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Introduction
Published in Robert Fried, Richard M. Carlton, Flaxseed, 2023
Robert Fried, Richard M. Carlton
The Flax Council of Canada also noted that there are other sources of dietary cyanide, including a metabolic by-product, thiocyanates, which can be found naturally in milk, beer and green vegetables. Thiocyanate is a breakdown product of the CNglcs and of glucosinolates found in millet and in cruciferous vegetables like cabbage, broccoli, cauliflower, kale, mustard, turnip, radish and horseradish.
Hypertension
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
Nitroprusside dilates veins and arteries to reduce preload and afterload, so it is very useful for heart failure in hypertensive patients. It is also indicated for hypertensive encephalopathy. With beta-blockers, nitroprusside is used for aortic dissection. Starting doses are titrated in small increments, and the maximum dose is given for 10 minutes or less, reducing risks of cyanide toxicity. Nitroprusside is quickly broken down into cyanide and its active moiety, nitric oxide. Then, the cyanide is detoxified into thiocyanate. Careful administration is required to avoid toxicity to the heart and CNS, signified by agitation, cardiac instability, seizures, and an anion gap metabolic acidosis. However, when given for more than 1 week or more than 3–6 days in renal-insufficient patients, thiocyanate accumulates. This causes abdominal pain, lethargy, tremor, and vomiting. If BP is reduced too quickly, there can be a transitory elevation of the hair follicles known as cutis anserina. After three consecutive days of treatment, thiocyanate levels are monitored. The drug is stopped if serum thiocyanate is higher than 12 mg/dL (2 mmol/L). The drug’s IV bag and tubing are wrapped in an opaque covering since nitroprusside is degraded by ultraviolet light.
Respiratory, endocrine, cardiac, and renal topics
Published in Evelyne Jacqz-Aigrain, Imti Choonara, Paediatric Clinical Pharmacology, 2021
Evelyne Jacqz-Aigrain, Imti Choonara
Sodium nitroprusside is a potent vasodilator with an almost instant effect when given intravenously. It is also very short-acting (seconds) and therefore capable of exquisite BP control. Continuous BP monitoring is mandatory. The drug undergoes rapid photo-degradation so the solution must be covered with aluminium foil. In vivo, cyanide is produced from its local breakdown in smooth muscle, which is then metabolised to thiocyanate in the liver. This is excreted by the kidney. Therefore it must be used with caution in patients with renal or hepatic failure. In the absence of organ failure, a clinical problem should not be expected unless the drug is used for more than 48 hours or so. After this time a worsening metabolic acidosis can be anticipated. It may be possible to measure thiocyanate levels in these circumstances, but usually the patient will be suitable for longer-acting drugs by this time.
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.
Thiocyanate toxicity: a teaching case
Published in Clinical Toxicology, 2022
C. James Watson, Daniel L. Overbeek, Gabriella Allegri-Machado, Mark D. Kellogg, Al Patterson, J. Brian McAlvin, Michele M. Burns
Thiocyanate is the byproduct generated by thiosulfate administered in cyanide toxicity. Antidotal nitrate therapy induces methemoglobinemia and facilitates dissociation of cyanide from mitochondrial cytochrome C oxidase, thereby limiting cellular asphyxiation. Thiosulfate subsequently converts the cyanide moiety to thiocyanate for renal excretion. Patients on nitroprusside infusions may receive thiosulfate for a similar purpose, as elevated cyanide concentrations are a known effect of nitroprusside [4,5].