Plants: Poisonous and Allergens
Poisonous plants have been known and used for
centuries. Socrates was forced to drink hemlock, and the
De Medicis and Borgias knew how to use plant poisons
to achieve their desired results.
There are many poisonous plants; the active ingredients
in most are alkaloids or glycosides. They act on the
CNS, on neuromuscular junctions, on the heart, on the
liver, and on basic metabolic processes (electron
transport and ATP synthesis).
Some of the poisonous plants presented in the text
chapter have come up earlier, for example as medicinal
plants when in small doses. We’ll skip those here.
Hemlocks
The two poison hemlocks are water hemlock (Cicuta
maculata and poison hemlock (Conium maculatum).
Both grow to a height range around 2m. Both are
members of the Umbelliferae, like the carrot.
The toxin in poison hemlock is an alkaloid, coniine
(there are other toxic alkaloids present, including
atropine). It is a neurotoxin, causing convulsions, a
paralysis advancing upwards from the lower limbs, and
eventually paralysis of the breathing apparatus and the
diaphragm. Death follows from suffocation.
Socrates’ death from hemlock poisoning was described
by Plato, and followed the pattern described.
The poison in water hemlock is different; it is an alcohol
called cicutoxin (from the genus name). Its effect is very
similar – violent convulsions followed by death.
Strychnos spp.
There are a number of species within the genus
Strychnos that are sources of strychnine, an extremely
bitter alkaloid that affects the basic function of nerve
cells. It blocks a protein involved in the chloride channel
of neurons.
Strychnos nox-vomica
Death occurs as a result of continuous muscle spasms,
convulsions that become continuously more severe, and
death either from exhaustion or uncontrollable
convulsions in the muscles of breathing.
The LD50 is ~1mg/Kg, or in the range of 20 – 40 mg, but
you can taste its bitterness in concentrations as low as 1
ppm (or that 1mg/Kg).
Strychnine has frequently appeared in the movies as a
method to kill, for example it was strychnine that
Norman Bates used in Hitchcock’s Psycho to kill both
his mother (the mummified figure sitting in a chair at the
end) and her lover.
Curare
Strychnos toxifera, below, with a stick insect on it, is a
main source for another potent alkaloid poison. It is a
main source for curare.
Curare, from Strychnos toxifera and Chondrodendron
tomentosum, is a paralytic that used in blowguns to kill
game (or members of opponent tribes). It is a group of
poisons, of which the most important is D-tubocurarine.
It is a muscle relaxant that blocks one of the two types of
acetylcholine receptors on post-synaptic nerve cells. It
kills prey (or humans) by blocking neuromuscular
junctions critical to breathing.
Curare is used as a relaxant for surgery. The source was
discovered by Richard Schultes in 1941, and a synthetic
form (intracostin) was developed in 1942 by Dr. Harold
Griffith. Now anesthesiologists use a variety of similar
drugs.
Richard Schultes
Dr. Harold Griffith
Milkweed cardiac glycosides
Various Asclepias species (the milkweeds) contain both
galitoxin and cardiac glycosides. The cardiac glycosides
have an effect similar to digitalis.
While the glycosides are poisonous to livestock and
humans, they are not poisonous to milkweed butterflies,
Danaus plexippus. The larvae (caterpillars) take up and
store the glycoside, and it is passed on through
metamorphosis to the adult butterfly.
You’ve already seen a picture of the result of this – a jay
throwing up only a few moments after eating a monarch
butterfly.
Your text has another excellent example: the rattlebox
moth caterpillar (male) that feeds on the rattlebox plant,
Crotalaria mucronata, but is unaffected and passes the
toxin on to protect the adult moth.
The female moth, when frightened, exudes a foam with
the toxin, monocrotaline, that potential predators avoid.
Protection for the female is a nuptial gift with sperm from
the male. It is spread throughout the female’s body
within minutes.
The female moth can even sense during courtship which
male will pass along the best level of protection. Spiders
are apparently the main predators from whom protection
is needed.
Crotolaria toxins are dangerous-to-fatal in humans and
other animals. The monocrotaline toxin induces
hypertension in the pulmonary arteries and cardiac
hypertrophy, both of which can be the cause of fatality.
Even so, it was introduced into the southern U.S.
because it improves soil conditions by adding fixed
nitrogen to soil. Oops! The toxicity to farm animals has
led to it now being considered in invasive, noxious
weed.
Plants also use chemical poisons against each other.
The chemical interaction is called allelopathy. In this
case, the chemicals are generally volatile, and include
terpenes or phenols.
Allelopathy has been suggested in many plant
interactions, but a few are well documented. One that
occurs locally is the interaction between black walnut
trees (Juglans nigra) and surrounding plants. A chemical
called juglone is washed off leaves by rainfall (it’s also in
the bark, walnut husks and roots), and poisons the
ground around the tree against germination or growth of
possible competitors. Some plants (tomatoes) are far
more susceptible than others.
On the right is another example of allelopathy that
occurs in California chaparral. Sagebrush (Artemesia
tridentata) releases monoterpenes into the surrounding
soil that inhibits the growth of seedlings and lowers the
respiration rates of both seedlings and mature plants.
That creates the bare zone around sagebrush plants
evident in the figure. In some cases the bare and
suppressed zone can extend almost 10m.
Common garden plants include a number of species that
are toxic. Rhododendrons range from short plants to
50m tall trees. You may know them as azalea.
The picture is of R. ponticum, which was known as a
hallucinogen and toxin as long ago as the golden age of
Greece. The toxin is a grayanotoxin. It is in the leaves,
pollen, nectar, and therefore honey derived from it.
Grayanotoxin (it has other names) is a diterpene that
binds to sodium channels in cell membranes. It leaves
exciteable cell membranes depolarized. The symptons
are: salivation, persperation, vomiting, dizzyness,
muscle weakness, and cardiac rhythm disruption. This
toxin is apparently not usually fatal.
Tulips and hyacinths (in flower soon or now) contain a
number of toxic glycosides.
Poinsetta (Euphorbia pulcherrima) is a member of the
Euphorbiaceae. It is named for the first American
ambassador to Mexico, Joel Poinsett, who brought the
plant from its native range in Mexico into the U.S. It’s
sap, according to general wisdom, is toxic. In fact it is an
allergen that may irritate skin and mucous membranes.
However, a relative in the same family, Ricinis
communis, or castor bean, is very toxic. The beans
contain ricin. Ingestion of one bean can kill a child, and
only a few will kill an adult. A lethal dose is 0.2mg. It is
considered to be the most potent plant toxin.
The beans are also the source for castor oil.
Ricin is a two-subunit protein. The A chain removes an
Adenine from ribosomal RNA, which then blocks protein
synthesis (and is eventually fatal). The B chain is a lectin
that binds to cell surface proteins, and is critical to get
the A chain inside the cell, where is does its damage.
A chain is blue
B chain is orange
A number of plants, e.g. barley, have the A chain, but no
B chain so that the A chain can’t get inside cells. Clearly,
you don’t get sick from eating barley (or drinking beer
made with malted barley).
Ricin has been investigated as a chemical weapon, and
was used at least once. The Russian KGB apparently
supplied ricin to the Bulgarian secret police, who used it
in a pellet fired by compressed gas into the leg of a
dissident, Georgi Markov, who died as a result.
Symptoms only appear slowly. They include: initially
nausea, vomiting, diarrhea, burning in the mouth and
throat; later retinal and intestinal hemorrhaging, liver
and kidney damage. Death is usually from kidney
failure. There is no known antidote.
Castor beans are “not all bad”. They, like soybeans, are
the source of an oil that is valuable in many industrial
processes and products. When you drive home tonight,
you will probably be sitting on automotive seats that are
made in part from hydrogenated oils of soy and castor
beans.
Although not usually fatal, some houseplants are ‘no fun’
and, to some degree, poisonous. Dumbcane
(Dieffenbachia spp.) and others in its family (e.g. jack-inthe-pulpit) contain calcium oxalate crystals that cause
swelling of the mouth, lips, tongue and throat. Difficulty
in speaking when suffering these symptoms is the
source of its name.
White snakeroot
White snakeroot (Eupatorium rugosum) is not
consumed by humans, but is sometimes consumed by
cattle. Its toxin is tremetol, an alcohol. Cattle suffer from
‘the trembles’ as a result – acetone breath (like diabetics
have with very high blood sugar), sluggishness, and
muscular weakness.
When a human eats the meat or drinks the milk of a
poisoned cow, the result is called milk disease. It killed
Nancy Hanks, Abraham Lincoln’s mother. In the 1800s it
was the cause of illness and many deaths.
The name of the disease relates to what it causes.
Tremetol blocks the liver from breaking down lactic acid.
Lactic acid accumulates in the blood, the pH of the
blood drops (acidosis, a characteristic of diabetes),
which leads to the “acetone breath”. Accumulating lactic
acid also at least in part blocks the Krebs cycle, leads to
a lowered amount of ATP, and produces the
sluggishness and muscle weakness.
Locoweeds – Oxytropis and Astragalus spp.
The name comes from the behaviour of poisoned
animals. Poisoning causes erratic behaviour,
aggression, lethargy, loss of balance, nervousness.
These are a mixed and conflicting bag of symptoms.
That’s because the active compound is a neurotoxin
called swainsonine. It inhibits a key enzyme in the Golgi
apparatus – a mannosidase. It is considered a possible
anti-cancer agent.
An Astragalus
Plants responsible for allergic reactions
Allergic reactions are responses of the immune system
to foreign substances. They represent a temporary
hypersensitivity to the agent.
The most important hypersensitivity reactions are hay
fever (and allergic rhinitis) with symptoms of runny
nose and nasal congestion, itchy and teary eyes, and
various types of dermatitis, with symptoms of reddening
of the skin and rashes.
As much as ¼ of the human population suffers from
hay fever, which has nothing to do with hay. Hay fever
is caused by allergic reaction to airborne pollen. That
pollen can come from grasses or, more commonly, from
ragweed (Ambrosia artemisifolia and A. trifida)
The problem gets its name from the timing that has
ragweed releasing pollen at the same time as hay ripens
(early-August to September or October). Each plant may
produce one billion pollen grains over a season.
The plant is monoecious; each plant has separated
male and female flowers. They are well adapted to
pioneer habitats, e.g. land bared for construction. You
will certainly be able to find some on or around land
cleared for construction, e.g. expansion of parking lots
before construction of the new engineering building.
The worst time of day for hay fever sufferers is mid
morning to early afternoon. Pollen disperses after the
day warms and relative humidity decreases. Usually the
worst is over by late afternoon, and rain is welcomed,
since it reduces the amount of pollen in the air.
How do you deal with hay fever allergies?
There are basically two ways:
1)Decrease the intensity of the symptoms using
antihistamines to decrease the histamine reaction
and/or decongestants to reduce the problems with
mucus produced as part of the histamine reaction.
2)Go through a long series of injections to become
desensitized to the pollen. The injections consist of
weakened extracts of pollen and cause an internal
immune reaction that blocks the IgE response of hay
fever.
Contact dermatitis is the other major allergic reaction.
The most common contact dermatitis is to poison ivy,
poison oak, and poison sumac. While their names seem
different, all are in the same genus, Toxicodendron.
Poison ivy,
T. radicans
The contact dermatitis is caused by an oil called
urushiol, from a Japanese word transliterated as urushi.
The oil (actually it’s a mixture of oils) is polymerized to
form the hard lacquer that protects Japanese
lacquerware.
The difference between poison ivy and poison oak is
the length of the side chains in the dominant catechols
in the urushiol: in poison ivy they are 15 carbon atoms
long, in poison oak the length is 17 carbons.
As you probably know, the urushiols are passed to you
by only brushing against the plant. The urushiol rapidly
binds to proteins in the skin, but can be spread by
rubbing or scratching the initial itch. The usual course is
a rash that lasts about 3 weeks, but a more severe
exposure (don’t ask, I’ve had personal experience)
produces blisters.
As a sort of warning, recognize and avoid the leaf
pattern: leaflets in threes, leaflet margins typically lobed,
but non-symmetrically. Plant size, and even, to some
degree, leaf shape is variable. Size you are probably
used to is as a ground dwelling plant. However, it can
grow as a woody vine to a few meters, and can be a
free-standing plant up to more than 1m. Leaf size can
range from a few centimeters in width and length to
around 25cm across. As they used to say on Hill Street
Blues, “be careful out there”.