Doses Of Cyanide Research Articles

Effects of Agro-based Adsorbents on the Biochemical Profiles of Wistar Rats Exposed to Cyanide

Background: Cyanide is a very toxic chemical that reacts with the ferric cytochrome oxidase in the mitochondrial system to form a stable complex. This complex inhibits the process of oxidative phosphorylation, thereby interrupting aerobic respiration in the organism. It is postulated that activated charcoal (AC) intercepts the ingested cyanide in the gastrointestinal tract before it is absorbed into the system. Methods: A single dose of 3 mg/kg body weight of potassium cyanide (KCN) was orally administered to the rats in each of the five groups, each consisting of 6 rats. After 15 minutes, all rats in each group were given AC from different agro-based materials. The control group (group 1) received standard commercial AC orally at 1 g/kg. group 2 received AC from plantain peels, group 3 received AC from castor oil seed shell, group 4 received AC from coconut shell and group 5 received a combination of AC from plantain peels, castor oil seed shell, and coconut shell. Blood samples were collected sequentially from rats in each group for biochemical assays using standard procedures. Results: The control group, which received KCN and standard commercial AC, exhibited the highest alanine transaminase (ALT) value (60.09±0.10 U/L) on day seven. Similarly, the highest aspartate transaminase (AST) value (196.28±0.72 U/L) was observed in the control group. Alkaline phosphate (ALP) levels followed a similar pattern. On day seven, the serum creatinine levels were 3.81±0.11 mg/dL for group 1 and 3.45±0.05 mg/dL for group 5. Subsequently, all biochemical parameters decreased after day 7, with the lowest levels recorded in rats that received AC derived from coconut shells. Conclusion: The administration of locally prepared agro-based adsorbents to Wistar rats after exposure to sublethal doses of cyanide significantly mitigated the effects of the cyanide on the liver, kidneys, and heart, as indicated by the biochemical parameters of the albino Wistar rats in the study.

Analysis of the toxicity and treatment methods of cyanide

Cyanide has historically been widely regarded as a highly toxic poison. In the 19th century, cyanide was used by terrorism to poison and manufacture chemical weapons. Due to occasional cyanide leakage incidents, cyanide has reappeared in peoples field of vision. It has developed a great interest in how this poison is viewed and handled. This research describes cyanide in detail in terms of source, history, use, and mechanism of action. At the same time, the relationship between the toxicity and dose of cyanide, the types of diseases caused by cyanide and their signs and symptoms are also explained. In addition, some of the main existing treatments and drugs are introduced, as well as the mechanism and principle of their functioning. The significance of this research lies in the systematic understanding of cyanide, helping people deepen their understanding of its toxicity and treatment, and providing new ideas for the development of cyanide antidotes.

Alteration in Cerebral Metabolism in a Rodent Model of Acute Sub-lethal Cyanide Poisoning.

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. Twenty rodents were divided into two groups: control (n = 10) and sub-lethal cyanide (n = 10). Cerebral microdialysis was performed during a 2mg/kg/h cyanide exposure to obtain real-time measurements of cerebral metabolic status. At the end of the exposure (90min), brain-isolated mitochondria were measured for mitochondrial respiration. Brain tissue ATP concentrations, acyl-Coenzyme A thioesters, and mitochondrial content were also measured. 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. 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.

Quantification of cyanide metabolite 2-aminothiazoline-4-carboxylic acid in postmortem dried blood spot samples by liquid chromatography–tandem mass spectrometry

2-Aminothiazoline-4-carboxylic acid (ATCA), which is produced by the reaction of cyanide with endogenous cystine, is a promising biomarker of cyanide exposure because of its physicochemical stability. Analysis of more stable metabolite than the toxic gas itself is sometimes useful for postmortem diagnosis of gas poisoning. Here, we developed and validated an approach that uses liquid chromatography coupled with electrospray ionization−tandem mass spectrometry for quantifying ATCA in dried blood spot (DBS) samples. The linearity of the calibration curve was good in the concentration range of 20–1500 ng/mL. Our method allows for repeatable and the accurate quantification of ATCA, with intra- and inter assay coefficients of variation of below 7.8 % and below 9.3 %, respectively. In addition, the concentration of ATCA in DBSs remained stable for at least one month when stored at −20°C. Our results indicated that our analytical approach can be used to determine past exposure to higher doses of cyanide. In a comparison of ATCA concentrations in DBSs obtained from cadavers with various causes of death, significantly higher ATCA concentrations were observed in fire victims than in non-fire victims, confirming that fire victims inhale large amounts of cyanide gas. Thus, here we extended the possible uses of DBS for quantification of ATCA to forensic toxicological testing for cyanide poisoning.

Sympathetic Modulation By Glucagon Like Peptide 1 And Melanocortin 4 Receptors In The Carotid Body Of Wistar Rats

Diabetes is a chronic metabolic disorder that occurs when there is raised levels of glucose in the blood (hyperglycemia) caused by either insulin deficiency or an inadequate response to insulin. Globally, the clinical problem of diabetes and obesity is huge (8.5% of total population) and this is reflected in Aotearoa by 6% of the population. Diabetes increases the likelihood of stroke, heart attack, vascular and visual disorders. Such a clinical tsunami makes understanding mechanisms of glucose homeostasis more critical than ever. An area that remains unexplained are the mechanisms by which sympathetic nervous activity (SNA) is heightened in diabetes as this contributes substantially to blood hyperglycaemia. Given the influential role of the carotid body (CB) in regulating SNA together with its ability to sense blood glucose, insulin and adrenaline, we tested the hypothesis that two newly revealed receptors from transcriptomic sequencing - glucagon-like peptide-1 (GLP1R) and melanocortin-4 (MC4R) located within the CB play a significant role in controlling SNA. The working heart-brainstem preparation was used to evaluate functionally the cardiovascular (SNA, heart rate, arterial pressure) and respiratory (phrenic nerve) activity in Wistar rats. The specific agonists and antagonists of GLP1R (Exendin-4 and Exendin-3, respectively) and MC4R (THIQ and HS014, respectively) were injected into the internal carotid artery (ICA) which, via the carotid body artery, perfuses the CB. Data are expressed 10 min post injection. The CB was stimulated with low doses of sodium cyanide (i.a.). Immunocytochemistry detected GLP1 and MC4 receptors localised to distinct cell groups within the carotid body. Stimulation of GLP1R within the CB inhibited the chemoreflex evoked sympathetic response (p<0.05) whilst it was augmented powerfully by the MC4R agonist (p<0.05) compared to baseline. In contrast, heart rate, arterial pressure and phrenic activity were unaffected. GLP1Rs antagonist alone increased the chemoreflex evoked sympathetic response above basline (p<0.05) while antagonising MC4Rs was without effect. Injections of vehicle did not alter either the chemoreflex evoked or basal SNA. For the first time, stimulation of metabolism-linked receptors – GLP1 and MC4 within the CB modulate SNA differentially. Our data purport endogenous secretion of GLP-1 within the CB affecting sympathetic activity. Our study provides novel targets within the CB that might be pharmacologically probed to control metabolism via modulation of SNA; such data may provide the much needed guidance for controlling blood glucose in diabetes.

Assessment of Some Biochemical Parameters in Vitreous Humor of Rabbits Exposed to Sodium Cyanide

Aim: The aim of this study was to assess some biochemical parameters in the vitreous humor of Rabbits exposed to sodium cyanide.&#x0D; Study Design: This study is an interventional study.&#x0D; Place and Duration of Study: This study was carried out at Animal House, Applied and Environmental Biology Department, Rivers State University, Port Harcourt, Rivers State, Nigeria, between April 2020 and November 2020.&#x0D; Methodology: A total of twelve (12) rabbits as indicated by Mead’s formula constituted the sample size. The study was divided into three groups including the control. 1 mg/kg sodium cyanide was administered to the rabbits orally in group one and vitreous humor was collected using standard procedure after thirty minutes. In group two the rabbits were put to death mechanically and 1 mg/kg sodium cyanide was administered to the rabbits after thirty minutes, vitreous humor was collected after thirty minutes using standard procedure. The rabbits in group three, control group, were put to death mechanically and nothing was given to the rabbits, then after thirty minutes vitreous humor was collected using standard procedure. Biochemical parameters investigated included vitreous glucose, total cholesterol, triglycerides, high density lipoprotein cholesterol, low density lipoprotein cholesterol, very low density lipoprotein cholesterol, total proteins (TP), albumin (ALB), total bilirubin, conjugated bilirubin, aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities. Data were expressed as mean ± SD. Statistical differences between groups were computed using Graph pad prism 7.0 version developed by Graph pad software, San Siago, Califonia, USA. Results were analyzed using analysis of variance (ANOVA) and significance between groups was taken at p&lt;.05.&#x0D; Results: Vitreous biochemical results showed significant (p&lt;.05) increase in levels of TC, LDL-C, AST, ALT, TB and CB in rabbits given 1 mg/kg sodium cyanide compared to control. Significant (p&lt;.05) decrease in levels of glucose, TP and ALB were also observed. This study also revealed that there was no significant (p&lt;.05) difference in biochemical results of rabbits given 1 mg/kg sodium cyanide thirty minutes after they were put to death mechanically compared to the control. It can be concluded that a lethal dose of sodium cyanide (1 mg/kg) may lead to alterations in vitreous biochemical parameters and this may enhance death differentiation due to sodium cyanide poisoning and other causes of death for example mechanical death. &#x0D; Conclusion: The findings of this study support a central role for vitreous humor biochemistry in many postmortem forensic and pathological evaluations and it could also be used for death differentiation in sodium cyanide poisoning.

Cyanide consumption minimisation and concomitant toxic effluent minimisation during precious metals extraction from waste printed circuit boards

Waste printed circuit boards (WPCBs) constitute a hazardous material with up to 40 different metals, including numerous many heavy metals and environmentally harmful metals. Most hydrometallurgical processing approaches use high concentrations of toxic reagents and generate significant amounts of harmful effluents. This research investigates the use of cyanide-starved glycine solution containing no free cyanide in the leachate to extract precious metals from WPCBs, with most of copper and base metals pre-removed by upstream glycine-only leaching. Under the optimised conditions, 90.1% Au, 89.4% Ag and 70.1% Pd were extracted together with 81.0% Cu and 15.0% Zn. The extraction of other base metals remained low at 8.3% for Al and <5% for Pb, Ni, Co, Fe and Sn, indicating a fairly good selectivity of the leaching system. By comparing with stoichiometric and intensive cyanidation, the cyanide-starved glycine system showed comparable or better performance on precious metals extraction, but cyanide use was reduced by >70% whereas the glycine can be reused. Analysis indicates that with an initial cyanide dose of 250 ppm, the leaching solution was starved of cyanide after 4 h with no free cyanide, which minimises safety and health risks significantly compared with traditional intensive cyanidation ([CN] > 3500 ppm). Glycine and cyanide dose, pH, and particle size dominated leaching kinetics, while staged addition of cyanide did not enhance the extractions. A significant (70–90%) reduction in required cyanide use and cyanide-bearing effluents can be achieved while performing polymetallic metal removal and allowing reagent recycling.

Screening of Cyanide-Utilizing Bacteria from Rumen and In Vitro Evaluation of Fresh Cassava Root Utilization with Pellet Containing High Sulfur Diet.

Two experiments were undertaken to screen for ruminal cyanide-utilizing bacteria (Experiment 1), and to evaluate the influence of fresh cassava root (FCR) and pellets containing high sulfur (PELFUR) on cyanide content, gas production parameters, in vitro degradability, and ruminal fermentation (Experiment 2). Experiment 1 was conducted in a completely randomized design (CRD) for the screening of cyanide-utilizing bacteria and the dietary treatments consisted of cyanide at 0, 150, 300, and 450 ppm. In Experiment 2, a 5 × 3 factorial arrangement in a completely randomized design was used for the in vitro study. Factor A was the level of FCR at 0, 260, 350, 440, and 530 g/kg of dry matter (DM) substrate, and factor B was the level of PELFUR at 0, 15, and 30 g/kg DM substrate. In Experiment 1, adding different doses of cyanide significantly affected cyanide-utilizing rumen bacterial growth (p < 0.05). Increasing the concentration of cyanide from 0 to 150 and 150 to 300 ppm resulted in increases in cyanide-utilizing rumen bacteria of 38.2% and 15.0%, respectively. In Experiment 2, no interaction effects were found between FCR and PELFUR doses on gas production parameters (p > 0.05). Increasing the FCR level to more than 260 g/kg of DM substrate could increase cumulative gas production (p < 0.05). Increasing doses of PELFUR from 15 to 30 g/kg increased the cumulative gas production when compared with that of 0 g PELFUR/kg of DM substrate (p < 0.05). The cyanide concentration in rumen fluid decreased with PELFUR (p < 0.05) supplementation. Degradability of in vitro DM and organic matter following incubation increased at 12 and 24 h due to PELFUR supplementation with FCR and increased additionally with 15 g PELFUR/kg of DM substrate (p < 0.05) in 440 g FCR/kg of DM substrate. Proportions of the total volatile fatty acids, acetic acid (C2), propionic acid (C3), and butyric acid among supplementations with FCR (p < 0.05) were significantly different. In conclusion, the present results represent the first finding of bacteria in the rumen that are capable of utilizing cyanide, and suggests that cyanide might function as a nitrogen source for bacterial cell synthesis. The inclusion of FCR of 530 g/kg with 30 g PELFUR/kg of DM substrate could increase the cumulative gas production, the bacterial population, the in vitro degradability, the proportion of C3, and the rate of the disappearance of cyanide.

Can isosorbide dinitrate oral spray serve as an immediate bridging therapy for a mass cyanide poisoning?

Objective 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. Methods 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. Results 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. Conclusion 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.

Quantification of amygdalin, prunasin, total cyanide and free cyanide in powdered loquat seeds

ABSTRACT Amygdalin, prunasin, total cyanide and free cyanide concentrations in 12 powdered loquat seeds were investigated. Loquat (Eriobotrya japonica) is a species of flowering plant in the family Rosaceae, and its fruit is quite popular in Japan. Amygdalin and prunasin were measured using LC–MS/MS. Total cyanide was measured by enzymatic treatment, steam distillation and colorimetric quantification using the pyridine–pyrazolone method. Free cyanide was measured without enzymatic treatment. The mean concentrations of amygdalin, prunasin, total cyanide and free cyanide in powdered loquat seeds were 5900, 760, 410 and 44 mg/kg, respectively. The range of each quantitative value was extensive. Seven out of twelve samples were at risk for exceeding the acute reference dose (ARfD) of cyanide.

Pharmacognostic Screening of Elaeis guineensis ( Aracaceae) Jacq. Oil and its Effect as an Antidote on Cyanide Poisoning

Introduction: Elaeis guinenesis is a perennial monocot belonging to the family Arecaceae. It is the source of the oil commonly called African palm oil or macaw fat which in traditional medicine has many uses&#x0D; Aim: This study is focused on the pharmacognostic screening of oil of Elaeis guineensis, and its antidotal effect on cyanide poisoning.&#x0D; Method: The extracted oil was subjected to various screening technique in order to determine its quality, purity and chemical constituents. The oil was macroscopically examined; acute toxicity test of Elaeis guineensis oil was carried out on rats. The oil was subjected to heating to determine the moisture content. Phytochemical analysis was also carried out on the palm oil extract. The physicochemical analysis was carried to determine the acid value, saponification value, ester value, hydroxyl value and iodine value. The Ld50 for the pure cyanide was carried out on the rats using “Up and Down” method. The antidotal study of Elaeis guineensis oil was carried out on the rats.&#x0D; Result: Macroscopic evaluation showed, the oil was in fresh condition, smooth texture, bright red colour, characteristic taste, oily appearance and a characterictic smell. The Phytochemical analysis showed the presence of flavonoids, phenols, tannins, saponnins, alkaloids, steroids and terpenoids. The physicochemical analysis showed that the oil has an acid value of 31.2, Saponification value of 194.8, Ester value 163.54, Peroxide value of 18.0, Hydroxyl Percentage of 2.07% and Free Fatty Acid of 3.65. The moisture content was calculated to be 0.2%. For the acute toxicity test on the oil using Lorkes method no death was recorded. The LD50 of the cyanide carried out on the rats showed that the lethal dose of cyanide is 5 mg/kg. The antidotal effect of Elaeis guineensis oil showed the absence of death on the group given oil extract alone and the groups that were poisoned and given the oil (antidote) within 4 minutes. Deaths were recorded for the groups that were administered antidotes after 8 minutes.&#x0D; Conclusion: Elaeis guineensis oil has counteracting effect on cyanide poisoning if administered within four minutes of cyanide ingestion.&#x0D;

Physiologically based pharmacokinetic modeling of hydrogen cyanide in humans following the oral administration of potassium cyanide and cyanogenic glycosides from food

Cyanogenic glycosides (CGs) are commonly found in some edible plants and seeds. After ingestion, CGs can release toxic hydrogen cyanide (HCN) in humans. At present, unfortunately, there is no tool capable of predicting the cyanide concentration in human blood and organs following oral administration of CG-containing food. The aim of this study was to develop a physiologically based pharmacokinetic (PBPK) model of cyanide following the ingestion of CG-containing food in humans. To develop this model, pharmacokinetic data concerning cyanide concentration levels in humans exposed to potassium cyanide (KCN) and CG-containing foods (persipan paste, linseed, cassava, and bitter apricot kernels) were obtained from published data. This study created a model structure consisting of four organ compartments including the lungs, kidneys, liver, and slowly perfused tissues by employing Berkeley Madonna software to extract three unknown parameters including the maximum velocity of rhodanese, the absorption rate constant, and the bioavailability for oral administration of KCN and the four CG-containing foods (equivalent a 6.8 mg dose of cyanide). The model was then validated by comparing the simulated results for the concentration-time courses of cyanide levels in venous blood with data from two clinical studies covering the oral administration of KCN and linseed at three other doses.

Metabolism of Cyanide by Glutathione To Produce the Novel Cyanide Metabolite 2-Aminothiazoline-4-oxoaminoethanoic Acid.

The direct analysis of cyanide (HCN or CN- inclusively symbolized as CN) to confirm exposure has major limitations due to cyanide's volatility, reactivity, and short half-life in biological fluids. These limitations have led to the exploration of cyanide detoxification products for indirect verification of cyanide exposure. Although cyanide interacts strongly with sulfur-containing molecules, to date, biomarkers resulting from the interaction of cyanide with glutathione (GSH; i.e., a biologically abundant sulfur-donating biomolecule) have yet to be discovered. In this study, we studied the interaction of CN and GSH to produce 2-aminothiazoline-4-oxoaminoethanioc acid (ATOEA). An LC-MS/MS method was developed and validated to analyze ATOEA from plasma, producing a linear range of 0.5-50 μM, a limit of detection of 200 nM, and excellent precision and accuracy. ATOEA concentrations were significantly elevated in the plasma of animals following cyanide exposure. Moreover, the production of ATOEA from cyanide exposure was confirmed by detection of both ATOEA and ATOEA-13C15N in rabbit plasma ( N = 11 animals) following administration of NaCN:K13C15N (1:1), with a similar amount of ATOEA and ATOEA-13C15N formed ( R2 = 0.9924, p < 0.05). The concentration of ATOEA increased with cyanide dose and then decreased rapidly when an antidote was administrated. This study definitively showed that ATOEA is produced from interaction of CN and GSH and can serve as a biomarker of cyanide exposure.

A Review on Ingested Cyanide: Risks, Clinical Presentation, Diagnostics, and Treatment Challenges.

Cyanide, a metabolic poison, is a rising chemial threat and ingestion is the most common route of exposure. Terrorist organizations have threatened to attack the USA and international food and water supplies. The toxicokinetics and toxicodynamics of oral cyanide are unique, resulting in high-dose exposures, severe symptoms, and slower onset of symptoms. There are no FDA-approved therapies tested for oral cyanide ingestions and no approved intramuscular or oral therapies, which would be valuable in mass casualty settings. The aim of this review is to evaluate the risks of oral cyanide and its unique toxicokinetics, as well as address the lack of available rapid diagnostics and treatments for mass casualty events. We will also review current strategies for developing new therapies. A review of the literature using thePRISMA checklist detected 7284 articles, screened 1091, and included 59 articles or other reports. Articles referenced in this review were specific to risk, clinical presentation, diagnostics, current treatments, and developing therapies. Current diagnostics of cyanide exposure can take hours or days, which can delay treatment. Moreover, current therapies for cyanide poisoning are administered intravenously and are not specifically tested for oral exposures, which can result in higher cyanide doses and unique toxicodynamics. New therapies developed for oral cyanide exposures that are easily delivered, safe, and can be administered quickly by first responders in a mass casualty event are needed. Current research is aimed at identifying an antidote that is safe, effective, easy to administer, and has a rapid onset of action.

Identification of specific metabolic pathways as druggable targets regulating the sensitivity to cyanide poisoning.

Cyanide is a potent toxic agent, and the few available antidotes are not amenable to rapid deployment in mass exposures. As a result, there are ongoing efforts to exploit different animal models to identify novel countermeasures. We have created a pipeline that combines high-throughput screening in zebrafish with subsequent validation in two mammalian small animal models as well as a porcine large animal model. We found that zebrafish embryos in the first 3 days post fertilization (dpf) are highly resistant to cyanide, becoming progressively more sensitive thereafter. Unbiased analysis of gene expression in response to several hours of ultimately lethal doses of cyanide in both 1 and 7 dpf zebrafish revealed modest changes in iron-related proteins associated with the age-dependent cyanide resistance. Metabolomics measurements demonstrated significant age-dependent differences in energy metabolism during cyanide exposure which prompted us to test modulators of the tricarboxylic acid cycle and related metabolic processes as potential antidotes. In cyanide-sensitive 7 dpf larvae, we identified several such compounds that offer significant protection against cyanide toxicity. Modulators of the pyruvate dehydrogenase complex, as well as the small molecule sodium glyoxylate, consistently protected against cyanide toxicity in 7 dpf zebrafish larvae. Together, our results indicate that the resistance of zebrafish embryos to cyanide toxicity during early development is related to an altered regulation of cellular metabolism, which we propose may be exploited as a potential target for the development of novel antidotes against cyanide poisoning.

Carbon Monoxide and Cyanide Poisoning in the Burned Pregnant Patient: An Indication for Hyperbaric Oxygen Therapy.

Carbon monoxide (CO) is a small molecule poison released as a product of incomplete combustion. Carbon monoxide binds hemoglobin, reducing oxygen delivery. This effect is exacerbated in the burned pregnant patient by fetal hemoglobin that binds CO 2.5- to 3-fold stronger than maternal hemoglobin. With no signature clinical symptom, diagnosis depends on patient injury history, elevated carboxyhemoglobin levels, and alterations in mental status. The standard of care for treatment of CO intoxication is 100% normobaric oxygen, which decreases the half-life of CO in the bloodstream from 5 hours to 1 hour. Hyperbaric oxygen (HBO2) is a useful adjunct to rapidly reduce the half-life of CO to 20 minutes and the incidence of delayed neurologic sequelae. Because of the slow disassociation of CO from hemoglobin in the fetus, there is a far stronger indication for HBO2 in the burned pregnant patient than in other burn patient populations.Cyanide intoxication is often a comorbid disease with CO in inhalation injury from an enclosed fire, but may be the predominant toxin. It acts synergistically with CO to effectively lower the lethal doses of both cyanide and CO. Diagnosis is best made in the presence of high lactate levels, carboxyhemoglobin concentrations greater than 10%, injury history of smoke inhalation from an enclosed fire, and alterations in consciousness. While treatment with hydroxocobalamin is the standard of care and has the effect of reducing concomitant CO toxicity, data indicate cyanide may also be displaced by HBO2.Carbon monoxide and cyanide poisoning presents potential complications impacting care. This review addresses the mechanism of action, presentation, diagnosis, and treatment of CO and cyanide poisonings in the burned pregnant patient and the use of HBO2 therapy.

English

Cyanide contents of locally processed cassava based products (CBP) in Ilorin-West urban markets, Nigeria was estimated and compared to established safety levels. Hence, 29 locally processed cassava products samples were randomly collected from retail outlets and tested for hydrogen cyanide content, pH, titratable acidity (TTA), water absorption capacity (WAC) and least gelation capacity (LGC) following standard procedures. Results from the survey showed that hydrogen cyanide contents of the CBP ranged from 3.36 to 37.73 mg/kg. Titratable acidity ranged between 0.22 and 1.79 × 10-3 (% w/w); the pH of the samples was between 4.55 and 6.75; WAC ranged from 1.46 to 5.82 g/ml, while the LGC was from 8.07 to 38.08%. Twenty five out of the 29 CBP samples collected had hydrogen cyanide content above the maximum safe level (10 mg/kg), the TTA was low, while the pH was high. These problems might be due to poor processing methods adopted by the processors. Continuous exposure of consumers to sub-lethal dose of hydrogen cyanide may lead to serious health hazards. Key words: Cassava, cyanide, Ilorin, market, survey.

Does diathermy smoke contaminate processed salvaged blood in cardiac surgery?

A cell salvage device is used in cardiac surgery with the aim of reducing allogeneic blood transfusion. Suction of blood from the operating field used for the device is often accompanied by diathermy smoke. There is limited published research to know if this blood is then contaminated with clinically significant levels of harmful chemicals from this smoke. Postoperative cardiac surgery patients are already physiologically vulnerable, making the optimization of salvaged blood worth considering. Ten patients who had cardiac surgery using a cell salvage device from a single institution had samples taken from the processed blood just prior to transfusion. Samples were tested for carbon monoxide (CO), cyanide and benzene. Results were compared to preoperative co-oximetry results and normal adult laboratory reference ranges. Demographic data about the patients was collected, including the type of operation, gender, age, body mass index, smoking status and amount of salvaged blood collected and processed. Primary surgery was coronary artery bypass grafting (CABG) in three patients, mitral valve repair or replacement in three patients and one each of aortic valve replacement (AVR)/CABG, AVR/plication of the aorta, CABG/external wrapping of the aorta and valve-sparing root replacement. None were smokers. Neither the blood CO level prior to surgery nor in the processed salvaged blood was above the normal limit of 2% for non-smokers. There was no processed blood benzene found. Cyanide levels in the processed blood ranged from 1.8 to 44.1 μmol/l (where <8 μmol/l is considered within the normal adult laboratory limit). Despite the obvious limitations of the current study, it shows that cyanide levels can be found many times the normal level in processed salvaged blood. Whilst the total dose of cyanide is small, the potential impact may be clinically significant due to cyanide's effect on mitochondrial metabolism in the heart and brain.

Biosorption of Phenol and Cyanide from Synthetic/Simulated Wastewater by Sugarcane Bagasse—Equilibrium Isotherm and Kinetic Analyses

Sugarcane bagasse biosorbents were tested for biosorption of phenol and cyanide from synthetic/simulated wastewater. The influence of pH, biosorbent dose, temperature, contact time, and initial concentration of phenol and cyanide was investigated. At an optimum temperature 30 °C, pH 7, and the biosorbent dose of 40 g/L, 66.78% phenol and 79.30% cyanide were removed from binary aqueous solution containing 300 mg/L of phenol and 30 mg/L of cyanide. The equilibrium state was achieved after about 34 and 32 h, respectively, for phenol and cyanide at a temperature of 30 °C. The extended Freundlich model fits the binary equilibrium data suitably for both phenol and cyanide. The kinetic modeling results showed that fractal-like models and Brouser–Weron–Sototlongo for phenol and cyanide were capable to provide realistic explanation of biosorption kinetic. Biosorption of phenol and cyanide followed pseudo-second-order kinetics, indicating chemisorption to be the mechanism of biosorption. The present study provides a new insight for the removal of phenol and cyanide onto sugarcane bagasse.

On the verge of a respiratory-type panic attack: Selective activations of rostrolateral and caudoventrolateral periaqueductal gray matter following short-lasting escape to a low dose of potassium cyanide

Intravenous injections of potassium cyanide (KCN) both elicit escape by its own and facilitate escape to electrical stimulation of the periaqueductal gray matter (PAG). Moreover, whereas the KCN-evoked escape is potentiated by CO2, it is suppressed by both lesions of PAG and clinically effective treatments with panicolytics. These and other data suggest that the PAG harbors a hypoxia-sensitive alarm system the activation of which could both precipitate panic and render the subject hypersensitive to CO2. Although prior c-Fos immunohistochemistry studies reported widespread activations of PAG following KCN injections, the employment of repeated injections of high doses of KCN (>60µg) in anesthetized rats compromised both the localization of KCN-responsive areas and their correlation with escape behavior. Accordingly, here we compared the brainstem activations of saline-injected controls (air/saline) with those produced by a single intravenous injection of 40-µg KCN (air/KCN), a 2-min exposure to 13% CO2 (CO2/saline), or a combined stimulus (CO2/KCN). Behavioral effects of KCN microinjections into the PAG were assessed as well. Data showed that whereas the KCN microinjections were ineffective, KCN intravenous injections elicited escape in all tested rats. Moreover, whereas the CO2 alone was ineffective, it potentiated the KCN-evoked escape. Compared to controls, the nucleus tractus solitarius was significantly activated in both CO2/saline and CO2/KCN groups. Additionally, whereas the laterodorsal tegmental nucleus was activated by all treatments, the rostrolateral and caudoventrolateral PAG were activated by air/KCN only. Data suggest that the latter structures are key components of a hypoxia-sensitive suffocation alarm which activation may trigger a panic attack.