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Cyanide toxicity and their environmental impact are well known. Nevertheless, they are still used in the mining, galvanic and chemical industries. As a result of industrial activities, cyanides are released in various forms to all elements of the environment. In a natural environment, cyanide exists as cyanogenic glycosides in plants seeds. Too much consumption can cause unpleasant side effects. However, environmental tobacco smoke (ETS) is the most common source of cyanide. Live organisms have the ability to convert cyanide into less toxic compounds excreted with physiological fluids. The aim of this paper is to review the current state of knowledge on the behaviour of cyanide in the environment and its impact on the health and human life.

Simultaneous poisoning by carbon monoxide (CO) and hydrogen cyanide is the major cause of mortality in fire gas accidents. Here, we report on the invention of an injectable antidote against CO and cyanide (CN⁻) mixed poisoning. The solution contains four compounds: iron(III)porphyrin (FeIIITPPS, F), two methyl-β-cyclodextrin (CD) dimers linked by pyridine (Py3CD, P) and imidazole (Im3CD, I), and a reducing agent (Na₂S₂O₄, S). When these compounds are dissolved in saline, the solution contains two synthetic heme models including a complex of F with P (hemoCD-P) and another one of F with I (hemoCD-I), both in their iron(II) state. hemoCD-P is stable in its iron(II) state and captures CO more strongly than native hemoproteins, while hemoCD-I is readily autoxidized to its iron(III) state to scavenge CN⁻ once injected into blood circulation. The mixed solution (hemoCD-Twins) exhibited remarkable protective effects against acute CO and CN⁻ mixed poisoning in mice (~85% survival vs. 0% controls). In a model using rats, exposure to CO and CN⁻ resulted in a significant decrease in heart rate and blood pressure, which were restored by hemoCD-Twins in association with decreased CO and CN⁻ levels in blood. Pharmacokinetic data revealed a fast urinary excretion of hemoCD-Twins with an elimination half-life of 47 min. Finally, to simulate a fire accident and translate our findings to a real-life scenario, we confirmed that combustion gas from acrylic cloth caused severe toxicity to mice and that injection of hemoCD-Twins significantly improved the survival rate, leading to a rapid recovery from the physical incapacitation.

Cyanide (CN) is a well-known mitochondrial poison. CN poisoning may result from acute or long-term exposure to a number of CN compounds. Recent insight into the chemical affinities of the CN anion has increased our understanding of its toxicity and the mechanisms of antidotal actions, which, together with information on various exposure sources, are reviewed in the present article. A literature search in Scopus, Embase, Web of Science, PubMed, and Google Scholar for the period 2001–2024 revealed that the CN anion after exposure or degradation of CN compounds is distributed to vulnerable copper and iron-containing targets, especially in mitochondria, thus blocking the electron transport chain. Intake of cyanogenic compounds may exert subacute or chronic toxic effects, also because of the interaction with cobalt in vitamin B12. Antidotal agents exert their effects through the affinity of CN for cobalt- or iron-containing compounds. Research on CN interactions with metalloproteins may increase our insight into CN toxicity and efficient antidotal regimens.

Hydrogen sulfide is a highly toxic gas—second only to carbon monoxide as a cause of inhalational deaths. Its mechanism of toxicity is only partially known and no specific therapy exists for sulfide poisoning. We show in several cell types, including human inducible pluripotent stem cell (hiPSC)-derived neurons, that sulfide inhibited complex IV of the mitochondrial respiratory chain and induced apoptosis. Sulfide increased hydroxyl radical production in isolated mouse heart mitochondria and F 2 -isoprostanes in brains and hearts of mice. The vitamin B 12 analog cobinamide reversed the cellular toxicity of sulfide and rescued Drosophila melanogaster and mice from lethal exposures of hydrogen sulfide gas. Cobinamide worked through two distinct mechanisms: direct reversal of complex IV inhibition and neutralization of sulfide-generated reactive oxygen species. We conclude that sulfide produces a high degree of oxidative stress in cells and tissues and that cobinamide has promise as a first specific treatment for sulfide poisoning.

Copper mining generates large quantities of waste, tailings, and acid outflows causing long-term environmental impacts and potential threats to human health. Valea Şesei is the largest tailing impoundment in Romania, created by flooding the valley (known as Valea Şesei) of the Metalliferous Mountains (a division of the Apuseni Mountains) with copper mining waste. The present study (i) estimated the total volume of tailings in this area; (ii) screened the concentration of 65 elements (rare earth and platinum group elements, alkali metals and alkali earth metals, transition and post-transition metals and metalloids) and cyanide concentrations in wastewater samples collected from tailing impoundment; (iii) evaluated the toxicity of these water samples using five in vitro bioassays employing human cells isolated from healthy donors and a short-term (1 h) exposure model. The sampled waters were highly acidic (pH 2.1–4.9) and had high electrical conductivity (280–1561 mS cm −1 ). No cyanides were detected in any sample. Water samples collected from the stream (AMD) inflowing to the tailing impoundment were characterized by the greatest concentrations of alkali metals, alkaline earth metals, transition and post-transition metals, metalloids, rare earth elements, and noble metal group. At other sites, the elemental concentrations were lower but remained high enough to pose a relevant risk. The greatest magnitude of in vitro toxic effects was induced by AMD. Observed alterations included redox imbalance in human neutrophils followed by lipid peroxidation and decreased cell survival, significant aggregation of red blood cells, and increased prothrombin time. The study highlights that Valea Şesei is a large sink for toxic elements, posing environmental and health risks, and requiring action to prevent further release of chemicals and to initiate restoration of the area.

Artisanal and small-scale gold mining (ASGM) is the largest source of anthropogenic Hg emissions on the planet. In addition, Hg-contaminated tailings are often reprocessed with sodium cyanide (NaCN) to extract the residual gold remaining in the material. This leads to the formation of mercury cyanide (Hg(CN)2) complexes, which are often discharged in untreated form into local drainages, leading to large amounts of free cyanide being released. However, data on mercury-cyanide interactions are scarce. In this study, we investigated the impact of cyanide and Hg bioavailability in zebrafish when added as Hg(CN)2. Different concentrations of Hg(CN)2 and NaCN were used, leading to an LC50 of 0.53 mg.L−1 for NaCN and 0.16 mg.L−1 for Hg(CN)2. Analyzing free cyanide concentrations in aquarium water, >40% dissociation was observed for NaCN and about 5% for Hg(CN)2. The accumulation of total Hg (THg) in the brain, gills, muscle and kidney was quantified. All fish exposed to Hg(CN)2 had higher THg levels than their controls and kidney was the tissue with higher Hg(CN)2 accumulation. Histological effects on the kidney and gills of both cyanides in D. rerio tissues were investigated, suggesting renal alterations in fish exposed to Hg(CN)2 and showing hyperplasia in the gills of animals exposed to NaCN and Hg(CN)2. The results alert to the risks of the presence of these complexes in aquatic environments.

Although cyanide’s biological effects are pleiotropic, its most obvious effects are as a metabolic poison. Cyanide potently inhibits cytochrome c oxidase and potentially other metabolic enzymes, thereby unleashing a cascade of metabolic perturbations that are believed to cause lethality. From systematic screens of human metabolites using a zebrafish model of cyanide toxicity, we have identified the TCA-derived small molecule glyoxylate as a potential cyanide countermeasure. Following cyanide exposure, treatment with glyoxylate in both mammalian and non-mammalian animal models confers resistance to cyanide toxicity with greater efficacy and faster kinetics than known cyanide scavengers. Glyoxylate-mediated cyanide resistance is accompanied by rapid pyruvate consumption without an accompanying increase in lactate concentration. Lactate dehydrogenase is required for this effect which distinguishes the mechanism of glyoxylate rescue as distinct from countermeasures based solely on chemical cyanide scavenging. Our metabolic data together support the hypothesis that glyoxylate confers survival at least in part by reversing the cyanide-induced redox imbalances in the cytosol and mitochondria. The data presented herein represent the identification of a potential cyanide countermeasure operating through a novel mechanism of metabolic modulation.

Premise of the Study The maintenance of adaptive polymorphisms within species requires fitness trade‐offs reflecting selection for each morph. Cyanogenesis, the ability to produce hydrogen cyanide (HCN) after tissue damage, occurs in >3000 plant species and exists as a discrete polymorphism in white clover. This polymorphism is spatially distributed in recurrent clines, with higher frequencies of cyanogenic plants in warmer climates. The HCN autotoxicity hypothesis proposes that cyanogenic plants are selected against where frosts are common, as freezing liberates HCN and could impair cellular respiration. Methods We tested the HCN autotoxicity hypothesis using a freezing chamber to examine survival, tissue damage, and physiological recovery as assessed via chlorophyll fluorescence following mild and severe freezing treatments. We utilized 65 genotypes from a single polymorphic population to eliminate effects of population structure. Key Results Cyanogenic plants did not differ from acyanogenic plants in survival, tissue damage, or recovery following freezing. However, plants producing either of the two required cyanogenic precursors had lower survival and tissue damage after freezing than plants lacking both precursors. Conclusions These results suggest that freezing‐induced HCN toxicity is unlikely to be responsible for the maintenance of the cyanogenesis polymorphism in white clover. However, energetic trade‐offs associated with costs of producing the cyanogenic precursors may confer a fitness benefit to acyanogenic plants under stressful climatic conditions. The lack of evidence for HCN toxicity suggests that cyanogenic clover uses physiological mechanisms mediated by β‐cyanoalanine synthase and alternative oxidase to maintain cellular function in the presence of HCN.

Hydrogen cyanide (HCN) occurs in living organisms and in the environment. This is a widely known poison but is also considered as a gasotransmitter. For most higher plants, microorganisms and animals HCN is toxic, especially at elevated concentrations. However, plants’ sensitivity to this compound is lower than animals’ due to the activity of an alternative oxidase in the mitochondrial respiration chain. All higher plants synthesize HCN as a co-product during the final step of ethylene biosynthesis, whilst some plant species release it from cyanogenic compounds, accumulated for diverse physiological purposes. This molecule is used as a toxic bomb against herbivores, as a source of nitrogen in N-deficient plants, or as a regulator of seed dormancy state. The toxicity of HCN is mainly due to the inhibition of the activity of several metalloenzymes: iron-containing enzymes, molybdoenzymes and enzymes that contain zinc or copper. HCN impacts cellular metabolism by modulation of the reactive oxygen species and reactive nitrogen species levels, and via modifications of proteins ( S -cyanylation, oxidation). The aim of this work is to describe the dual (toxic and signalling) mode of cyanide action in plants at a cellular level.

Potassium cyanide (KCN) is a highly lethal poison with cyanide anions having an inhibitory effect on complex IV of the mitochondrial respiratory chain, leading to stoppage in electron transport and eventually cessation of aerobic respiration within the cell. Tardigrades are a group of small invertebrates, most well known for their exceptional resistance to environmental stressors, including exposure to aqueous solution of KCN. In this study, specimens of the tardigrade Paramacrobiotus experimentalis were subjected to KCN exposures of various concentrations and durations, as well as repeated exposures. The resulting reactions have been observed, both by observing its movements and through ultrastructure analysis using transmission electron microscope (TEM). Obtained results confirm high tolerance of tardigrades to KCN. After an initial period of debilitation, tardigrades gradually return to full activity. Statistically significant relationships between time needed for recovery and KCN concentration, duration of exposure and number of consecutive exposure episodes have been found. However, no significant relationship between KCN exposure and long-term survival has been found. Analysis using TEM has found changes in midgut and storage cells of exposed animals, including mitochondrial damage and evidence of autophagy. Finally, a new protocol for tardigrade exposure to KCN has been devised.