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A 77‐year‐old professional gold craftsman ingested a white powder used in goldsmithing, mistaking the powder for a health supplement. He detected a strange taste and immediately fell sick, reported the incident to 911, and was taken to the emergency room. He died approximately 8.5 h post‐ingestion despite treatment. There were no significant findings in the autopsy, the victim's heart blood sample, gastric contents, and the white powder the victim had taken were submitted to the department of forensic toxicology. Using scanning electron microscopy energy dispersive X‐ray analysis, potassium and gold (Au) were detected in the white powder. Ion chromatography analysis detected cyanide. Concentrations of cyanide were 0.5 mg/L in heart blood and 13.3 mg/L in gastric contents. Qualitative and quantitative analyses of Au in the heart blood sample and gastric contents using inductively coupled plasma‐optical emission spectrometry detected concentrations of 79.8 mg/L and 2010.1 mg/L, respectively. Au and cyanide synergistically enhance cytotoxicity through inhibition of detoxification and increasing intracellular accumulation. In the present case, the detected blood cyanide concentration was sub or minimally lethal, and the blood Au concentration was high. The cause of the victim's death was the combined toxicity of Au and cyanide. [ABSTRACT FROM AUTHOR]

Late-onset Alzheimer's disease (LOAD) is a chronic, multifactorial, and progressive neurodegenerative disease that associates with aging and is highly prevalent in our older population (≥65 years of age). This hypothesis generating this narrative review will examine the important role for the use of sodium thiosulfate (STS) as a possible multi-targeting treatment option for LOAD. Sulfur is widely available in our environment and is responsible for forming organosulfur compounds that are known to be associated with a wide range of biological activities in the brain. STS is known to have (i) antioxidant and (ii) anti-inflammatory properties; (iii) chelation properties for calcium and the pro-oxidative cation metals such as iron and copper; (iv) donor properties for hydrogen sulfide production; (v) possible restorative properties for brain endothelial-cell-derived bioavailable nitric oxide. Thus, it becomes apparent that STS has the potential for neuroprotection and neuromodulation and may allow for an attenuation of the progressive nature of neurodegeneration and impaired cognition in LOAD. STS has been successfully used to prevent cisplatin oxidative-stress-induced ototoxicity in the treatment of head and neck and solid cancers, cyanide and arsenic poisoning, and fungal skin diseases. Most recently, intravenous STS has become part of the treatment plan for calciphylaxis globally due to vascular calcification and ischemia-induced skin necrosis and ulceration. Side effects have been minimal with reports of metabolic acidosis and increased anion gap; as with any drug treatment, there is also the possibility of allergic reactions, possible long-term osteoporosis from animal studies to date, and minor side-effects of nausea, headache, and rhinorrhea if infused too rapidly. While STS poorly penetrates the intact blood–brain barrier(s) (BBBs), it could readily penetrate BBBs that are dysfunctional and disrupted to deliver its neuroprotective and neuromodulating effects in addition to its ability to penetrate the blood–cerebrospinal fluid barrier of the choroid plexus. Novel strategies such as the future use of nano-technology may be helpful in allowing an increased entry of STS into the brain. [ABSTRACT FROM AUTHOR]

Little is known about how pharmacological and toxicological knowledge evolves. The aim of this study was to investigate the changes in the presentation of the poison hydrogen cyanide in sixteen German-language pharmacology and toxicology textbooks from 1878 to 2020. The categories of structure, molecular mechanism of action, occurrence, effects, resorption, areas of application, lethal dose, acute symptoms of intoxication, treatment of hydrogen cyanide poisoning, and recommended therapeutic preparations were evaluated. The knowledge on the structure, lethal dosage, and occurrence of hydrogen cyanide has remained constant. In contrast, knowledge on molecular mechanism of action and recommended preparations of the poison has changed dramatically. Until 1944, the binding of hydrogen cyanide to hemoglobin was considered the mechanism of action, whereas from 1951 onwards, the interaction of hydrogen cyanide with the Fe3+ of cytochrome oxidase was described. The number of preparations containing hydrogen cyanide decreased into obsolescence until 1951. The areas of application of hydrogen cyanide also show a change, as from 1919 onwards, mainly industrial areas of application of the poison are described instead of medical ones, and from 1951 onwards, criminalistic areas of application are also mentioned. Thus, pharmacological and toxicological knowledge develops non-linearly, molecular mechanism and uses being the most dynamic areas, whereas the knowledge about hydrogen cyanide's chemical structure, lethal dose, and occurrence remained constant. Older pharmacology and toxicology textbooks were better than newer ones at discussing changes in scientific concepts. Pharmacology and toxicology textbooks also mostly failed to discuss the misuse of hydrogen cyanide (Zyklon B) during the Nazi regime, missing an important opportunity to showcase the ethical responsibility of pharmacology and toxicology. Thus, future pharmacology and toxicology textbooks should improve on discussing the development of pharmacological and toxicological concepts and the ethical responsibility of the discipline. [ABSTRACT FROM AUTHOR]

An alternative biomarker for assessing the cyanide levels in postmortem materials is crucial for investigating acute cyanide intoxication. Herein, an aptamer–ligand biorecognition system with high specificity was developed to detect acute cyanide poisoning via its secondary metabolite, 2-amino-2-thiazoline-4-carboxylic acid (ATCA). Potential aptamers were screened from a random library of 66-base single-stranded DNA using GO-SELEX, with individual aptamers being identified through single-stranded DNA sequencing. Molecular docking was employed to predict the affinity of these aptamers toward ATCA and selected counter-targets; these predictions were confirmed using thermodynamic analysis with an isothermal titration calorimeter. Owing to its label-free biomolecular binding interactions, Apt46 exhibited the highest affinity against ATCA and notable selectivity against structurally similar counter-targets. Thus, an amino-tagged Apt46 binding aptamer was attached to a carbon electrode modified with EDC–NHS-activated graphene oxide. The binding of Apt46 to ATCA was quantified by measuring current changes using differential pulse voltammetry. The aptasensor achieved a detection limit of 0.05 µg/mL and demonstrated suitability for detecting ATCA across various biological matrices, with the high recovery percentages ranging from 92.29 to 114.22%. Overall, the proposed ATCA aptasensor is promising for identifying ATCA metabolites in cases of acute cyanide exposure. [ABSTRACT FROM AUTHOR]

D-penicillamine is used as the mainstay of chelation therapy for Wilson's disease and for heavy metal intoxication. D-penicillamine itself has been noted to cause several systemic side effects as well as symptoms related to the skin. Common cutaneous side effects such as acute hypersensitivity reactions, elastic fiber abnormalities, and bullous diseases have been occasionally described. Herein, we report a case of a 23-year-old Thai female with gold intoxication who developed Stevens–Johnson syndrome (SJS) following the treatment of D-penicillamine. To our knowledge, D-penicillamine-induced SJS is exceptionally rare. To raise awareness of potentially fatal cutaneous adverse drug reaction triggered by D-penicillamine, published literature regarding SJS induced by this agent has also been reviewed. D-penicillamine should be regarded as a possible culprit in patients presenting with SJS following D-penicillamine administration and should be promptly discontinued. [ABSTRACT FROM AUTHOR]

Despite established exposure limits and safety standards, and the availability of carbon monoxide (CO) alarms, each year an estimated 50,000 people in the United States visit emergency departments for CO poisoning. Carbon monoxide poisoning can occur from brief exposures to high levels of CO or from longer exposures to lower levels. If the CO exposure is sufficiently high, unconsciousness and death occur quickly, and without symptoms. With non-lethal exposures to CO, common symptoms include headaches, nausea and vomiting, dizziness, general malaise, and altered mental status. Some patients may have chest pain, shortness of breath, and myocardial ischemia, and may require mechanical ventilation and treatment of shock. Individuals poisoned by CO often develop brain injury. As with brain injury from non-CO causes such as traumatic brain injury, the clinical expression of brain injury caused by CO poisoning includes the domains of cognition, affect, neurological, and somatic. Common problems are neurological: imbalance, motor weakness, neuropathies, hearing loss, tinnitus, Parkinson's-like syndrome, vestibular, gaze, auditory processing, cognitive, anxiety and depression, posttraumatic stress, personality change, persistent headaches, dizziness, sleep problems, and others. In addition, some will have cardiac or other problems. While breathing oxygen hastens the removal of carboxyhemoglobin (COHb), hyperbaric oxygen (HBO2) hastens COHb elimination and favorably modulates inflammatory processes instigated by CO poisoning, an effect not observed with breathing normobaric oxygen. Hyperbaric oxygen improves mitochondrial function, inhibits lipid peroxidation transiently, impairs leukocyte adhesion to injured microvasculature, and reduces brain inflammation caused by CO-induced adduct formation of myelin basic protein. Based upon supportive randomized clinical trials in humans and considerable evidence from animal studies, HBO² should be considered for all cases of acute symptomatic CO poisoning. Hyperbaric oxygen is indicated for CO poisoning complicated by cyanide poisoning, often concomitantly with smoke inhalation. [ABSTRACT FROM AUTHOR]

Purpose: Forensic verification of cyanide (CN) poisoning by direct CN analysis in postmortem blood is challenging due to instability of CN in biological samples. CN metabolites, thiocyanate (SCN−) and 2-aminothiazoline-4-carboxylic acid (ATCA), have been proposed as more stable biomarkers, yet it is unclear if either is appropriate for this purpose. In this study, we evaluated the behavior of CN biomarkers in postmortem swine and postmortem blood to determine which serves as the best biomarker of CN exposure. Methods: CN, SCN−, and ATCA were measured in postmortem swine (N = 8) stored at 4 °C and postmortem blood stored at 25 °C (room temperature, RT) and 37 °C (typical human body temperature, HBT). Results: Following CN poisoning, the concentration of each CN biomarker increased well above the baseline. In postmortem swine, CN concentrations declined rapidly (t1/2 = 34.3 h) versus SCN− (t1/2 = 359 h, 15 days) and ATCA (t1/2 = 544 h, 23 days). CN instability in postmortem blood increased at RT (t1/2 = 10.7 h) and HBT (t1/2 = 6.6 h). SCN− and ATCA were more stable than CN at all storage conditions. In postmortem swine, the t1/2s of SCN− and ATCA were 15 and 23 days, respectively. While both the t1/2s of SCN− and ATCA were relatively lengthy, endogenous levels of SCN− were much more variable than ATCA. Conclusion: While there are still questions to be answered, ATCA was the most adept forensic marker of CN poisoning (i.e., ATCA produced the longest half-life, the largest increase above baseline levels, and most stable background concentrations). [ABSTRACT FROM AUTHOR]

Simple Summary: Both wild (Sorghum halepense) and cultivated Sorghum (Sorghum bicolor) species are commonly used for animal feeding. However, sorghum plants naturally produce dhurrin, a cyanogenic glycoside releasing cyanide; this extremely toxic molecule potentially causes lethal toxicoses, particularly in ruminants. This was the case in a number of farms located in Northwest Italy during August 2022, under weather conditions (drought, tropical temperatures) known to increase plants' dhurrin content. Sixty-six bovines died after grazing Sorghum pastures (Sorghum bicolor or Sorghum halepense) or being fed with Sorghum-containing hay (Sorghum halepense). The reported clinico-pathological findings clearly indicated cyanide poisoning, and chemical analysis revealed high concentrations of dhurrin in the plant materials. The successful management of such toxicosis should rely on the prompt removal of the contaminated fodder and the administration of the antidote sodium thiosulphate. Dhurrin content should be carefully monitored, particularly in the hot season, and both farmers and veterinarians should be made aware of the risks associated with feeding cattle even with cultivated Sorghum, particularly if grown under adverse climatic conditions. Sorghum plants naturally produce dhurrin, a cyanogenic glycoside that may be hydrolysed to cyanide, resulting in often-lethal toxicoses. Ruminants are particularly sensitive to cyanogenic glycosides due to the active role of rumen microbiota in dhurrin hydrolysis. This work provides an overview of a poisoning outbreak that occurred in 5 farms in Northwest Italy in August 2022; a total of 66 cows died, and many others developed acute toxicosis after being fed on either cultivated (Sorghum bicolor) or wild Sorghum (Sorghum halepense). Clinical signs were recorded, and all cows received antidotal/supportive therapy. Dead animals were subjected to necropsy, and dhurrin content was determined in Sorghum specimens using an LC–MS/MS method. Rapid onset, severe respiratory distress, recumbency and convulsions were the main clinical features; bright red blood, a bitter almond smell and lung emphysema were consistently observed on necropsy. The combined i.v. and oral administration of sodium thiosulphate resulted in a rapid improvement of clinical signs. Dhurrin concentrations corresponding to cyanide levels higher than the tolerated threshold of 200 mg/kg were detected in sorghum specimens from 4 out of 5 involved farms; thereafter, such levels declined, reaching tolerable concentrations in September–October. Feeding cattle with wild or cultivated Sorghum as green fodder is a common practice in Northern Italy, especially in summer. However, care should be taken in case of adverse climatic conditions, such as severe drought and tropical temperatures (characterising summer 2022), which are reported to increase dhurrin synthesis and storage. [ABSTRACT FROM AUTHOR]

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Carbon monoxide (CO) and cyanide poisoning are frequent causes of morbidity and mortality in cases of house and industrial fires. The 14th edition of guidelines from the Undersea and Hyperbaric Medical Society does not recommend hyperbaric oxygen (HBO2) treatment in those patients who have suffered a cardiac arrest and had to receive cardiopulmonary resuscitation [1]. In this paper, we describe the case of a 31-year-old patient who received HBO treatment in the setting of cardiac arrest and survived. [ABSTRACT FROM AUTHOR]

This article discusses the Jessica Wongso cyanide coffee case, focusing on the doctrine of causality and the proof of criminal actions. The research analyzes the case using qualitative research methods and concludes that the doctrine of causality is crucial in determining the cause of prohibited effects. The judge relied on witness testimony, expert testimony, and evidence to prove Jessica's crime, resulting in a 20-year prison sentence. The article emphasizes the importance of these teachings in criminal law, despite the controversy surrounding the case. The use of indirect evidence in proving Jessica's guilt is also discussed, highlighting the role of evidence in the legal process. [Extracted from the article]

Key Clinical Message: We present a case of a 36‐year‐old woman with a history of three suicide attempts who had ingested approximately 40 bitter almonds in a suicidal act, leading to her admission to the emergency department of a regional hospital due to complaints of vomiting. Upon arrival, she exhibited confusion, and her vital signs were recorded as follows: pulse rate = 117 beats/min, blood pressure = 160/85 mmHg, oxygen saturation = 95%, respiratory rate = 16, temperature = 37°C. The patient venous blood gas analysis manifested severe metabolic acidosis (pH = 6.92, pO2 = 43 mmHg, HCO3 = 8.6 mmol/L, pCO2 = 42.7 mmHg, base excess = −25.9 mmol/L). Four hours later, she became unconscious and she was intubated. Gastric lavage and a single dose of 60 g of activated charcoal and sodium bicarbonate were administered. In the referral hospital, sodium nitrite was given due to the severity of the poisoning, and norepinephrine infusion was initiated to manage hypotension. Within a day, the patient regained consciousness, underwent extubation, and after 72 h was discharged and subsequently transferred to psychiatric care for further treatment. This case underscores the critical, life‐threatening implications of cyanide toxicity following the ingestion of bitter almonds, highlighting the efficacy of supportive measures such as gastric lavage, activated charcoal, and sodium bicarbonate. Furthermore, it emphasizes the successful application of sodium nitrite monotherapy in managing this condition. [ABSTRACT FROM AUTHOR]

Introduction: Cyanide exposure can occur in various settings such as industry and metallurgy. The primary mechanism of injury is cellular hypoxia from Complex IV (CIV) inhibition. This leads to decreased ATP production and increased reactive oxygen species production. The brain and the heart are the organs most affected due to their high metabolic demand. While the cardiac effects of cyanide are well known, the cerebral effects on cellular function are less well described. We investigated cerebral metabolism with a combination of brain respirometry, microdialysis, and western blotting using a rodent model of sub-lethal cyanide poisoning. Methods: Twenty rodents were divided into two groups: control (n = 10) and sub-lethal cyanide (n = 10). Cerebral microdialysis was performed during a 2 mg/kg/h cyanide exposure to obtain real-time measurements of cerebral metabolic status. At the end of the exposure (90 min), brain-isolated mitochondria were measured for mitochondrial respiration. Brain tissue ATP concentrations, acyl-Coenzyme A thioesters, and mitochondrial content were also measured. Results: The cyanide group showed significantly increased lactate and decreased hypotension with decreased cerebral CIV-linked mitochondrial respiration. There was also a significant decrease in cerebral ATP concentration in the cyanide group and a significantly higher cerebral lactate-to-pyruvate ratio (LPR). In addition, we also found decreased expression of Complex III and IV protein expression in brain tissue from the cyanide group. Finally, there was no change in acyl-coenzyme A thioesters between the two groups. Conclusions: The key finding demonstrates mitochondrial dysfunction in brain tissue that corresponds with a decrease in mitochondrial function, ATP concentrations, and an elevated LPR indicating brain dysfunction at a sub-lethal dose of cyanide. [ABSTRACT FROM AUTHOR]

3-mercaptopyruvate sulfurtransferase (3-MST) plays the important role of producing hydrogen sulfide. Conserved from bacteria to Mammalia, this enzyme is localized in mitochondria as well as the cytoplasm. 3-MST mediates the reaction of 3-mercaptopyruvate with dihydrolipoic acid and thioredoxin to produce hydrogen sulfide. Hydrogen sulfide is also produced through cystathionine beta-synthase and cystathionine gamma-lyase, along with 3-MST, and is known to alleviate a variety of illnesses such as cancer, heart disease, and neurological conditions. The importance of cystathionine beta-synthase and cystathionine gamma-lyase in hydrogen sulfide biogenesis is well-described, but documentation of the 3-MST pathway is limited. This account compiles the current state of knowledge about the role of 3-MST in physiology and pathology. Attempts at targeting the 3-MST pathway for therapeutic benefit are discussed, highlighting the potential of 3-MST as a therapeutic target. [ABSTRACT FROM AUTHOR]

The article "Survival in Carbon Monoxide-Associated Cardiac Arrest" discusses a case study of a patient treated with hyperbaric oxygen therapy and Cyanokit for carbon monoxide poisoning following cardiac arrest. The patient sustained permanent brain injury but was able to live independently after one year. The author, Dr. Neil B. Hampson, emphasizes the limited survival benefits of hyperbaric oxygen therapy for patients with carbon monoxide-associated cardiac arrest, suggesting that transferring such patients long distances for treatment may not significantly improve outcomes. [Extracted from the article]

Hydroxocobalamin administration is not uncommon during the initial medical assistance of fire victims, so it should always be included in the differential diagnosis when evaluating orange-red discoloration with mucosal involvement and chromaturia in this context. Changes in the skin coloration is a common and potentially serious reason for dermatological consultations in hospitalized patients. When evaluating a fire victim developing sudden and asymptomatic orange-red discoloration, one should first investigate the possible administration of hydroxocobalamin as treatment for cyanide poisoning.[1] We present three cases of women in their 80s developing sudden generalized orange-red discoloration. [Extracted from the article]

Cyanide—a fast-acting poison—is easy to obtain given its widespread use in manufacturing industries. It is a high-threat chemical agent that poses a risk of occupational exposure in addition to being a terrorist agent. FDA-approved cyanide antidotes must be given intravenously, which is not practical in a mass casualty setting due to the time and skill required to obtain intravenous access. Glyoxylate is an endogenous metabolite that binds cyanide and reverses cyanide-induced redox imbalances independent of chelation. Efficacy and biochemical mechanistic studies in an FDA-approved preclinical animal model have not been reported. Therefore, in a swine model of cyanide poisoning, we evaluated the efficacy of intramuscular glyoxylate on clinical, metabolic, and biochemical endpoints. Animals were instrumented for continuous hemodynamic monitoring and infused with potassium cyanide. Following cyanide-induced apnea, saline control or glyoxylate was administered intramuscularly. Throughout the study, serial blood samples were collected for pharmacokinetic, metabolite, and biochemical studies, in addition, vital signs, hemodynamic parameters, and laboratory values were measured. Survival in glyoxylate-treated animals was 83% compared with 12% in saline-treated control animals (p  < .01). Glyoxylate treatment improved physiological parameters including pulse oximetry, arterial oxygenation, respiration, and pH. In addition, levels of citric acid cycle metabolites returned to baseline levels by the end of the study. Moreover, glyoxylate exerted distinct effects on redox balance as compared with a cyanide-chelating countermeasure. In our preclinical swine model of lethal cyanide poisoning, intramuscular administration of the endogenous metabolite glyoxylate improved survival and clinical outcomes, and ameliorated the biochemical effects of cyanide. [ABSTRACT FROM AUTHOR]

Treatment of CH‐diazomethane sulfonamides with tert‐butyl nitrite produces novel sulfamoyl cyanide N‐oxides which dimerize to form furoxanes. When the reaction is performed in the presence of a dipolarophile, an olefin or an alkyne, dipolar cycloaddition takes place to deliver isoxazolines or isoxazoles, respectively. [ABSTRACT FROM AUTHOR]

Objective: Vitamin B17 tablets are sold (online) as an alternative cancer therapy medication. Its use however is not benign, given that it is metabolised into hydrogen cyanide. We aimed to measure the number of calls received by the New South Wales Poisons Information Centre (NSW PIC) regarding Amygdalin exposures. Methods: A retrospective review of all amygdalin/cyanogenic glycoside product ingestion exposure calls to NSW PIC between 2015 and 2022. Results: There were 120 unique exposure calls. Eighty‐two (68%) were regarding minor exposures, with the remaining 38 (32%) of calls involving patients who had either a signifcant history or symptoms to prompt referral to hospital or were already seeking advice from a treating hospital clinican. Conclusion: There is a significant burden of concern generated from the misuse of cyanogenic glycoside products for cancer prevention and treatment, which can result in hospital admission carrying significant health risk and expenditure. [ABSTRACT FROM AUTHOR]

Cassava is the world's most essential food root crop, generating calories to millions of Sub-Saharan African subsistence farmers. Cassava leaves and roots contain toxic quantities of the cyanogenic glycoside linamarin. Consumption of residual cyanogens results in cyanide poisoning due to conversion of the cyanogens to cyanide in the body. There is a need for acyanogenic cassava cultivars in order for it to become a consistently safe and acceptable food, and commercial crop. In recent years, the CRISPR/Cas system, has proven to be the most effective and successful genome editing tool for gene function studies and crop improvement. In this study, we performed targeted mutagenesis of the MeCYP79D1 gene in exon 3, using CRISPR/Cas9, via Agrobacterium-mediated transformation. The vector design resulted in knockout in cotyledon-stage somatic embryos regenerated under hygromycin selection. Eight plants were recovered and genotyped. DNA sequencing analysis revealed that the tested putative transgenic plants carried mutations within the MeCYP79D1 locus, with deletions and substitutions being reported upstream and downstream of the PAM sequence, respectively. The levels of linamarin and evolved cyanide present in the leaves of mecyp79d1 lines were reduced up to seven-fold. Nevertheless, the cassava linamarin and cyanide were not completely eliminated by the MeCYP79D1 knockout. Our results indicate that CRISPR/Cas9-mediated mutagenesis is as an alternative approach for development of cassava plants with lowered cyanide content. [ABSTRACT FROM AUTHOR]

A narrative review of the literature was conducted to determine if the administration of methylene blue (MB) in humans has potential risks. Studies were identified from MEDLINE, Web of Science, Scopus, and Cochrane. MB is a diagnostic substance used during some diagnostic procedures and also a part of the treatment of several diseases including methemoglobinemia, vasoplegic syndrome, fosfamide-induced encephalopathy, and cyanide intoxication, and the detection of leaks or position of parathyroid corpuscles during surgery. Although the use of MB is historically justified, and it ought to be safe, because it originated as a diagnostic material, the basic toxicological characteristics of this substance are unknown. Despite reports of severe adverse effects of MB, which could significantly exceed any possible benefits evaluated for the given indication. Therefore, the clinical use of MB currently represents a controversial problem given the heterogeneity of available data and the lack of preclinical data. This is in conflict with standards of safe use of such substances in human medicinal practice. The toxic effects of the application of MB are dose-dependent and include serious symptoms such as hemolysis, methemoglobinemia, nausea and vomitus, chest pain, dyspnoea, and hypertension. Some countries regard MB as harmful because of the resulting skin irritation and triggering of an adverse inflammatory response. MB induced serotoninergic toxicity clinically manifests as neuromuscular hyperactivity. This review aims to summarize the current understanding concerning the indications for MB administration and define the potential adverse effects of MB. [ABSTRACT FROM AUTHOR]

To identify the pattern of myoglobin compared to hemoglobin blockade by the combustion products contained in the fire smoke using computational chemistry tools. The myoglobin unavailability can be a determining factor of the severity and consequences of smoke poisoning, generating the inability of patients to attempt evacuate themselves, compromising myocardial function, leading to crush syndrome-like effects and increasing of multi-organ failure to the victims of mass burn casualties event. In this study, it was used quantum chemical calculations performed with the Gaussian program suite using DFT/B3LYP/6-311G level of theory to optimize molecular geometries, calculate the molecular electrostatic potential, and obtain the vibrational spectrum. These calculations were applied to the myoglobin and hemoglobin model, thus studying their binding to the essential components of toxic fire smoke. Comparing the structural descriptors - frontier molecular orbitals, energy difference, electric dipole moment (µ), was obtained the highest values as belonging to hydrogen cyanide (2.9), which may explain its increased reactivity, meaning strong interaction with both myoglobin and hemoglobin, followed by hydrochloric acid (1.03) and carbon monoxide (0.122). Within the framework of complex intoxication generated by the inhalation of fire smoke, myoglobin is blocked in a temporal manner and according to a very similar pattern to hemoglobin. It follows that the significant rhabdomyolysis found in these patients is due not only to hypoxemia but also to the primary unavailability of myoglobin, and myocardial damage is also multifactorial. Although slightly discussed, the calculation of different structural and geometric descriptors for hydrochloric acid reveals for hydrochloric acid high values, suggesting binding affinities comparable to those of carbon monoxide. Molecular modeling programs allow for new approaches and can identify parameters or areas of their reference that influence the management of patients intoxicated with fire smoke components. [ABSTRACT FROM AUTHOR]

Cyanide is a prevalent, lethal chemical. Possible sources of exposure include products of combustion, plant material, industry, chemical warfare and terrorism. Retrospective review of UK Poisons Information Database of telephone enquiries to the National Poisons Information Service between 1st January 2008 and 31st December 2019 where cyanide poisoning was considered a possibility. Data extracted included demographics, exposure source, clinical features, Poisoning Severity Score, lactate concentration and antidotes given. A total of 1,252 cases of suspected cyanide poisoning were identified, 239 (19%) involved children under 10 years. The commonest sources of exposure were ingestion of plant material (437 cases; 35%) and smoke inhalation (399; 32%). Smoke inhalation caused the majority of severe and fatal cases (139; 71%). Clinical features associated with fatal outcomes were cardiac arrest (OR 36.4; 95% CI 14.4–92.2), hypotension (15.8; 7.0–35.9), coma (10.8; 5.6–21.0) and lactic acidosis (7.8; 4.1–14.8). 110 patients (9%) were given an antidote and 40 patients (3%) died. Lactate concentrations correlate with Poisoning Severity Score category (r = 0.6, p < 0.0001). Serum lactate <2.0 mmol/L was associated with Poisoning Severity Score None or Minor (sensitivity 76%; specificity 86%) and >11.0 mmol/L was associated with fatal outcome (sensitivity 74%; specificity 80%). 61 cases (5%) had severe carboxyhaemoglobin toxicity (COHb >30%). This was associated with a fatal outcome (OR 7.0; 95% CI 1.5-33.7) and there was positive correlation between carboxyhaemoglobin and Poisoning Severity Score, r = 0.57, p < 0.0001. Most cases of ingestion of plant material involved children under five years and resulted in no or mild symptoms. In adults smoke inhalation was associated with the most severe poisoning. The lactate cut-off values associated with each severity score calculated in this study are lower than the values used by NPIS on TOXBASE. Analytical conformation of cyanide exposure was unavailable in the majority of case, limiting the strength of these conclusions. [ABSTRACT FROM AUTHOR]

Summary: A 45‐year‐old man attended to a warehouse fire involving burning plastic, without wearing full protective equipment. He subsequently presented to hospital with shortness of breath and his trachea was intubated for airway protection due to initial concerns of inhalational injury. However, a post‐intubation bronchoscopy was normal. The patient's serum lactate level was normal on admission but was increased when measured 14 h after the initial event and accompanied by a metabolic acidosis. Transdermal cyanide poisoning was suspected given this delayed biochemical presentation and the absence of another apparent cause. A handheld chemical detector detected a high level of toxins on the patient's skin. Clinical improvement was not observed after the first dose of intravenous hydroxocobalamin, which was administered before full body decontamination. After decontamination and the administration of a second dose of hydroxocobalamin, the patient's acid–base status rapidly improved and serum lactate level returned to normal. Clinicians should have a high index of suspicion for transdermal cyanide poisoning in patients presenting after exposure to a fire. [ABSTRACT FROM AUTHOR]

Despite the risk of cyanide poisoning a suitable antidote that can be administered at a reasonable quantity to a large number of individuals is not yet available. This study was carried out to determine the possible hepatoprotective effect of ethanolic extract of Aframomum melegueta seed against cyanide-induced liver injury and its possible antidote effect. Thirty male rats divided into five groups were used for this study. Group 1, received neither cyanide nor the seed extract (Normal control), Groups 2-5 were administered cyanide orally by gavage in form of KCN at a concentration of 4 mg/kg body weight according to body weights as follows; Group 2, received cyanide only (positive control). Group 3 received cyanide and sodium thiosulphate (500 mg/kg body weight) a standard cyanide antidote. (Standard control). Group 4 and 5 were co-treated with cyanide and different doses of the extract three times weekly for the duration of the experiment. Cotreatment with A. melegueta restored the weight loss and the activities of AST, ALT. ALP to levels compared to that obtained in the normal control. In addition co-treatment with A. melegueta modulated the cyanide mediated depletion of the antioxidant capacities of the rats that were exposed to cyanide and the increasing lipid peroxidation profile. The results indicated that ethanolic extract of A.melegueta seed ameliorated cyanideinduced hepatoxicity in rats through their free radical-scavenging mechanisms. [ABSTRACT FROM AUTHOR]

Cyanide is a poison widely used in cases of suicide or homicide. Although various methods to identify and quantify this substance are reported in the literature, they are mainly validated on biological fluids (e.g., blood and urine). In the present study, the Anion‐Exchange Liquid Chromatography with Pulsed Amperometric Detection (IC‐PAD) method was validated on blood and, for the first time, on gastric content, and organs (brain, lung, and liver). For each matrix, linearity, accuracy, precision, limit of detection (LOD), lower limit of quantification (LLOQ), matrix interferences, and carryover were assessed. The samples were extracted by steam distillation in acid environment for the following analysis by IC‐PAD. Furthermore, cyanide values found in two real poisoning cases are reported. For each investigated matrix, the analytical method satisfied all acceptance criteria for validation: it showed a good precision and accuracy, selectivity, and sensitivity with no carryover and matrix interference. The extraction by steam distillation in acid environment REDUCED the interference of the matrices and ALLOWED to perform the analysis with good precision and accuracy. In case #1, analysis showed a blood cyanide concentration of 0.99 μg/ml. In case #2, cyanide concentrations were 1.3 μg/g in brain, 0.8 μg/g in lung, 1.6 μg/g in liver, and 1.2 μg/g in gastric content. The cyanide concentrations found in the two reported cases have been suitable to cause death by poisoning. [ABSTRACT FROM AUTHOR]

The detoxifying abilities of the humic acids and its antioxidant capacity have led to an increased interest in its use as feed additive in livestock production. This research assessed the physiological and antioxidant response of West African dwarf (WAD) goats to cassava peels based diets containing different levels of sodium humate. The experimental design was a completely randomized design, with four treatment diets containing sodium humate at 0, 5, 10 and 15 g/kg diet (Control, 5HNa, 10HNa and 15HNa). Twenty (20) WAD bucks were divided into four (4) groups of five (5) animals and assigned to the four experimental diets. Data was collected on haematological parameters, serum indices and oxidative stress biomarkers and statistically analyzed using the GLM of SPSS (version 23). Result revealed that sodium humate in cassava peels based diets of WAD goats did not affect (p > 0.05) the haematological parameters measured. Total protein increased (p < 0.05) in cassava peels based diet containing 5 g/kg diet (6.43 mg/dL) of sodium humate compared to the other groups (5.50, 5.75 and 5.99 mg/dL for control, 10HNa and 15HNa groups respectively). Also, sodium humate in cassava peels based diets reduce (p < 0.05) glucose level in the blood compared to the control. Serum aluminum increased (p < 0.05) in 10HNa group (0.33 µgL-1) compared to the 5HNa group (0.30 µgL-1) but not in the control and 15HNa groups (0.31 µgL-1, respectively). Albumin concentration increased (p < 0.05) in all sodium humate groups (5.23, 5.50 and 5.48 mg/dL for %HNa, 10HNa, and 15HNa, respectively) compared to the control (3.50 mg/dL). Uric acid increased (p < 0.05) with the increasing amount of sodium humate in the cassava peels based diets. In conclusion, to address the concerns of possible cyanide poisoning and mycotoxins in the mixed diets containing cassava peels, up to 15 g/kg diet of sodium humate could be used as additive to improve the physiological and antioxidant capacity of the animals. [ABSTRACT FROM AUTHOR]

An association between proper chromosome segregation and intact mitochondria has been extensively reported. This could be related to the effects on the progression of cell division of altered energy production, increased oxidative stress, and deregulated calcium homeostasis. However, evidence for a direct relationship is still lacking. The present study was aimed at investigating the possible effect of mitochondrial dysfunction on chromosomal instability as detected in primary human cells treated with the mitochondrial poison carbonyl cyanide 3-chlorophenyl hydrazone (CCCP). Chromosome instability was analyzed in anaphase and interphase cells to follow the fate of chromosome damage during the progression of mitosis and the subsequent cell cycle. Through the combination of cytogenetic approaches and molecular analyses, i.e. morphological cell analysis, formation and characterization of micronucleus content, Comet assay, and gene expression, it was demonstrated that the prevalent DNA damage associated with CCCP treatment was the induction of chromosome loss, while primary DNA damage was not detected. No alterations in the shape of anaphase cells were observed nor induction of multipolar spindles. The proper activation of mitotic checkpoint was maintained. A linear dose–response curve characterizing the CCCP effects suggested that multiple cellular targets could be affected by the CCCP-induced mitochondrial dysfunctions triggering aneuploidy. Conversely, a steep increase was induced by the positive control vinblastine, known to have tubulin as a unique target. In addition, the effect of CCCP on mitochondrial function was demonstrated by changes in mitochondrial DNA copy number and in the expression of genes involved in mitochondrial maintenance. Overall, these results indicate that the mitochondrial poison CCCP may induce aneugenic effects. [ABSTRACT FROM AUTHOR]

The problem of cyanide poisoning may be addressed with addition of feed additives with potentials for detoxification. This research was conducted to assess the performance, rumen microbial and faecal egg counts of West African dwarf (WAD) goats fed cassava peel based diets. Twenty WAD bucks were fed cassava peel based diets supplemented with sodium humate at 0, 5, 10 and 15 g/kg diet for a period of 87 days. The experiment was laid out in a completely randomised design. Data was collected on growth performance indices, rumen microbial count, apparent nutrient digestibility and faecal egg count and statistically analysed using SPSS. Results showed addition of sodium humate to cassava peels based diets improved (p<0.05) daily weight gain, feed conversion ratio and dry matter digestibility. Faecal egg count in WAD goats decreased (p<0.05) with addition of sodium humate in the diet. Increasing amount of sodium humate linearly decreased (p<0.05) protozoa count in the rumen of WAD goats. In conclusion, 5 g/kg diet of sodium humate is sufficient to ensure improved performance of WAD goats on cassava peel based diets. [ABSTRACT FROM AUTHOR]

An original kinetic spectrophotometric procedure was developed for the determination of hydrogen cyanide (HCN) in the whole blood of fire victims. Cyanide poisoning by smoke inhalation is common in forensic medicine, but the blood HCN of fire victims has not been studied in detail so far. In this research project, we developed a simple, fast, sensitive, and selective quantification method for both free and metabolized HCN based on the kinetics of cyanide reaction with ninhydrin. The method was linear in range, from 0.26 to 2.6 μg mL−1, with a coefficient of determination of r = 0.994. A high molar absorptivity of 4.95 × 105 L mol−1 cm−1 was calculated under the reaction conditions. The limit of quantification was 0.052 μg mL−1; the detection limit was 0.012 μg mL−1 and the standard error was ±2.7%. This micro method proved to be accurate, sensitive, and selective and has been successfully applied to the analysis of blood samples, allowing rapid monitoring of blood cyanide in several fire victims. [ABSTRACT FROM AUTHOR]

Hydrogen cyanide and methanethiol are two toxic gases that inhibit mitochondrial cytochrome c oxidase. Cyanide is generated in structural fires and methanethiol is released by decaying organic matter. Current treatments for cyanide exposure do not lend themselves to treatment in the field and no treatment exists for methanethiol poisoning. Sodium tetrathionate (tetrathionate), a product of thiosulfate oxidation, could potentially serve as a cyanide antidote, and, based on its chemical structure, we hypothesized it could react with methanethiol. We show that tetrathionate, unlike thiosulfate, reacts directly with cyanide in vitro under physiological conditions, and based on rabbit studies where we monitor cyanide poisoning in real-time, tetrathionate likely reacts directly with cyanide in vivo. We found that tetrathionate administered by intramuscular injection rescues >80% of juvenile, young adult, and old adult mice from exposure to inhaled hydrogen cyanide gas that is >80% lethal. Tetrathionate also rescued young adult rabbits from intravenously administered sodium cyanide. Tetrathionate was reasonably well-tolerated by mice and rats, yielding a therapeutic index of ∼5 in juvenile and young adult mice, and ∼3.3 in old adult mice; it was non-mutagenic in Chinese Hamster ovary cells and by the Ames bacterial test. We found by gas chromatography-mass spectrometry that both tetrathionate and thiosulfate react with methanethiol to generate dimethyldisulfide, but that tetrathionate was much more effective than thiosulfate at recovering intracellular ATP in COS-7 cells and rescuing mice from a lethal exposure to methanethiol gas. We conclude that tetrathionate has the potential to be an effective antidote against cyanide and methanethiol poisoning. [ABSTRACT FROM AUTHOR]

Widespread access to the Internet has an increasing influence on how suicides are committed. On websites such as eBay® or Amazon.com®, highly toxic substances including cyanides are available for purchase. In the last 5 years, a few fatal intoxications associated with Internet shopping and buying "suicide kits" have been reported. The epidemiology of intoxications reported by the American Association of Poison Control Centers between 2000 and 2018 shows that about 10% of all exposures to cyanide were related to suicide attempts and intentional ingestion of this substance. In order to determine the cyanide concentration in four fatal intoxication cases associated with Internet shopping, a headspace gas chromatography with dual-column/dual-flame ionization detection method was validated and applied to casework. The method was linear in range, from 1 to 50 mg/L, with a coefficient of determination of 0.999 (R2). The limit of quantification was 1.0 mg/L; the detection limit was 0.5 mg/L. Intra- and interday validation precision and accuracy did not exceed 10% and 15%, respectively. Recovery and matrix effect values ranged from 94.8% to 103.8% and from −5.2% to 3.8%, respectively. The cyanide concentrations were determined in biological fluids (blood, urine, bile, vitreous humor and gastric content) and postmortem tissue samples (spleen, kidney, liver and brain). The headspace gas chromatographic method, which is routinely used in clinical and forensic toxicology to quantify ethanol with its congeners (methanol, acetone, isopropanol, n -propanol and n -butanol), can also be applied to determine the cyanide concentrations in intoxication cases. The global problem of a high number of suicides each year requires increasing and more restrictive control of highly toxic substances available online as well as careful monitoring of human exposure to cyanide. This old and well-known poison is being increasingly used nowadays for suicidal purposes; therefore, the determination of cyanide in biological samples is still important in terms of clinical and forensic toxicology. [ABSTRACT FROM AUTHOR]

Cyanide poisoning is one of the most dangerous poisonings, it can be absorbed into the body through the mouth, inhalation and through the skin. A 32-year-old female patient was admitted to our poison control center because of high fever, severe vomiting, and seizures. Physical examination found that the patient was drowsy, had a high fever of 40 degrees Celsius, pulse of 140 beats/minute, and increased tendon and bone reflexes. Exploiting the patient's information, it was discovered that the patient bought Cyanide to drink with the intention of committing suicide. The patient was quickly treated with gastric lavage and activated charcoal. Echocardiography recorded EF: 35%, reduced movement of the entire myocardium. CK blood test: 4562 U/L. The patient's condition rapidly deteriorated and the patient was made ECMO, IHD and CVVHDF. After 3 days of treatment, the patient's condition did not improve, so the family asked for the patient to go home. This article aims to describe the rapidly progressing and severe damage to the heart and muscles of patients with cyanide poisoning. [ABSTRACT FROM AUTHOR]

Cyanide poisoning most commonly occurs from smoke inhalation, less commonly by oral ingestion for suicide or homicide. There are rare cases of intravenous or subcutaneous parenteral cyanide. We report a fatal case of intramuscular cyanide used as a homicidal agent. A 35-year-old female was assaulted and injected with an unknown substance in her left buttock using a syringe. She was unresponsive at ED arrival and underwent immediate endotracheal intubation. After near normal vital signs at arrival (BP 130/83 mmHg, HR 102 bpm), she rapidly became hypotensive and bradycardic with worsening acidosis (pH 6.95, lactate 7.7 mmol/L). Despite vasopressors, hydroxocobalamin, and sodium thiosulfate, she succumbed. Plasma cyanide concentrations from blood drawn 1 and 4 h post exposure were both in the lethal range (3.4 and 4.1 mg/L, respectively). Our case demonstrates that intramuscular injection can result in fatal cyanide poisoning, resulting in rapid absorption, severe toxicity, and death. [ABSTRACT FROM AUTHOR]

Cyanide is a highly toxic agent that has been frequently used for suicide in South Korea. It is also used in various industrial fields, such as metal plating, in which many accidental cyanide intoxications have occurred. To overcome the disadvantages of conventional cyanide analysis methods, a simple and fast method for the analysis of cyanide in whole blood using ion chromatography (IC) with amperometric detection was developed in this study. Whole blood samples were deproteinized, diluted, and analyzed using an IC–amperometric detection system. The limits of detection and quantitation were 0.1 and 0.2 mg/L, respectively. The method showed good linearity in the range of 0.2 to 50 mg/L with R2 > 0.99. The intra‐ and inter‐assay precision and accuracy values were <10%. The established method was successfully applied to analyze whole blood samples from three cyanide intoxication cases. [ABSTRACT FROM AUTHOR]

Cyanide is a rapid acting, lethal, metabolic poison and remains a significant threat. Current FDA-approved antidotes are not amenable or efficient enough for a mass casualty incident. The objective of this study is to evaluate short and long-term efficacy of intramuscular aqueous dimethyl trisulfide (DMTS) on survival and clinical outcomes in a swine model of cyanide exposure. Anesthetized swine were instrumented and acclimated until breathing spontaneously. Potassium cyanide infusion was initiated and continued until 5 min after the onset of apnea. Subsequently, animals were treated with intramuscular DMTS (n = 11) or saline control (n = 10). Laboratory values and DMTS blood concentrations were assessed at various time points and physiological parameters were monitored continuously until the end of the experiment unless death occurred. A subset of animals treated with DMTS (n = 5) were survived for 7 days to evaluate muscle integrity by repeat biopsy and neurobehavioral outcomes. Physiological parameters and time to apnea were similar in both groups at baseline and at time of treatment. Survival in the DMTS-treated group was 90% and 30% in saline controls (p = 0.0034). DMTS-treated animals returned to breathing at 12.0 ± 10.4 min (mean ± SD) compared to 22.9 ± 7.0 min (mean ± SD) in the 3 surviving controls. Blood collected prior to euthanasia showed improved blood lactate concentrations in the DMTS treatment group; 5.47 ± 2.65 mmol/L vs. 9.39 ± 4.51 mmol/L (mean ± SD) in controls (p = 0.0310). Low concentrations of DMTS were detected in the blood, gradually increasing over time with no elimination phase observed. There was no mortality, histological evidence of muscle trauma, or observed adverse neurobehavioral outcomes, in DMTS-treated animals survived to 7 days. Intramuscular administration of aqueous DMTS improves survival following cyanide poisoning with no observed long-term effects on muscle integrity at the injection site or adverse neurobehavioral outcomes. [ABSTRACT FROM AUTHOR]

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Acetone cyanohydrin (ACH), an organic cyanide, is mainly used in the production of methyl methacrylate (MMA), and it also exists in cassava roots, the main calorie source in some tropical countries. ACH can decompose spontaneously or enzymatically into acetone and highly toxic hydrogen cyanide (HCN) and be potentially toxic to its contacts. Given that limited forensic studies and case reports on fatal ACH poisoning are available, herein, we present a report of two fatal cases of ACH poisoning in which the two victims, with postmortem cyanide blood concentrations of 4.22 μg/ml and 4.07 μg/ml, suffered from acute poisoning of ACH due to a traffic accident. Furthermore, a literature review of cyanide poisoning case reports from 2000 to 2020 was carried out, and 28 subjects with cyanide poisoning were presented, including the age, sex, cause of poisoning, autopsy findings and the cyanide concentration in the blood. ACH poisoning lacks specific and reliable autopsy findings for diagnosis, and relevant toxicological studies are necessary. Due to the chemical properties of ACH that allow it to easily decompose, the toxicological analysis of acetone and cyanide in biological samples is essential for the diagnosis of ACH poisoning. [ABSTRACT FROM AUTHOR]

Dispersive-micro solid phase extraction (d-µSPE) has gained increasing attention due to its convenience, effectiveness, and flexibility for sorbent selection. Among a various selection of materials, magnetic carbon nanotubes (Mag-CNTs) is a promising d-µSPE sorbent with excellent separation efficiency in addition to its high surface area and adsorption capability. In this work, two different surface-modified Mag-CNTs, Mag-CNTs-COOH and Mag-CNTs-SO3H, were developed to facilitate d-µSPE (Mag-CNTs/d-µSPE). The cyanide metabolite, 2-aminothiazoline-4-carboxylic acid (ATCA), was selected to evaluate their extraction performance using gas chromatography–mass spectrometry (GC–MS) analysis. The Mag-CNTs-COOH enabled a one-step derivatization/desorption approach in the workflow; therefore, a better overall performance was achieved. Compared to the Mag-CNTs-SO3H/d-µSPE and SPE workflow, the one-step desorption/derivatization approach improved the overall extraction efficiency and reduced solvent consumption and waste production. Both Mag-CNTs/d-µSPE workflows were validated according to ANSI/ASB 036 guidelines and showed excellent analytical performances. The limit of detection (LOD) and limit of quantitation (LOQ) of ATCA in synthetic urine were 5 and 10 ng/mL, respectively, and that in bovine blood were achieved at 10 and 60 ng/mL. The SPE method's LOD and LOQ were also determined at 1 and 25 ng/mL in bovine blood samples. The Mag-CNTs/d-µSPE methods demonstrated great potential to extract polar and ionic metabolites from biological matrices. The extraction processes of ATCA described in this work can provide an easier-to-adopt procedure for potential routine forensic testing of the stable biomarker in cyanide poisoning cases, particularly for those cases where the cyanide detection window has passed. [ABSTRACT FROM AUTHOR]

In this proof-of-concept study, the aim was to evaluate the short-term clinical effectiveness of isosorbide dinitrate (ISDN) oral spray in non-anaesthetized cyanide-poisoned swine. A comparative study was conducted using domestic swine. Animals were intravenously poisoned with potassium cyanide (KCN), either 2 mg/kg or 4 mg/kg dose. Two control groups (one for each cyanide dose) were not further treated. Two other groups (one for each cyanide dose) were treated within 1 min after poisoning with ISDN oral spray: 3 spray actuations (averaging a total of 3.75 mg) after the lower cyanide dose and 4 spray actuations (averaging a total of 5.0 mg) after the higher dose. The study outcomes were clinical score, time to death, and blood tests including pH, lactate, and methemoglobin levels. All the animals started to convulse within 20 to 30 sec after KCN poisoning, then became unresponsive and hemodynamically depressed after another 20 to 30 sec. After the KCN 2 mg/kg dose, 3 of 4 control animals survived, while all treated animals survived. Compared with control animals, ISDN-treated animals displayed significantly better clinical scores starting 5 min after KCN poisoning. Acidosis was significantly more pronounced in the untreated animals. After the KCN 4 mg/kg dose, similar survival rates were observed for control and ISDN-treated groups (1/4), but treated animals had longer time to death and better pH and lactate levels. ISDN oral spray administration following KCN poisoning in this porcine model did not result in statistically significant increased survival. However, based on clinical scores and clinical laboratory values, ISDN may benefit as a bridging countermeasure until currently-available specific cyanide antidotes can be administered. Further research is warranted to better characterize this potential role of ISDN in cyanide poisoning. [ABSTRACT FROM AUTHOR]

“Caution is advised while decontaminating a victim of poisoning. Over enthusiasm may result in the patient, not the poison” – John Morrision Poisoning has been known to mankind since time immemorial and the study of various poisons and their effects has always fascinated mankind. References to poisons and various instances of poisoning are available in Indian Shastras, Egyptian Papyari and Sumerian writings.1 Since then many substances considered advantages and disadvantages in the form of food or poisons have been discovered. Those substances which are used unfortunately to take away the man’s life or cause ill health have been changing. Some of the great persons who were poisoned to death are Chatrapati Shivaji Maharaj,2-3 whose bed was poisoned, Socrates, who was made to drink Hemlock (Conium maculatum) and Rasputin who was poisoned with cyanide and then shot. Aluminum phosphide poisoning, a rodenticide is also posing a formidable challenge and is on the way for taking the number one position. As poisoning trends go on changing, it is necessary to know the poisoning trends from time to time. [ABSTRACT FROM AUTHOR]

In case of mild to moderate cyanide poisoning, especially when standard antidote kits are not readily available, plasmapheresis can be utilized as an alternative option alongside supportive measures. [ABSTRACT FROM AUTHOR]

This letter, published in the Journal of Medical Toxicology, comments on a case report of serotonin syndrome caused by methylene blue. The authors highlight the use of hydroxocobalamin as an alternative therapy for vasodilatory shock, as it also inhibits nitric oxide synthase. They suggest that hydroxocobalamin may have been a better choice in this case due to the risk of serotonin syndrome with methylene blue. The authors note that the choice of therapy depends on patient-specific risk factors and that both agents have their own adverse effects. [Extracted from the article]

Azide is a highly toxic chemical agent to human being. Accidental, but also intentional exposure to azide occurs. To be able to confirm azide ingestion, we developed a method to identify and quantify azide in biological matrices. Cyanide was included in the method to evaluate suggested in vivo production of cyanide after azide ingestion. Azide in biological matrices was first derivatized by propionic anhydride to form propionyl azide. Simultaneously, cyanide was converted into hydrogen cyanide. After thermal rearrangement of propionyl azide, ethyl isocyanate was formed, separated together with hydrogen cyanide by gas chromatography (GC) and detected using a nitrogen phosphorous detector (NPD). The method was linear from 1.0‐100 µg/mL for both analytes, and azide was stable in human plasma at −20°C for at least 49 days. Azide was measured in the gastric content of two cases of suspected azide ingestion (case 1:1.2 mg/mL, case 2:1.5 mg/mL). Cyanide was only identified in the gastric content of case 1 (approximately 1.4 µg/mL). Furthermore, azide was quantified in plasma (19 µg/mL), serum (24 µg/mL), cell pellet (21 µg/mL) and urine (3.0 µg/mL) of case 2. This method can be used to confirm azide and cyanide exposure, and azide concentrations can be quantified in several biological matrices. [ABSTRACT FROM AUTHOR]

Cyanide-based blood poisoning can seriously damage fire victims and cause death if not detected quickly. Previous conventional methods require laboratory equipment, which are expensive and increase the duration of the analysis. Here, a simple origami based microfluidic device was introduced for point of need detection of blood cyanide concentration in people involved in fire. The device is made of four layers of paper. Each layer was in the size of 1 × 1 cm folded on each other. In this work, the blood sample was acidified by trichloroacetic acid to separate cyanide from methaemoglobin in the form of HCN gas. The produced gas released into borate buffer to recover free cyanide ions which interacted with the Pt complex ([Pt(p-MeC6H4)2(phen)]) used as a receptor in this study. Optimized conditions were applied to have a suitable interaction causing the color of the receptor to change from yellow to colorless. The color changes were recorded by a smartphone, and the sensor response was calculated by the routine image analysis software. The assay was capable of determining cyanide ions at different concentrations in the range of 1.0 to 100.0 µmol L−1. The detection limit of these determination was equal to 0.4 µmol L−1. The assay responses were not affected by the interfering species. As a practical analysis, the proposed sensor was applied to determine cyanide ions in the blood sample of 20 studied fire survivors and 10 controls with high accuracy. [ABSTRACT FROM AUTHOR]