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Prussic Acid Poisoning

Last Updated: February 23, 2010

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Fact Sheet Written by:

Gary Strickland, Extension Educator Agriculture/4-H/CED

Glenn Selk, Extension Animal Reproduction Specialist

Hailin Zhang, Director of Soil, Water, Forage Analytical Laboratory

D.L. Step, DVM, Associate Professor Veterinary Clinical Sciences

And Provided by

Oklahoma State University


It was discovered in the early 1900s that under certain conditions, sorghum is capable of releasing hydrocyanic acid (HCN or prussic acid), which makes them potentially dangerous for grazing. In the plant, HCN is attached to a larger molecule, a cyanogenic glucoside called dhurrin. Dhurrin itself is harmless, as it is simply a compound consisting of a sugar and a non-sugar molecule. However, a two-step enzymatic process results in two hydrolysis products with the final one being HCN. Generally, for this process to occur the plant has to be damaged as the glucosides and degradative enzymes are compartmentally separated within the plant cells. This damage may occur through the chewing action of an animal, a hard freeze where plant cell walls are ruptured, or through mechanical action such as that caused by a swather and its crimpers. Once ingested by an animal, the HCN is released in the rumen and readily absorbed into the bloodstream. HCN does not prevent oxygen from being transported by hemoglobin, but does prevent the body cells from receiving oxygen. The site of this inhibition is believed to be the cellular electron transport system where cyanide (CN) blocks the utilization of oxygen. Thus, the animal dies from asphyxiation at the cellular level. Animals affected by prussic acid poisoning exhibit a characteristic bright red blood just prior to and during death.

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