Cyanogenic glycosides are compounds produced naturally by over 2,500 species of plants, functioning as a defense mechanism against herbivores and pathogens. These nitrogen-containing metabolites are found in various plant parts, including leaves, stems, roots, and seeds. The compounds are not inherently harmful in their stored form, but they rapidly convert into a toxic substance when the plant tissue is disturbed. Understanding this conversion is important for safely preparing and consuming many common food sources worldwide.
Chemical Conversion to Toxins
The mechanism relies on a two-component system that keeps the potentially harmful glycosides separated from the enzymes that activate them. The glycosides are stable molecules, consisting of a sugar component attached to an \(\alpha\)-hydroxynitrile structure. In an intact plant cell, the glycosides are typically stored in the vacuole, while the activating enzyme is kept in a different cellular compartment.
When the plant tissue is physically damaged, such as through chewing or crushing, the cellular compartments break, allowing the glycosides and the activating enzyme to mix. This initiates a rapid enzymatic hydrolysis, primarily catalyzed by \(\beta\)-glucosidases, such as linamarase. This first step cleaves the sugar molecule from the glycoside, yielding an unstable intermediate compound known as a cyanohydrin.
The resulting cyanohydrin spontaneously decomposes. The final step is the breakdown of the cyanohydrin into a carbonyl compound, such as an aldehyde or ketone, and the volatile toxin, hydrogen cyanide (HCN). This release of HCN is the core risk associated with consuming these plant products.
Hydrogen cyanide is a potent cellular poison that interferes with the body’s ability to use oxygen. The cyanide ion rapidly binds to the iron atom found in cytochrome \(c\) oxidase, an enzyme complex located in the mitochondria. By binding to this enzyme, cyanide blocks the final step of the electron transport chain, the process cells use to produce energy from oxygen. This inhibition of aerobic respiration leads to cellular asphyxiation, as tissues cannot extract oxygen from the blood, causing rapid system failure.
Common Dietary Sources and Exposure
Cyanogenic glycosides are widely distributed across the plant kingdom, appearing in several important food crops. The tropical root crop cassava (Manihot esculenta), also known as manioc or yuca, is the most significant source globally, with its toxicity primarily due to the glycoside linamarin. Cassava varieties are classified as “sweet” or “bitter” based on their cyanogen content, with bitter varieties containing higher concentrations that necessitate extensive processing.
Another common source is the seeds of stone fruits, such as apricots, cherries, peaches, and plums, which contain the glycoside amygdalin. Bitter almonds, distinct from the sweet almonds typically consumed, also contain high levels of amygdalin, which is responsible for their characteristic taste. Other foods, like certain varieties of lima beans and sorghum, are recognized as dietary sources of these compounds.
Exposure levels are influenced by geographical location and dietary habits, particularly where these plants form a primary food source. In parts of Africa, for instance, cassava is a staple food, and reliance on it means that any lapse in traditional processing can lead to chronic or acute exposure risks. Immature bamboo shoots, common in Asian cuisine, contain the glycoside taxiphyllin and require proper preparation. The concentration of these compounds can also vary widely based on the specific cultivar, climate, and the age of the plant part.
Mitigating Risk Through Processing
Traditional food preparation methods are effective at reducing or eliminating the cyanogenic risk. The goal of processing is twofold: allowing the activating enzymes to break down the glycosides and facilitating the removal of the volatile hydrogen cyanide gas. This process has been developed over centuries in cultures that rely on cyanogenic plants for sustenance.
Methods like grating or pounding the raw material, such as cassava tubers, are performed first to intentionally damage the tissue and mix the glycosides with the \(\beta\)-glucosidase enzyme. Once the enzymatic reaction begins, subsequent steps focus on removal. Soaking the grated plant material in water for prolonged periods, often several days, allows the water-soluble glycosides and the liberated hydrogen cyanide to leach out.
Boiling and cooking are effective, as the heat facilitates the spontaneous decomposition of the unstable cyanohydrins into HCN, which readily volatilizes into the air. Drying, whether by sun or oven, is another mechanism that allows the gas to escape. Fermentation, which involves exposing the plant material to microorganisms, is also utilized because the microflora can contribute to the degradation of the hydrolytic enzymes and the cyanogens themselves.
Symptoms of Cyanide Poisoning
Exposure to high levels of hydrogen cyanide results in acute poisoning, characterized by a rapid onset of severe, non-specific symptoms. Since the toxin impairs cellular oxygen use, the effects are most pronounced in the central nervous system and the cardiovascular system. Initial symptoms often include headache, confusion, nausea, and vomiting.
As exposure worsens, the person may experience rapid breathing and a fast pulse rate, followed by a decline in blood pressure and mental status. In severe cases, the inhibition of cellular respiration can quickly lead to seizures, loss of consciousness, coma, and cardiac arrest. The acute lethal dose of hydrogen cyanide for humans is generally reported to be between 0.5 to 3.5 milligrams per kilogram of body weight.
Beyond the immediate, life-threatening effects of acute poisoning, chronic exposure to lower levels of cyanogens can cause health problems. This long-term exposure, often resulting from consuming insufficiently processed foods like cassava, is associated with neurological disorders. These chronic effects can include conditions that affect motor skills and interfere with thyroid function, as the body’s detoxification product, thiocyanate, can disrupt iodine uptake.