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PubMed1994

The utilization of thiocyanate as a nitrogen source by a heterotrophic bacterium: the degradative pathway involves formation of ammonia and tetrathionate.

A Gram-negative soil bacterium (isolate 26B) has been shown to utilize up to 100 mM thiocyanate as a source of nitrogen when supplied with glucose as the source of carbon and energy. During growth of isolate 26B with thiocyanate as the source of nitrogen, no ammonia, nitrate, nitrite, cyanide, cyanate, sulfate, sulfite, sulfide or carbonyl sulfide was detected in the growth medium. Growth of the bacterium on 14C-labelled thiocyanate (1.6 microCi) and glucose, yielded 14C-labelled carbon dioxide (0.9 microCi). The addition of 2.9 mM thiocyanate to a bacterial suspension in phosphate buffer (50 mM, pH 7.4) resulted in the utilization of 2.1 mM thiocyanate and the production of 2.0 mM ammonia. This activity was inducible and only occurred after growth of the bacterium with thiocyanate as the source of nitrogen. Tetrathionate (0.7 mM) was detected in the medium after the utilization of thiocyanate (2.4 mM) by a suspension of the bacterium in phosphate buffer, and thiosulfate (1.0 mM) was detected as an intermediate. The addition of sulfide or thiosulfate to the bacterial suspension also resulted in the formation of tetrathionate. The utilization of both of these compounds appeared to be constitutive. A pathway for thiocyanate utilization by isolate 26B is proposed which involves the hydrolysis of thiocyanate to produce cyanate and sulfide. The cyanate then undergoes further hydrolysis to form ammonia and carbon dioxide. The sulfide is ultimately oxidized to tetrathionate via a pathway which includes thiosulfate.

Ammonia↗

PubMedDate not supplied

[Thiocyanate--a biologically active ion of veterinary and medical relevance].

Thiocyanate-ions are ubiquitous in living nature. They are important for the cell-function and the ongoing of vital functions. Therefore they are an essential factor in both, animal and human being. The Thiocyanate-ions are brought in alimentary but also built by the organism itself. Beneath the guarantee for many different body-functions Thiocyanate-ions are an important part of the immune response. To that belongs their involvement in H2O2-Thiocyanate Peroxidase-Systems. Furthermore Thiocyanate-ions are agents for cell-protection and for the repair-mechanism of the host in the struggle with toxic substances of germs. Therefore they also have a tumour-prophylactic effect. Thiocyanate-ions participate at physiochemical reactions which due the protein-conformation. There are hypothesis that a deficiency of Thiocyanate-ions may be a co-factor for causative agents of diseases such as Cystic Fibrosis and Transmissible Spongiform Encephalopathia. References for calculations of the alimentary balance are given, if deficiency of Thiocyanate-ions occurs. From the view of an optimal animal-feeding the sufficient alimentary supply of Thiocyanate-ions and their precursors is mentioned.

Animal Feed↗

PubMed1994

Thiocyanate levels of mainly dietary origin in serum and urine from a human population sample in Port Harcourt, Nigeria.

Thiocyanate levels were determined in serum and urine samples obtained from a human population sample of healthy non-smoking volunteers (aged between 14 and 30 years) of both sexes known to eat gari-based meals at least once a day. The samples were collected before and 3-4 hours after a gari- or rice-based meal. The values obtained before the test meals showed a wide variation, ranging between 39.20 +/- 1.95 to 160.95 +/- 8.06 mumol/l of serum, and 81.92 +/- 9.78 to 294.01 +/- 14.70 mumol/l of urine. For each volunteer, the serum and urine thiocyanate were affected by the test meals. Average increases of 18 and 20% were observed for serum and urine thiocyanate, respectively, following a gari-based meal. A rice-based meal produced, on the average, 10% decrease in both serum and urine thiocyanate. No significant effect of sex or age on the thiocyanate levels was observed. The gari samples used in the study, as well as random samples from the locality of study, had no detectable thiocyanate but contained between 0.013 and 0.015 mg cyanide per kg of gari. These findings indicate that conversion to thiocyanate is a significant pathway in the metabolism of HCN and contributes significantly to thiocyanate found in body fluids and tissues of man. In addition, support is provided for the possible involvement of the sulphur-transferases in the process of cyanide detoxication.

Adolescent↗

PubMed1987

Detoxication of cyanide in the chicken by conversion to thiocyanate, as influenced by the availability of transferable sulphur.

The urinary excretion of thiocyanate by hens after dosage with cyanide (30 mumol) has been studied in a series of acute experiments involving 6 hr urine collection periods. More than half of the dose could be recovered as thiocyanate when cyanide was given by intravenous infusion and the rate of excretion closely paralleled plasma thiocyanate concentration. Little cyanide was excreted directly. The excretion of thiosulphate fell by an amount that suggested that availability of sulphane sulphur might limit the extent of conversion. However, neither thiosulphate nor sulphur amino acids enhanced thiocyanate excretion when they were infused together with cyanide; indeed, thiocyanate excretion decreased as the level of sulphur compound given was increased. Both nitrite and sulphite depressed thiocyanate excretion also but they differed in their effects on plasma thiocyanate levels and the pattern of urinary excretion. Comparison of excretion from both sides of the kidneys separately emphasised the importance of the first pass of cyanide in its conversion to thiocyanate. The results suggest that although sulphur availability may be limited the in vivo production of sulphite also restricts cyanide detoxication.

Animals↗

PubMed1984

Serum and tissue thiocyanate concentrations in growing pigs fed cassava peel or corn based diets containing graded protein levels.

Thiocyanate concentrations of serum, liver, kidney, spleen and longissimus dorsi were determined in 64 growing Large White x Landrace pigs offered 8 experimental isocaloric diets containing different levels of cassava peel and crude protein. Cassava peel increased serum thiocyanate on day 60 (P less than 0.01) and day 90 (P less than 0.01) of the trial, while the crude protein level increased it (P less than 0.05) on days 30 and 90, respectively. Interaction of the two factors was significant on day 30 (P less than 0.05) and day 90 (P less than 0.05). There was a correlation between cyanide intake and serum thiocyanate level. Coefficient of determination revealed that cyanide alone accounted for 28.5; 60.6 and 48.8% variation in serum thiocyanate on days 30, 60 and 90, respectively. Liver, spleen and longissimus dorsi thiocyanate were affected by dietary protein intake (P less than 0.05). Thiocyanate concentration was higher (P less than 0.05) on cassava peel diet. Generally, crude protein at 5% reduced organ and muscle thiocyanate concentrations. A diet containing 112.2-117.3 mg/kg hydrocyanic acid (HCN) affected serum but not organ and muscle thiocyanate in protein-sufficient diets.

Analysis of Variance↗

PubMed1991

Lactoperoxidase-catalyzed oxidation of thiocyanate by hydrogen peroxide: 15N nuclear magnetic resonance and optical spectral studies.

To establish the agent(s) responsible for the activity of the lactoperoxidase (LPO)/SCN-/H2O2 system, the oxidation of thiocyanate with hydrogen peroxide, catalyzed by lactoperoxidase, has been studied by 15N NMR and optical spectroscopy at different concentrations of thiocyanate and hydrogen peroxide and at different pHs. The formation of hypothiocyanite ion (OSCN-) as one of the oxidation products correlated well with the activity of the LPO/SCN-/H2O2 system and was maximum when the concentrations of the H2O2 and SCN- were nearly the same and the pH was less than 6.0. At [H2O2]/[SCN-] = 1, OSCN- decomposed very slowly back to thiocyanate. When the ratio [H2O2]/[SCN-] was above 2, formation of CN- was observed, which was confirmed by 15N NMR and also by changes in the optical spectrum of LPO. The oxidation of thiocyanate by H2O2 in the presence of LPO does not take place at pH greater than 8.0. Since thiocyanate does not bind to LPO above this pH, the binding of thiocyanate to LPO is considered to be prerequisite for the oxidation of thiocyanate. Maximum inhibition of oxygen uptake by Streptococcus cremoris 972 bacteria was observed when hydrogen peroxide and thiocyanate were present in equimolar amounts and the pH was below 6.0.

Animals↗

PubMed1987

A study of serum thiocyanate concentrations in office workers as a means of validating smoking histories and assessing passive exposure to cigarette smoke.

Patients in clinical practice often falsely report their smoking status. To see if this was so in occupational surveys we have validated smoking histories (using a serum thiocyanate assay) in 206 randomly sampled office workers who completed a smoking questionnaire administered by a doctor. Past and present cigarette consumption was determined with an assessment of exposure to passive cigarette smoke at home and at work in the non-smokers. Serum thiocyanate concentrations were measured by the ferric nitrate method. All smoking groups showed mean thiocyanate concentrations greater than non-smokers except those smoking five or fewer cigarettes a day. There was a significant increase in plasma thiocyanate with increasing smoking (p less than 0.01). Non-smokers with and without exposure to passive smoke could not be separated by thiocyanate concentration. In our hands serum thiocyanate concentrations identified moderate and heavy smokers but could not distinguish between non-smokers, light smokers, and passive smokers. Fourteen non-smokers had serum thiocyanate concentrations higher than 70 mumol/l which were still raised on a repeat sample. On a further questionnaire two admitted to smoking. To help confirm non-smoking status, expired carbon monoxide levels were also checked in this group. One person had a level of 22 ppm and subsequently admitted to smoking. In the others the levels were less than or equal to 10 ppm. Using a combination of serum thiocyanate assay and exhaled breath carbon monoxide levels, non-smoking was confirmed in 98% of those stating that they were non-smokers. In non-smokers exposure to passive cigarette smoke was much more likely to occur at work than at home.

Environmental Exposure↗

PubMedDate not supplied

Umbilical cord thiocyanate and thyroid function in intrauterine growth-restricted infants of the smoking gravida.

OBJECTIVE: We evaluated maternal and umbilical cord thiocyanate and thyroid function in intrauterine growth-restricted infants of smoking mothers. STUDY DESIGN: One hundred six mother-infant pairs were studied and divided into four groups: smokers with appropriate for gestational age infants (n = 37), smokers with intrauterine growth-restricted infants (n = 19), nonsmokers with appropriate for gestational age infants (n = 33), and nonsmokers with intrauterine growth-restricted infants (n = 17). Sera from mothers were analyzed for thiocyanate levels. Serum from umbilical cord blood was analyzed for thiocyanate, thyroxine, resin triiodothyronine uptake, and thyroid-stimulating hormone. The free thyroxine index was then calculated. RESULTS: A significant correlation was found between maternal and umbilical cord thiocyanate levels (r = 0.90, p < 0.0001). Maternal and umbilical cord thiocyanate concentrations correlated with increased maternal cigarette use. For appropriate for gestational age and intrauterine growth-restricted infants, mean maternal and umbilical cord thiocyanate levels were not significantly different. The umbilical cord thiocyanate level did not correlate with thyroid function or birth weight. The umbilical cord thyroxine level was lower in nonsmokers than in smokers. CONCLUSION: Thiocyanate was not more concentrated in the intrauterine growth-restricted infant and did not correlate with thyroid function or birth weight. The thyroxine level was decreased significantly in intrauterine growth-restricted infants born to nonsmoking mothers. Further studies are necessary to evaluate the effects of smoking on thyroid function and on fetal growth and development.

Case-Control Studies↗

PubMed1990

Microbial transformation of thiocyanate.

Thiocyanate is present in appreciable concentration in coal carbonization wastewater along with other toxicants like phenols, cyanide, sulphide and ammonia. This paper encompasses studies on biodegradation of thiocyanate by a microbial consortium obtained from a biological treatment plant receiving coal carbonization wastewater. Effects of secondary toxicants and growth stimulants on thiocyanate oxidation by the consortium, and thiocyanate transformation in actual and partially treated coal carbonization waste, have also been studied. Results indicate that the consortium can degrade thiocyanate up to 1400 mg litre(-1) in batch culture with 10 mg litre(-1) of initial inoculum within a period of 6 days. Phenol above 500 mg litre(-1) and cyanide at 10 mg litre(-1) completely inhibits thiocyanate oxidation. Sulphide at 32 mg litre(-1) and ammonia at 4000 mg litre(-1) at neutral pH prolongs thiocyanate oxidation from 3 to 6 days and from 4 to 7.5 days, respectively. These studies reveal that elimination of phenolics, their oxidized products, ammonia, cyanides and sulphides is a pre-requisite for effective thiocyanate removal from the waste by the consortium. Bacteria of the genera Pseudomonas and Bacillus dominate the consortium.

Journal Article↗

PubMed1979

Kinetics of elimination of thiocyanate in 7 healthy subjects and in 8 subjects with renal failure.

The concentration of thiocyanate in the serum of eight test subjects with renal failure and seven healthy control subjects was measured, as it declined with time, after oral doses of thiocyanate or i.v. injections of nitroprusside had been administered. Additional measurements were taken, on the healthy subjects only, of the concentrations of thiocyanate in the urine, and also of the influence of an increased chloride intake on the rate of elimination of thiocyanate. For the healthy subjects an elimination half-life of between one and five days (mean c. 3 days) was found. Increasing the chloride elimination rate to approximately twice normal did not significantly speed up the rate of thiocyanate elimination. The amounts of thiocyanate which had been administered as doses reappeared almost exclusively in the urine. For the subjects with renal failure, the elimination half-life had a mean value of approximately nine days. The elimination constants were found to be proportional to the creatinine-clearance rates. The ke value at a creatinine-clearance of zero ml/min was approximately 15% of the ke value at a creatinine-clearance rate of 120 ml/min. The distribution volumes for thiocyanate were greater for the patients with renal failure than for the healthy subjects. The conclusions for therapies using nitroprusside are discussed.

Adult↗

PubMed1995

Effect of thiocyanate on AMPA receptor mediated responses in excised patches and hippocampal slices.

The binding affinity of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors for [3H]AMPA is increased 10-30-fold by the chaotropic anion thiocyanate. The present experiments tested if thiocyanate alters AMPA receptor mediated current fluxes and if any such effects are reflected in the waveform of synaptic responses. Currents were measured after a step application of glutamate or AMPA to patches excised from pyramidal cells of hippocampal slice cultures. Application of 1 mM AMPA produced responses with an average peak amplitude of 86 pA at -50 mV and a 10-90% rise time of 1.7 +/- 0.1 ms; the responses desensitized to a steady-state level below 10% of the peak current with a time constant of 11.1 +/- 0.7 ms. Glutamate in presence of D-amino-phosphonopentanoate produced similar responses which were inhibited by 6-cyano-7-nitro-quinoxaline-dione and enhanced by aniracetam or cyclothiazide and thus are characteristic for AMPA receptors. Thiocyanate accelerated the decay of AMPA responses two-fold and reduced the peak current by 30-50% with an EC50 of 3.2 mM which is comparable to its EC50 for enhancing binding. Effects on the desensitization of glutamate induced responses were much smaller and only evident at the highest thiocyanate concentration; no effect was seen on response amplitude. Binding and physiological effects can be adequately explained by assuming that thiocyanate enhances conversion from the sensitive to the desensitized state of the receptor and reduces ligand dissociation from the desensitized state. Synaptic responses were measured in disinhibited hippocampal slices. Perfusion with 20 mM sodium thiocyanate increased the slope of the field excitatory postsynaptic potential by 44.9 +/- 4.2% and reduced its decay time by 10.4 +/- 4.3%. The former effect appears to result at least in part from an increase in transmitter release since it was accompanied by a decrease in paired-pulse facilitation and was reduced in magnitude after enhancing transmitter release. The decrease in the decay time constant points to an effect of thiocyanate on AMPA receptors in situ which is similar to that seen in excised patches. These results demonstrate that an increase in binding affinity may be indicative of reduced rather than enhanced current flow through AMPA receptors. In addition, the results provide further evidence that the kinetics of the AMPA receptor channel contribute significantly to at least the decay phase of fast excitatory synaptic responses.

Animals↗

PubMed1998

Characterization of the interaction between bovine pancreatic trypsin inhibitor and thiocyanate by NMR.

The interaction between Bovine Pancreatic Trypsin Inhibitor and thiocyanate was studied using NMR spectroscopy following several experimental approaches. The chemical shift variations of the BPTI protons in the absence and in the presence of increasing thiocyanate concentrations (up to 0.2 M) were significant (> 0.05 ppm) for 30 protein protons belonging to 20 residues. The largest deviation, 0.2 ppm, was observed for the amide backbone proton of Arg42 in the absence of thiocyanate and in the presence of 40 molar equivalents of thiocyanate. The influence of the presence of thiocyanate on the electrostatic potential surrounding the protein was demonstrated by NOESY spectra selective at the water frequency: the presence of SCN- favours acid catalysed exchange and disfavours base catalysis. However, a specific effect of thiocyanate was pointed out since the comparison of the chemical shifts in the presence of 40 molar equivalents of KSCN and KCl, respectively, showed much more as well as larger deviations compared to measurements in the absence of salt. A dissociation constant, KD, for a 1/1 complex between BPTI and thiocyanate was calculated from chemical shifts measurements: KD = 89 +/- 8 mM. A second value, KD = 99 +/- 10 mM, was extracted from SC15N relaxation time measurements.

Animals↗

PubMed1997

Effect of thiocyanate on microtubule assembly in rat brain during postnatal development.

The effects of feeding thiocyanate (a goitrogen derived from thioglucosides, which are naturally occurring in certain foods) to female rats throughout gestation and lactation on a microtubule assembly of pups during postnatal development were examined. Microtubules, which are important components of the neuronal cell cytoskeleton, may serve as markers of neurite growth. A progressive increase with age in the initial rate of microtubule assembly was apparent in both untreated control and thiocyanate-treated rat pups in the cerebrum, cerebellum and brainstem. Thiocyanate treatment did not alter the tubulin content at any of the developmental stages studied (7, 14 and 21 days postnatal). However, examination of the microtubule assembly revealed a markedly reduced polymerization of tubulin into microtubules in brain regions of thiocyanate-treated rats compared with untreated controls. The effect of thiocyanate on microtubule assembly was evident at all three ages (7, 14 and 21 days). Thiocyanate-induced hypothyroidism increased the lag period for initiation of assembly and also altered the initial rate of microtubule formation. This study suggests that a partial suppression of thyroid function by thiocyanate, as evidenced by a decrease in circulating concentrations of thyroxine, could bring about alterations in microtubule formation during brain development and suggests the possibility of an impairment in the process of microtubule metabolism.

Analysis of Variance↗

PubMed1989

Binding of thiocyanate to lactoperoxidase: 1H and 15N nuclear magnetic resonance studies.

The binding of thiocyanate to lactoperoxidase (LPO) has been investigated by 1H and 15N NMR spectroscopy. 1H NMR of LPO shows that the major broad heme methyl proton resonance at about 61 ppm is shifted upfield by addition of the thiocyanate, indicating binding of the thiocyanate to the enzyme. The pH dependence of line width of 15N resonance of SC15N- in the presence of the enzyme has revealed that the binding of the thiocyanate to the enzyme is facilitated by protonation of an ionizable group (with pKa of 6.4), which is presumably distal histidine. Dissociation constants (KD) of SC15N-/LPO, SC15N-/LPO/I-, and SC15N-/LPO/CN- equilibria have been determined by 15N T1 measurements and found to be 90 +/- 5, 173 +/- 20, and 83 +/- 6 mM, respectively. On the basis of these values of KD, it is suggested that the iodide ion inhibits the binding of the thiocyanate but cyanide ion does not. The thiocyanate is shown to bind at the same site of LPO as iodide does, but the binding is considerably weaker and is away from the ferric ion. The distance of 15N of the bound thiocyanate ion from the iron is determined to be 7.2 +/- 0.2 A from the 15N T1 measurements.

Animals↗

PubMedDate not supplied

Biokinetic evaluation and modeling of continuous thiocyanate biodegradation by Klebsiella sp.

Biokinetics for autotrophic degradation of thiocyanate using batch culture of Klebsiella sp. were evaluated both analytically and numerically. A sequential approach with an analytical method followed by a numerical approximation was used to evaluate and to ensure the accuracy of the parameter estimation. The nonlinear least-squares method with a 95% confidence interval was employed. The growth conditions were maintained at pH 7 and 38 degrees C for all experiments. With an automated incubation and turbidity reader, a total of 16 different initial thiocyanate concentrations, ranging from 10 to 300 mg L(-1), were used to develop a kinetic expression of specific growth rate as a function of substrate concentration. The biodegradation of thiocyanate with Klebsiella sp. followed a substrate inhibition pattern. Three identical automated bioreactors with working volumes of 1.5 L, equipped with sterilizable sampling ports, were also used for the numerical approximation of the biokinetic parameters in batch mode. A fourth order Runge-Kutta method was used to approximate the substrate inhibition kinetics of the Klebsiella sp. utilizing thiocyanate. Although the kinetic coefficients estimated by analytical and numerical methods were not statistically different at a 0.05 alpha level, model responses of numerical approximation generated a better prediction of changes in thiocyanate and cell mass concentrations. The hypothetical maximum growth rate, micro m, half saturation coefficient, Ks, microbial yield coefficient, Y, cell mass decay rate coefficient, kd, and substrate inhibition coefficient, Ksi, were evaluated as being 0.62 +/- 0.05 d(-1), 85 +/- 8 mg SCN- L(-1), 0.076 +/- 0.011 mg cell mass (mg SCN)(-1), 0.03 +/- 0.002 d(-1), and 131 +/- 22 mg SCN- L(-1), respectively. The calculated maximal substrate concentration, Sm, and apparent maximum specific growth rate, micro'm, were 105.5 +/- 8.7 mg SCN- L(-1) and 0.24 +/- 0.01 d(-1), respectively. Using these estimated parameters, the theoretical performance of the continuous operation was also illustrated, which depicts the residual thiocyanate and Klebsiella sp. concentrations in the non-steady and steady states at different hydraulic retention times (HRTs). Assuming the influent concentration of 250 mg SCN- L(-1), the expected treatment efficiency ranged from 94.9% to 69.4% between 20 and 5 days HRT, respectively. Klebsiella sp. was expected to be washed out at 4.8 days HRT, thus resulting in no treatment of thiocyanate.

Hydrolysis↗

PubMed1970

The oxidation of reduced nicotinamide nucleotides by hydrogen peroside in the presence of lactoperoxidase and thiocyanate, iodide or bromide.

Lactoperoxidase (EC 1.11.1.7) catalysed the oxidation of NADH by hydrogen peroxide in the presence of either thiocyanate, iodide or bromide. In the presence of thiocyanate, net oxidation of thiocyanate occurred simultaneously with the oxidation of NADH, but in the presence of iodide or bromide, only the oxidation of NADH occurred to a significant extent. In the presence of thiocyanate or bromide, NADH was oxidized to NAD(+) but in the presence of iodide, an oxidation product with spectral and chemical properties distinct from NAD(+) was formed. Thiocyanate, iodide and bromide appeared to function in the oxidation of NADH by themselves being oxidized to products which in turn oxidized NADH, rather than by activating the enzyme. Iodine, which oxidized NADH non-enzymically, appeared to be an intermediate in the oxidation of NADH in the presence of iodide. NADPH was oxidized similarly under the same conditions. An assessment was made of the rates of these oxidation reactions, together with the rates of other lactoperoxidase-catalysed reactions, at physiological concentrations of thiocyanate, iodide and bromide. The results indicated that in milk and saliva the oxidation of thiocyanate to a bacterial inhibitor was likely to predominate over the oxidation of NADH.

Alcohol Oxidoreductases↗

PubMed2006

Association between recurrent aphthous stomatitis and salivary thiocyanate levels.

The aim of this work was to investigate the association between recurrent aphthous stomatitis (RAS) and salivary thiocyanate levels. The sample comprised men and women of age ranging from 15 to 55 years, who were allocated to four groups: 28 patients in RAS active phase (group 1); 28 patients in RAS remission phase (group 2); 29 smokers (group 3); 26 non-smokers without RAS (group 4). Samples of whole saliva mechanically stimulated were collected, and thiocyanate levels were measured. The results were analyzed by ANOVA and paired t-test. Mean salivary thiocyanate values were 0.55 mM, 0.64 mM, 2.36 mM and 0.96 mM in groups 1 (active RAS), 2 (remission RAS), 3 (smokers) and 4 (control), respectively. There was no significant difference in thiocyanate levels when groups 1 and 2 were compared with group 4. Group 3 showed a significantly higher thiocyanate concentration when compared with groups 1, 2 and 4 (P < 0.05). There was no significant difference in thiocyanate levels between groups 1 and 2 (P > 0.05). It is therefore suggested that there is no association between RAS and salivary thiocyanate levels.

Adolescent↗

PubMed1999

Simple method for determination of thiocyanate in urine.

BACKGROUND: It would be useful to develop a simple kit method for determination of thiocyanate in urine, which could be used to monitor cyanide overload in cassava-consuming populations. METHODS: The method was based on the quantitative oxidation of thiocyanate in acid permanganate at room temperature in a closed vial with liberation of HCN, which reacted with a picrate paper. For semiquantitative analysis in the field, the colored picrate paper was matched with a color chart prepared using known amounts of KSCN. In the laboratory, a more accurate result was obtained by elution of the colored complex in water and measurement of the absorbance at 510 nm. Over the range 0-100 mg/L, there was a linear relationship given by the equation: thiocyanate content (mg/L) = 78 x absorbance. RESULTS: The picrate thiocyanate method gave no interference with urine samples containing protein at less than 7 g/L, 21 amino acids, histamine, glucose, NaCl, urea, blood, and linamarin. For 53 urine samples analyzed by an accurate column method and the thiocyanate picrate method, a regression line gave very good agreement (r(2) = 1. 000). Quantitative recoveries of thiocyanate added to urine samples were obtained with the picrate method. CONCLUSIONS: A simple picrate kit for determination of thiocyanate in urine was developed and is available free of charge for workers in developing countries.

Adult↗