Dr. Ted McCollum, Extension Beef Cattle Specialist with Texas A&M AgriLife Extension Service, explains that prussic/cyanide levels when there is a frost/freeze event is one of the most confusing and misleading statements in most extension and popular press articles. Here’s the skinny on the actual facts brought to you by thee Dr. McCollum:
“The cyanide(prussic acid) in plants does not exist in a free, liberated state. The cyanide is part of a larger molecule called a cyanogenic glycoside. In members of the sorghum family this compound is Dhurrin; in chokecherries, wild cherries, mountain mahogany, among others, and the kernels of almonds, peaches, apricots and apples this is Amygdalin (laetrile) and Prunasin; in cassava, white clover, flax and lima beans this is Linamarin. These compounds themselves are harmless; the breakdown and liberation of the cyanide is the insult.
A hand grenade represents a “potential” explosion. As long as the pin is in place and the lever (trigger) has not been released that “potential” is not realized; the grenade is harmless. But when the pin is pulled and the trigger is released and the fuse activates and catalyzes the explosion, the potential is realized and potential harm ensues. The cyanogenic glycoside is like the hand grenade. As long as the cyanogenic glycoside remains intact there is only the potential for toxicity; this is sometimes referred to as “cyanide potential”. In order for the potential to be realized, something has to trigger the enzymatic action to liberate the cyanide molecule from the glycoside. The beta-glucosidase enzymes that liberate cyanide from the parent glycoside are found in the plant tissue. In the intact plant tissue, the cyanogenic glycosides are found in vacuoles while the enzymes are found in the cytosol. In order for the cyanide to be released the plant tissue must be damaged so that the glycosides and the enzymes come together. The enzymes are also produced by ruminal microbes. Cutting, crimping, mastication, trampling, hail damage, and frost/freeze disrupt cellular structure and allow the glycosides and enzymes to mix and liberate cyanide from the parent glycoside. Introduction into the ruminal environment presents the glycosides to the microbial enzymes and releases cyanide.
So back to the grenade, the cyanogenic glycoside is the grenade and represents “potential toxicity”. The damage to the plant tissue or introduction to the ruminal environment pulls the pin and releases the trigger. The subsequent mixing of the glycoside with the enzymes activates the fuse and catalyzes the release of cyanide and a possibly toxic insult.
Back to the freeze/frost —
First, freeze/frost causes tissue damage and will indeed result in an increase in the “free” cyanide present in plant tissue (In fact, when analyzing cyanide in the lab, the forage samples are first frozen in order to release all of the cyanide; simply analyzing cyanide on fresh samples only indicates what is “free” in the tissue). But remember, when the animal bit, chewed and swallowed that same forage into the ruminal environment just hours before the freeze or frost, the same cascade of events occurred as when the standing forage was exposed freeze/frost a few hours later. The potential for toxicity was always there, different events pulled the pin and released the trigger. So, in order for a freeze/frost to increase toxicity for ruminants (more later) as is stated in the many pubs, the freeze/frost would have to actually stimulate dhurrin (cyanogenic glycoside) synthesis by the plant. In other words, the freeze/frost would have to stimulate the plant to make more hand grenades. I have searched for research to prove that freeze/frost increases dhurrin synthesis (specifically dhurrin since that is the glycoside in sorghums, sudans, johnsongrass) in the plant. It is not there. I recently contacted Dr. Ros Gleadow from Australia who works in the area of cyanogenensis in plants and her response to my query was quote “Dhurrin is not synthesised in response to frost.”
So, the plant does not make more hand grenades in response to frost/freeze which goes back to Dr. Halliburton’s comment which I have reworded with my interpretation of his meaning – The potential toxicity after the freeze was the same as the day before the freeze.
I think some of the misinterpretation and source of information in the pubs stems from studies of long ago where the researchers collected plant samples before and after a freeze and analyzed the cyanide content of the forage tissue. However, they did not freeze the samples before they analyzed them. So, they did not release all of the cyanide before analyses. They found that the amount of “Free” cyanide was higher after the freeze. This is indeed true. BUT, they did not measure “cyanide potential” which is the real concern and as far as I have discerned, if they had measured cyanide potential they would have found no difference before and after the freeze.
We typically deal with ruminants in these grazing forage situations. Ruminants are typically more susceptible to cyanide toxicity because (1) ruminal microbial beta-glucosidase activity, (2) ruminal pH near neutrality – the optimum pH for beta-glucosidase activity.
What about nonruminants? Typically less susceptible to cyanide toxicity (1) no microbial activity in the first stage of digestion (2) acid pH in first stage of digestion slows/eliminates beta-glucosidase activity in ingested forages. So when the nonruminant is ingesting forage with “cyanide potential”, they have some protection because the enzymatic activities that release cyanide are suppressed or absent.
BUT, following a freeze/frost, the possibility for toxicity in a nonruminant may increase. The frost or freeze has liberated the cyanide and the animal will be ingesting free cyanide. The other “protective” mechanisms – no microbial digestion, acid pH in stomach – have been circumvented.”