POISONOUS PLANTS - INFO

 POISONOUS PLANTS

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This lists those plants which are particularly poisonous or harmful in one way or another.

It must be remembered that most plants are poisonous in some way, even the humble potato (if green). These are not listed here.

Only the plants that are particularly nasty and very poisonous are herein listed.


WHY ARE PLANTS MAKING POISONS?

The question which must be asked is why are plants making chemicals or compounds that are poisonous to mammals?

It must be remembered that for millions of years plants have endured a constant battle from predators: things from the animal (and insect) kingdom that are trying to devour them. They have had to develop a defence against this onslaught. Some plants have come up with mild poisons or distasteful bitterness that deter animals from eating them whilst others have gone the whole hog and produced toxic poisons that will kill any animal that even dares nibble on a leaf.

They have accomplished this by natural selection: a plant that, by random chance, has happened to produce a distasteful or poisonous substance gets to propagate another day, proliferating that trait, whilst those same plants that have not invented this trait lose out (are eaten into oblivion) and eventually die off over millennia.

But then the question must arise how did the plant just happen to invent a substance that was in some way either injurious (or beneficial) to those animals that were consuming it? Well, it can happen by chance, and this seems to be the conventional view: The plant, by chance (using its genetic material), produces multitudinous new and novel compounds, many having no effect whatsoever on either the plant or the potential devourer: these possess neutral selective pressure. They may or may not propagate, the plant could easily lose the ability to produce that chemical. Some invented compounds benefit the plant directly and exhibit some useful property of advantage to the plant (positive selection pressures), these compounds will be welcomed and even amplified by the plant. Some compounds are harmful to predators, and thus also of advantage to the plant, these too will be kept or amplified by the plant. Then other compounds may be injurious to the plant itself; these will die out naturally. Whilst others still may produce some nutrient or chemical that is beneficial to its predator, so the predator, rather than eating it all, farmed it, thus propagating it. You could classify that as natural selection too. Moreover, some plants may produce a chemical that makes the imbibers' brain feel very happy or pleasantly strange; the propagation and protection of these too would have been encouraged by 'farmers' (The word 'farmer' is here used in the broadest possible sense; it could even include other animals beside hominids - after all, if a compound affects their brains, it can affect their behaviour too - much as Toxoplasma does to rats (they lose their fear of cats and are eaten by them. The cats become infected, and pass on the Toxoplasma in their faeces to other mammals including rats, thus propagating Toxoplasma - a sinister but clever ploy that seems to have been evolved by Toxoplasma).

But can it just be chance alone that a plant just happens to produce a toxic chemical out of pure luck, out of the millions of compounds it could have produced by chance? Did plants really try inventing trillions of different compounds and just kept the 100,000 or so that were beneficial in some way to its survival, shedding the 99.9999% of the rest in natural selection? I think not, and this is where I probably diverge from the conventional viewpoint. Not only would such a shotgun blunderbuss approach have been a huge waste of (synthesizing) energy, but it could even be counter-productive - many of the chemicals it produced might have been poisonous to itself!

When the chemical structures of a lot of the substances produced in plants (that are required by the plants) are compared with those in animals, some remarkable similarities and relationships become apparent.

CONSIDER THE FOLLOWING:

Indole acetic acid. a plant phyto-hormone or auxin, is related to tryptamine.

Tryptophan is a tryptamine similar in chemical structure to serotonin, a neurotransmitter required by animals.

Bufotenine is a tryptophan-like substance produced by certain toads and mushrooms (note both kingdoms are represented here) that is poisonous to mammals and has hallucinogenic properties.

Psilocybin produced by the psilocybin mushrooms is also related to tryptamines and is also a hallucinogen in mammals.

Yohimbine, a hallucinogen and indole-alkaloid (note the reference to indole acetic acid) produced by the Yohimbine tree (related to the Madder Family) is a serotonin antagonist in mammals, with a great many effects too numerous to list.

Cocaine, produced by the Opium poppy, is a tropane alkaloid, like atropine which is produced by the potato family of plants. Cocaine is a dopamine inhibitor. Dopamine is another neurotransmitter based on tryptophan.

Ergotamine is a poisonous ergot-family alkaloid produced by a certain fungus that is parasitic on cereal grains and grasses. Despite ergotamines chemical complexity, it is also plainly based, at least in part, on tryptamine. It possesses similarities to several neurotransmitters, serotonin, domamine and adrenaline and has the remarkable ability to act both as agonist and antagonist on a number of those neurotransitter receptors at the same time.

Strychnine, a poisonous alkaloid synthesized in the seeds of the strychnos nux vomica tree, is based on an indole acetic acid core with a confusion of multiply-fused rings, seven in all. It consists of two five-membered, four six-membered, and one seven-membered ring, very high for a 23-atom'd core (it does have extra atoms external to the ring). Strychnine acts on the glycine receptor in the spinal cord and brain. Curiously, Glycine is yet another neurotransmitter.

Reserpine, another indole-alkaloid, is synthesized in the roots of Rauwolfia Serpentina and blocks the uptake of noradrenaline and dopamine. Noradrenaline is both another neurotransmitter, and a hormone in mammals.

A rather remarkable compound that is synthesized in both plants and animals is beta-carboline, an alkaloid and founder-member of the class of alkaloids called beta-carboline alkaloids. Some beta-carbolines, notably pinoline and tryptoline, are manufactured within the human body and are implicated (along with melatonin) in our sleep/wake pattern. Many are selective inhibitors of enzyme monoamine oxidase type A and thus are monoamine oxidase inhibitors (MOAI's) within the human body.

Beta-carboline is directly related to tryptamine. Other beta-carolines, the harmines (a class of compounds synthesized in the non-native Syrian Rue plant and used as a hypnotic drink by rain-forest shamans) are mono-amineoxidase inhibitors, MAOI's. The Monoamine class of compounds include many neurotransmitters.

Tryptoline (aka Tetrahydro-β-carboline and Tetrahydronorharmane) is also a naturally produced derivative of Β-carboline.





Bryophyllin A is a bufadienolide found in both plant and animal kingdoms which was first found in some species of toads (hence the bufa in the name of the series of compounds). Later it was discovered in a Crassula species from Indonesia and some other members of the Bryophyllum Genus. It is a powerful insecticide, active against the third member of the kingdoms. What is very strange about this particular bufadienolide is the very unusual triangular cage (bottom left) formed by three oxygen atoms straddling a phenyl group bonded at the apex by another carbon atom. This same cage-like structure, but with the cage straddling 1,2,4 positions, is also to be found in the extremely irritant Daphnane-type of Phorbol Resiniferatoxin, which is found in Resin Spurge (Euphorbia resinafera) (a non-native). Resiniferatoxin is a neurotoxin and the most irritant substance known, nearly 100,000 times more irritant that capsaicin the irritant in chili peppers.

Other bufadienolides omit this structure. Bufadienolides are characterised by a steroidal frame (the four fused rings) with an added lactone ring (top right). Steroids are, of course, compounds vital to the functioning of mammals, and are found in a variety of (mostly highly poisonous) forms in hundreds of different plants. If ingested, steroid look-e-likees in plants may interfere with the normal operation of resident steroids in mammals.

So, are all these just coincidences? A substance that just happens to be required by a plant has almost the same chemical structure (with variations), as do substances which are synthesized by animals and that happen to have a similar chemical structure to substances required by the animal kingdom? Can it all just be pure coincidence? Or has there, at some time in the distant past, been some collusion between plant and animal kingdoms? A sharing of ancient genes that have since diversified into genes for synthesizing compounds with different functions, but similar structures?

So, how can these remarkable similarities in structure between certain substances shared by the plant and animal kingdom have come about? Well, we (plants and animals) are all of this Earth. [Actually, between you the reader, myself,  Fred Hoyle and a few others, I don't think we are totally of this Earth, but the same argument apples from wherever we ultimately derived].

I think we (the plant and animal kingdoms) shared (either now, or once in the distant past) a lot of useful genes. They could have swapped or shared genes by means of plasmids, circular bits of DNA, delivered by viruses. Or by a multitudinous variety of other methods of gene-swapping yet to be discovered by biologists [they are making revelatory findings about gene-swapping all the time - discoveries that they never suspected, nor predicted. It's all in the DNA. Perhaps only 10% of DNA is understood. What they previously thought was junk DNA turns out to have innovatory properties relevant to this topic that are still being interpreted. And introns (the non-protein-coding DNA between genes) are now recognised as being not so passive after all. DNA is turning out to be somewhat of a Gordian knot, its ancient secrets still to un-fold]. Of course, since DNA has itself been evolving, changing its function over time, we may never be able to fully un-ravel its mysteries [by looking at a car engine, could you, from first principles, deduce that it was once re-melted from Roman armour, and before that was once buried in the ground as yellow ochre?].

Although by now the plant and animal kingdoms seem to have diverged and crystallised into two separate kingdoms, it could be that some gene swapping or sharing is still occurring. We suffer viruses; so too do plants. Might one or two viruses be ambivalent about which kingdom they infect? There are millions of viruses out there. Mankind knows of just some small sub-fraction of the total number of virii. Could these ambivalent viruses (if they exist, and I see no reason why they couldn't) be swapping some genes between both kingdoms even now?

I believe they could.

Why - Hoooooom, why, I could be a prime example...
The Ent, Truebeard.


TOXINS and PATHOGENS, the never-ending war.
The synthesis of toxins by plants is not always a well targeted affair, for not only are several intermediate compounds fabricated (as would be expected anyway) but a whole plethora of 'wrongly' assembled molecules are sometimes generated in, what must be, a stochastic generation process. A scattergun approach. Whilst this may seem counter-productive to us, to the plant trying to protect itself from invading pathogens and hungry beasts it matters not as long as all or most of these compounds are poisonous. In fact, it can be of huge benefit to the plant not to selectively manufacture just one toxin, but rather a bizarre selection. The attacking microorganisms or famished creature could, by natural selection, develop resistance to one certain toxin, but is most unlikely to develop resistance to a huge arsenal of haphazardly assembled toxins.


PLANT TOXINS - should we try to avoid consuming them?
Some edible plants have been producing poisons in their cells for a very long time, and mammals including humans have been consuming them for millennia. Of course, it is only certain poisonous plants that we eat, and then we dont eat too much of them. Take parsley for instance. The leaves contain toxic furanocoumarins but still we eat it, oblivious to the toxins. If we ate too much, then we may indeed poison ourselves, but we don't eat parsley as a vegetable, just as a salad and meal-dressing; we have learnt the hard way not to eat large quantities of it. It isn't sold as a vegetable like spinach or kale or cabbage, but sold more like lettuce (which also contains toxins).

But even spinach, kale or cabbage contain toxins. We just limit ourselves to not eating so much as to poison ourselves.

It is impossible to avoid eating toxins; they are present, to a greater or lesser extent, in almost everything we eat.

Should we try to avoid eating any plants that contain toxins?
The answer must surely be an emphatic 'no - definitely not'. We have grown up with these toxins.

Could the toxins we consume in food be of benefit to us?
The answer is almost certainly 'yes' (but only in moderation). We have co-evolved with these toxins in our diet. For some toxins our bodies may have learnt to limit or neutralise their poisonous effects, others may be of benefit to our bodies in complex ways as yet unknown (the toxins are usually present in only very small doses). But some toxins really are bad, and our bodies may not yet have learnt how to deal with them effectively. Another 100,000 years of evolution may solve the problem for those toxins, but new ones that are equally as bad will surely have been evolved by plants in that time. It is a never ending war.

[The author thinks that these toxins are now so essential to mammals that some mass extinctions may be attributable to their lack. There are two fungii currently causing the mass death of both amphibians and bats; the spread of both these fungi in populations of bats and frogs is the cause of much world-wide concern. No one knows why bats and frogs are suddenly susceptible to certain fungi. No one knows how to prevent both the spread of the infection, nor how to prevent the death of the animals concerned. In the case of bats, the fungus is Geomyces destructans, which, unusual amongst fungi, grows only in the cold, between 5C and 14C].

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But the author has a theory...

Many toxins in plants are fungicidal; active against fungal growth. This helps the plant being invaded by mycellium itself, for it is extremely vulnerable; standing fixed as it is in damp soil, unable to move and get out of the way of either fungal spores or underground mycellia.

Many plants around the world are also in marked decline; their habitats disappearing. Some regions have lost some species of plant altogether, whilst other regions are experiencing a large reduction in population.

But what if the bats normally got their fungicidal protection from this particular fungus by eating flies that usually came into contact with a plant producing a fungicide effective against this fungus? If bats and frogs got their fungicidal protection in roundabout ways like this, then it is no wonder that no one has spotted this yet. What is more, if this is the case, then scientists are highly unlikely to spot this route of fungal protection now in its' complete absence!

Why does everyone not get athletes foot (a fungal disease) when exposed to it?
Could those that don't get it have a diet rich in the anti-fungal toxins produced by a certain plant that they normally eat, which others who are susceptible to athletes foot don't eat? And which plant, of the hundreds that we consume, might that be? There are many candidates. Hundreds of plants produce hundreds of differing toxins that have anti-fungal properties (amongst their many other and varied properties).

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This theory demonstrates in one small way how ecosystems could be linked in ways as yet un-known, and also presents one small example of how plant toxins may be beneficial to us in ways totally un-suspected.


PLANT SECONDARY METABOLITES
Many plants modulate their secondary metabolites based upon the enemies around them and the conditions or circumstances in which they find themselves. These could be climatic conditions or soil chemistry conditions. There is little point in expending energy to produce toxins that is required for growing when there are no enemies or adverse conditions with which to cope. The obverse is that there is a need to divert resources to produce some extra secondary metabolites or toxins if there are 'enemies' about. That is how the variation in secondary metabolite or toxin production comes about in many plants.

For instance: Potatoes go green if left in the Sun. The green bits (actually chlorophyll) is where the greatest concentration of deadly poisonous solanines (in the case of potatoes) are produced, presumably to defend against the exposed tubers from being eaten by all and sundry (worms, and the like).

Another source of variability in the plant secondary metabolite production is genetic variability between plants of the same species. More variability could be due to the place where they are growing. Under stressful conditions (heat, sun, lack of water, lack of nutrients) or perhaps due to poisonous heavy metals in the soil or lack of essential trace elements plants will modulate their secondary metabolite response. Other stressful conditions could include attack by mammals, insects, fungi, virii, bacteria or external RNA (RNAex, which is free-swimming in the environment ready to infiltrate plants [or other life-forms] where they then travel all the way through the organism adding genetic snippets to each copy of nuclear DNA).

Most toxins taste bitter. This is both an adaption by humans to warn themselves of poisonous constituents, and is perhaps also a ploy employed by the plants to warn everyone: after all, the aim of being poisonous is to AVOID being eaten, rather than to kill or disable any organisms that eat the plants. But it is a two-way process, the plants 'learn' to make poisonous substances that their enemies can detect without consuming too much; and mammals learn to perceive poisonous substances as bitter, and un-palatable. Of course, there are exceptions: there is still some learning to be done by both plants and by mammals/insects.

The obverse is that substances that taste sweet are usually not poisonous. But beware! There are some exceptions! (And dont forget that plants produce many substances, not just one at a time...). For instance Lead Acetate is sweet, but toxic (however note that no plant as far as the Author is aware produces lead acetate). The Romans used it to sweeten their beverages, and it slowly sent them bananas [due to heavy metal poisoning]).

Don't forget, most substances are poisonous: it is the dose that maketh the poison. With some substances, it is just micrograms that will kill you. Other substances, like water, may take a few litres before your cells lyse...

And then there's the Mammalian response. Everyone is different, we all make different substances ourselves and have different responses to external substances, as do mammals differ from us. What may prove poisonous to one person may prove benign to another. Saying whether a plant is poisonous or not is fraught with huge difficulty.


WHO (WORLD HEALTH AUTHORITY) TOXICITY CLASSES

The WHO recognises four Toxicity Classes for Toxins:
  • Class Ia: Extremely Hazardous.   [LD50  <5mg /kg]
  • Class Ib: Highly Hazardous.        [LD50  5mg - 50mg /kg]
  • Class II: Moderately Hazardous.  [LD50  50mg - 500mg /kg]
  • Class III: Slightly Hazardous.       [LD50  >500mg /kg]
Where the LD50 values are the amount of any toxin needed to kill 50% of the dosed rats, measured in milligrams per kilogram of their body weight. Thus, this Toxicity rating does not correspond with how toxic any particular plant might be, because the amount of toxin in any particular plant varies a great deal. Therefore the category 'Extremely Poisonous Plants' may not correlate well with 'Extremely Hazardous Toxins' - for the corresponding plant may have much more of a less hazardous toxin.

Also, rats are not always good models for the toxicity of poisons in humans, which depends on the particular toxin. Human studies of toxicity would be highly un-ethical; rat data is the next best thing.

It should be noted that the TOXICITY ratings given in this website do NOT adhere to these WHO Toxicity Classses, but in many cases are mere guesses based on estimated toxicity. The Author accepts no responsibility whatsoever for any consequences whatsoever resulting from touching, burning, smoking, drinking or eating any part of any plant. ! DO NOT TOUCH OR IMBIBE PLANTS !

 DEADLY POISONOUS PLANTS - INFO

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To specifically search this website for extremely poisonous plants, then add the search term: toxicity?severe .

 EXTREMELY POISONOUS PLANTS - INFO

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high

To specifically search this website for still deadly poisonous plants, then add the search term: toxicity?high .

 POISONOUS PLANTS - INFO

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To specifically search this website for still poisonous plants, then add the search term: toxicity?medium .

 MILDLY POISONOUS PLANTS - INFO

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Note that there is no such category as 'Non-Poisonous': most things to excess are bad for you; you can die from drinking too much water (it is poisonous in excess).

Low Toxicity or Mildly Poisonous plants can still make the imbiber seriously ill, and may even cause death if too much is ingested! The reader is not supposed to eat these plants!

To specifically search this website for mildly poisonous plants, then add the search term: toxicity?lowish .

NO RATING on TOXICITY - INFO

Danger by Toxicity - No Rating

This either means that the risk posed by any Toxicity is non-existent, or that the Author has been unable to find out if there is any risk (and it is possibly therefore either lowish or non-existent).

But do not assume that there is no danger at all. Even otherwise edible potatoes can kill if they are green! And other folk may be allergic to one plant and suffer anaphylactic shock whereas most folk are un-affected.



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