Why talk about these troublesome plants?
If you use plants at all in your workings, you need to know something about those plants that are poisonous or troublesome. If for no other reason, so you can identify their effects or at least know to avoid that herb in the store. Even if you never wild harvest, you still need to know what herbs have strong effect, because many of them CAN be purchased at your local herb shop.
I will not discuss the ethics of poisoning, because I think that's not relevant. This is about the plants themselves, and which need to be handled carefully.
This includes herbs that cause allergic reactions, plants that cause contact dermatitis/irritation, and plants that can cause other undesirable effects.
I will be showcasing herbs at this space periodically that are known to be either poisonous or noisome. I will start with the best known and the most widely available, at least in my area. (Zone 6, Temperate, USA, suburban area, 30 miles from a major (mid-western) world city) I can't really cover world-wide here, so I will stick (for now) with western herbalism and US availability. IF you have valuable information about toxic or suspect plants that you are familiar with that I haven't mentioned, feel free to post what you know.
This topic will also have discussion about these plants and handling precautions.
What I will provide are basic info for identifying the plant, scientific and common names that I'm familiar with, a few good pictures of the plant, and it's qualities, for good and ill. I will even cover healing AND magickal applications, but mostly magickal because I that's what I know best. What healing qualities will be either practical first-aid stuff, or abstract informational and the latter will be clearly marked.
A witch cannot heal with herbs if he/she/hir doesn't know which herbs can harm as well.
--Paraphrased Scott Cunningham, who paraphrased an old witch's rhyme.
We at this board do not condone using plants to harm others. If you do so, you do so at your own recognizance, and we are not responsible. This info is provided for entertainment/informational purposes only. We are not doctors. Do not take candy or medical advice from strangers.This is has been a public service announcement on behalf of the board. Now, back to our regularly scheduled crowfoot.[/size]
Nature's Bite: Plants to handle with Care
-
Shaman of Bliss
- Banned Member
- Posts: 366
- Joined: Thu Jan 04, 2007 11:20 am
- Gender: Female
- Location: Canada
Common Foxglove
Description
The best-known species is the Common Foxglove, Digitalis purpurea. It is a biennial, often grown as an ornamental plant due to its showy flowers, that range in colour from purples through to whites, with variable marks and spotting. The first year of growth produces only the long, basal leaves. In the second year, the erect leafy stem 0.5-2.5 m tall develops.
Toxicity
The entire plant is a poison (including the roots and seeds), although the leaves of the upper stem are particularly potent, with just a nibble being enough to potentially cause death.
Early symptoms of ingestion include;
• nausea,
• vomiting,
• anorexia,
• diarrhea,
• abdominal pain,
• wild hallucinations,
• delirium,
and
• severe headache.
Depending on the severity of the toxicosis the victim may later suffer;
• irregular and slow pulse,
• tremors,
• various cerebral disturbances, especially of a visual nature (unusual color visions with objects appearing yellowish to green, and blue halos around lights),
• convulsions,
and
• deadly disturbances of the heart.
There have been instances of people confusing digitalis with the harmless Symphytum (comphrey) plant (which is often brewed into a tea) with fatal consequences. Other fatal accidents involve children drinking the water in a vase containing digitalis plants. Drying does not reduce the toxicity of the plant. The plant is toxic to animals including all classes of livestock, as well as cats and dogs.
Digitalis poisoning can cause heart block and bradycardia (lowered heart rate) and tachycardia (increased heart rate). It is often quoted around the Internet that only bradycardia is associated with digitalis poisoning, but that is not true. It can cause either, depending on the dose and the condition of one's heart. It should however be noted, that electric cardioversion (to "shock" the heart) is generally not indicated in ventricular fibrillation in digitalis toxicity, as it can increase the dysrhythmia in digitalis toxicity.
Source;
http://en.wikipedia.org/wiki/Foxglove
Description
The best-known species is the Common Foxglove, Digitalis purpurea. It is a biennial, often grown as an ornamental plant due to its showy flowers, that range in colour from purples through to whites, with variable marks and spotting. The first year of growth produces only the long, basal leaves. In the second year, the erect leafy stem 0.5-2.5 m tall develops.
Toxicity
The entire plant is a poison (including the roots and seeds), although the leaves of the upper stem are particularly potent, with just a nibble being enough to potentially cause death.
Early symptoms of ingestion include;
• nausea,
• vomiting,
• anorexia,
• diarrhea,
• abdominal pain,
• wild hallucinations,
• delirium,
and
• severe headache.
Depending on the severity of the toxicosis the victim may later suffer;
• irregular and slow pulse,
• tremors,
• various cerebral disturbances, especially of a visual nature (unusual color visions with objects appearing yellowish to green, and blue halos around lights),
• convulsions,
and
• deadly disturbances of the heart.
There have been instances of people confusing digitalis with the harmless Symphytum (comphrey) plant (which is often brewed into a tea) with fatal consequences. Other fatal accidents involve children drinking the water in a vase containing digitalis plants. Drying does not reduce the toxicity of the plant. The plant is toxic to animals including all classes of livestock, as well as cats and dogs.
Digitalis poisoning can cause heart block and bradycardia (lowered heart rate) and tachycardia (increased heart rate). It is often quoted around the Internet that only bradycardia is associated with digitalis poisoning, but that is not true. It can cause either, depending on the dose and the condition of one's heart. It should however be noted, that electric cardioversion (to "shock" the heart) is generally not indicated in ventricular fibrillation in digitalis toxicity, as it can increase the dysrhythmia in digitalis toxicity.
Source;
http://en.wikipedia.org/wiki/Foxglove
-
Shaman of Bliss
- Banned Member
- Posts: 366
- Joined: Thu Jan 04, 2007 11:20 am
- Gender: Female
- Location: Canada
Potato
*The last picture is an image of Potato fruits, which are produced by mature potato plants, and are highly toxic.*
Description
Potato plants grow high to the ground and bear yellow to silver flowers with yellow stamens.
Potatoes are cross-pollinated mostly by bumblebees that carry pollen from other potato plants, but a substantial amount of self-fertilizing occurs as well. Any potato variety can also be propagated vegetatively by planting tubers, pieces of tubers, cut to include at least one or two eyes, or also by cuttings, a practice used in greenhouses for the production of healthy seed tubers.
Some commercial potato varieties do not produce seeds at all (they bear imperfect flowers) and are propagated only from tuber pieces. Confusingly, these tubers or tuber pieces are called "seed potatoes".
After potato plants flower, some varieties will produce small green fruits that resemble green cherry tomatoes. Each fruit can contain up to 300 true seeds. One can separate seeds from the fruits by putting them in a blender on a slow speed with some water, then leaving them in water for a day so that the seeds will sink and the rest of the fruit will float. All new potato varieties are grown from seeds, also called "true seed" or "botanical seed" to distinguish it from seed tubers.
Potato fruit contains large amounts of the toxic alkaloid solanine, and is therefore unsuitable for consumption.
Toxicity
Potatoes contain glycoalkaloids, toxic compounds, of which the most prevalent are solanine and chaconine.
Cooking at high temperatures (over 170 °C or 340 °F) partly destroys these.
The concentration of glycoalkaloid in wild potatoes suffices to produce toxic effects in humans. Glycoalkaloids occur in the greatest concentrations just underneath the skin of the tuber, and they increase with age and exposure to light.
Glycoalkaloids may cause;
• headaches,
• diarrhea,
• cramps,
and in severe cases,
• coma and death.
however, poisoning from potatoes occurs very rarely.
Light exposure also causes greening, thus giving a visual clue as to areas of the tuber that may have become more toxic; however, this does not provide a definitive guide, as greening and glycoalkaloid accumulation can occur independently of each other. Some varieties of potato contain greater glycoalkaloid concentrations than others; breeders developing new varieties test for this, and sometimes have to discard an otherwise promising cultivar.
Breeders try to keep solanine levels below 200 mg/kg (200 ppmw). However, when these commercial varieties turn green, even they can approach concentrations of solanine of 1000 mg/kg (1000 ppmw). In normal potatoes, however, analysis has shown solanine levels may be as little as 3.5% of the breeders' maximum, with 7–187 mg/kg being found.
The National Toxicology Program suggests that the average American consumes at most 12.5 mg/day of solanine from potatoes (note that the toxic dose is actually several times this, depending on body weight).
Dr. Douglas L. Holt, the State Extension Specialist for Food Safety at the University of Missouri - Columbia, notes that no reported cases of potato-source solanine poisoning have occurred in the U.S. in the last 50 years and most cases involved eating green potatoes or drinking potato-leaf tea.
Solanine is also found in other plants, mainly in the mostly-deadly nightshade family, which includes a minority of edible plants including the potato and the tomato, and other typically more dangerous plants like tobacco.
This poison affects the nervous system causing;
• weakness
and
• confusion.
Solanine
Solanine is a glycoalkaloid poison found in species of the nightshade family, such as potatoes. It can occur naturally in any part of the plant, including the leaves, fruit, and tubers. It is very toxic even in small quantities. Solanine has both fungicidal and pesticidal properties, and it is one of the plant's natural defenses.
Solanine in potatoes;
Solanine occurs naturally in all nightshades, including tomatoes, capsicum, tobacco and eggplant, as well as plants from other species. However, the most ingested solanine is from the consumption of potatoes.
Potatoes naturally produce solanine and chaconine, a related glycoalkaloid, as a defense mechanism against insects, disease, and predators. Potato leaves and stems and shoots are naturally high in glycoalkaloids.
When potato tubers are exposed to light, they turn green and increase glycoalkaloid production. This is a natural defense to help prevent the uncovered tuber from being eaten. The green colour is from chlorophyll, and is itself harmless. However, it is an indication that increased level of solanine and chaconine may be present.
Some diseases, such as potato blight, can dramatically increase the levels of glycoalkaloids present in potatoes. Mechanically damaged potatoes also produce increased levels of glycoalkaloids. This is believed to be a natural reaction of the plant in response to disease and damage.
Commercial varieties of potatoes are screened for solanine levels, and most have a solanine content of less than 0.2 mg/g.
However, potatoes that have been exposed to light and started to green can show concentrations of 1 mg/g or more. In these situations a single unpeeled potato can result in a dangerous dose.
In potato tubers 30–80% of the solanine develops in and close to the skin.
Showing green under the skin strongly suggests solanine build-up in potatoes although each process can occur without the other. A bitter taste in a potato is another, potentially more reliable indicator of toxicity.
Deep-frying potatoes at 170°C (306°F) is known to effectively lower glycoalkaloid levels, whereas microwaving is only somewhat effective and boiling has no effect.
Source;
http://en.wikipedia.org/wiki/Potato#Tox ... n_potatoes
http://en.wikipedia.org/wiki/Solanine
*The last picture is an image of Potato fruits, which are produced by mature potato plants, and are highly toxic.*
Description
Potato plants grow high to the ground and bear yellow to silver flowers with yellow stamens.
Potatoes are cross-pollinated mostly by bumblebees that carry pollen from other potato plants, but a substantial amount of self-fertilizing occurs as well. Any potato variety can also be propagated vegetatively by planting tubers, pieces of tubers, cut to include at least one or two eyes, or also by cuttings, a practice used in greenhouses for the production of healthy seed tubers.
Some commercial potato varieties do not produce seeds at all (they bear imperfect flowers) and are propagated only from tuber pieces. Confusingly, these tubers or tuber pieces are called "seed potatoes".
After potato plants flower, some varieties will produce small green fruits that resemble green cherry tomatoes. Each fruit can contain up to 300 true seeds. One can separate seeds from the fruits by putting them in a blender on a slow speed with some water, then leaving them in water for a day so that the seeds will sink and the rest of the fruit will float. All new potato varieties are grown from seeds, also called "true seed" or "botanical seed" to distinguish it from seed tubers.
Potato fruit contains large amounts of the toxic alkaloid solanine, and is therefore unsuitable for consumption.
Toxicity
Potatoes contain glycoalkaloids, toxic compounds, of which the most prevalent are solanine and chaconine.
Cooking at high temperatures (over 170 °C or 340 °F) partly destroys these.
The concentration of glycoalkaloid in wild potatoes suffices to produce toxic effects in humans. Glycoalkaloids occur in the greatest concentrations just underneath the skin of the tuber, and they increase with age and exposure to light.
Glycoalkaloids may cause;
• headaches,
• diarrhea,
• cramps,
and in severe cases,
• coma and death.
however, poisoning from potatoes occurs very rarely.
Light exposure also causes greening, thus giving a visual clue as to areas of the tuber that may have become more toxic; however, this does not provide a definitive guide, as greening and glycoalkaloid accumulation can occur independently of each other. Some varieties of potato contain greater glycoalkaloid concentrations than others; breeders developing new varieties test for this, and sometimes have to discard an otherwise promising cultivar.
Breeders try to keep solanine levels below 200 mg/kg (200 ppmw). However, when these commercial varieties turn green, even they can approach concentrations of solanine of 1000 mg/kg (1000 ppmw). In normal potatoes, however, analysis has shown solanine levels may be as little as 3.5% of the breeders' maximum, with 7–187 mg/kg being found.
The National Toxicology Program suggests that the average American consumes at most 12.5 mg/day of solanine from potatoes (note that the toxic dose is actually several times this, depending on body weight).
Dr. Douglas L. Holt, the State Extension Specialist for Food Safety at the University of Missouri - Columbia, notes that no reported cases of potato-source solanine poisoning have occurred in the U.S. in the last 50 years and most cases involved eating green potatoes or drinking potato-leaf tea.
Solanine is also found in other plants, mainly in the mostly-deadly nightshade family, which includes a minority of edible plants including the potato and the tomato, and other typically more dangerous plants like tobacco.
This poison affects the nervous system causing;
• weakness
and
• confusion.
Solanine
Solanine is a glycoalkaloid poison found in species of the nightshade family, such as potatoes. It can occur naturally in any part of the plant, including the leaves, fruit, and tubers. It is very toxic even in small quantities. Solanine has both fungicidal and pesticidal properties, and it is one of the plant's natural defenses.
Solanine in potatoes;
Solanine occurs naturally in all nightshades, including tomatoes, capsicum, tobacco and eggplant, as well as plants from other species. However, the most ingested solanine is from the consumption of potatoes.
Potatoes naturally produce solanine and chaconine, a related glycoalkaloid, as a defense mechanism against insects, disease, and predators. Potato leaves and stems and shoots are naturally high in glycoalkaloids.
When potato tubers are exposed to light, they turn green and increase glycoalkaloid production. This is a natural defense to help prevent the uncovered tuber from being eaten. The green colour is from chlorophyll, and is itself harmless. However, it is an indication that increased level of solanine and chaconine may be present.
Some diseases, such as potato blight, can dramatically increase the levels of glycoalkaloids present in potatoes. Mechanically damaged potatoes also produce increased levels of glycoalkaloids. This is believed to be a natural reaction of the plant in response to disease and damage.
Commercial varieties of potatoes are screened for solanine levels, and most have a solanine content of less than 0.2 mg/g.
However, potatoes that have been exposed to light and started to green can show concentrations of 1 mg/g or more. In these situations a single unpeeled potato can result in a dangerous dose.
In potato tubers 30–80% of the solanine develops in and close to the skin.
Showing green under the skin strongly suggests solanine build-up in potatoes although each process can occur without the other. A bitter taste in a potato is another, potentially more reliable indicator of toxicity.
Deep-frying potatoes at 170°C (306°F) is known to effectively lower glycoalkaloid levels, whereas microwaving is only somewhat effective and boiling has no effect.
Source;
http://en.wikipedia.org/wiki/Potato#Tox ... n_potatoes
http://en.wikipedia.org/wiki/Solanine
-
Shaman of Bliss
- Banned Member
- Posts: 366
- Joined: Thu Jan 04, 2007 11:20 am
- Gender: Female
- Location: Canada
Deadly Nightshade-Bellandona
Description
The species has dull green leaves and bell-shaped flowers that are purple, these yield black, shiny berries measuring approximately 1 cm in diameter. The yellow form, Atropa belladonna var. lutea, has pale yellow flowers and fruit. The berries are sweet, but the seeds contain toxic alkaloids. It is an herbaceous plant, and can grow to be approximately five metres tall. The leaves have an oily, "poison ivy"-like feel.
When Belladonna is in its first stages of growing the star shaped base of the berries is barely visible.
Toxicity
Belladonna is one of the most toxic plants found in the Western hemisphere. Children have been poisoned by eating as few as three berries. Ingestion of a leaf of the Belladonna can be fatal to an adult.
The root of the plant is generally the most toxic part, though this can vary from one specimen to another.
Belladonna leaves, if handled carelessly, can cause pus filled blisters.
All parts of the plant contain tropane alkaloids. The berries pose the greatest danger to children because they look attractive and have a somewhat sweet taste.
Symptoms of belladonna poisoning are the same as those for atropine (a tropane alkaloid), and include;
• dilated pupils,
• tachycardia,
• hallucinations,
• blurred vision,
• loss of balance,
• a feeling of flight, staggering,
• a sense of suffocation,
• paleness followed by a red rash,
• flushing, husky voice,
• extremely dry throat,
• constipation,
• urinary retention,
and
• confusion.
The skin can completely dry out and slough off.
The plant's deadly symptoms are caused by atropine's disruption of the parasympathetic nervous system's ability to regulate non-volitional/subconscious activities such as sweating, breathing, and heart rate. Heartbeat and breathing can become extremely irregular, and fatal cases have a rapid pulse that turns feeble.
The antidote for belladonna poisoning is physostigmine or pilocarpine, the same as for atropine.
Atropa belladonna is toxic to many domestic animals and livestock; Belladonna poisoning can lead to colic, depression, weakness, and lack of coordination in horses, with fatalities reported even for small amounts from 1 to 10 pounds (0.5 to 5 kg). Many animals, such as rabbits, birds and deer, seem to eat the plant without suffering harmful effects, though dogs and cats are affected.
The poison;
Atropine
Atropine is a tropane alkaloid extracted from the deadly nightshade (Atropa belladonna) and other plants of the family Solanaceae. It is a secondary metabolite of these plants and serves as a drug with a wide variety of effects. It is a competitive antagonist for the muscarinic acetylcholine receptor. It is classified as an anticholinergic drug. Being potentially deadly, it derives its name from Atropos, one of the three Fates who, according to Greek mythology, chose how a person was to die.
The antidote;
physotigmine;
Physostigmine (also known as eserine) is a parasympathomimetic, specifically, a reversible cholinesterase inhibitor obtained from the Calabar bean. It can also be obtained from Streptomyces griseofuscus . By interfering with the metabolism of acetylcholine, physostigmine indirectly stimulates both nicotinic and muscarinic receptors.
It is available in the U.S. under the trade names Antilirium, Eserine Salicylate, Isopto Eserine, and Eserine Sulfate
pilocarpine;
Pilocarpine is a muscarinic alkaloid obtained from the leaves of tropical American shrubs from the genus Pilocarpus
Pilocarpine is available under several trade names such as:
Diocarpine (Dioptic), Isopto Carpine (Alcon), Miocarpine (CIBA Vision), Ocusert Pilo-20 and -40 (Alza), Pilopine HS (Alcon), Salagen (MGI Pharma), Scheinpharm Pilocarpine (Schein Pharmaceutical), and Timpilo (Merck Frosst).
Sources;
http://en.wikipedia.org/wiki/Deadly_nightshade
http://en.wikipedia.org/wiki/Atropine
http://en.wikipedia.org/wiki/Physostigmine
http://en.wikipedia.org/wiki/Pilocarpine
Description
The species has dull green leaves and bell-shaped flowers that are purple, these yield black, shiny berries measuring approximately 1 cm in diameter. The yellow form, Atropa belladonna var. lutea, has pale yellow flowers and fruit. The berries are sweet, but the seeds contain toxic alkaloids. It is an herbaceous plant, and can grow to be approximately five metres tall. The leaves have an oily, "poison ivy"-like feel.
When Belladonna is in its first stages of growing the star shaped base of the berries is barely visible.
Toxicity
Belladonna is one of the most toxic plants found in the Western hemisphere. Children have been poisoned by eating as few as three berries. Ingestion of a leaf of the Belladonna can be fatal to an adult.
The root of the plant is generally the most toxic part, though this can vary from one specimen to another.
Belladonna leaves, if handled carelessly, can cause pus filled blisters.
All parts of the plant contain tropane alkaloids. The berries pose the greatest danger to children because they look attractive and have a somewhat sweet taste.
Symptoms of belladonna poisoning are the same as those for atropine (a tropane alkaloid), and include;
• dilated pupils,
• tachycardia,
• hallucinations,
• blurred vision,
• loss of balance,
• a feeling of flight, staggering,
• a sense of suffocation,
• paleness followed by a red rash,
• flushing, husky voice,
• extremely dry throat,
• constipation,
• urinary retention,
and
• confusion.
The skin can completely dry out and slough off.
The plant's deadly symptoms are caused by atropine's disruption of the parasympathetic nervous system's ability to regulate non-volitional/subconscious activities such as sweating, breathing, and heart rate. Heartbeat and breathing can become extremely irregular, and fatal cases have a rapid pulse that turns feeble.
The antidote for belladonna poisoning is physostigmine or pilocarpine, the same as for atropine.
Atropa belladonna is toxic to many domestic animals and livestock; Belladonna poisoning can lead to colic, depression, weakness, and lack of coordination in horses, with fatalities reported even for small amounts from 1 to 10 pounds (0.5 to 5 kg). Many animals, such as rabbits, birds and deer, seem to eat the plant without suffering harmful effects, though dogs and cats are affected.
The poison;
Atropine
Atropine is a tropane alkaloid extracted from the deadly nightshade (Atropa belladonna) and other plants of the family Solanaceae. It is a secondary metabolite of these plants and serves as a drug with a wide variety of effects. It is a competitive antagonist for the muscarinic acetylcholine receptor. It is classified as an anticholinergic drug. Being potentially deadly, it derives its name from Atropos, one of the three Fates who, according to Greek mythology, chose how a person was to die.
The antidote;
physotigmine;
Physostigmine (also known as eserine) is a parasympathomimetic, specifically, a reversible cholinesterase inhibitor obtained from the Calabar bean. It can also be obtained from Streptomyces griseofuscus . By interfering with the metabolism of acetylcholine, physostigmine indirectly stimulates both nicotinic and muscarinic receptors.
It is available in the U.S. under the trade names Antilirium, Eserine Salicylate, Isopto Eserine, and Eserine Sulfate
pilocarpine;
Pilocarpine is a muscarinic alkaloid obtained from the leaves of tropical American shrubs from the genus Pilocarpus
Pilocarpine is available under several trade names such as:
Diocarpine (Dioptic), Isopto Carpine (Alcon), Miocarpine (CIBA Vision), Ocusert Pilo-20 and -40 (Alza), Pilopine HS (Alcon), Salagen (MGI Pharma), Scheinpharm Pilocarpine (Schein Pharmaceutical), and Timpilo (Merck Frosst).
Sources;
http://en.wikipedia.org/wiki/Deadly_nightshade
http://en.wikipedia.org/wiki/Atropine
http://en.wikipedia.org/wiki/Physostigmine
http://en.wikipedia.org/wiki/Pilocarpine
-
Shaman of Bliss
- Banned Member
- Posts: 366
- Joined: Thu Jan 04, 2007 11:20 am
- Gender: Female
- Location: Canada
Castor Oil Plant
Description
The castor oil plant, Ricinus communis, is a plant species of the Euphorbiaceae and the sole member of the genus Ricinus and of the subtribe Ricininae. Its seed is the castor bean which, despite its name, is not a true bean.
Castor seed is the source of castor oil, which has a wide variety of uses. The seeds contain between 40% and 60% oil that is rich in triglycerides, mainly ricinolein. They also contain ricin, a poison, which is also present in lower concentrations throughout the plant.
Toxicity
The toxicity of raw castor beans is well-known, and reports of actual poisoning are relatively rare.
Children could conceivably die from as few as three beans; adults may require eight or more.
As an example of the rarity of castor bean poisoning, in recent years there have only been two cases reported in all of England, and in both the victims recovered uneventfully.
In February, 2008, a 57-year-old man in Las Vegas, Nevada, called for medical assistance from an Extended Stay hotel. Ricin and castor beans were subsequently found in the man's room.
Castor seeds have been found in Egyptian tombs dating back to 4000 BC. Herodotus and other Greek travelers have noted the use of castor seed oil for lighting and body ointments.
The poison;
Ricin
The protein ricin (pronounced /ˈraɪsɨn/) is a toxin extracted from the castor bean (Ricinus communis).
The U.S. Centers for Disease Control (CDC) gives a possible minimum figure of 500 micrograms for the lethal dose of Ricin in humans if exposure is from injection or inhalation.
A pinhead-sized amount can kill an adult.
Sources;
http://en.wikipedia.org/wiki/Castor_Oil_Plant
http://en.wikipedia.org/wiki/Ricin
Description
The castor oil plant, Ricinus communis, is a plant species of the Euphorbiaceae and the sole member of the genus Ricinus and of the subtribe Ricininae. Its seed is the castor bean which, despite its name, is not a true bean.
Castor seed is the source of castor oil, which has a wide variety of uses. The seeds contain between 40% and 60% oil that is rich in triglycerides, mainly ricinolein. They also contain ricin, a poison, which is also present in lower concentrations throughout the plant.
Toxicity
The toxicity of raw castor beans is well-known, and reports of actual poisoning are relatively rare.
Children could conceivably die from as few as three beans; adults may require eight or more.
As an example of the rarity of castor bean poisoning, in recent years there have only been two cases reported in all of England, and in both the victims recovered uneventfully.
In February, 2008, a 57-year-old man in Las Vegas, Nevada, called for medical assistance from an Extended Stay hotel. Ricin and castor beans were subsequently found in the man's room.
Castor seeds have been found in Egyptian tombs dating back to 4000 BC. Herodotus and other Greek travelers have noted the use of castor seed oil for lighting and body ointments.
The poison;
Ricin
The protein ricin (pronounced /ˈraɪsɨn/) is a toxin extracted from the castor bean (Ricinus communis).
The U.S. Centers for Disease Control (CDC) gives a possible minimum figure of 500 micrograms for the lethal dose of Ricin in humans if exposure is from injection or inhalation.
A pinhead-sized amount can kill an adult.
Sources;
http://en.wikipedia.org/wiki/Castor_Oil_Plant
http://en.wikipedia.org/wiki/Ricin
-
Shaman of Bliss
- Banned Member
- Posts: 366
- Joined: Thu Jan 04, 2007 11:20 am
- Gender: Female
- Location: Canada
Monk's Hood
Description
These herbaceous perennial plants are chiefly natives of the mountainous parts of the northern hemisphere, growing in moisture retentive but well draining soils on mountain meadows. Their dark green leaves lack stipules. They are palmate or deeply palmately lobed with 5–7 segments. Each segment again is 3-lobed with coarse sharp teeth. The leaves have a spiral or alternate arrangement. The lower leaves have long petioles.
These are handsome plants, the tall, erect stem being crowned by racemes of large and eye-catching blue, purple, white, yellow or pink zygomorphic flowers with numerous stamens. They are distinguishable by having one of the five petaloid sepals (the posterior one), called the galea, in the form of a cylindrical helmet; hence the English name monkshood. There are 2–10 petals, in the form of nectaries. The two upper petals are large. They are placed under the hood of the calyx and are supported on long stalks. They have a hollow spur at their apex, containing the nectar. The other petals are small and scale like or non forming. The 3–5 carpels are partially fused at the base.
Toxcity
In a few minutes after the introduction of a poisonous dose of aconite, marked symptoms supervene. The initial signs of poisoning are referable to the alimentary canal. There is a sensation of;
• burning,
• tingling,
and
• numbness in the mouth,
and
• burning in the abdomen.
Death usually supervenes before a numbing effect on the intestine can be observed. After about an hour, there is
• severe vomiting,
motor weakness
and
cutaneous sensations similar to those above described soon follow.
The pulse and respiration steadily fail, death occurring from asphyxia. As in strychnine poisoning, the patient is conscious and clear-minded to the last.
The only post-mortem signs are those of asphyxia. The treatment is to empty the stomach by tube or by a non-depressant emetic.
The physiological antidotes are atropine and digitalis (Foxglove) or strophanthin, which should be injected subcutaneously in maximal doses.
Alcohol, strychnine, and warmth must also be employed. It must be noted that these "antidotes" are historical ones, as few toxicological centers today would recommend warmth, digitalis, or strychnine for any poisonings.
The above description of poisoning is characteristic of an oral administration. It should however be noted that aconitine may be easily absorbed through the skin, and poisoning may occur through this route simply by picking the leaves without the use of gloves; the toxin in the sap is absorbed through the skin. The sap oozing from eleven picked leaves will cause cardiac symptoms for a couple of hours. In this event, there will be no gastrointestinal effects. Tingling will however start at the point of absorption, and extend up the arm to the shoulder, after which the heart will start to be affected. The tingling will be followed by numbness which is fairly unpleasant.
As remarked above, atropine is an antidote.
Atropine is a constituent of Belladonna. [Terribly ironic, no?]
Canadian actor, Andre Noble died in July 2004 from poisoning following the accidental consumption of aconite from Monkshood during a camping trip.
Sources;
http://en.wikipedia.org/wiki/Monkshood
Description
These herbaceous perennial plants are chiefly natives of the mountainous parts of the northern hemisphere, growing in moisture retentive but well draining soils on mountain meadows. Their dark green leaves lack stipules. They are palmate or deeply palmately lobed with 5–7 segments. Each segment again is 3-lobed with coarse sharp teeth. The leaves have a spiral or alternate arrangement. The lower leaves have long petioles.
These are handsome plants, the tall, erect stem being crowned by racemes of large and eye-catching blue, purple, white, yellow or pink zygomorphic flowers with numerous stamens. They are distinguishable by having one of the five petaloid sepals (the posterior one), called the galea, in the form of a cylindrical helmet; hence the English name monkshood. There are 2–10 petals, in the form of nectaries. The two upper petals are large. They are placed under the hood of the calyx and are supported on long stalks. They have a hollow spur at their apex, containing the nectar. The other petals are small and scale like or non forming. The 3–5 carpels are partially fused at the base.
Toxcity
In a few minutes after the introduction of a poisonous dose of aconite, marked symptoms supervene. The initial signs of poisoning are referable to the alimentary canal. There is a sensation of;
• burning,
• tingling,
and
• numbness in the mouth,
and
• burning in the abdomen.
Death usually supervenes before a numbing effect on the intestine can be observed. After about an hour, there is
• severe vomiting,
motor weakness
and
cutaneous sensations similar to those above described soon follow.
The pulse and respiration steadily fail, death occurring from asphyxia. As in strychnine poisoning, the patient is conscious and clear-minded to the last.
The only post-mortem signs are those of asphyxia. The treatment is to empty the stomach by tube or by a non-depressant emetic.
The physiological antidotes are atropine and digitalis (Foxglove) or strophanthin, which should be injected subcutaneously in maximal doses.
Alcohol, strychnine, and warmth must also be employed. It must be noted that these "antidotes" are historical ones, as few toxicological centers today would recommend warmth, digitalis, or strychnine for any poisonings.
The above description of poisoning is characteristic of an oral administration. It should however be noted that aconitine may be easily absorbed through the skin, and poisoning may occur through this route simply by picking the leaves without the use of gloves; the toxin in the sap is absorbed through the skin. The sap oozing from eleven picked leaves will cause cardiac symptoms for a couple of hours. In this event, there will be no gastrointestinal effects. Tingling will however start at the point of absorption, and extend up the arm to the shoulder, after which the heart will start to be affected. The tingling will be followed by numbness which is fairly unpleasant.
As remarked above, atropine is an antidote.
Atropine is a constituent of Belladonna. [Terribly ironic, no?]
Canadian actor, Andre Noble died in July 2004 from poisoning following the accidental consumption of aconite from Monkshood during a camping trip.
Sources;
http://en.wikipedia.org/wiki/Monkshood
-
Shaman of Bliss
- Banned Member
- Posts: 366
- Joined: Thu Jan 04, 2007 11:20 am
- Gender: Female
- Location: Canada
Hemlock
Description
Conium is a genus of two species of perennial herbaceous flowering plants in the family Apiaceae, native to Europe and the Mediterranean region (C. maculatum), and to southern Africa (C. chaerophylloides).
By far the most familiar species is Conium maculatum (Hemlock or Poison Hemlock), the most common of several species of hemlock noted for their toxicity. It is a herbaceous biennial plant which grows between 1.5–2.5 m tall, with a smooth green stem, usually spotted or streaked with red or purple on the lower half of the stem. The leaves are finely divided and lacy, overall triangular in shape, up to 50 cm long and 40 cm broad. The flowers are small, white, clustered in umbels up to 10–15 cm across. The plant is often mistaken for fennel, parsley or wild carrot although the characteristic stem hairs of the wild carrots are missing. The Conium root is fleshy, white and often unbranched and can be mistaken for parsnip. When crushed, the leaves and root emit a rank, unpleasant odour often compared to that of parsnips.
Conium maculatum has been introduced and naturalised in many other areas, including much of Asia, North America and Australia. Poison hemlock is often found on poorly drained soils, particularly near streams, ditches, and other surface water.
A useful trick to determine whether a plant is poison hemlock rather than fennel, which it resembles, is to crush some leaves and smell the result. Fennel smells like anise or liquorice, whereas the smell of poison hemlock is often described as mouse-like or musty. Considering the high toxicity of poison hemlock, if the plant cannot be identified it must be discarded.
Conium is used as a food plant by the larvae of some Lepidoptera species including Silver-ground Carpet.
Poison hemlock flourishes in the spring, when most other forage is gone. All plant parts are poisonous but once the plant is dried, the poison is greatly reduced, however not gone completely. Hemlock is also known as "poison parsley" or "spotted parsley".
Poison hemlock is sometimes confused with water hemlocks in the related genus Cicuta, but are readily distinguished by the less finely divided leaves of the latter; the leaf veins of poison hemlock also run through the tips of the teeth, but those of the water hemlock run through the notches in between the teeth. The poison hemlock's root is long, white, and fleshy. It is unbranched and can usually be distinguished from the water hemlock's roots that are made up of several tubers.
Toxicity
The most important and toxic of these is coniine. Coniine is a neurotoxin, which disrupts the workings of the peripheral nervous system and is toxic to people and all classes of livestock. Coniine causes death by blocking the neuromuscular junction in a manner similar to curare; this results in an ascending muscular paralysis with eventually paralysis of the respiratory muscles which results in death due to lack of oxygen to the heart and brain. Death can easily be prevented by artificial ventilation until the effects have worn off.
The poison;
Coniine
Coniine is a poisonous alkaloid found in poison hemlock and the Yellow Pitcher Plant, and contributes to hemlock's fetid smell. It is a neurotoxin which disrupts the peripheral nervous system. It is toxic to all classes of livestock and humans; less than 0.2g (0.007oz) is fatal to humans, with death caused by respiratory paralysis.
Socrates was put to death by way of this poison in 399 BC.
The story of Socrates
In ancient Greece, hemlock was used to poison condemned prisoners. The most famous victim of hemlock poisoning is the philosopher Socrates. After being condemned to death for impiety in 399 BC, Socrates was given a potent solution of the hemlock plant. Plato described Socrates' death in the Phaedo [1]:
"The man … laid his hands on him and after a while examined his feet and legs, then pinched his foot hard and asked if he felt it. He said ‘No’; then after that, his thighs; and passing upwards in this way he showed us that he was growing cold and rigid. And then again he touched him and said that when it reached his heart, he would be gone. The chill had now reached the region about the groin, and uncovering his face, which had been covered, he said — and these were his last words — 'Crito, we owe a cock to Asclepius. Pay it and do not neglect it.' 'That,' said Crito, 'shall be done; but see if you have anything else to say.' To this question he made no reply, but after a little while he moved; the attendant uncovered him; his eyes were fixed. And Crito when he saw it, closed his mouth and eyes."
Although many have questioned whether this is a factual account, careful attention to Plato's words, modern and ancient medicine, and other ancient Greek sources point to the above account being consistent with Conium poisoning.
Sometimes the characteristic red spots found on the stem and branches are referred to as "the blood of Socrates" in reference to his death.
Sources;
http://en.wikipedia.org/wiki/Poison_Hemlock
http://en.wikipedia.org/wiki/Coniine
Description
Conium is a genus of two species of perennial herbaceous flowering plants in the family Apiaceae, native to Europe and the Mediterranean region (C. maculatum), and to southern Africa (C. chaerophylloides).
By far the most familiar species is Conium maculatum (Hemlock or Poison Hemlock), the most common of several species of hemlock noted for their toxicity. It is a herbaceous biennial plant which grows between 1.5–2.5 m tall, with a smooth green stem, usually spotted or streaked with red or purple on the lower half of the stem. The leaves are finely divided and lacy, overall triangular in shape, up to 50 cm long and 40 cm broad. The flowers are small, white, clustered in umbels up to 10–15 cm across. The plant is often mistaken for fennel, parsley or wild carrot although the characteristic stem hairs of the wild carrots are missing. The Conium root is fleshy, white and often unbranched and can be mistaken for parsnip. When crushed, the leaves and root emit a rank, unpleasant odour often compared to that of parsnips.
Conium maculatum has been introduced and naturalised in many other areas, including much of Asia, North America and Australia. Poison hemlock is often found on poorly drained soils, particularly near streams, ditches, and other surface water.
A useful trick to determine whether a plant is poison hemlock rather than fennel, which it resembles, is to crush some leaves and smell the result. Fennel smells like anise or liquorice, whereas the smell of poison hemlock is often described as mouse-like or musty. Considering the high toxicity of poison hemlock, if the plant cannot be identified it must be discarded.
Conium is used as a food plant by the larvae of some Lepidoptera species including Silver-ground Carpet.
Poison hemlock flourishes in the spring, when most other forage is gone. All plant parts are poisonous but once the plant is dried, the poison is greatly reduced, however not gone completely. Hemlock is also known as "poison parsley" or "spotted parsley".
Poison hemlock is sometimes confused with water hemlocks in the related genus Cicuta, but are readily distinguished by the less finely divided leaves of the latter; the leaf veins of poison hemlock also run through the tips of the teeth, but those of the water hemlock run through the notches in between the teeth. The poison hemlock's root is long, white, and fleshy. It is unbranched and can usually be distinguished from the water hemlock's roots that are made up of several tubers.
Toxicity
The most important and toxic of these is coniine. Coniine is a neurotoxin, which disrupts the workings of the peripheral nervous system and is toxic to people and all classes of livestock. Coniine causes death by blocking the neuromuscular junction in a manner similar to curare; this results in an ascending muscular paralysis with eventually paralysis of the respiratory muscles which results in death due to lack of oxygen to the heart and brain. Death can easily be prevented by artificial ventilation until the effects have worn off.
The poison;
Coniine
Coniine is a poisonous alkaloid found in poison hemlock and the Yellow Pitcher Plant, and contributes to hemlock's fetid smell. It is a neurotoxin which disrupts the peripheral nervous system. It is toxic to all classes of livestock and humans; less than 0.2g (0.007oz) is fatal to humans, with death caused by respiratory paralysis.
Socrates was put to death by way of this poison in 399 BC.
The story of Socrates
In ancient Greece, hemlock was used to poison condemned prisoners. The most famous victim of hemlock poisoning is the philosopher Socrates. After being condemned to death for impiety in 399 BC, Socrates was given a potent solution of the hemlock plant. Plato described Socrates' death in the Phaedo [1]:
"The man … laid his hands on him and after a while examined his feet and legs, then pinched his foot hard and asked if he felt it. He said ‘No’; then after that, his thighs; and passing upwards in this way he showed us that he was growing cold and rigid. And then again he touched him and said that when it reached his heart, he would be gone. The chill had now reached the region about the groin, and uncovering his face, which had been covered, he said — and these were his last words — 'Crito, we owe a cock to Asclepius. Pay it and do not neglect it.' 'That,' said Crito, 'shall be done; but see if you have anything else to say.' To this question he made no reply, but after a little while he moved; the attendant uncovered him; his eyes were fixed. And Crito when he saw it, closed his mouth and eyes."
Although many have questioned whether this is a factual account, careful attention to Plato's words, modern and ancient medicine, and other ancient Greek sources point to the above account being consistent with Conium poisoning.
Sometimes the characteristic red spots found on the stem and branches are referred to as "the blood of Socrates" in reference to his death.
Sources;
http://en.wikipedia.org/wiki/Poison_Hemlock
http://en.wikipedia.org/wiki/Coniine
Thanks for all the posts Shaman.Shaman Of Bliss wrote:Deadly Nightshade-Bellandona
...
Belladonna leaves, if handled carelessly, can cause pus filled blisters
...
I agree, Belladonna is very dangerous, although I wouldn't worry about
handling the leaves of the plants as was stated.
Let's not forget the *positive* uses of this plant as well. Atropine, which is
a muscarinic antagonist, can counteract substances which over-stimulate
muscarinic acetylcholine receptors (an overdose of such substances can
kill). For example, belladonna will counteract some of the effects of fly
agaric (and vice versa, to an extent).
In a bind it's action can also be used to increase dangerously low
blood-pressure and heart-rate.
However, please, do *not* *ever* try to administer such treatments
yourself; *EVER*.
Wikipedia is a *great* resource for information, however, it's a good
idea to always double-check any 'facts' you find therein. It's not as if
master herbalists and botanists have enough spare time to scrutinise
every single detail in every article.
I still think that the best way to get to know any plant is through
(safe and reasonable) personal experience.
cheers,
T. Guy.
P.S. great idea for a thread JCrowfoot.
