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Like many plants, ragwort has evolved a chemical arsenal to protect itself from unwanted attention from animals seeking to make a meal out of it. Its first line of defence are chemicals, which have an acrid smell and a very bitter flavour. Most grazing animals will be repelled by these two weapons and will leave the ragwort plants alone. However, if this first line of defence fails, ragwort has an arsenal of ‘STEALTH CHEMICAL WARFARE’ agents at its disposal.
Ragwort is not unique in this respect. It is believed that as many as 3% (ca 6000 plants) of the world’s flowering plants have evolved this stealth mode of defence through the use of a group of chemicals called Pyrrolizidine Alkaloids (PAs). Common Ragwort (Senecio jacobaea) has at least eight of these defence chemicals (EHC 80 p 322) distributed within the sap throughout the whole of the plant.
The level of these tasteless, odourless, defence chemicals in ragwort is tiny; typically 0.016% of the plants weight (EHC 80 p 51) but perhaps the most surprising thing about PAs is that THEY ARE NOT POISONOUS!! Yes, you read that correctly, PAs are not poisonous by themselves.
Remember, that this is the plant’s STEALTH CHEMICAL WARFARE. Having failed to put off attack by smell and bitterness, the plant’s ‘fall back defence’ is to disable and kill its attackers. PAs are the perfect weapon to achieve this. Stable and unreactive, PAs pass undigested into the blood stream. Because PAs do not ‘do’ anything, the body’s defences are not triggered. The stable PAs are allowed to circulate throughout the whole of the animal’s body. If the animal is a lactating female, some of the PAs will be included in the milk but a large proportion will simply be urinated away.
So far, plenty of ‘stealth’ but no ‘warfare’. The PAs will be freely circulating in the body of the animal and through its milk will also be circulating in the bodies of the animal’s offspring. The almost unbelievable fact about PAs is that they are turned into aggressive toxins by the animal’s own body. The ticking bomb is triggered in the animal’s liver by its own enzymatic processes.
The liver is the ‘chemical factory’ of the body. PAs entering the liver in the blood stream are converted by natural metabolic processes (mixed function oxidases EHC 80 p 20) into reactive toxins called Pyrrolic derivatives. These derivatives rapidly attack the nucleus of the nearest cells. Once attacked, the liver cell fails to function correctly and eventually dies. PAs circulating in the blood stream are able to cross the placental barrier and are then able to attack the liver of the developing foetus. The various Pyrrolic derivatives are able to attack liver cells (hepatocytes) and have also been shown to be carcinogenic, mutagenic and teratogenic. Although Pyrrolic derivatives are able to attack most cells within the body, they are so reactive, they tend to attack the first cell they encounter, and this is generally the liver cells where they were formed.
However, the liver is a large organ capable of repair and regeneration. The loss of one or two hepatocytes is never going to be a life threatening issue. But the animal does not know that it has been damaged, so it is not possible for it to learn or evolve strategies of defence. If the animal continues to take in PAs its liver continues to be destroyed cell by cell - likewise that of its offspring. As overall liver function and capacity begins to fail the animal ceases to operate at peak performance and becomes subject to predation. If the animal survives predation, eventually its liver fails through overload and the animal dies a lingering and miserable death.
The use of PAs allows plants the ability to disadvantage and eventually destroy any would be predators that ignore the smell and bitterness of its leaves.
How much PA is required to damage or kill an animal?
The answer is complex and is influenced by three key aspects:-
- How large is the animal - or more correctly - its liver. Obviously it takes a lot more PA to kill 70% of a horse’s liver than it takes to kill the same percentage of a human’s liver.
- How well the animal’s PA metabolic processes function. Some animals lack high levels of the metabolic activity that converts the PAs to the toxic derivatives.
- The timescale over which the PAs are consumed. If a lethal dose is spread out over a very long period of time, then the liver’s own ability to repair and regenerate may compensate for the damage and the animal may survive with little more than being ‘off colour’ for that period of time.
Other less well documented factors such as age, the cocktail of PAs involved and other demands made on the animals body all influence the impact of PAs on an animals health.
Complicating the issue still further is the ability of a single appropriate exposure to PAs to lead to a relentlessly progressive course and eventually kill the animal, more than 18 months after exposure (EHC 80 p 98). Humans developing jaundice from PA damage have a 74% probability of death within 18 months of the poisoning. Even when the dose is insufficient to kill, severe ill health from extensive liver damage or cirrhosis can destroy the quality of life.
Hooper and Scanlan (1977) studied the long-term effects of feeding very low levels of PAs to pigs. The feeds contained as little as 0.004% body weight of dried PA containing plant. Over 90% of the animals died from liver and lung disease caused by PAs and showed signs of kidney damage. The animals surviving 136 days showed liver damage after slaughter. (EHC 80 p 85).
In many cases, it is not how much is required to kill an animal, it is how little is required to harm or damage it that should be the issue for consideration and this is amplified massively by the fact that the damage caused by PAs is cumulative.
Of most significant alarm should be the fact, that when the UK Food Standards Agency were asked in July 2003 what the safe daily intake level was for PAs, THEY COULD NOT GIVE AN ANSWER. The FSA are responsible for publishing safe daily limits for all hazardous substances that might be presented through the human food chain, yet to date, they have not seen fit to publish a safe figure. So although foods can be assayed for PAs; without meaningful safety limits, no decisions can be made as to the safety of foods shown to contain PAs.
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