bioToxins found in Popular Jamaican

Botanic Foods.Oraine reid18080241

Objectives Should be able to define Bio-toxins List the bio-toxins present in several

popular Jamaican Botanical Foods Understand the mechanism by which

these toxins are able to act on the human body.

Give preventative measures that can be taken against the effect of these toxins.

What are Biotoxins A naturally produced toxic compound

which shows pronounced biological activity and presumably has some adaptive significance to the organism which produces it

Toxin Purpose and Function Toxins - metabolic products produced �

by living organisms for the purpose of repelling or killing

Plant Toxins (Phytotoxins)• Large array of chemicals, many species of

plants.• Toxins include: alkaloids, pyrrolizidine

alkaloids, terpenoids, amino acids, others.

Popular Jamican Botanical Foods

Ackee Bitter yam Potato Cassava Nutmeg Castor oil plant

Solanum tuberosum: Potato

glycoalkaloids Toxic glycoalkaloids are found in the

whole plant of potato Solanum tuberosum, and also in majority of other species from family Solanaceae, e.g. tomato or aubergine - Solanum melongena

These alkaloids are so called steroid glycoalkaloids (SGA), or pseudoalkaloids, because their precursors are not aminoacids like in genuine alkaloids

Glycoalkaloids are termostable, so you cannot destroy them by cooking, frying or drying. They bear temperatures higher than 300°C. But during cooking potatoes in water majority of alkaloids pass to water

Solanin – in fresh unpeeled tubers there can be concentration of solanin more than 100 mg/kg.

The limit for potatoes determined to eat is 200 mg/kg.

But at about 150 mg/kg, the taste starts to be bitter and in higher concentration this taste discourages to eat them.

Types of Glycoalkaloids

Were are they found? Glycoalkaloids are

usually found at low levels. They can be higher in certain cases if the vegetable is still: • green • damaged • starting to sprout 

Toxic effects of glycoalkaloids: They posses two mechanisms of action:

- First: they disturb cell membranes containing steroid substances (an effect similar to those in saponines)

- Second: they inhibit serum cholinesterase too (similar to organophosphates)

Mechanism Acetylcholine is a neurotransmitter (a

chemical which transmits nerve impulses or signals) in the brain and the peripheral nervous system. The enzyme cholinesterase functions to break down acetylcholine. When cholinesterase is inhibited, the continued presence of acetylcholine over-stimulates the post-synaptic nerve cell, causing the symptoms of poisoning that characterize the anti-cholinesterases.

Early signs: of intoxication are colic, diarrhoea with blood in excrements, apathy, halucinations. Then follow seizures, coma and respiration paralysis

Toxic dose: is 2-5 mg/kg of body weight and lethal dose between 3-6 mg/kg body weight.

Other group of glycoalkaloids in potatoes are

leptins. They are natural pesticides and genetics try to put the gene for leptins to other plants to protect them.

Tubers also contain so called protease inhibitors, which dissociate trypsine, chymotrypsine, kathepsine D and karboxypeptidases. These inhibitors can be removed and destroyed by exposure to heat

Factors that have effect on toxicity levels

o Maturity• The highest concentrations of glycoalkaloids are usually

associated with areas that are undergoing high metabolic activity, such as potato flowers, young leaves, sprouts, peels and the area around the potato 'eyes'. Small immature tubers are normally high in glycoalkaloids since they are still metabolically active.

o Exposure to light• Exposure to light has a significant effect on the

concentration of both total and individual glycoalkaloids. Potatoes that become sunburned during growth and start to 'green', owing to lack of soil cover, tend to taste very bitter as a result of their high glycoalkaloid content. In retail outlets, tubers may be displayed under fluorescent lighting and this can increase glycoalkaloid concentration. Studies have indicated that replacing fluorescent lights

with mercury lighting for potatoes on display would significantly reduce glycoalkaloid content and improve food safety.

Storage temperature• Storage at very low temperatures (0 - 5°C)

results in more bitter-tasting potatoes and thus more glycoalkaloids than storage at higher temperatures (up to 20°C.

Injury/damage• Any type of injury or damage to the tuber will

result in the accumulation of glycoalkaloids. Disease, insect attack or rough handling, during or after harvest, will all initiate glycoalkaloid synthesis (as it is a defence response).

Control options Processing

• Peeling: In normal tubers, potato glycoalkaloids appear to be concentrated in a small 1.5-mm layer immediately under the skin, therefore, with normal tubers, peeling will remove between 60% - 95% of the glycoalkaloids present.

• Unfortunately, peeling or slicing also elicits a stress response in the tubers and causes a slow rise in glycoalkaloid levels. If long delays occur before subsequent processing, glycoalkaloids can accumulate.

Cooking• The heat stability of glycoalkaloids means that only high

temperature processing, such as deep frying, has any significant effect on levels in potatoes.

COMPARISON BETWEEN POTATOES

AFFECTED NOT AFFECTED

Dioscorea dumetorum: Bitter yam

Bitter yam (Dioscorea dumetorum)

There are approximately ten types of Jamaican yams known

The edible, mature, cultivated yam does not contain any toxic principles. 

The Jamaican yam tuber has a brown or black skin which resembles the bark of a tree and off-white, purple, white, yellow and sometimes red flesh, depending on the variety.

STUCTURE OF TOXINS

 Bitter principles tend to accumulate in immature tuber tissues.

Wild forms of D. dumetorum do contain bitter principles, and hence are referred to as bitter yam.

The bitter principle has been identified as the alkaloid dihydrodioscorine.

These are water-soluble alkaloids,

MECHANISM This compound is a convulsant alkaloid and it

causes central nervous system paralysis in animals.

An extract of dihydrodioscorine produces a long lasting hypotension and contraction of the smooth muscle fibers of the intestine both in vivo and in vitro when administered to animals (Oliver-Bever, 1989).

This explains the use of Dioscorea species for the preparation of poison bit for fishing, hunting and preparation of insecticide

CassavaManihot utilissima

Toxicity of the plant : The leaves and roots contain free and bound forms of the cyanogenic glycoside linamarin, which is converted to cyanide in the presence of linamarinase, a naturally occurring enzyme in cassava or via exposure to the atmosphere. Two varieties Sweet - contains as little as 20 milligrams of cyanide (CN) per kilogram of fresh rootsBitter - may produce more than 50 times as much (1 g/kg)

Lethal dose : One dose of pure cassava cyanogenic glucoside (40mg) is sufficient to kill even a cow. Hence about 300 grams of fresh root is enough to kill an adult human and about 125 grams of fresh root would be enough to kill a child

Mechanism of action: The carrier of toxicity is HCN, released from

glucoside in blood It binds to haemoglobin and methaemogobin

and forms cyanhaemoglobin and cyanmethaemoglobin respectively

Cyanides and cyanic acid act as neurotoxins and they also bind to several proteins damaging enzyme systems.

They decrease tissue breathing, block cytochromoxidase (HCN binds to Fe and Cu), cause tissue suffocation, because oxygen is not passed on to tissues, blood is oversaturated by oxygen and is of bright brick red colour

BiotransformationDissociation of cyanogenic glucosides goes on in two steps

oFirst, β-D-glucopyranose is dissociated due to action of enzyme called β-D-glucosidase and α hydroxynitrile is formedoThis substance is dissociated to HCN and aldehyde or ketone due to enzyme hydroxynitrillyase Dissociation of cyanogenic glucosides: R1 O- β-glucopyranose R1 OH

C C + glucose R2 C= N + H2O R2 C = N cyanogenic glucoside α-hydroxynitrile

β –glucosidase

R1 OH R1

C C = O + HCN R2 C= N + H2O R2

Aldehyde and ketone

α-hydroxynitrile α-hydroxynitrillyase

In normal plant tissues free HCN doesn’t occur

Described dissociation takes place in mechanically damaged tissues, where glucosides and enzyme, normally stored separately, come into touch and start to react together

Released HCN must be detoxified in plant or in animal somehow - product of detoxification is thiocyanate SCN-

The enzyme sulphurtransferases is used to detoxify HCN released in plants or animals.

Myristica fragrans: Nut meg

Myristica fragrans:Nut meg

It is a tropical evergreen tree found in East and West Indes. Contains a number of methylenedioxy-substituted compounds, including

myristicin, elemicin, and safrole It also contains elemycin, eugenol,

and methyleugenol.

{Weil, Andrew. Nutmeg as a Narcotic. 1965. 19(3), 194-217

Mechanism The only known mechanism of

metabolization of these compounds is the detoxification of safrole to piperonylic acid, a reaction which also shows the capability of oxidizing olefinic side chains.

If this same degenerative process will act on myristicin, or elemicin, then a possible intermediate (a vinyl alcohol) could undergo transamination.

Myristicin produces MMDA which is metabolised to form TMA. MMDA has a higher potency than TMA

Elemicin undergoes oxidation of its oleficin side chain to produce TMA (3,4,5-trimethoxyamphetamine), a psychotropic drug agent

Traditional use: • As a spice in foods• As a traditional medicine for diarrhoea

Toxic part of the plant: seeds (nutmeg) and, to a lesser extent, the aril (mace)

Lethal dose: Humans: 1-3 nutmegs (5-15g) for adults, 2 nutmegs for children

Animals: oral dose of 24mg nutmeg oil per kg body weight

Clinical features of poisoning:symptoms are usually seen within 3-6 hours after ingestion and vary according to the dose taken and the variability between different samples of nutmegs

intoxication resembles anti-cholinergic intoxication i.e profuse sweating, flushed face, dry mouth, burning epigastric pain, tachycardia, restlessness, giddiness, hallucinations.

Alocasia macrorrhiza: cocoa

Toxic part of the plant: all parts Main toxic constituent/s:

all parts of the plant contain specialized cells containing bundles of needle-like calcium oxalate crystals and toxic proteins

Mode of action: When the plant is chewed the sharp crystals injure the mucous

membrane allowing toxic proteins to penetrate

Lethal dose: The extreme oropharyngeal response generally limits the amount of

plant ingested and oxalate absorbed through the oral mucosa is unlikely to cause systemic poisoning.

Symptoms: Eating parts of the plant causes a severe burning in mouth and throat.

Other symptoms may include: Redness, swelling, pain, burning pain of the tongue and mucous membranes,

profuse salivation, dysphagia Swelling can rarely cause obstruction and respiratory compromise Loss of speech may last several days and swelling more than a week

Treatment of poisoning: wipe out the mouth with a cold, wet cloth and give milk to drink antihistamines, mouthwashes, antiseptics and steroids may be used

References: http://en.wikipedia.org/wiki/Alocasia [3 July 2008]; Jayaweera DMA. Medicinal plants used in Ceylon. Part 1. Colombo: The National Science Foundation, 2006; Lucas GN, De Silva TUN. Poisonous plants of Sri Lanka. Colombo: Sri Lankan College of Paediatricians, 2006

The scanning electron microscopic images of Alocasia macrorrhiza

•Upper picture: a calcium oxalate druse in the mesophyll cells of a leaf.

•Middle picture: calcium oxalate needles (raphids) in cells of a root tuber.

•Lower picture: silicate bodies of silicate cells in the epidermis. 

CASTOR OIL PLANTRicinus communis

Traditional use:

Pure castor oil has been used since ancient times to loosen the stool and remove waste products in the intestines and colon.

This thick liquid is rich in fatty acids, thereby making it a natural emollient perfect for moisturizing.

It has been applied internally and externally as a remedy for various kinds of medical conditions and ailment

Toxic part of the plant: seeds are the most toxic part (leaves are also poisonous)

Lethal dose: 1mg/kg pure ricin in man Ingestion of a single well chewed bean has caused death

1-3 seeds can be fatal to a child2-4 seeds cause severe poisoning in an adult

poisoning is unlikely if seeds are swallowed without chewing

RICIN Ricin is a toxic glycoprotein (with

several minor variants) belonging to the type II group of ribosome inactivating proteins (type II RIP) found in the seeds (beans) of the castor oil plant.

It is composed of two polypeptide chains of approximately 30 kDa joined by a disulfide bond.

Blighia sapida: Ackee

Ackee Blighia sapida Ackee fruit causes profound

hypoglycemia due to hypoglycin A, a toxic compound contained in the fruit.

Ackee fruit is produced biannually by the tropical evergreen tree,Blighia sapida

Unripe fruit and the water used to cook it are toxic and cause Jamaican vomiting sickness when ingested

 Metabolism of hypoglycin yields methylenecyclopropylacetyl-CoA (MCPA-CoA). Acyl-CoA dehydrogenase will accept MCPA-CoA as a substrate. This causes a removal of a proton from the a-carbon to yield an intermediate that

irreversibly inactivates acyl-CoA dehydrogenase by reacting covalently with FAD on the enzyme.

MCPA-CoA exerts its effect by inhibiting several coenzyme A dehydrogenases which are essential for gluconeogenesis

Depletion of glucose reserves and the inability of cells to regenerate glucose leads to hypoglycemia.

Statistics Between the years 1880 – 1955, there

evolved an illness that was found predominantly in Jamaica.

In 1955 the causative factor of JVS was isolated, a non proteinogenic amino acid, hypoglycin A, so named due to its ability to induce severe hypoglycemia.

Concentrations within the arilli ranges from over 1000 ppm in the immature fruit to less than 0.1 ppm in the fully mature fruit 

Conclusion Jamaican culture is filled with a diverse

amount of indigenous botanical plants that are consumed by the population.

The consumption of these plants and their derivatives have caused and have the potential to cause several chronic illnesses.

It is important that the contents of these foods are known and necessary precautionary measures be taken to reduce the effects by toxins.