The distinction between the terms ‘medicinal’ and ‘poisonous’ is sometimes smaller than one might believe. There is generally fine correlation between the total poison ingested and the rigorousness of the clinical symptoms.

Classification of Plant Toxins

Plant toxins are food components of plant origin that may be low-molecular-weight endogenous toxins or products of secondary metabolism. Products of secondary metabolism are species specific and are responsible for the particular characteristics of plant. They include plant pigments, flavours, and compounds that serve to protect the plants. Some of these secondary metabolic products cause toxicity to the individual when taken orally. These substances may be growth inhibitors, neurotoxins, carcinogens, and teratogens⁴. These are classified based on their structural and chemical properties. Plant toxins can be classified as follows:

a) Alkaloids

These are organic compounds containing nitrogen in heterocyclic ring, basic in nature and derived from amino acid, most of which exhibit strong physiological activity. For example, colchicines, nicotine, aconitine, taxine, cocaine and many others.

Some common toxins from this class include:

· Indole alkaloids: beta-carbolines like harmine active on the central nervous system⁵

· Pyrrolizidine: veno occlusive disease of the liver⁶

· Tropanes: atropine, scopolamine, hyoscyamine active on the autonomous nerve system

· Glycoalkaloid: The greatest worry for glycoalkaloid toxicity is its acute toxicity. There have been many reported cases of human poisonings (sometimes fatal) due to the ingestion of greened, damaged or sprouted potatoes as a consequence of high levels of glycoalkaloid i.e. solanine^7,8

· Vicine/covicine: important in G-6PD deficiency and fauvism (haemolytic anaemia)

b) Glycosides

These substances are consisting of a nonsugar moiety i.e. aglycone to which one or more sugar chains is bound.

· Cyanogenic glycosides release prussic acid. The cyanide ions (CN-) attach to the mitochondrial cytochrome oxidase and in this way blocks electron transport. The clinical symptoms of acute cyanide intoxication can include: rapid respiration, drop in blood pressure, rapid pulse, dizziness, headache, stomach pains, vomiting, diarrhoea, mental confusion, stupor, cyanosis with twitching and convulsions followed by terminal coma⁹.

· Cardiac glycosides such as digitoxin from foxglove. Digoxin inhibits the enzyme Na-K-ATPase. Vomiting, confusion, changes in colour perception and in particular, cardiac arrhythmias are dominant symptoms.

· Goitrogenic glycosides: too much ingestion and simultaneous iodine deficiency may lead to thyroid disorders.

· Mustard seed oil glycosides: After splitting of the sugar, irritating mustard oils were released.

c) Tannins

These substances have the capability to precipitate proteins. They make the skin tough by deception of the proteins in the skin.

d) Proteins

A number of protein toxins produced by plants enter eukaryotic cells and inhibit protein synthesis enzymatically¹⁰. Examples of poisonous proteins include ricin (castor plant)¹¹, abrin (rosary pea) and white acacia. Lathyrism occurs due to a toxic amino acid that mimics glutamate¹².

e) Oxalic acid and oxalates

These substances may be present in trichomes or in raphides (needle-like structures). They can provoke mechanical irritation. Ingested oxalate will be absorbed. Oxalate in blood binds calcium to form the insoluble calcium oxalate. Severe hypocalcaemia with tetany can occur.

f) Anti-vitamins

Some substances work against the vitamins, e.g. thiaminases in horsetails and bracken (breakdown of thiamine) and anti-vitamin K such as coumarins.

g) Photosensitising and contact-sensitising substances

St. John’s wort with hypericin and hogweed causes photoallergy. Poison ivy is known in North America. Many of the active substances are phenols, furano-coumarins or derivatives of these, which causes allergy to sunlight.

h)Volatile oils

Volatile oils are liquid substances formed in special oil cells, glands, hairs, or channels. They are all soluble in alcohol. At certain concentrations, some are irritant (forming blisters) and emetic. Some volatile oils are nephrotoxic¹³.

Plant toxins:

The following table entails about different phytotoxins, their source and effect on human physiology (Table 1).

Table 1: Different Plant toxins

S.No.	Plant Toxins with common name	Phytoconstituents	Action	Reference
1.	Manihot esculenta (Bitter cassava)	Linamarin and lotaustralin	Severe Calcific Pancreatitis, Chronic Pancreatitis	14, 15
2.	Andromeda floribunda (Mountain andromeda)	Andromedotoxin	Paralysis, Death
3.	Lathyrus sativus (grass pea)	amino acid ODAP	Neurolathyrism A Neurodegenerative Disease	16
4.	Phaseolus vulgaris (white beans)	Phytohaemagglutinin	Nausea, Vomiting, Diarrhoea	17
5.	Myristica fragrans	Myristicin and elemicin	Neurotoxic Effects	18, 19
6.	Avocado persea spp.	Persin	Equinecolic, Resp. Distress, Fluid Accumulate around Heart	20
7.	Actea rubra	Cardiogenic toxins	Menstrual Cramping Cardiac Arrest, Death	21
8.	Asparagus.	Berries	Nausea, Vomiting, Diarrhoea	22
9.	Convolvula arvensis	Convolmine	Insomnia, Diuretic	23
10.	Helleborus niger	Protoanemonin, ranunculin	Oral Ulceration, Gastroenteritis, Hematemesis	24, 25
11.	Helenium.spp	Glycosides and sesquiterpene lactones	Muscle Tremor, Dehydration, Cough, Pneumonia
12.	Hippomane mancinella	Latex	Allergic Dermatitis	26
13.	Chelidonium majus	Coptisine	CNS Sedative, Dermatitis, Eye Irritation	27, 28
14.	Atropa belladonna, Hyocyamus niger	Atropine	Blurred Vision, Tachycardia, , Staggering, Headache, Rash, Flushing, Dry Mouth and Throat, Urinary Retention, Constipation, Hallucinations, Delirium, Convulsions	29, 30
15.	Colchicum autumnale	Colchicine	Anemia, Muscular Weakness, Respiratory Failure	31
16.	Robinia pseudocadia	Glycoprotein- abrin, lectin	Colieic Pain, Constipation, Diarrhoea, Muscle Weakness, Ataxia	32
17.	Cerbera odollam	Cerberin	Disturbance of Heart Beat	33
18.	Cytisus scoparius	Sparteine	Depress Heart and Nervous System	34
19.	Saponaria officinalis	Saponins	Hepatopathy, Git Disturbances	22
20.	Amianthium, Anticlea, Stenanthium, Toxicoscordion and Zigadenus	Toxic alkaloid	Fatal To Human And Animal	35
21.	Petridium aquilinum	Thiaminase	GIT Cancer, Enzootic Haematuria, Thrombocytopaenia, Depression, Blindness, Decreased Platelets	36
22.	Fagopyrum Esculentum	Fagopyrin, dianthroquin Ones	Fagopyrin, Dianthroquin Ones	37
23.	Solanum tuberosum	Solanine, atropine	Bloating,Diarrhoea	38, 39
24.	Ranunculus .spp	Oily glycoside, ranunculln	Increased Salivation, Reddening Of Mucous Membrane	40
25.	Caladium .spp	Tropane alkaloids	Constipation, Resp Failure, Mydriasis, Muscle Weakness, Tachycardia	41
26.	Ricinus communus	Ricin, lectin	Diarrhea, Pyrexia, Depression, Anorexia, Bloat, Hypovolemic Shock	42
27.	Jacobaea vulgaris	Jacobine, Jaconine	Skin Allergy
28.	Kalanchoe delagoensis	bufadienolide cardiac glycosides	Cardiac Poisoning	43
29.	Lolium temulentum	Temuline and loblline	Causes Toxicity	44
30.	Oenanthe crocata	Oenanthotoxin	Neurotoxin	45
31.	Physostigma venenosum	physostigmine	Nausea, Vomiting, Diarrhea, Anorexia, Dizziness, Headache, Stomach Pain, Sweating, Dyspepsia And Seizures	46
32.	Pteridium aquilinum	Ptaquiloside	Carcinogenic	47
33.	Quercus	Tannic acid	Gastroenteritis, Heart Trouble, Contact Dermatitis And Kidney Damage	48
34.	Sanguinaria canadensis	Sanguinarine	Blocking The Action Of Na+/K+-Atpase Transmembrane Proteins	27
35.	Solanum dulcamara	Solanine	Fatigue, Paralysis, Convulsions, And Diarrhea	49
36.	Taxus baccata	Taxane	Seed Toxic If Chewed	50
37.	Veratrum	Veratridine	Rapid Cardiac Failure And Death If Ingested	51
38.	Zantedeschia	Oxalates	Irritation To Mouth And Throatvomiting And Diarrhoea	52

MECHANISM OF ACTION OF PLANT TOXIN

Neurotoxins

The neuroactive alkaloids can function either as agonists which excite a neuroreceptor or as antagonists which would block a certain neuroreceptor. Receptors on neuron cells are another major target for many of alkaloids, which structurally resemble the endogenous neurotransmitters such as glutamate, acetylcholine, dopamine, noradrenalin, and adrenaline. Some alkaloids inhibit the enzymes that break down neurotransmitters, such as cholinesterase and monoamine oxidase. Neurotoxins also have an effect on significant ion channels of neuronal cells, such as Na⁺, K⁺ and Ca²⁺ channels, whichever by activating or inactivating them eternally. This activities stop neuronal signal transduction and block the activity of the central nervous system and neuromuscular. The sodium, potassium ion ATPase that is an important ion pump in neuronal and other cells to maintain an ion gradient important for action potentials and transport mechanisms^{53- 56}.

Inhibitors of cellular respiration

Cellular respiration, which occur in mitochondria and produces ATP, is another susceptible target in animals, in view of the fact that ATP is essential for all cellular and organ functions. Many plant toxins can attack this target with HCN, which binds to iron ions of the terminal cytochrome oxidase in the mitochondrial respiratory chain^{53, 54}. HCN does not occur in a free form, but is stored as Cyanogenic glucoside in plant cell vacuoles. When plants are injured, the content of the vacuoles gets into contact with enzymes, such as β-glucosidase and nitrilase due to ruptured cellular matrix. These enzymes hydrolyse and Cyanogenic glucoside releases extremely toxic HCN. The Diterpene atractyloside is a potent inhibitor of the mitochondrial ADP/ATP transporter and thus inhibits the ATP supply of a cell⁵⁷.

Cytotoxins

Many phyto constituents are regarded as cytotoxins as they obstruct important cellular functions. Biomembrane are prime target of such compounds which are involved in the import and export of metabolites and ions in cells^{53, 54}. Membrane fluidity and integrity can be severely disturbed by both steroidal and triterpenoids saponins. Saponins are usually stored as inactive bidesmosidic saponins in plant vacuoles; on injury and destruction, they are transformed into the active monodesmosidic saponins, which are amphiphilic with detergent activities⁵⁷. Several enzymes , proteins, DNA/RNA and related processes are other important targets of such compounds. A number of strong plant toxins inhibit ribosomal protein biosynthesis, such as the alkaloid emetine , amanitins, and the lectins. These toxins can attach to cells by their B-chain, the haptomer, whereas the A-chain is taken up by endocytosis into the cytosol, where it blocks protein biosynthesis^{53, 54}. The elements of the cytoskeleton, especially microtubules and actin filaments, are also vulnerable targets in animal cells. A number of plant toxins are known as microtubule poisons, such as colchicine, podophyllotoxin, vinblastine, chelidonine, noscapine, cucurbitacins and taxol. These poisons are known to block cell division, vesicle transport and microtubules. Several secondary compounds can covalently bind to proteins, such as aldehydes, epoxides, secondary compounds with exocyclic methylene groups, with SH groups or reactive double or triple bonds^{57, 58, 59}. These protein modifications influence the three- dimensional structure of proteins and can inhibit their function. Therefore, many poisons with such properties have neurotoxic and cytotoxic properties or are irritants to skin and mucosal tissue.

Toxins of skin and mucosal tissues

Skin and mucosal tissues of animals are also affected by several toxins. Diterpene, which resemble the endogenous signal compounds diacylglycerol (DAG), an activator of the key enzyme protein kinase^{53, 54}. These diterpenes are classified as phorbol esters and they stimulate protein kinase. When they come in contact of skin, mucosal tissues or eye they cause severe painful inflammation, with ulcers and blister formation. Furanocoumarins can penetrate the skin and intercalate dermal cells. When the skin is exposed to sun light, the Furanocoumarins alkylate DNA, which kills the cells and induces strong blister formation and necrosis. Many species of the Ranunculaceae accumulate the glycoside ranunculin in the vacuole. It splits into the active protoanemonin, which can alkylate proteins and DNA, which causes skin and mucosal irritation, followed by a severe inflammation. The proteases or other noxious proteins of plants further worsen the condition by their damaging activity.

TOXICOLOGICAL EFFECTS OF PLANT TOXINS

Phytodermatitis and Phytophotodermatitis

Some substances secreted from plants have an irritant effect on the skin after being irradiated by UV light e.g. hogweed (Heracleum sphondylium), giant hogweed (Heracleum mantegazzianum) and rue (Ruta graveolens). Fig, mango and many other trees known to cause irritation skin on contact. Phytophotodermatitis also known as dermatitis pratensis that is identified clinically by strange red stripes at the site of contact (forearms, hands, legs, face) that is exposed to the sun. The skin lesions are similar to burns. There is a delay between the skin contact and the first signs of irritation. Phytophotodermatitis should not be confused with contact allergy or with photoallergic reactions such as polymorphous light eruption, persistent light reaction or solar urticaria. The treatment consists of thorough cleansing of the skin and application of a steroid cream. Celery, parsnips, figs, and parsley foods should be avoided by people with photodermatitis, e.g. in SLE because of containing large amounts of psoralens.

Berloque dermatitis, triggered by perfumes containing bergamot oil, is a known state in dermatology. There is generally residual pigmentation. Phytoconstituents such as 8-methoxypsoralen and similar furano-coumarins from Ammi majus known as psoralens are photodynamic substances. They absorb UV light, become activated and then cause cell damage by inhibiting DNA synthesis. These are used in PUVA therapy of psoriasis as psoralens with Ultraviolet A.

Phytoallergy

Hay fever caused by pollen from ragweed, birch, hazel, timothy grass and rye grass are common case of phytoallergy. Urticaria resulting from eating strawberries and allergy to peanuts are some other recognised allergy conditions due to phytoconstituents. Some phytoconstituents cause certain forms of extrinsic allergic alveolitis. Pyrethrum allergy is a known problem on the plantations of Chrysanthemum cineriaefolium in many countries. The Japanese cedar (Cryptomeria japonica) is a source of annual misery because of the massive amounts of highly allergenic pollen in every spring. A Phytoallergic problem has increased greatly in recent decades.

A different allergic mechanism occurs in regions with poison ivy (Rhus toxicodendron, T. rydbergii), poison oak (Rhus juglandifolia) and poison sumac (Rhus vernix). The active ingredient is urushiol. Its first exposer of sap to the skin, has no noticeable clinical effect. Urushiol acts as a hapten, however. It binds to proteins in the skin, creating new epitopes. Upon subsequent contact pronounced pruritic dermatitis develops.

Food poisoning

Food poisonings provoked by plant toxins mainly due to consumption of foods such as beans that are partially cooked, some cultivars of potatoes, and ingestion of herbs selected from the wild not wished-for for human use such as poisonous berries and mushrooms. Acute poisoning cases caused by plant toxins are occasionally ignored because the symptoms of toxicity can be rather non-specific. Earlier, acute poisoning from a high consumption of glycoalkaloid, such as solanine, from potatoes has been misdiagnosed as microbial food poisoning⁶⁰. The amount of eating of food plants containing toxins that will be responsible for food poisoning depends on many factors such as individual susceptibility, the cooking methods and the levels of toxin in the plant that may vary according to the species and geographical environment.

CONCLUSION:

Plants grow up in an extremely competitive environment. Insects, microbes and herbivores continually intimidate plants. In order to existence, each plant must produce secondary metabolites to protect them. Plant toxins are found widely in edible plants; apart from harmful effect, these also have nutritious and beneficial to health. These substances may be alkaloid, glycoside, proteins, tannins etc. These toxins are problem in correlation with different diseases, and they may be a risk as bioterror weapons. Still, It serve as superb tools to study cellular and other mechanisms, and enhanced knowledge about the plant toxins may give us new products for use in medicine.

ACKNOWLEDGEMENT:

The authors are thankful to Director, University Institute of Pharmacy, Pt. Ravishankar Shukla University, Raipur (C.G.) India for providing all necessary facilities for carrying out this work and University Grants Commission (UGC/MRP 39-169/2010 (SR)) and (UGC-RA 70-371/2012) for financial assistance.

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Received on 09.04.2013

Modified on 22.04.2013

Accepted on 10.05.2013

Research J. Pharmacology and Pharmacodynamics. 5(5): September–October 2013, 283-288