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Battlefield Chemical Inhalation Injury
Published in Jacob Loke, Pathophysiology and Treatment of Inhalation Injuries, 2020
Synonyms for cyanide (AC) include hydrocyanic acid, hydrogen cyanide, and prussic acid. Its formula is HCN; vapor density 0.93; specific gravity 0.69; boiling point 25.7°C. Cyanide is a colorless gas (or liquid) with a peach-kernel or bitter-almond odor. Although it can be detected by trained observers at slightly less than toxic levels, because of the rapidity of onset of toxic symptoms this substance is regarded as having poor warning properties (Braker et al., 1977).
Asphyxia due to Metabolic Poisons
Published in Burkhard Madea, Asphyxiation, Suffocation,and Neck Pressure Deaths, 2020
Hydrogen cyanide is an extremely toxic gas (or liquid – hydrocyanic acid), which prevents tissue utilization of oxygen by binding to cytochrome oxidase, resulting in inhibition of cellular respiration. This binding occurs very rapidly and may cause death within minutes [22]. The expectation of a rapid death is probably a major reason for the ingestion of cyanide salts to commit suicide. However, the availability of hydrogen cyanide is limited and therefore such suicides are mostly seen in groups with ready access to it, such as scientists, jewellers and metal workers, a pattern that has been reported for decades and still remains unchanged [10]. Despite the awareness of its toxicity, workplace exposure causing non-intentional poisoning continues to contribute to the cyanide death toll. In addition, hydrogen cyanide can be formed in toxic concentrations in fires, and even if certain plastics have been banned because of a high production of cyanide upon combustion, many fire victims still show high blood cyanide levels. The high toxicity has also attracted interest by terrorists, and several attempts of mass killings have been reported, the most well-known being that in a Tokyo underground station in 1995, where bags of sulfuric acid and sodium cyanide were found in a restroom. When mixed, these would produce deadly hydrogen cyanide (HCN) gas.
Pharmacological actions of chemical constituents
Published in C. P. Khare, Evidence-based Ayurveda, 2019
Common cyanogenic glycosides include amygdalin, found in bitter almonds and peach karnels, and prunasin, which occurs in wild cherry (Prunus serotina) bark. Cyanogenic glucosides are capable of generating hydrocyanic acid, which is a violent poison. But hydrolysis of the glycosides in the digestive tract or by the liver leads to a slow release of hydrocyanic acid, which can be detoxified by the body.
Molecular mechanism of amygdalin action in vitro: review of the latest research
Published in Immunopharmacology and Immunotoxicology, 2018
Przemysław Liczbiński, Bożena Bukowska
Amygdalin is a representative of chemical organic compounds of cyanogenic glycosides with a molecular formula of C20H27O11 (Figure 1) and a molecular mass of 457.42 g/mol. Amygdalin is composed of benzaldehyde, hydrocyanic acid and two glucose molecules (D-mandelonitrile-β-D-glucoside-6-β-glucoside). It is a widespread compound in the environment, occurring in seeds of many plants, including black cherries, peaches, plums, apples, apricots, etc1. Amygdalin is not a toxic compound but hydrogen cyanide (HCN), which is formed during the enzymatic hydrolysis, has toxic properties. Years of research on the effects of amygdalin have shown its wide range of properties, including its supportive function in treatment of asthma, bronchitis, leprosy or colorectal cancer. Due to the presence of benzaldehyde in the amygdalin molecule it has analgesic properties2. Anticancer activity of amygdalin is still controversial and has been subject to a lot of research. This ability may be associated with enzymatic hydrolysis, which results in hydrocyanic acid release3.
Cassava toxicity, detoxification and its food applications: a review
Published in Toxin Reviews, 2021
Anil Panghal, Claudia Munezero, Paras Sharma, Navnidhi Chhikara
Mechanism: Cyanogenic glycoside and hydrolyzing enzymes are particularly stored separately in different compartments of plant cells. Glycosides are present in cell vacuoles and β-glucosidases and hydroxynitrile lyases enzymes are present in mesophyllic cells. Cyanogenic glycoside and its breakdown products cyanohydrins and HCN are responsible for the potential toxicity of cassava (Figure 2). Hydrolysing enzymes ingested as food component is inactivated by low pH of the stomach and mammalian tissues contain no significant amounts of β-glucosidase. Kobawila et al. 2005 suggested that ingested intact cyanogenic glycosides might be metabolized by β-glucosidases from the bacterial microflora of the gastrointestinal tract. Cyanide toxicity is the main reason underlying the reduced consumption of cassava and safety issues (Montagnac et al.2009). Plants secrete such substances for their self-defense from predators or other stress factors. The toxic compound cyanide secreted are glucosides (≥90% linamarin and ≤10% lotaustralin; Figure 3), cyanohydrins, free hydrocyanic acid (HCN), small amount of flavonoid glycosides and hydroxycoumarin for their defense is present throughout the plant (Delia et al.2016). The leaves contain cyanide in range of 53–1300 mg/kg and roots contain 10–500 mg/kg of the dry matter (Wobeto et al.2007). This variability might be due to differences in variety, soil composition, geographical location, environmental conditions, age, and part of the plant. Depending on the cyanide level in the root parenchyma tissue, cassava is categorized as sweet and bitter varieties. Sweet variety of cassava contains small amount of cyanogens as compared to the bitter variety; on the contrary, no correlation between the cyanide level and the bitterness of cassava (Balagopalan et al.1988, Bokanga 2000, Vetter 2000). Bitter varieties are more resistant to pest, pathogens, and are high yielding (Mader 2005).
Antitumor Action of Amygdalin on Human Breast Cancer Cells by Selective Sensitization to Oxidative Stress
Published in Nutrition and Cancer, 2019
Muayad Mehdi Abboud, Wajdy Al Awaida, Hakam Hasan Alkhateeb, Asia Numan Abu-Ayyad
Amygdalin C20H27NO11 is a cyanogenic glycoside compound derived from the aromatic amino acid phenylalanine (1). This natural product is mainly present in the seeds of apricot, peach, bitter almond, plum, and apple (2). Laetrile is simpler semisynthetic form produced by a chemical modification of amygdalin. Both amygdalin and laetrile can be hydrolyzed to yield common components of D-glucuronic acid and L-mandelonitrile (3,4). The latter is further broken down to produce benzaldehyde and hydrocyanic acid. The generation of hydrocyanic acid from amygdalin is performed by the enzyme β-glucosidase, which shows 1,000 – 3,000 times higher activity in tumor cells than in normal cells (5). This difference in enzyme activity permits tumor cells to accumulate excessive amounts of liberated hydrocyanic acid with antineoplastic activity. A further detoxification of hydrocyanic acid to thiocyanate requires another enzyme called rhodanese (6), which is more active in normal tissues but has almost negligible activity in cancer cells (7). Thus, it was proposed that a combination of abundant cyanide-liberating β-glucosidase activity together with a deficiency of the cyanide-detoxifying rhodanese activity, could provide a selective advantage for the killing of cancer cells by amygdalin without having substantial harmful effects on normal cells (5). By taking advantage of this interesting cell-killing approach, many attempts have been made to use amygdalin as an anticancer agent against human tumors. The earliest human trial was dated back to 1845 in Russia, when positive results were reported on the first treatment of cancer patient with amygdalin (8). In 1920, a similar attempt to treat cancer patients with amygdalin was conducted in the USA; but the drug was considered too toxic and its use to treat human cancer was abandoned. Later on, a more soluble and less toxic form of amygdalin was developed in 1950, which was commercially referred to as laetrile (9). However, at high doses even the laetrile itself could have adverse effects due to possible development of liver injury, damaged nerves, fever, and coma (10). These side effects appear to depend on the route of laetrile administration, with oral uptake showing much higher toxicity than the intravenous, intraperitoneal, or intramuscular injection (10). Furthermore, recent epidemiological studies on animal experiments found little antitumor activity of laetrile, which was supported by the failure of this compound to show effective anticancer therapy during human trials (11). These disappointing clinical data together with the potential of developing toxicity have discouraged the Food and Drug Administration (FDA) in the USA from approving laetrile as an anticancer agent in human therapy (11).