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POISONOUS PLANTS Treat unknown plants with respect , and teach your children to do the same . M any plants are poisonous to varying degrees. M any plant poisons are either alkaloids or steroid s , - PowerPoint PPT Presentation


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Treat unknown plants with respect, and teach your children to do the same.

Many plants are poisonous to varying degrees.

Many plant poisons are either alkaloids or steroids, a potential source of drugs or commercial poisons for use as insecticides, herbicides and fungicides.

Use of plant poisons in the capital punishment well known from the story: death of Greek Philosopher Socrates- sentenced to drink the juice of poison hemlock Conium maculatum.Plants cannot escape their predators-need protection from herbivores.

Some have physical defenses:- thorns, prickles, hairs, bristles.

BUT most common protection is chemicals.

Natural selectionhas produced many chemical compounds to keep away herbivores-during thousands of years.

Tannins- emerged relatively early in the evolutionary history of plants.

More complex molecules-Polyacetylenes are found in younger groups of plants like Asterales.

Consumption of such plants may produce negative effects-mild discomfort to death.Same poisonous compounds may be of medicinal value.

Many unanswered questions about this chemical defence system.. Questions include: Which plants have which type of defenses? (2)Which herbivores are the plants defended against?

(3)What are the chemical structures of the compounds that provide defense?

(4)What are the potential medical uses of these compounds?

An active area of research with important implications in the field of medicinal chemistry.

Human fatalities caused by poisonous plants-especially from accidental ingestion.Poisonous Food PlantsMany food plants toxic unless processed, or are toxic at certain stages of their life.

Apple(Malus domestica)-Seeds mildly poisonous, contain small amount ofamygdalin, a cyanogenic glycoside.

Quantity contained usually not enough to be dangerous to humans, but if enough seeds ingested can prove fatal.Cassava(Manihot esculenta)Roots +Leaves contain 2cyanogenic glucosides;linamarin&lotaustralin- decomposed bylinamarase-a naturally occurringenzyme in cassava, liberating HCN.

Sweet or Bitter Varieties signify absence or presence of toxic levels of cyanogenic glucosides.

Sweet' cv can produce 20 mg ofCN/kg of fresh roots-bitter ones produce more 1 g/kg. Toxin very high indrought conditions.

40mg of pure cassava cyanogenic glucoside sufficient to kill a cow.

Causes severe calcific Pancreatitis in humans-chronic (inflammation of pancreas).

Processing (soaking, cooking, fermentation) of roots necessary to remove the toxins & avoid getting sick. "Low-level CN exposure associated with the development ofgoiter & tropical ataxic neuropathy-a nerve damaging disorder; renders a person unsteady & uncoordinated.

Severe CN poisoning-associated with outbreaks of a debilitating, irreversible paralytic disorder called KONZO -in some cases death. Incidence of KONZO & Tropical Ataxic Neuropathy can be as high as 3 % in some areas.

For smaller-rooted sweet varieties-cooking sufficient to eliminate all toxicity.

CN is carried away in the processing water.

Larger-rooted, bitter var. used for production of flour or starch must be processed to remove cyanogenic glucosides.

Industrial production of cassava flour, even at the cottage level, may generate enough CN & cyanogenic glycosides in the effluents to have a severe environmental impact.

Cherry(Prunus cerasus), + otherPrunusspecies -peach(P. persica),plum(P. domestica),almond (P. dulcis), &apricot(P. armeniaca)-Leaves + seeds contain Cyanogenic Glycosides.Indian pea (Lathyrus sativus)

Legume from Asia & East Africa insurance crop for use during famines.

Produces a high-protein seed.

Seeds contain variable amounts of ODAP (-N-Oxalyl-L-,- diaminopropionic acid) a neurotoxicamino acid.ODAP causes paralysisif eaten over a long period.

Considered as the cause of disease Neurolathyrism, a neurodegenerative disease causes paralysis of the lower body & emaciation(weight loss) of gluteal muscle. Disease seen to occur afterfaminesin Europe (France, Spain, Germany), North Africa & South Asia.

Still prevalent in Eritrea, Ethiopia & parts of Afghanistan ifLathyrusseed exclusive or main source of nutrients for long.Nutmeg(Myristicafragrans)

-ContainsMyristicin - a naturally occurringinsecticide&acaricidewith possible neurotoxiceffects onneuroblastomacells.

Psychoactiveproperties at doses much higher than used incooking.

Raw producesanticholinergic-like symptoms, attributed to myristicin &elemicin (a phenylpropene).Myristicin intoxication causes condition between waking - dreaming; euphoria is reported, nausea often experienced.

Users report bloodshot eyes memory disturbances.

Induces hallucinogenic effects like visual distortions.

Intoxication peak reaching- may take 7 hours, effects can be felt for 24 hours, with lingering effects lasting up to 72 hours. Kidney beanorcommon bean (Phaseolus vulgaris)

Toxic compound phytohaemagglutinin (alectin) -in many varieties of common bean especially red kidney beans.

Lectin - number of effects on cell metabolism.

Induces mitosis, affects cell membrane transport & permeabilityto proteins. Primary symptoms of poisoning-nausea, vomiting, diarrhea

Onset from 1 - 3 hours after consumption of improperly prepared beans, symptoms typically resolve within a few hours.

]Consumption of as few as 4 or 5 raw kidney beans sufficient to trigger symptoms.

Phytohaemagglutinin can be deactivated by cooking beans at 100C for 10 minutes- (degrades toxin).

For dry beans initial soak of at least 5 hours in water required; the soaking water is discarded.

Lower cooking temperatures may have the paradoxical effect of potentiating the toxic effect of haemagglutinin.

Beans cooked at 80C are reported to be up 5 times as toxic as raw beans.Outbreaks of poisoning associated with the use ofslow cookers, the low cooking temperatures-unable to degrade the toxin.

Lima beanorbutter bean (Phaseolus lunatus)

Raw beans contain dangerous amounts of linamarin, a cyanogenic glucoside.Lupin - Some varieties have edible seeds

Sweet Lupins less toxic alkaloids lupinine & sparteine; Bitter have more.

Onions and Garlic. Alliums- containthiosulphate, in high doses toxic to dogs, cats + other livestock.Potato(Solanum tuberosum)

Contain toxic compounds called Glyco-alkaloids -most prevalent solanine&chaconine.

Solanine found also in Atropa belladonna("deadly nightshade") & Hyoscyamus niger("henbane").

Concentration of glycoalkaloid in wild potatoes suffices to produce toxic effects in humans.

Toxin affects - nervous system, causingheadaches,diarrhea, intense digestive disturbances,cramps, weakness & confusion, in severe casescoma / death. Poisoning from cultivated potatoes very rare -toxic compounds in general concentrated in the green portions & fruits, cultivated potato varieties contain lower toxin levels.

Cooking at high temperatures (over 170 C) partly destroys the toxin.

Exposure to light, physical damage & age increase glycoalkaloid content within the tuber, highest concentrations occurring just underneath the skin. Tubers exposed to light turn green from chlorophyllsynthesis-a visual clue to areas of the tuber that may have become more toxic.

Not a definite guide, as greening & glycoalkaloid accumulation can occur independently of each other.

Some potato cv contain greater glycoalkaloid concentrations than others; breeders developing new varieties test for this, and sometimes have to discard an otherwise promisingcv.

Breeders keep solanine levels below 200mg/kg.If commercial varieties turn green-they can approach concentrations of solanine of 1000mg/kg.

Americans consume 12.5mg/day of solanine from potatoes (toxic dose actually several times this, depending on body weight).

No reported cases of potato-source solanine poisoning, and most cases involved eating green potatoes or drinking potato-leaf tea.

Rhubarb(Rheum rhaponticum)

Petioles edible-leaves contain notable quantities of oxalic acid- a Nephrotoxic & corrosive acid- present in many plants.

Symptoms of poisoning-kidney disorders, convulsions & coma, Rarely fatal.

LD50(median lethal dose) for pure oxalic acid is about 25 grams for a 65kg human. Oxalic acid content in leaves varies.

Typical value 0.5%- if 5kg of extremely sour leaves consumed - reach anLD50of oxalic acid.

Cooking leaves with soda can make them more poisonous by producing solubleoxalates.

Leaves are believed to also contain an unidentified toxin- might be an anthraquinone glycoside(also called senna glycosides).In petioles-amount of oxalic acid much lower;about 2-2.5% of the total acidity which is dominated by malic acid.

Even raw stalks may not be hazardous.

Tart taste of raw stalks is so strong as to be unpalatable to many.Tomato(Solanum lycopersicum).

Leaves + stems containsolanine-toxic if ingested, causing digestive upset & nervous excitement.

Use of tomato leaves as a tea (tisane) has been responsible for at least