Determination of cyanide in whole blood, erythrocytes, and plasma.

Lundquist, Per‐G.; Rosling, Hans; Sörbo, Bo

doi:10.1093/clinchem/31.4.591

Cited by 128 publications

(56 citation statements)

References 2 publications

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“…Subcutaneous injection could potentially cause a rapid absorption and distribution of CN, versus a slower uptake of CN through the digestive tract. If a large dose of cyanide was rapidly absorbed into the erythrocytes, as suggested by Lundquist et al (25), our data would suggest that the sequestered CN is only slowly released back into rat plasma for transport to tissues to be metabolized. Whole blood concentrations were also measured in multiple samples from each individual animal for the duration of the current study versus multiple animals at each time point in previous studies (3,23).…”

Section: Discussionsupporting

confidence: 57%

“…Cyanide conversion to ATCA was calculated as a percentage by dividing the maximum concentration of ATCA in each model over the total maximum concentration of cyanide, thiocyanate and ATCA. Considering that cyanide is distributed in the range of 70 -96% in the red blood cells, with the remainder in the plasma (25,34), it was estimated that 0.10 -0.78%, 2.46 -9.19% and 0.60 -3.7% of the cyanide dose was converted to ATCA in rats, rabbits and swine, respectively. Although the calculation of the percentage of cyanide conversion to ATCA from the current study is meant to be a rough estimate and further studies should be undertaken to accurately determine the amount of cyanide converted to ATCA, our calculations are significantly lower than previously reported estimates of 15 -20% (6) and are likely even overestimated for swine and rabbits, due to SCN 2 failing to reach a maximum.…”

Section: Discussionmentioning

confidence: 99%

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Cyanide Toxicokinetics: The Behavior of Cyanide, Thiocyanate and 2-Amino-2-Thiazoline-4-Carboxylic Acid in Multiple Animal Models

Bhandari

Oda

Petrikovics

et al. 2014

Journal of Analytical Toxicology

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Cyanide causes toxic effects by inhibiting cytochrome c oxidase, resulting in cellular hypoxia and cytotoxic anoxia, and can eventually lead to death. Cyanide exposure can be verified by direct analysis of cyanide concentrations or analyzing its metabolites, including thiocyanate (SCN(-)) and 2-amino-2-thiazoline-4-carboxylic acid (ATCA) in blood. To determine the behavior of these markers following cyanide exposure, a toxicokinetics study was performed in three animal models: (i) rats (250-300 g), (ii) rabbits (3.5-4.2 kg) and (iii) swine (47-54 kg). Cyanide reached a maximum in blood and declined rapidly in each animal model as it was absorbed, distributed, metabolized and eliminated. Thiocyanate concentrations rose more slowly as cyanide was enzymatically converted to SCN(-). Concentrations of ATCA did not rise significantly above the baseline in the rat model, but rose quickly in rabbits (up to a 40-fold increase) and swine (up to a 3-fold increase) and then fell rapidly, generally following the relative behavior of cyanide. Rats were administered cyanide subcutaneously and the apparent half-life (t1/2) was determined to be 1,510 min. Rabbits were administered cyanide intravenously and the t1/2 was determined to be 177 min. Swine were administered cyanide intravenously and the t1/2 was determined to be 26.9 min. The SCN(-) t1/2 in rats was 3,010 min, but was not calculated in rabbits and swine because SCN(-) concentrations did not reach a maximum. The t1/2 of ATCA was 40.7 and 13.9 min in rabbits and swine, respectively, while it could not be determined in rats with confidence. The current study suggests that cyanide exposure may be verified shortly after exposure by determining significantly elevated cyanide and SCN(-) in each animal model and ATCA may be used when the ATCA detoxification pathway is significant.

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Section: Discussionsupporting

confidence: 57%

Section: Discussionmentioning

confidence: 99%

Cyanide Toxicokinetics: The Behavior of Cyanide, Thiocyanate and 2-Amino-2-Thiazoline-4-Carboxylic Acid in Multiple Animal Models

Bhandari

Oda

Petrikovics

et al. 2014

Journal of Analytical Toxicology

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“…In the literature, erythrocyte to plasma ratios of at least 10:1 are frequently cited Rumack, 1983). These ratios were also confirmed by Lundquist et al (1985). In this study, cyanide concentrations in whole blood, plasma and erythrocytes were compared in 10 non-smoking subjects and five smoking subjects.…”

Section: Biomarkerssupporting

confidence: 58%

Acute health risks related to the presence of cyanogenic glycosides in raw apricot kernels and products derived from raw apricot kernels

Alexander

Barregård²,

Bignami³

et al. 2016

EFS2

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Amygdalin is the major cyanogenic glycoside present in apricot kernels and is degraded to cyanide by chewing or grinding. Cyanide is of high acute toxicity in humans. The lethal dose is reported to be 0.5-3.5 mg/kg body weight (bw). An acute reference dose (ARfD) of 20 lg/kg bw was derived from an exposure of 0.105 mg/kg bw associated with a non-toxic blood cyanide level of 20 micro mol (lM), and applying an uncertainty factor of 1.5 to account for toxicokinetic and of 3.16 to account for toxicodynamic inter-individual differences. In the absence of consumption data and thus using highest intakes of kernels promoted (10 and 60 kernels/day for the general population and cancer patients, respectively), exposures exceeded the ARfD 17-413 and 3-71 times in toddlers and adults, respectively. The estimated maximum quantity of apricot kernels (or raw apricot material) that can be consumed without exceeding the ARfD is 0.06 and 0.37 g in toddlers and adults, respectively. Thus the ARfD would be exceeded already by consumption of one small kernel in toddlers, while adults could consume three small kernels. However, consumption of less than half of a large kernel could already exceed the ARfD in adults.

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“…There are two primary detoxification mechanisms of ingested cyanide in the body. The minor one involves methemoglobin in the red blood cells, which temporarily neutralize cyanide by reversible reaction [52]. The major pathway proceeds by the conversion of cyanide to a less toxic thiocyanate (SCN).…”

Section: Cyanide Detoxificationmentioning

confidence: 99%

Toxicity Potential of Cyanogenic Glycosides in Edible Plants

Nyirenda¹

2021

Medical Toxicology

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Cyanogenic glycosides are natural phytotoxins produced by over 2000 plant species, many of which are consumed by humans. The important food crops that contain cyanogenic glycosides include cassava (Manihot esculenta), sorghum (Sorghum bicolor), cocoyam (Colocasia esculenta L. and Xanthosoma sagittifolium L.), bamboo (Bambusa vulgaris), apple (Malus domestica), and apricot (Prunus armeniaca). Cyanogenic glycosides and their derivatives have amino acid-derived aglycones, which spontaneously degrade to release highly toxic hydrogen cyanide (HCN). Dietary cyanide exposure has been associated with several health challenges such as acute cyanide poisoning, growth retardation, and neurological disorders. This chapter will introduce general cyanogenesis principles, highlight major food plants with lethal cyanide levels, and provide epidemiological-based health conditions linked to cyanide intake. Furthermore, strategies for elimination of cyanogens from food crops, such as processing technologies, will be discussed. Finally, the chapter will analyze the role of cyanogenic plants in ensuring food security among resource-poor communities.

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Determination of cyanide in whole blood, erythrocytes, and plasma.

Cited by 128 publications

References 2 publications

Cyanide Toxicokinetics: The Behavior of Cyanide, Thiocyanate and 2-Amino-2-Thiazoline-4-Carboxylic Acid in Multiple Animal Models

Cyanide Toxicokinetics: The Behavior of Cyanide, Thiocyanate and 2-Amino-2-Thiazoline-4-Carboxylic Acid in Multiple Animal Models

Acute health risks related to the presence of cyanogenic glycosides in raw apricot kernels and products derived from raw apricot kernels

Toxicity Potential of Cyanogenic Glycosides in Edible Plants

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