~ 1559 ~ International Journal of Chemical Studies 2018; 6(5): 1559-1561 P-ISSN: 2349–8528 E-ISSN: 2321–4902 IJCS 2018; 6(5): 1559-1561 © 2018 IJCS Received: 11-07-2018 Accepted: 15-08-2018 Asgar Ud Deen Ph.D. Scholar, Animal Nutrition Division, National Dairy Research Institute, Karnal, Haryana, India Vandana Kumari Ph.D. Scholar, Animal Nutrition Division, National Dairy Research Institute, Karnal, Haryana, India Amit N Sharma Ph.D. Scholar, Animal Nutrition Division, National Dairy Research Institute, Karnal, Haryana, India Goutam Mondal Senior Scientist, Animal Nutrition Division, National Dairy Research Institute, Karnal, Haryana, India Gaurav Pratap Singh MV Sc. Scholar, Animal Nutrition Division, National Dairy Research Institute, Karnal, Haryana, India Correspondence Asgar Ud Deen Ph.D. Scholar, Animal Nutrition Division, National Dairy Research Institute, Karnal, Haryana, India Understanding cyanogenic glycoside toxicity in livestock: A review Asgar Ud Deen, Vandana Kumari, Amit N Sharma, Goutam Mondal and Gaurav Pratap Singh Abstract Ingestion of high concentrations of cyanogenic glycosides from cyanophoric plants has resulted in mortality in numerous species of animals. Death has been reported more in grazing and browsing animal species such as cattle, sheep, and goats than in those usually kept under intensive system of management like pigs and poultry. This is because it’s possible to consume larger doses of the glycosides from fresh, cyanophoric plant materials than in processed products usually given to pigs and poultry. Under certain conditions, several plants can accumulate large quantities of cyanogenic glycosides which upon ingestion convert to prussic acid. The risk of prussic acid poisoning in livestock is substantially increased during periods of drought, and drought breaks, when stressed, stunted plants begin to grow. Prussic acid is a potent poison, once ingested, it enters the bloodstream of affected animals and is transported throughout the body. It then inhibits oxygen utilisation by disrupting the electron transport chain (ETC) of the mitochondria, so that the animal dies from asphyxia. The present review article is an attempt to understand the multiple facets of cyanide toxicity in livestock and the possible mitigation strategies. Keywords: cyanogenic glycoside, prussic acid poisoning, HCN 1. Introduction Glycosides in general are compounds that consists of a carbohydrate moiety (sugar) attached by an ester bond to a non-carbohydrate moiety (referred to as aglycone). The structure and/or properties of the aglycone moiety are used to identify the glycosides. Various examples are Saponins, Cyanogens, Glucosinolates, Vicine and Convicting. The cyanogenic glycosides may be defined chemically as glycosides of the α-hydroxynitriles and is a secondary metabolites of plants. They are amino acid-derived plant constituents. The biosynthetic precursors of the cyanogenic glycosides in plants are the different L-amino acids, which are hydroxylated to form N-hydroxylamino acids which are then converted into nitriles and are further hydroxylated and glycosylated to form cyanogenic glycosides (Vetter, 2000) [2] . All known cyanogenic glycosides are β-linked, mostly with D-glucose. In animals they are not toxic unless hydrolyzed by dilute acids, plant enzymes or rumen microorganisms to form free HCN. Cyanide toxicity is also called as Prussic Acid Poisoning. The β-glucosidases enzymes are found in plant cytoplasm, while glycosides are stored in plant vacuoles, any damage from chewing or wilting allows the contact of the enzyme with its substrate and subsequently broken down to form HCN. The conversion of cyanogens to HCN is enhanced when there is damage to plant cell (crushing, mastication, wilting or freezing stress). Leaves of cherry, cyanogenic acacia species and young sorghum leaves have frequently caused death in grazing animals. 2. Incriminating sources There are at least 2650 species of plants that produce cyanogenic glycosides (Cheeky and Peter, 1989). These plants also possess a corresponding hydrolytic enzyme (β-glycosidase), which are brought together when the cell structure of the plant is disrupted by a predator, with subsequent breakdown to sugar and a cyanohydrin, which rapidly decomposes to hydrogen cyanide (HCN) and an aldehyde or a ketone (Hosel, 1981; Moller and Seigler, 1999) [3, 7] . The glycosides, cyanohydrins and hydrogen cyanide are collectively known as cyanogens. This combination of cyanogenic and hydrolytic enzyme is the means by which cyanogenic plants are protected against predators (Moller and Seigler, 1999) [7] . The best characterized