives the corresponding α-aminonitriles, which are versatile synthetic intermediates of various compounds such as amino acids and unsymmetrical 1,2-diamines, in excellent yields. This reaction is clean and should be an environmentally benign and useful process.
405 citations
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TL;DR: Results suggest that extracellular GLU accumulation and subsequent activation of GLU receptors were involved in the NaCN response, and that a general elevation in cytoplasmic calcium does not necessarily predict neurodegeneration.
Abstract: Because hypoxic/ischemic neurodegeneration appears to be in part linked to glutamate neurotoxicity, we measured intracellular calcium (Ca2+i) levels in cultured hippocampal neurons during exposure to toxic doses of glutamate (GLU) and to an anoxic environment simulated by sodium cyanide (NaCN). Changes in Ca2+i produced by cyanide greatly exceeded those induced by GLU. The NaCN response was mimicked when oxidative metabolism was also disrupted by sodium azide, oligomycin, or dinitrophenol. Noncompetitive NMDA receptor antagonists and enzymatic GLU degradation abolished the GLU-induced Ca2+i increases and attenuated those produced by NaCN. Only NaCN-induced increases were blocked when dantrolene and ruthenium red were applied to prevent release from intracellular pools. All responses were reduced proportionally in the absence of added external calcium. These results suggest that extracellular GLU accumulation and subsequent activation of GLU receptors were involved in the NaCN response. During such metabolic compromise, however, GLU-induced elevations of Ca2+i were enormously amplified. In parallel toxicity studies, NaCN was not neurotoxic despite the large elevations in Ca2+i, indicating that a general elevation in cytoplasmic calcium does not necessarily predict neurodegeneration.
277 citations
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TL;DR: The results indicate that the carotid chemoreceptor function in Wistar rats in normal while functional aortic chemoreceptors are absent in them.
Abstract: Carotid and aortic chemoreceptor function was studied in normal Wistar rats. Sodium cyanide, lobeline HCl, and doxapram HCl in the doses of 2–400 mug/kg injected into the external carotid artery st...
229 citations