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 LD 50 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-in- the-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”.