Although HCN is a weak acid and normally not considered corrosive, it has a corrosive effect under two special conditions: (1) water solutions of HCN cause transcrystalline stress-cracking of carbon steels under stress even at room temperature and in dilute solution; (2) water solutions of HCN containing sulfuric acid as a stabilizer severely corrode steel above 40 °C and stainless steels above 80 °C.
燃烧热：
642 kJ/mol
汽化热：
25.2 kJ/mol
电离电位：
13.60 eV
聚合：
Can polymerize explosively at 50-60 °C or in the presents of traces of alkali.
Reports of ingestion of cyanides by humans and reports of occupational exposure ... indicate that cyanide is transformed into thiocyanate. ... Conversion of cyanide to thiocyanate is enhanced when cyanide poisoning is treated by intravenous administration of a sulfur donor ... . The sulfur donor must have a sulfane sulfur, a sulfur bonded to another sulfur (e.g., sodium thiosulfate). During conversion by rhodanese, a sulfur atom is transferred from the donor to the enzyme, forming a persulfide intermediate. The persulfide sulfur is then transferred from the enzyme to cyanide, yielding thiocyanate. Thiocyanate is then readily excreted in the urine as the major metabolite. Once thiocyanate is formed, it is not converted back to cyanide. /Cyanide/
The metabolism of cyanide has been studied in animals. The proposed metabolic pathways ... are (1) the major pathway, conversion to thiocyanate by either rhodanese or 3-mercaptopyruvate sulfur transferase; (2) conversion to 2-aminothiazoline-4-carboxylic acid; (3) incorporation into a 1-carbon metabolic pool; or (4) combining with hydroxocobalamin to form cyanocobalamin (vitamin B12). Thiocyanate has been shown to account for 60 to 80% of an administered cyanide dose while 2-aminothiazoline-4-carboxylic acid accounts for about 15% of the dose. /Cyanide/
Although cyanide can interact with substances such as methemoglobin in the bloodstream, the majority of cyanide metabolism occurs within the tissues. Cyanide is metabolized in mammalian systems by one major route and several minor routes. The major route of metabolism for hydrogen cyanide and cyanides is detoxification in the liver by the mitochondrial enzyme rhodanese, which catalyses the transfer of the sulfane sulfur of thiosulfate to the cyanide ion to form thiocyanate ... . About 80% of cyanide is detoxified by this route. The rate-limiting step is the amount of thiosulfate. While rhodanese is present in the mitochondria of all tissues, the species and tissue distributions of rhodanese are highly variable. In general, the highest concentrations of rhodanese are found in the liver, kidney, brain, and muscle, but the supply of thiosulfate is limited. Rhodanese is present in rat nasal mucosal tissues, particularly in the olfactory region, at a 7-fold higher concentration (on a per milligram of mitochondrial protein basis) than in the liver. Dogs have a lower overall activity of rhodanese than monkeys, rats, and rabbits. A number of other sulfur transferases can also metabolize cyanide, and albumin, which carries elemental sulfur in the body in the sulfane form, can assist in the catalysis of cyanide to thiocyanate as well. Cyanide and thiocyanate can also be metabolized by several minor routes, including the combination of cyanide with hydroxycobalamin (vitamin B12a) to yield cyanocobalamin (vitamin B12) and the non-enzymatic combination of cyanide with cystine, forming 2-iminothiazoline-4-carboxylic acid, which appears to be excreted without further change. /Cyanide/
While absorbed cyanide is principally excreted as thiocyanate in the urine, traces of free hydrogen cyanide may also be excreted unchanged in the lungs, saliva, sweat, or urine, as carbon dioxide in expired air, or as beta-thiocyanoalanine in saliva and sweat. /Cyanide/
Organic nitriles are converted into cyanide ions through the action of cytochrome P450 enzymes in the liver. Cyanide is rapidly absorbed and distributed throughout the body. Cyanide is mainly metabolized into thiocyanate by either rhodanese or 3-mercaptopyruvate sulfur transferase. Cyanide metabolites are excreted in the urine. (L96)
IDENTIFICATION AND USE: Hydrogen cyanide is a colorless or pale blue liquid or gas with a faint bitter almond like odor. Hydrogen cyanide is used primarily in the production of substances such as adiponitrile, methyl methacrylate, chelating agents, cyanuric chloride, methionine and its hydroxylated analogues, and sodium and potassium cyanide. Hydrogen cyanide is also used as a fumigant in ships, railroad cars, large buildings, grain silos, and flour mills, as well as in the fumigation of peas and seeds in vacuum chambers. Hydrogen cyanide is formed during the incomplete combustion of nitrogen-containing polymers, such as certain plastics, polyurethanes, and wool. Hydrogen cyanide is also present in cigarette smoke. HUMAN STUDIES: The primary targets of cyanide toxicity in humans are the cardiovascular, respiratory, and central nervous systems. The endocrine system is also a potential target for long term toxicity, as a function of continued exposure to thiocyanate, which prevents the uptake of iodine in the thyroid and acts as a goitrogenic agent. Sequelae after severe acute intoxications may include neuropsychiatric manifestations and Parkinson type disease. Cyanide from tobacco smoke has been implicated as a contributing factor in tobacco alcohol amblyopia. Long term exposure to lower concentrations of cyanide in occupational settings can result in a variety of symptoms related to central nervous system effects. Cyanides are weakly irritating to the skin and eye. ANIMAL STUDIES: The principal features of the toxicity profile for cyanide are its high acute toxicity by all routes of administration, with a very steep and rate-dependent dose effect curve, and chronic toxicity, probably mediated through the main metabolite and detoxification product, thiocyanate. The toxic effects of cyanide ion in humans and animals are generally similar and are believed to result from inactivation of cytochrome oxidase and inhibition of cellular respiration and consequent histotoxic anoxia. The primary targets of cyanide toxicity in animals are the cardiovascular, respiratory, and central nervous systems. The endocrine system is also a potential target for long-term toxicity, as a function of continued exposure to thiocyanate, which prevents the uptake of iodine in the thyroid and acts as a goitrogenic agent. In a 13 week repeated-dose toxicity study in which cyanide was administered in drinking-water, there were no clinical signs associated with central nervous system effects or histopathological effects in the brain or thyroid of rats or mice. There were slight changes in the reproductive tract in male rats. The examination of neurotoxicity in this study was limited to clinical observation and optical microscopy in autopsy. The few available studies specifically intended to investigate neurotoxicity, while reporting adverse effects at exposure levels of 1.2 mg cyanide/kg body weight per day in rats and 0.48 mg cyanide/kg body weight per day in goats, suffer from weaknesses that preclude their quantitative assessment. In relation to characterization of concentration-response for repeated-dose toxicity for inhalation (relevant principally to the occupational environment), in three separate studies in rats, there were no adverse systemic effects in rats exposed to acetone cyanohydrin, which is rapidly hydrolyzed to hydrogen cyanide at physiological pH, at concentrations up to 211 mg/cu m (corresponding to a concentration of 67 mg hydrogen cyanide/cu m). The steepness of the dose effect curve is illustrated by the observation of 30% mortality among rats exposed part of the day to 225 mg acetone cyanohydrin/cu m (71 mg hydrogen cyanide/cu m). ECOTOXICITY STUDIES: Adverse effects of exposure to the low concentrations of cyanide that are generally present in the general environment (<1 ug/cu m in ambient air; <10 ug/L in water) are unlikely.
Organic nitriles decompose into cyanide ions both in vivo and in vitro. Consequently the primary mechanism of toxicity for organic nitriles is their production of toxic cyanide ions or hydrogen cyanide. Cyanide is an inhibitor of cytochrome c oxidase in the fourth complex of the electron transport chain (found in the membrane of the mitochondria of eukaryotic cells). It complexes with the ferric iron atom in this enzyme. The binding of cyanide to this cytochrome prevents transport of electrons from cytochrome c oxidase to oxygen. As a result, the electron transport chain is disrupted and the cell can no longer aerobically produce ATP for energy. Tissues that mainly depend on aerobic respiration, such as the central nervous system and the heart, are particularly affected. Cyanide is also known produce some of its toxic effects by binding to catalase, glutathione peroxidase, methemoglobin, hydroxocobalamin, phosphatase, tyrosinase, ascorbic acid oxidase, xanthine oxidase, succinic dehydrogenase, and Cu/Zn superoxide dismutase. Cyanide binds to the ferric ion of methemoglobin to form inactive cyanmethemoglobin. (L97)
来源:Toxin and Toxin Target Database (T3DB)
毒理性
致癌物分类
对人类无致癌性（未列入国际癌症研究机构IARC清单）。
No indication of carcinogenicity to humans (not listed by IARC).
Exposure to high levels of cyanide for a short time harms the brain and heart and can even cause coma, seizures, apnea, cardiac arrest and death. Chronic inhalation of cyanide causes breathing difficulties, chest pain, vomiting, blood changes, headaches, and enlargement of the thyroid gland. Skin contact with cyanide salts can irritate and produce sores. (L96, L97)
Cyanide as hydrogen cyanide is rapidly absorbed (within seconds) following inhalation exposure. Humans retained 58% of hydrogen cyanide in the lungs after inhaling the gas through normal breathing.
Once cyanide is absorbed, it is rapidly distributed by the blood throughout the body. Tissue levels of hydrogen cyanide were 0.75, 0.42, 0.41, 0.33, and 0.32 mg/100 g of tissue in the lung, heart, blood, kidney, and brain, respectively, in a man who died following inhalation exposure to hydrogen cyanide gas. ... In another case, tissue cyanide levels from a man who died from inhalation of hydrogen cyanide were reported as 0.5 mg per 100 mL of blood and 0.11, 0.07, and 0.03 mg/100 g in the kidney, brain, and liver, respectively. Urinary cyanide levels were reported as 0.2 mg/100 mL, and 0.03 mg/100 g were found in the gastric contents ... .
Rats exposed /by inhalation/ to hydrogen cyanide gas at 356 or 1,180 ppm died within 10 and 5 minutes, respectively. Samples taken immediately after respiration stopped showed that the pattern of tissue distribution of cyanide did not vary with the concentration used. In averaging data for both dose groups, tissue concentrations, reported as ug/g wet weight (ww), were 4.4 in the lungs, 3.0 in the blood, 2.15 in the liver, 1.4 in the brain, and 0.68 in the spleen. Thus, the highest cyanide concentrations were observed in the lung.
Rabbits exposed /by inhalation/ to hydrogen cyanide at 2,714 ppm for 5 minutes had cyanide levels of 170/100 mL in blood and 48 ug/100 mL in plasma, and tissue levels (in units of ug/100 g) of 0 in the liver, 6 in the kidney, 50 in the brain, 62 in the heart, 54 in the lung, and 6 in the spleen. ... Six rabbits exposed dermally (area not reported) to 33.75 mg CN/kg as hydrogen cyanide had blood and serum cyanide levels of 310 and 144 ug/dL, respectively, and tissue levels (ug/100 g) of 26 in liver, 66 in kidney, 97 in brain, 110 in heart, 120 in lungs, and 21 in the spleen.
Investigation of the CH3 + NO reaction in shock waves
摘要：
AbstractThe reaction of CH3 + NO was investigated behind incident shock waves at temperatures between 1300 K and 2080 K. The formation of H atoms and of HCN was studied by time resolved UV absorption and by IR‐emission. OH measurements of Hoffmann et al. were reevaluated with the rate constant of this work. The rate constant for the reaction of CH3 + NO can be expressed byk = (4.0 ± 0.8)·1012 exp (−(8500 ± 500) K/T) cm3 mol−1 s−1.HCN was found to be the main final product of the reaction of CH3 + NO in the temperature range covered. The contribution of the H forming channels is around 20–25% to the main channel.
Electronic Effects in Asymmetric Catalysis: Structural Studies of Precatalysts and Intermediates in Rh-Catalyzed Hydrogenation of Dimethyl Itaconate and Acetamidocinnamic Acid Derivatives Using <i>C</i><sub>2</sub>-Symmetric Diarylphosphinite Ligands
作者：T. V. RajanBabu、Branko Radetich、Kamfia K. You、Timothy A. Ayers、Albert L. Casalnuovo、Joseph C. Calabrese
DOI：10.1021/jo9901182
日期：1999.5.1
largely unaffected by electronic effects, which suggests that other explanations have to be sought for the electronic amplification of enantioselectivity. One possibility is a change in the diastereomeric equilibrium between the initially formed [substrate]Rh(+)[phosphinite] complexes as a function of electronic effect of the ligand. In the Rh-catalyzed hydrogenation of dimethyl itaconate, we have examined
Ethics and Foreign Policy: The Antinomies of New Labour's ‘Third Way’ in Sub-Saharan Africa
作者：Rita Abrahamsen、Paul Williams
DOI：10.1111/1467-9248.00312
日期：2001.6
This article explores how New Labour has attempted to implement its ideas about a ‘third way’ foreign policy in sub-Saharan Africa. Through an examination of British foreign policy practices, we explore whether New Labour has succeeded in finding a ‘third way’ between traditional views of socialism and capitalism in Africa. In particular, the article focuses on New Labour's attempts to build peace, prosperity and democracy on the African continent. We conclude that although New Labour's claims to add an ‘ethical dimension’ to foreign policy have succeeded in giving Britain a higher profile in the international arena, the implementation of such a policy is intrinsically difficult. These difficulties in turn arise from the antinomies embodied in New Labour's policy, or more specifically from the tension between the liberal internationalism of the third way and traditional concerns for the national interest, as well as the contradictions inherent in a commitment to both political and economic liberalism.
Disparate effects of non-steroidal anti-inflammatory drugs on apoptosis in guinea-pig gastric mucous cells: inhibition of basal apoptosis by diclofenac
作者：Miranda Ashton、Peter J Hanson
DOI：10.1038/sj.bjp.0704497
日期：2002.1
Non‐steroidal anti‐inflammatory drugs (NSAIDs) induce apoptosis in gastrointestinal cancer cell lines. Similar actions on normal gastric epithelial cells could contribute to NSAID gastropathy. The present work therefore compared the actions of diclofenac, ibuprofen, indomethacin, and the cyclo‐oxygenase‐2 selective inhibitor, NS‐398, on a primary culture of guinea‐pig gastric mucous epithelial cells.
Cell number was assessed by staining with crystal violet. Apoptotic activity was determined by condensation and fragmentation of nuclei and by assay of caspase‐3‐like activity. Necrosis was evaluated from release of cellular enzymes.
Ibuprofen (250 μM for 24 h) promoted cell loss, and apoptosis, under both basal conditions and when apoptosis was increased by 25 μM N‐Hexanoyl‐D‐sphingosine (C6‐ceramide).
Diclofenac (250 μM for 24 h) reduced the proportion of apoptotic nuclei from 5.2 to 2.1%, and caused inhibition of caspase‐3‐like activity, without causing necrosis under basal conditions. No such reduction in apoptotic activity was evident in the presence of 25 μM C6‐ceramide.
The inhibitory effect of diclofenac on basal caspase‐3‐like activity was also exhibited by the structurally similar mefenamic and flufenamic acids (1–250 μM), but not by niflumic acid.
Inhibition of superoxide production by the cells increased caspase‐3‐like activity, but the inhibitory action of diclofenac on caspase activity remained. Diclofenac did not affect superoxide production.
Diclofenac inhibited caspase‐3‐like activity in cell homogenates and also inhibited human recombinant caspase‐3.
In conclusion, NSAIDs vary in their effect on apoptotic activity in a primary culture of guinea‐pig gastric mucous epithelial cells, and the inhibitory effect of diclofenac on basal apoptosis could involve an action on caspase activity.
British Journal of Pharmacology (2002) 135, 407–416; doi:10.1038/sj.bjp.0704497
非甾体抗炎药（NSAIDs）可诱导胃肠癌细胞系凋亡。类似的作用对正常胃上皮细胞可能导致NSAIDs导致的胃病。因此本研究比较了双氯芬酸、布洛芬、吲哚美辛以及环氧化酶-2选择性抑制剂NS-398对实验用豚鼠胃黏膜上皮细胞培养物的作用。
通过结晶紫染色评估细胞数量。通过细胞核凝缩、破碎和caspase-3样活性测定评估凋亡活性。通过细胞酶释放评估坏死。
布洛芬（250 μM，24小时）在基底条件和C6-神经酰胺（25 μM）增加凋亡条件下均促进细胞丢失及凋亡。
双氯芬酸（250 μM，24小时）将凋亡细胞核比例从5.2%降低至2.1%，抑制caspase-3样活性，且在基底条件下不引起坏死。但在C6-神经酰胺存在下，没有观察到凋亡活性的显著下降。
双氯芬酸对基底caspase-3样活性的抑制作用也被结构相似的甲氯芬酸和氟芬酸（1-250 μM）表现出，但尼美舒利酸没有表现出这种抑制。
抑制细胞中超氧物的产生会增加caspase-3样活性，但双氯芬酸对caspase活性的抑制作用仍然存在。双氯芬酸不影响超氧物的产生。
双氯芬酸抑制细胞匀浆中的caspase-3样活性，并且抑制人重组caspase-3。
结论：NSAIDs对豚鼠胃黏膜上皮细胞原代培养物凋亡活性的影响不同，双氯芬酸对基底凋亡的抑制作用可能涉及对caspase活性的作用。
British Journal of Pharmacology (2002) 135, 407–416; doi:10.1038/sj.bjp.0704497
Novel synthetic route to perfluoroallyl cyanide (PFACN) reacting perfluoroallyl fluorosulfonate with cyanide
作者：Sergey N. Tverdomed、Markus E. Hirschberg、Romana Pajkert、Klaus Hintzer、Gerd-Volker Röschenthaler
DOI：10.1016/j.jfluchem.2018.03.003
日期：2018.6
perfluoroallyl cyanide CF2CFCF2CN (PFACN) is presented. This includes the addition – elimination reaction of cyanide anion with perfluoroallyl fluorosulfate CF2CFCF2OSO2F (PFAFS). The reaction conditions, factorsaffecting the reactivity and regioselectivity of the process, the choice of reagent as well as the course of competitive reactions are discussed, too.
Catalytic Promiscuity of Ancestral Esterases and Hydroxynitrile Lyases
作者：Titu Devamani、Alissa M. Rauwerdink、Mark Lunzer、Bryan J. Jones、Joanna L. Mooney、Maxilmilien Alaric O. Tan、Zhi-Jun Zhang、Jian-He Xu、Antony M. Dean、Romas J. Kazlauskas
DOI：10.1021/jacs.5b12209
日期：2016.1.27
esterase substrates and six lyase substrates found higher catalytic promiscuity among the ancestral enzymes (P < 0.01). Ancestral esterases were more likely to catalyze a lyase reaction than modern esterases, and the ancestral HNL was more likely to catalyze ester hydrolysis than modern HNL's. One ancestral enzyme (HNL1) along the path from esterase to hydroxynitrilelyases was especially promiscuous
