-
Marine Pollution Bulletin Sep 2022
Topics: Animals; Embryo, Nonmammalian; Potassium Cyanide; Sea Urchins
PubMed: 35872477
DOI: 10.1016/j.marpolbul.2022.113965 -
Indian Pediatrics Jul 1992
Topics: Child; Child, Preschool; Female; Humans; Male; Poisoning; Potassium Cyanide
PubMed: 1428143
DOI: No ID Found -
BMJ Case Reports Jul 2019While potassium cyanide poisoning has been well described, the toxicity of potassium gold cyanide is less well understood. This case describes an 84-year-old man who...
While potassium cyanide poisoning has been well described, the toxicity of potassium gold cyanide is less well understood. This case describes an 84-year-old man who presented after an intentional ingestion of 0.5-1 teaspoons of potassium gold cyanide. Despite antidotal therapy, the patient rapidly developed severe lactic acidosis, multiorgan dysfunction and ultimately expired. While the patient's clinical findings were consistent with acute cyanide poisoning, a serum cyanide level was below the toxic threshold. Previous reports have suggested that gold toxicity may also contribute to the effects of potassium gold cyanide, and may have played a role in the patient's rapid decline. In addition to treatment of cyanide toxicity, management of acute gold toxicity should also be considered in potassium gold cyanide ingestion.
Topics: Acidosis, Lactic; Aged, 80 and over; Cyanates; Gold; Gold Compounds; Humans; Male; Potassium Cyanide; Suicide
PubMed: 31350229
DOI: 10.1136/bcr-2019-229947 -
Immunological Investigations Mar 1993The exact mechanism by which deposited C5b-9 complexes kill Gram-negative bacteria is unclear. It has been proposed that during complement activation the membrane attack...
The exact mechanism by which deposited C5b-9 complexes kill Gram-negative bacteria is unclear. It has been proposed that during complement activation the membrane attack complex triggers an energy dependent process in Gram-negative bacteria that mediates destruction of the inner membrane. This observation in part resulted from the survival of Gram-negative bacteria that were incubated with an uncoupler (DNP) or an inhibitor (KCN) of oxidative phosphorylation during complement activation. In a reexamination of this issue we employed potassium cyanide (KCN) to block energy dependent pathways and observed a dose dependent inhibition of C9 uptake on E. coli J5 during serum incubation, suggesting that cyanide was interfering with complement activation. To verify the effect on complement activation we chose specifically to study the effects of KCN on the C3 convertase of the classical pathway. Sensitized sheep erythrocytes were employed as our model system. This system allowed us to construct a series of stable intermediates that were used to test the effect of cyanide on the formation and activity of precursors of the classical pathway C3 convertase. The data illustrate that the concentrations of potassium cyanide that inhibit complement killing of J5 also inhibit C3 convertase activity on sensitized sheep erythrocytes. The results of this study refute the principal observation made by other investigators, that potassium cyanide protects bacteria from complement killing by inhibiting bacterial energy dependent pathways that spark inner membrane destruction. A better scenario is that the organisms survive because cyanide inhibits complement activation.
Topics: Animals; Complement Activation; Complement C3-C5 Convertases; Complement C9; Cytotoxicity, Immunologic; Dose-Response Relationship, Drug; Escherichia coli; Humans; Potassium Cyanide
PubMed: 8505069
DOI: 10.3109/08820139309063396 -
Chemical Research in Toxicology Jun 2021Smoke inhalation from a structure fire is a common route of cyanide poisoning in the U.S. Cyanide inhibits cellular respiration, often leading to death. Its rapid...
Smoke inhalation from a structure fire is a common route of cyanide poisoning in the U.S. Cyanide inhibits cellular respiration, often leading to death. Its rapid distribution throughout the body can result in injuries to multiple organs, and cyanide victims were reported to experience myocardial infarction and other cardiac complications. However, molecular mechanisms of such complications are yet to be elucidated. While FDA-approved CN antidotes such as sodium thiosulfate and hydroxocobalamin are clinically used, they have foreseeable limitations during mass casualty situations because they require intravenous administration. To facilitate the development of better antidotes and therapeutic treatments, a global view of molecular changes induced by cyanide exposure is necessary. As an exploratory pursuit, we performed oligonucleotide microarrays to establish cardiac transcriptomes of an animal model of nose-only inhalation exposure to hydrogen cyanide (HCN), which is relevant to smoke inhalation. We also profiled cardiac transcriptomes after subcutaneous injection of potassium cyanide (KCN). Although the KCN injection model has often been used to evaluate medical countermeasures, this study demonstrated that cardiac transcriptomes are largely different from that of the HCN inhalation model at multiple time points within 24 h after exposure. Pathway analysis identified that HCN-induced transcriptomes were enriched with genes encoding mediators of pathways critical in modulation of cardiac complications and that a large number of such genes were significantly decreased in expression. We utilized the upstream regulatory analysis to propose drugs that can be potentially employed to treat cyanide-induced cardiac complications.
Topics: Animals; Heart Injuries; Hydrogen Cyanide; Inhalation Exposure; Injections, Subcutaneous; Male; Mice; Potassium Cyanide
PubMed: 33914522
DOI: 10.1021/acs.chemrestox.0c00467 -
International Journal of Toxicology Sep 2016The Food and Drug Administration Animal Rule requires evaluation of cardiovascular and central nervous system (CNS) effects of new therapeutics. To characterize an adult...
The Food and Drug Administration Animal Rule requires evaluation of cardiovascular and central nervous system (CNS) effects of new therapeutics. To characterize an adult and juvenile mouse model, neurobehavioral and cardiovascular effects and pathology of a single sublethal but toxic, 8 mg/kg, oral dose of potassium cyanide (KCN) for up to 41 days postdosing were investigated. This study describes the short- and long-term sensory, motor, cognitive, and behavioral changes associated with oral dosing of a sublethal but toxic dose of KCN utilizing functional observation battery and Tier II CNS testing in adult and juvenile mice of both sexes. Selected tissues (histopathology) were evaluated for changes associated with KCN exposure with special attention to brain regions. Telemetry (adult mice only) was used to evaluate cardiovascular and temperature changes. Neurobehavioral capacity, sensorimotor responsivity or spontaneous locomotor activity, and rectal temperature were significantly reduced in adult and juvenile mice at 30 minutes post-8 mg/kg KCN dose. Immediate effects of cyanide included bradycardia, adverse electrocardiogram arrhythmic events, hypotension, and hypothermia with recovery by approximately 1 hour for blood pressure and heart rate effects and by 2 hours for body temperature. Lesions consistent with hypoxia, such as mild acute tubular necrosis in the kidneys corticomedullary junction, were the only histopathological findings and occurred at a very low incidence. The mouse KCN intoxication model indicates rapid and completely reversible effects in adult and juvenile mice following a single oral 8 mg/kg dose. Neurobehavioral and cardiovascular measurements can be used in this animal model as a trigger for treatment.
Topics: Administration, Oral; Animals; Behavior, Animal; Blood Pressure; Brain; Cardiovascular System; Disease Models, Animal; Electrocardiography; Female; Heart Rate; Lethal Dose 50; Male; Mice; Mice, Inbred Strains; Nervous System; Neurons; Potassium Cyanide
PubMed: 27170681
DOI: 10.1177/1091581816646974 -
Comparative Medicine Oct 2018Cyanide is a readily available and potentially lethal substance. Oral exposure can result in larger doses, compared with other routes. Currently, there are no antidotes...
Cyanide is a readily available and potentially lethal substance. Oral exposure can result in larger doses, compared with other routes. Currently, there are no antidotes specific for use in the treatment of oral cyanide poisoning, and studies cannot be done in humans. We report on a new large animal model of oral cyanide toxicity to evaluate potential antidotes. Six female swine (; weight, 45 to 55 kg) were anesthetized, intubated, and instrumented. Animals received a KCN bolus of either 5 or 8 mg/kg delivered via orogastric tube. Time to apnea was recorded; parameters monitored included heart rate, respiratory rate, blood pressure, pulse oximetry, end-tidal CO2, arterial blood gasses, and lactate concentrations. The Welch test was used to calculate confidence intervals, mean, and standard deviation, and a Kaplan-Meier survival curve was used to compare survival between the 2 groups. At baseline, all animals in both groups were similar. Animals in the 5-mg/kg group had a more rapid time to apnea (5.1 ± 2.1 min), longer time to death (48.5 ± 38.1 min), and a greater rate of survival than the 8-mg/kg group (apnea, 10.6 ± 10.7 min; death, 26.1 ± 5.8 min). All animals displayed signs of toxicity (acidemia, hyperlactatemia, hypotension, apnea). We here report a large animal (swine) model of oral cyanide poisoning with dose-dependent effects in regard to time to death and survival rate. This model likely will be valuable for the development of medical countermeasures for oral cyanide poisoning.
Topics: Administration, Oral; Animals; Disease Models, Animal; Female; Kaplan-Meier Estimate; Monitoring, Physiologic; Potassium Cyanide; Swine
PubMed: 30208987
DOI: 10.30802/AALAS-CM-18-000041 -
Nature Apr 1953
Topics: Cyanides; Genetics; Potassium Cyanide; Smell; Solutions
PubMed: 13054678
DOI: 10.1038/171698b0 -
Human Toxicology Mar 1988The pharmacokinetics of intravenously injected potassium cyanide have been studied in Beagle bitches. In the period up to about 80 min after dosing, blood levels fell in...
The pharmacokinetics of intravenously injected potassium cyanide have been studied in Beagle bitches. In the period up to about 80 min after dosing, blood levels fell in a manner consistent with first-order elimination kinetics. Thereafter blood cyanide concentrations fell at a slower rate, indicating that a second phase of slower elimination had been entered.
Topics: Animals; Cyanides; Dogs; Female; Injections, Intravenous; Metabolic Clearance Rate; Potassium Cyanide
PubMed: 3378806
DOI: 10.1177/096032718800700214 -
The Tokai Journal of Experimental and... Dec 2013Hydrogen cyanide possesses a high acid-dissociation constant of 9.14, favoring its vaporization and depletion from the culture media at physiological pH, which may cause...
BACKGROUND
Hydrogen cyanide possesses a high acid-dissociation constant of 9.14, favoring its vaporization and depletion from the culture media at physiological pH, which may cause the cyanide toxicity unstable in vitro.
OBJECTIVE
We investigated whether adjustment of culture medium pH stabilizes cyanide concentration and decreases the effective concentration of potassium cyanide (KCN).
METHODS
Murine fibroblast cells were exposed to different concentrations of KCN in media maintained at pH 7.4 or 9.2, in the presence or absence of hydroxocobalamin. After incubation for 1 h, we evaluated medium pH, cyanide concentration, cytochrome activity, and cell viability.
RESULTS
Cyanide concentration decreased to 18.8% in pH 7.4 medium compared to 83.2% in pH 9.2 medium. A significant decrease in cytochrome activity was observed at 40 mM and 1.25 mM KCN in pH 7.4 and pH 9.2 media, respectively. In pH 9.2 medium, dose-dependent cytotoxicity of KCN and antidotal effects of hydroxocobalamin were observed.
CONCLUSION
Adjustment of culture medium pH to 9.2 could stabilize cyanide concentration and decrease the effective concentration of KCN, allowing stable evaluation of KCN toxicity and antidotal efficacy.
Topics: Animals; Antidotes; Cell Survival; Cells, Cultured; Culture Media; Cytochromes; Dose-Response Relationship, Drug; Fibroblasts; Hydrogen-Ion Concentration; Hydroxocobalamin; Mice; Potassium Cyanide; Toxicity Tests; Volatilization
PubMed: 24318282
DOI: No ID Found