Thiocyanate poisoning

Experimental studies with southern armyworm larvae and thiocyanate — one of the in vivo cyanide metabolites — showed that 5000 mg thiocyanate/kg diet reduced pupation by 77%, completely inhibited oviposition, and reduced adult emergence by 80% (Brattsten et al. 1983), strongly suggesting that thiocyanate poisoning is the primary effect of high dietary cyanide levels in southern army worms. 

The drug must be administered as a controlled continuous infusion, and the patient must be closely observed. Most hypertensive patients respond to an infusion of 0.25-1.5 flg/kg/min. Higher infusion rates are needed to produce controlled hypotension in normotensive patients under surgical anesthesia. Infusion of nitroprusside at rates >5 flg/kg/min over a prolonged period can cause cyanide and/or thiocyanate poisoning. Patients receiving other antihypertensive medications usually require less nitroprusside to lower blood pressure. If infusion rates of 10 pg/kg/min do not produce adequate reduction of blood pressure within 10 minutes, the rate of administration of nitroprusside should be reduced to minimize potential toxicity. 

The thiosulfate reaction with cyanide to give thiocyanate is the basis for the use of thiosulfate as an antidote in cyanide poisoning ... 

Compounds such as hydrogen sulfide and cyanides are the most common metal surface poisoners occurring in process units subject to aqueous-phase hydrogen attack. In many process units, these compounds can be effectively eliminated and hydrogen diffusion stopped by adding ammonium polysulfides and oxygen to the process streams which converts the compounds to polysulfides and thiocyanates, provided the pH is kept on the alkaline side. 

Mercury (Mercuric) Sulfocyanate (Mercuric thiocyanate, Mercuric rhodamide). Hg(SCN)2, mw 316.77, white powd mp (decompn), poisonous si sol in w (0.07g/100g at 25°), sol in ale and in NH3 NH4 salts. Can be prepd by pptn of Hg nitrate with Amm sulfocyanate and subsequent soln in a large quant of hot w, followed by crystn. Used in prepn of Pharaoh s Serpent and other fireworks (Ref 4)... 

After acidification with H3PO3 the extremely poisonous HCN and H2S formed may be evaporated by refluxing under a fume hood subsequently the thiocyanate can be titrated [10, 11]. The degradation of the polysulfide in the reactions at Eqs. (35) and (36) results in discoloration of the solutions. 

We have studied the hydrogenolysis of 2-(perfluorohexyl)ethane thiocyanate to 2-(perfluorohexyl)ethane thiol. It was discovered that perfluoroalkyl thiocyanates can be reduced to thiols and co-product hydrogen cyanide with molecular hydrogen in the presence of a carbon-supported palladium-tin catalyst. This result is surprising since it is known that palladium and other gronps 8 to 10 metal catalysts are poisoned by the product thiol, traces of hydrogen snlfide byprodnct, and the hydrogen cyanide co-product. For that reason, we characterized the catalyst to understand why it was so robust under conditions that would normally poison snch a catalyst. 

It is apparent that a new synthetic methodology, preferably catalytic, is needed for the synthesis of this important class of 2-(perfinoroalkyl)ethane thiols. In this context, a variety of catalysts was examined to determine if they wonld catalyze the hydrogenolysis of 2-(perfinorohexyl)ethane thiocyanate. In the conrse of this study, much to our surprise, it was discovered that a carbon supported Pd-Sn would catalyze the reaction. It is known that palladium and other group Vtll metal catalysts are poisoned by the product thiol, traces of hydrogen sulfide byproduct, and the hydrogen cyanide co-prodnct (6), but our observations are that this catalyst is surprisingly robust in the reaction medium. 

The subjects of this chapter are the exploration of the scope and hmitations of the new Pd-Sn catalyzed hydrogenolysis route for the synthesis of thiols via 2-(perfluoroalkyl)ethane thiocyanate, the characterization of the surprisingly active and robust Pd-Sn catalysts, and the attempted correlation of the characterization of the catalysts with observed onset of hydrogenolysis reactivity and snrprisingly long lifetime in the presence of known catalyst poisons. ... 

The disulfide intermediate was also hydrogenolyzed very efficiently at about 2-3 times the rate of the thiocyanate in selected solvents such as tetrahydrofuran at a lower temperature and pressure, as illustrated in Table 15.2. Of course, in the disulfide hydrogenolysis, no hydrogen cyanide was available as a coproduct to poison the palladium catalyst. 

It is well known that palladium on carbon catalysts are poisoned by hydrogen cyanide and thiol products or hydrogen sulfide (6). Therefore, it was of interest to investigate the reduction of perfluoroalkyl thiocyanates as a function of tin concentration, keeping the concentration of palladium and reaction conditions constant. Figure 15.1 delineates the % conversion vs. Sn/Pd ratio, under the same reaction conditions of 175°C, 700 psig H2 for 2 hours with 5% Pd on carbon catalysts in ethyl acetate solvent at a 1000 1 substrate catalyst molar ratio. The increase in... 

Bitter almond odor associated with patient suggests cyanide poisoning, metabolic acidosis, cyanide (blood) or thiocyanate (blood or urine) levels. 

Methaemoglobin forming compounds should be used cautiously in victims suffering from concurrent carbon monoxide poisoning or hypoxia. The second approach calls for provision of additional sulfur groups to enhance the detoxification of cyanide and thiocyanate by endogenous rhodanese this comes about by giving sodium thiosulphate. 

CobaltCII) sulfate monohydrate, 7 231 Cobalt sulfide, poisons in representative reactions, 5 258t CobaltCII) sulfide, uses, 7 241t CobaltCII) thiocyanate, uses, 7 241t Cobalt tin alumina blue spinel, formula and DCMA number, 7 348t... 

HCN is a systemic poison toxicity is due to inhibition of cytochrome oxidase, which prevents cellular utilization of oxygen. Inhibition of the terminal step of electron transport in cells of the brain results in loss of consciousness, respiratory arrest, and ultimately, death. Stimulation of the chemoreceptors of the carotid and aortic bodies produces a brief period of hyperpnea cardiac irregularities may also occur. The biochemical mechanisms of cyanide action are the same for all mammalian species. HCN is metabolized by the enzyme rhodanese which catalyzes the transfer of sulfur from thiosulfate to cyanide to yield the relatively nontoxic thiocyanate. 

The metabolism of cyanide has been studied in animals. The proposed metabolic pathways shown in Figure 2-3 are (1) the major pathway, conversion to thiocyanate by either rhodanese or 3-mercapto-pyruvate sulfur transferase (2) conversion to 2-aminothiazoline-4-carboxylic acid (Wood and Cooley 1956) (3) incorporation into a 1-carbon metabolic pool (Boxer and Richards 1952) or (4) combining with hydroxocobalamin to form cyanocobalamin (vitamin B12) (Ansell and Lewis 1970). Thiocyanate has been shown to account for 60-80% of an administered cyanide dose (Blakley and Coop 1949 Wood and Cooley 1956) while 2-aminothiazoline-4-carboxylic acid accounts for about 15% of the dose (Wood and Cooley 1956). The conversion of cyanide to thiocyanate was first demonstrated in 1894. Conversion of cyanide to thiocyanate is enhanced when cyanide poisoning is treated by intravenous administration of a sulfur donor (Smith 1996 Way 1984). 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... 

Cyanide antagonists help convert cyanide to thiocyanate. Sodium thiosulfate is commonly used in cases of cyanide poisoning, (Bonsall 1984 Mengel et al. 1989 Schubert and Brill 1968 Sylvester et al. 

Acute poisoning only occurs when the detoxification mechanism is overwhelmed. This reaction is enhanced by giving sodium thiosulfate and sodium nitrate intravenously as 20% solutions in a 3 1 ratio, which is a recommended antidote for acute cyanide poisoning. It is the thiocyanate metabolite that causes chronic disease when cyanide forage is ingested over an extended period. 

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