Technetium-Labeled Compounds
Garimella V. S. Rayudu, Lelio G. Colombetti in Radiotracers for Medical Applications, 2019
The intensity of color of the thiocyanate complex (in organic solvents) is quite high, and determinations can be carried out with good sensitivity and precision.78 The reduction is slow, but can be hastened using auxiliary reducing agents such as Sn(II) or Ti(III). However, formation of species lower than Tc(V) is encountered with the use of these reducing agents. A better procedure is to use ascorbic acid as a reductant, with Fe(III) to prevent formation of lower oxidation states. Under these conditions, reduction takes a few minutes. Determinations are possible in the presence of rhenium and molybdenum; the former is reduced very slowly and the latter absorbs at 450 nm, whereas the technetium complex at 513 nm. There appears to be considerable doubt as to the nature of the technetium thiocyanate complex.
The Toxic Environment and Its Medical Implications with Special Emphasis on Smoke Inhalation
Jacob Loke in Pathophysiology and Treatment of Inhalation Injuries, 2020
Although hydrogen cyanide may be present in fires associated with plastic polymers, the chemical diagnosis of cyanide poisoning is difficult, and there is no rapid method for determination of cyanide blood levels in most hospital clinical laboratories. Furthermore, hydrogen cyanide acts quickly at the cellular level, and the half life for cyanide is approximately 1 hr (Clark et al., 1981). Also, cyanide is metabolized in the body to a less toxic thiocyanate compound and excreted in the urine. Serum thiocyanate levels have been used as an indication of cyanide exposure (Levine and Radford, 1978), but because of the long half life of thiocyanate (4-8 days), a serum thiocyanate level evaluates previous cyanide exposure and may not reflect a particular acute cyanide exposure.
Measurement of Exposure and Dose
Samuel C. Morris in Cancer Risk Assessment, 2020
Smoking is such an important confounding factor in epidemiological studies of environmental carcinogenesis and self-reporting is so often inaccurate (perhaps the product of self-deception on the part of smokers), that a biomarker which can provide a definite and quantitative measure of smoking is highly desirable. Moreover, a marker that could provide a quantitative measure of passive smoking—the involuntary exposure of nearby people to side-stream cigarette smoke—would also be of use. Some nicotine is excreted in the urine; it can be measured in the saliva, also. The rate of nicotine metabolism varies as much as fourfold among smokers, however, so nicotine levels in urine, while specific, do not provide an accurate quantitative indicator unless calibrated in each individual. Levels of cotinine, the major metabolite of nicotine, vary much less than residual nicotine levels; measured in urine, cotinine provides both a specific and relatively accurate quantitative measure of exposure to tobacco smoke. Thiocyanate, a metabolite of hydrogen cyanide (a component of cigarette smoke) has also been suggested as a biomarker for exposure to tobacco smoke; but cyanide is also a component of leafy vegetables, some nuts, and beer, so its metabolite is not specific to cigarette smoke (HHS, 1986).
Intramuscular sodium tetrathionate as an antidote in a clinically relevant swine model of acute cyanide toxicity
Published in Clinical Toxicology, 2020
Tara B. Hendry-Hofer, Alyssa E. Witeof, Patrick C. Ng, Sari B. Mahon, Matthew Brenner, Gerry R. Boss, Vikhyat S. Bebarta
Either of the two sulfane sulfurs of sodium tetrathionate, Na2S4O6, can react directly with cyanide, yielding thiocyanate, sulfate, and sodium thiosulfate. Thiosulfate, in turn, acts as a substrate for the enzyme rhodanese, again generating thiocyanate. Tetrathionate thereby neutralizes two moles of cyanide, compared to thiosulfate (Figure 1) [16–18]. Sodium tetrathionate was first examined in 1910 in a study indicating efficacy in a rabbit model of cyanide toxicity [19]. It was later shown to be 1.5–3.3 fold more potent then thiosulfate in treating mice, rats, and dogs with cyanide poisoning. These studies lacked proper controls and were done in animal models not clinically relevant by today’s standards [20–22]. Thus, these early studies indicate sodium tetrathionate is minimally toxic and efficacious against cyanide toxicity [20–22]. Based on these data and tetrathionate’s ability to neutralize two cyanide molecules, we hypothesized it would be efficacious against cyanide poisoning when delivered intramuscularly (IM) following cyanide exposure. The objective of our study was to evaluate the efficacy of IM sodium tetrathionate compared to saline control on survival and clinical outcomes in swine after acute systemic cyanide poisoning.
Activated neutrophil carbamylates albumin via the release of myeloperoxidase and reactive oxygen species regardless of NETosis
Published in Modern Rheumatology, 2020
Shuichiro Nakabo, Koichiro Ohmura, Shuji Akizuki, Kosaku Murakami, Ran Nakashima, Motomu Hashimoto, Hajime Yoshifuji, Masao Tanaka, Tsuneyo Mimori
A previous study showed that protein carbamylation was induced by cyanate, which is synthesized from thiocyanate by MPO and hydrogen peroxide at inflammatory sites [3]. Thiocyanate naturally exists in the human body and serum thiocyanate levels in a healthy population were reported to be 111.2 ± 92.1 μM [12]. It is produced from several chemical compounds, such as glucosinolate and cyanide, the origins of which are the dietary intake of vegetables from the genus Brassica [13] and cigarette smoking [14], respectively. Therefore, once MPO and hydrogen peroxide are released, protein carbamylation may be induced elsewhere. Since MPO and hydrogen peroxide abundantly exist in neutrophils, we speculated that neutrophils are the key player in protein carbamylation in the milieu of inflammation.
Evaluation of aqueous dimethyl trisulfide as an antidote to a highly lethal cyanide poisoning in a large swine model
Published in Clinical Toxicology, 2022
Tara B. Hendry-Hofer, Carter C. Severance, Subrata Bhadra, Patrick C. Ng, Kirsten Soules, Dennean S. Lippner, Diane M. Hildenberger, Melissa O. Rhoomes, Jessica N. Winborn, Brian A. Logue, Gary A. Rockwood, Vikhyat S. Bebarta
The behavior of DMTS (Figure 3) indicates that DMTS partitions quickly into tissue and subsequently slowly leaches into the blood. Recently Bhadra et al. showed relatively large blood concentrations of dimethyl disulfide (DMDS) in swine following IM administration of DMTS [26], suggesting DMTS is converted rapidly to DMDS. DMDS is the primary breakdown product of DMTS. While DMDS was not measured in these blood samples, we suspect the rapid conversion of DMTS to DMDS is one of the main benefits of DMTS, as this likely contributes to the overall pool of readily available sulfane sulfur. Enhancing the conversion of cyanide to thiocyanate and reducing the toxic effects of cyanide. However, it is difficult to know how much cyanide is converted to thiocyanate by DMTS given the rapid conversion of DMTS to DMDS and the body’s natural physiological ability to convert cyanide to thiocyanate via endogenous rhodanese [14,15].
Related Knowledge Centers
- Cyanate
- Halide
- Oxygen
- Potassium Thiocyanate
- Sulfur
- Salt
- Ion
- Conjugate
- Thiocyanic Acid
- Sodium Thiocyanate