This, in turn, activates mechanisms as a result of which the cell expels Na+ ions and absorbs calcium. Although a considerable increase in calcium concentration is buffered by sarcoplasmic reticulum, a local
increase in calcium concentrations leads to an increase in the force of myocardium contraction. A similar mechanism of inducing an intracellular inflow of calcium, induced by ciguatoxin, is observed in cells of intestinal endothelium. It contributes to the enhanced secretion and is manifested by diarrhea (Lehane and Lewis 2000).
Ciguatoxin intoxication is characterized by gastrointestinal disorders (vomiting, diarrhea and contractions of abdominal cavity organs), neurological symptoms (headaches and nausea, ataxia, sensibility disorders, muscular and joint pains), itching of the skin of palm, feet and lips, as well as less common cardiovascular symptoms (arrhythmia, bradycardia or tachycardia, reduced blood pressure) (Watters 1995, Isbister and Kiernan 2005). There is no antidote in the case of ciguatoxin poisoning, only adjunct therapy is undertaken. Since ciguatoxin is very soluble in fats, its absorption from the intestine is rapid and considerable. Nevertheless, early occurrence of vomiting and diarrhea may facilitate the removal of some amount of the toxin before its absorption (Lehane and Lewis 2000). There is some evidence that calcium channel blocker type drugs such as nifedipine and verapamil are effective in treating some of the symptoms that remain after the initial sickness passes, such as poor circulation and shooting pains through the chest. These symptoms are due to the cramping of arterial walls caused by maitotoxin. Ciguatoxin lowers the threshold for opening voltage-gated sodium channelsin synapses of the nervous system (Davis et al. 1986).
2.2. Shellfish Toxins:
Shellfish poisoning is caused by a group of toxins produced by planktonic algae (dinoflagellates, in most cases) on which shellfish feed. Numerous shellfish toxins have been described around the world; included here are toxins currently regulated by the FDA (Deeds 2012).
2.2.1.Paralytic shellfish poisoning (PSP):
PSP is caused by water-soluble alkaloid neurotoxins that are collectively referred to as saxitoxins or paralytic shellfish toxins (PSTs). They absorb active toxins or non-toxic form with food, and the latter are hydrolyzed in the gastrointestinal tract of the shellfish to the active forms (Isbister and Kiernan 2005, Watters 1995). Saxitoxin and its derivative, i.e. gonyatoxin, block sodium channels susceptible to tetrodotoxin, thus blocking Na+ penetration to the cellsâ interior, which disturbs nervous conductance and leads to motor and sensory nervous abnormality (Isbister and Kiernan 2005). The symptoms include gastrointestinal disorders appearing in the first 30â”60 min, followed by sensation disorders manifested by pinching and numbness of tongue and lips which, with time, expands to the face, neck, fingers and toes. In most fatal cases, death occurs within the first 12 h (Lehane and Olley 2001, Meier and White 1995).
2.2.2. Diarrhetic shellfish poisoning (DSP):
DSP is caused by a group of lipid-soluble polyether toxins that includes okadaic acid, the dinophysistoxins, and a series of fatty acid esters of okadaic acid and the dinophysistoxins (collectively known as DSTs). Okadaic acid is a strong inhibitor of phosphatases, enzymes closely linked with metabolic processes in cells. Diarrhea in humans is suggested to be induced by excessive phosphorylation of proteins that control the secretion of sodium through the cells of intestinal epithelium (Hallegraeff et al. 1995).
2.2.3. Neurotoxic shellfish poisoning (NSP):
NSP is caused by a group of lipid-soluble polyether toxins called brevetoxins. NSP-causing toxins in shellfish include intact algal brevetoxins and their metabolites (collectively known as NSTs). Poisoning occurs after consumption of shellfish containing
brevetoxin produced by dinofllagellates Karenia brevis. Its effect on an organism consists mainly in the stimulation of sodium channels in the cell wall [Novak, 1998]. Symptoms include gastrointestinal disorders as well as sensation disorders in the form of pinching and numbness of lips, tongue and throat. Vertigo, muscular pains and alternating sensation of warmth and cold are also likely to occur (Hughes and Merson 1976).
2.2.4. Amnesic shellfish poisoning (ASP):
ASP is caused by the neurotoxin domoic acid (DA), a water-soluble, non-protein, excitatory amino acid. Isomers of domoic acid have been reported, but are less toxic than domoic acid itself. Domoic acid is a water soluble, thermostable amino acid produced by microscopic alga of the genus Nitzschia (Isbister and Kiernan 2005). Its activity is based on the inhibition of adenyl cyclase activity in cellular membranes (Nijjar and Grimmelt 1994) and changes in the structure of myelin sheath of axons (Schumued and Slikker 1999). Domoic acid demonstrates neurotoxic, immunotoxic and genotoxic activity (Dizer et al. 2001). Its neurotoxic properties are manifested by neuronal degeneration and necrosis of hippocampus regions and amygdala region.
2.2.5. Azaspiracid shellfish poisoning (AZP):
AZP is caused by the lipid-soluble toxin azaspiracid and several derivatives (AZAs). To date, more than 30 AZA analogs have been identified, with three analogs routinely monitored in shellfish. AZP symptoms include nausea, vomiting, severe diarrhea and contractions of abdominal cavity organs (Satake et al.1998).
Scombroid food poisoning is a food borne illness that results from eating spoiled (decayed) fish (Clark et al. 1999). Scombrotoxin is a combination of substances, histamine prominent among them. There are 3 elements that are required for histamine fish poisoning to occur. Firstly, the fish must have high levels of free histidine present. Secondly, certain bacteria that produce the enzyme histidine decarboxylase, particularly Morganella morganii, Klebsiella pneumoniae or other Enterobacteriaceae must be present in the fish (Bjornsdottir et al. 2009). This enzyme is responsible for the conversion of histidine to histamine (Smolinska et al. 2014). Lastly, there must be some form of inappropriate handling or temperate abuse that allows the multiplication of these bacteria and thus the production of histamine. As histamine is heat stable, cooking does not reduce the risk of illness (Smolinska et al. 2014). Scombrotoxin poisoning is closely linked to the accumulation of histamine in these fish (Benner 2012).
Symptom onset is rapid, usually within minutes to a few hours after consumption of the implicated fish (Heymann 2004). Symptoms may vary for different individuals depending on underlying medical conditions and medications but can include flushing of the face, neck and upper arms, oral numbness and/or burning, metallic taste, headache, itchy rash, hives, nausea, vomiting, diarrhoea and difficulties swallowing. The illness is generally self-limiting and recovery usually occurs within 24 hours. When required, antihistamines are used to treat symptoms (Lehane and Olley 1999).
Tetrodotoxin, frequently abbreviated as TTX, is a potent neurotoxin. Its name derives from Tetraodontiformes, an order that includes pufferfish, porcupinefish, ocean sunfish or mola, and triggerfish, several species that carry the toxin. Although tetrodotoxin was discovered in these fish and found in several other animals (e.g., blue-ringed octopus, rough-skinned newt (Hogan 2008), and Naticidae (Hwang 1991)) it is actually produced by certain symbiotic bacteria, such as Pseudoalteromonas tetraodonis, certain species of Pseudomonas and Vibrio, as well as some others that reside within these animals.
TTX is extremely toxic. The toxin can enter the body by ingestion, injection, or inhalation, or through abraded skin (Patocka and Stredav 2002). The mechanism of toxicity is through the blockage of fast voltage-gated sodium channels. Tetrodotoxin is quite specific in blocking the Na+ ion channel and therefore the flow of Na+ ions while having no effect on K+ ions. Binding to the channel is relatively tight (Kd =10-10 nM). Whereas the hydrated sodium ion binds reversibly on a nanosecond time-scale, tetrodotoxin is bound for tens of seconds.
Tetrodotoxin, much larger than the sodium ion, acts like a cork in a bottle, preventing the flow of sodium until it slowly diffuses off. A mortal dose of tetrodotoxin is but a single milligram. Tetrodotoxin competes with the hydrated sodium cation and enters the Na+-channel where it binds. It is proposed that this binding results from the interaction of the positively charged guanidino group on the tetrodotoxin and negatively charged carboxylate groups on side chains in the mouth of the channel. Saxitoxin, a natural product from dinoflagellates, acts in a similar way and is also a potent nerve poison.
If we assume that there are carboxylate groups also on the intracellular side of the pore why doesnât the tetrodotoxin also block Na+ from leaving the cell when the cell reestablishes equilibrium (Noda et al. 1986).
Plasma membrane with ion channels and hydrated sodium ion and tetrodotoxin
Symptoms typically develop within 30 minutes of ingestion, but may be delayed by up to four hours; however, death once occurred within 17 minutes of ingestion (Clark et al. 1999). Paresthesia of the lips and tongue is followed by hypersalivation, sweating, headache, weakness, lethargy, incoordination, tremor, paralysis, cyanosis, aphonia, dysphagia, seizures, dyspnea, bronchorrhea, bronchospasm, respiratory failure, coma, and hypotension. Gastroenteric symptoms are often severe and include nausea, vomiting, diarrhea, and abdominal pain. Cardiac arrhythmias may precede complete respiratory failure and cardiovascular collapse.
No antidote has been developed for Tetrodotoxin. Therapy is supportive and based on symptoms, with aggressive early airway management. If ingested, treatment can consist of emptying the stomach, feeding the victim activated charcoal to bind the toxin, and taking standard life-support measures to keep the victim alive until the effect of the poison has worn off. Alpha adrenergic agonists are recommended in addition to intravenous fluids to combat hypotension. Anticholinesterase agents have been used with mixed success (Clark et al. 1999).
5. Mushroom poisoning:
Mushroom poisoning (also known as mycetism) refers to harmful effects from ingestion of toxic substances present in a mushroom. These symptoms can vary from slight gastrointestinal discomfort to death. The toxins present are secondary metabolites produced in specific biochemical pathways in the fungal cells. Mushroom poisoning is usually the result of ingestion of wild mushrooms after misidentification of a toxic mushroom as an edible species. The most common reason for this misidentification is close resemblance in terms of colour and general morphology of the toxic mushrooms species with edible species. There are many folk traditions concerning the defining features of poisonous mushrooms (Hall 2003).
The severity of mushroom poisoning may vary, depending on the geographic location where the mushroom is grown, growth conditions, the amount of toxin delivered, and the genetic characteristics of the mushroom. Boiling, cooking, freezing, or processing may not alter some mushroomâs toxicity. Mushroom exposure in children is an infrequent but perennial problem for parents and clinicians. Parental anxiety is generally high because of fears of unknown or untoward effects. The challenges for clinicians are to identify such poisonings, to discern whether poisoning has taken place, to order appropriate diagnostic studies, and to prescribe reasonable therapy. The varied nature of mushroom toxicities, their ubiquitous distribution, and the relative infrequency of the ingestions make these challenges difficult to meet (Diaz 2005a).
Each poisonous mushroom species contains 1 or more toxins, which may be classified on the basis of the mushroomâs physiologic and clinical effects in humans, the target organ toxicity, and the time to symptom onset.
Cyclopeptides include amatoxins and Amanita phalloides (death cap), Amanita virosa (destroying angel), Amanita verna(foolâs mushroom), Amanita bisporigera, Galerina autumnalis (autumn skullcap), and Galerina sulcipes are the most common mushrooms implicated in liver injury and death amongst the amatoxin-containing mushrooms.
Gyromitrin is a volatile hydrazine derivative synthesized by certain species of false morel (Gyromitra esculenta) and is easily confused with the early false morel (Verpa bohemica). Gyromitrin poisoning typically occurs after ingestion of the toxin-containing mushrooms but may also result from inhalation of the cooking vapors during their preparation.
Orellanine is a nephrotoxic compound that is synthesized by several species ofCortinarius mushrooms. Orellanine-containing species include Cortinarius orellanusand Cortinarius speciosissimus, both of which are commonly found in Europe and Japan but not in North America. Cortinarius species that may contain small amounts of orellanine include Cortinarius gentilis, Cortinarius rainierensis, andCortinarius splendens henrici; however, there are very few confirmed cases ofCortinarius -induced renal failure in North America (Judge 2010).
Psilocybin and psilocin are elaborated by a number of mushroom genera, includingPsilocybe cubensis, Psilocybe semilanceata (Liberty cap) , Panaeolus cyanescens(previously referred to as Copelandia species), Gymnopilus spectabili (Big Laughing Jim), Conocybe cyanopus, Psathyrella foenisecii, and several species of Pluteus. Psilocybin and psilocin are serotonin (5-HT2) agonists and, when ingested, cause psychedelic effects similar to those of lysergic acid diethylamide (LSD).
Mushrooms that contain muscarine are commonly found in yards, parks, and wooded areas throughout the United States, Europe, and Asia. Species from the genera Clitocybe and Inocybe (see the images below) are most commonly responsible for muscarinic mushroom poisoning in the United States. Clitocybe dealbata (the sweating mushroom) may be confused with the edible fairy ring champignon (Marasmius oreadus) or sweetbread mushroom (Clitopilus prunulus). Other muscarine-containing mushrooms include species from the genera Boletus, Mycena, and Omphalotus. Muscarine stimulates M1 and M2 types of postganglionic cholinergic receptors (muscarinic receptors) in the autonomic nervous system. This action results in parasympathetic stimulation similar to that caused by the release of endogenous acetylcholine at postganglionic receptors of smooth muscle and exocrine glands.
Muscarine-containing mushrooms typically produce cholinergic symptoms such as sweating, facial flushing, salivation, lacrimation, vomiting, abdominal cramps, diarrhea, urination, and miosis; occasionally, bradycardia, hypotension, and dizziness develop (Benjamin 1995).
There are no specific antidotes available for muscarinic mushroom toxicity. As in this report, patients with severe symptoms and signs may require atropine, hemodynamic monitoring and aggressive fluid management for the reversal of symptoms (Stallard and Edes 1989, Diaz 2005b, Goldfrank 2011, Erguven 2007). George and Hegde studied Muscarinic Toxicity Among Family Members After Consumption of Mushrooms and reported that patients with muscarinic mushroom toxicity have early onset of symptoms and they respond well to atropine and symptomatic supportive care (George and Hegde 2013).
5.6. Muscimol and Ibotenic Acid:
Amanita muscaria (fly agaric) and Amanita pantherina (panthercap) mushrooms synthesize ibotenic acid and muscimol, both of which are excitatory neurotoxins and may be mildly hallucinogenic.
Ibotenic acid is structurally similar to glutamic acid and acts as an agonist at the glutamic acid receptors (NMDA receptors) in the CNS.
A few species of mushrooms, including Coprinopsis atramentaria (formerly known as Coprinus atramentarius), commonly referred to as inky cap or tipplerâs bane and mistaken for the edible Coprinus comatus (shaggy mane), produce coprine, an amino acid that is metabolized to 1-aminocyclopropanol in the human body. This metabolite blocks acetaldehyde dehydrogenase, and in the presence of alcohol, acetaldehyde builds up, resulting in a disulfiram reaction.
Other nephrotoxic mushrooms, such as Amanita smithiana and Amanita proxima,have also been associated with an acute oliguric renal failure. Amanita smithianamay be mistaken for the matsutake mushroom (Tricholoma magnivelare) by foragers. These mushrooms cause vomiting and diarrhea 1-12 hours after ingestion, followed by a transient elevation of transaminases, then oliguric renal failure in 3-6 days.
5.9. Bronchoalveolar Allergic Syndrome:
An immune reaction is believed to be the cause of the bronchoalveolar allergic syndrome seen after inhalation of spores of some puffball (Lycoperdon) mushroom species.
Ingestion of Paxillus involutus may result in the acute onset of abdominal pain, nausea, vomiting, and diarrhea within 30 minutes to 3 hours of ingestion, followed by an immune complex-mediated hemolytic anemia with hemoglobinuria, oliguria, anuria, and acute renal failure.
5.11. Gastro-Intestinal Toxins:
Hundreds of mushrooms contain toxins that can cause Gastro-Intestinal symptoms (eg, nausea, vomiting, diarrhea, and abdominal pain) similar to those observed with more dangerous mushrooms. They include Chlorophyllum molybdites (green gill), Boletus piperatus (pepper bolete), and Agaricus arvensis (horse mushroom), among many others.
5.12. Erythromelalgia Syndrome:
Two species of mushrooms, Clitocybe acromelaga (in Japan) and Clitocybe amoenolens (in Europe), cause a painful burning sensation with reddening of the skin several days after eating them. In Europe, the Clitocybe amoenolens mushroom has been mistaken for the edible mushroom Lepista inversa. The suspected toxin is acromelic acid A.
Aflatoxins are naturally occurring mycotoxins that are produced by Aspergillus flavus and Aspergillus parasiticus, species of fungi. The name, aflatoxin, was created around 1960 after the discovery that the source of “Turkey ‘X’ disease” was Aspergillus flavus toxins (Wannop 1961). Aflatoxins are toxic and among the most carcinogenic substances known (Hudler 1998). After entering the body, aflatoxins may be metabolized by the liver to a reactive epoxide intermediate or hydroxylated to become the less harmful aflatoxin M1. The main feed sources of aflatoxins are peanut meal, maize and cottonseed meal. Many researchers reported that there was a linear relationship between the amount of aflatoxin M1 in milk and aflatoxin B1 in feed consumed by animals (Bakirci 2001).
At least 14 different types of aflatoxin are produced in nature (Boutrif 1998). Aflatoxin B1 is considered the most toxic and is produced by both Aspergillus flavus and Aspergillus parasiticus. Aflatoxin G1 and G2 are produced exclusively by A. parasiticus. While the presence of Aspergillus in food products does not always indicate that harmful levels of aflatoxin also are present, it does imply a significant risk in consumption. Aflatoxins M1, M2 originally were discovered in the milk of cows that fed on moldy grain. In addition to aflatoxins B1 and B2, A. flavus also produces many other mycotoxins such as cyclopiazonic acid, kojic acid, beta-nitropropionic acid, aspertoxin, aflatrem and aspergillic acid (Goto 1996).
The fungus A. flavus is a weak and opportunistic plant pathogen, affecting many agricultural crops such as maize (corn), cotton, groundnuts (peanuts), as well as tree nuts such as Brazil nuts, pecans, pistachio nuts, and walnuts. Preharvest contamination of these crops with aflatoxins is common. A. flavus also causes the spoilage of post harvest grains during storage. Because A. flavus lacks host specificity (St Leger 2000), it can attack seeds of both monocots and dicots, and seeds produced both above ground (corn) as well as below the ground (peanuts). Under weather conditions favorable for its growth, A. flavus can cause ear rot on maize, resulting in significant economic losses to farmers (Richard 2003, Robens and Cardwell 2003, Robens and Cardwell 2005).
Aflatoxin B1 has been associated with child growth impairment (Gong et al. 2002, Gong et al. 2004, Shouman et al. 2012), suppressed immune function (Turner et al. 2003), hepatomegaly (Gong et al. 2012), and death due to acute poisoning (Probst et al. 2007).
6.1. Factors Affecting Aflotoxins Biosynthesis:
Many biotic and abiotic environmental factors influence aflatoxin biosynthesis (Bennett 1988, Kale 1996, Kale 1991, Yabe 1988, Demain 1988) including nutritional factors such as carbon and nitrogen source; environmental effects such as water activity and temperature; physiological conditions such as pH (Cotty 1988) and bioreactive agents (Payne 1988, Guo 2005).
The best-known nutritional factors affecting aflatoxin biosynthesis are carbon and nitrogen sources (Adye and Mateles 1964, Bennett 1979, Luchese and Harrigan 1993). The relationship of carbon source and aflatoxin formation has been well established. Simple sugars such as glucose, sucrose, fructose, and maltose support aflatoxin formation, while peptone, sorbose, or lactose does not (Payne 1998, Buchanan and Lewis 1984). Woloshuk et al. reported the connection between alpha amylase activity and aflatoxin production in A. flavus (Woloshuk 1997).
Nitrogen is closely linked to aflatoxin production (Payne 1998). Asparagine, aspartate, alanine, ammonium nitrate, ammonium nitrite, ammonium sulfate, glutamate, glutamine, and proline containing media support aflatoxin production; while sodium nitrate and sodium nitrite containing media do not (Davis 1967, Reddy 1871, Reddy 1979). Nitrate was reported to have a suppressive effect on aflatoxin production, and overexpression of aflR gene by additional copies of aflR overcomes the negative regulatory effect on aflatoxin pathway gene transcription (Chang 1973).
Aflatoxin formation is directly affected by temperature Optimal aflatoxin production is observed at temperatures near 30 Â°C (28 Â°C to 35 Â°C). When temperature increases to above 36 Â°C, aflatoxin production is nearly completely inhibited (Schroeder and Hein 1968, Diener and Davis 1970, Roy 1989, OBrian 2007).
The conditions of high humidity and warm temperatures can give rise to the highest levels of aflatoxins in food (Adams and Moss 2005). They are toxic, immunosuppressive, mutagenic, teratogenic and carcinogenic compounds to animals and humans (Piva et al. 1995, Peraica et al. 1999, Kocabas and Sekerel 2003).
Aflatoxin biosynthesis in A. flavus occurs in acidic media, but is inhibited in alkaline media (Cotty 1988).
Severe aflatoxin outbreaks in corn have been documented to occur under hot weather and drought conditions (Sanders 1984, Cotty 2007) . The possible scenarios may include a combination of these factors: (I) the plant defense mechanism is weakened under water stress conditions; (II) higher insect feeding and associated injuries to plant tissues, thus providing entry opportunities for fungal invasion; and (III) more fungal spores dispersed into the air under dry climate.
6.1.6. Oxidative Stress Condition:
Oxidative stress and aflatoxin biosynthesis are related in A. parasiticus (Jayashree 2000a, Mahoney and Molyneux 2004, Kim 2006, Reverberi 2006). Oxidative stress induces aflatoxin formation in A. parasiticus (Jayashree 2000b). Treatment of A. flavus with tert-butyl hydroperoxide, or gallic acid induced significant increases in aflatoxin production (Kim 2006). Similar treatment of A. parasiticus also induced aflatoxin production (Reverberi 2006, Reverberi 2005). Hydrolysable tannins significantly inhibit aflatoxin biosynthesis, with the main anti-aflatoxigenic constituents in these tannins being gallic acid (Mahoney and Molyneux 2004).
6.1.7. Development Stage:
Sporulation and sclerotial formation are associated with secondary metabolism (Bennett 1986, Chang 2002, Hicks 1997, Calvo 2002). Spore formation and secondary metabolite formation occur at about the same time (Trail 1995, Hicks 1997). Some mutants that are deficient in sporulation are unable to produce aflatoxins (Bennett 1988) and some compounds that inhibit sporulation in A. parasiticus also inhibit aflatoxin formation (Reib 1982).
6.1.8. Plant Metabolites:
Plant metabolites play some role on aflatoxin formation (Zeringue and Bhatnagar 1993, Zeringue 1996, Zeringue 2002, Greene-McDowelle 1999). Wright et al. reported that, at certain conditions, n-decyl aldehyde reduces not only fungal growth of A. parasiticus but also aflatoxin production by over 95% compared with control (Wright 2000). The 13(S)-hydroperoxide derivative of linoleic acid, the reaction product of lipoxygenase (encoded by L2 LOX gene from maize), is reported to reduce aflatoxin production (Wilson 2001).
7. Pyrrolizidine alkaloids:
Pyrrolizidine alkaloids (PAs; sometimes referred to as necine bases) are a group of naturally occurring alkaloids based on the structure of pyrrolizidine. Pyrrolizidine alkaloids are produced by plants as a defense mechanism against insect herbivores. More than 660 PAs and PA N-oxides have been identified in over 6,000 plants, and about half of them exhibit hepatotoxicity (Radominska-Pandya 2010).
Aside from ingesting the plants directly, PAs may be consumed by eating honey collected by bees that visit PA-containing plants (mainly species of Senecio) and by drinking milk or eating eggs produced by animals that have consumed PA-containing plants. In honey originating from species of Senecio, the total concentration of PAs was 0.3-3.2 micrograms per kilogram. PAs could be detected in the concentration range of 30-70 micrograms per kilogram in honey from the Alpine foothills of Switzerland. No cases of PA poisoning have been attributed to ingestion of tainted honey or milk (Roder 1995). Eggs have been implicated as a source of PA toxicity in a case involving use of unregulated grain feed containing some Heliotropium (Edgar and Smith 2000).
The PAs, which have minimal toxicity in their original form, are metabolized in the liver and can become toxic metabolites, depending on the PA and on the particular condition of the liver enzymes (Huxtable and Cooper 2000). Pyrrolizidine alkaloids became an issue of safety concern in relation to herbal medicine about 20 years ago, when an herb enthusiast consumed comfrey (Symphytum officinale) on a daily basis and suffered liver damage (Stickel and Seitz 2000). A new concern arose with use of another popular herb: coltsfoot (Tussilago farfara). Coltsfoot was widely used for coughs in Europe and America, and has also been used by the Chinese for the same purpose. There was a report from Switzerland in 1988 of liver damage leading to death of a newborn due to consumption of coltsfoot tea by the mother during pregnancy (Roulet et al. 1988).
8. Phytohaemagglutinin (Red kidney bean poisoning):
Lectins are widely used reagents for the study of glycoconjugates in solution and on cells, and for cell characterization and separation (Sharon 2008). Next to this, lectins are also used as tools for novel techniques such as in a microarray for a high-throughput analysis of glycans and glycoproteins (Hu et al. 2012), and in new data-storing techniques, where carbohydrates are used as hardware for information coding (Gabius et al. 2011).
Phytohaemagglutinin (PHA, or phytohemagglutinin) is a lectin found in plants, especially legumes. PHA actually consists of two closely related proteins, called leucoagglutinin (PHA-L) and PHA-E. The letters E and L indicate these proteins agglutinate Erythrocytes and Leukocytes. Phytohaemagglutinin has carbohydrate-binding specificity for a complex oligosaccharide containing galactose, N-acetylglucosamine, and mannose (Hamelryck et al. 1996).
This form of food poisoning is a chemical intoxication and is apparently due to the presence of high levels of phytohaemagglutinins in the beans. Haemagglutinins (lectins) are proteins or glycoproteins, capable of binding to specific carbohydrate residues (Pusztai 1986), which have been detected in a wide variety of leguminous seeds including soybeans (Glycine max), lentils (Lens esculenta), lima beans (Phaseolus lunatus) and red kidney beans (Phaseolus vulgaris) (Liener 1974).
The main cause is a toxin called âphytohaemagglutininâ or kidney bean lectin. This is a sugar based protein (glycoprotein) which is found in many types of beans which includes cannellini beans and broad beans. But some of the highest concentrations of this toxin are found in red kidney beans. This toxin is killed if red kidney beans are cooked at a high enough temperature and for the right length of time. It is also important that red kidney beans are prepared correctly before use which means soaking them for at least 8 hours before hand.
These symptoms appear around 2 to 3 hours after the kidney beans have been eaten. However, it only takes a few beans to cause the following symptoms: Nausea,Vomiting, Diarrhoea, Abdominal pains. These symptoms appear soon after consumption but, they also disappear quickly as well.
Most cases resolve themselves within a few hours. But there have been cases which have required admittance to hospital. This is usually been due to the quantity of beans consumed and dehydration. Persistent vomiting or diarrhoea can result in a depletion of fluids, and electrolytes which need to be replaced. This can be done at home via an âoral re-hydrationâpowder which can be purchased at a local pharmacy (http://www.medic8.com/healthguide/food-poisoning/red-kidney-bean-toxins.html). Inactivation of the toxin in beans may be achieved by soaking overnight followed by boiling in fresh water for at least 10 min (Bender and Reaidi 1982). Heating beans at a lower temperature is reported to result in an increase in levels of lectin (Bender and Reaidi 1982), hence the observation that beans cooked at 82 Â°C (which were still palatable) were toxic whereas those cooked at 91 Â°C were not (Coffey et al. 1985).
Zacharko-Siembida et al. Studied and demonstrated that red kidney bean lectin increased the serotonin reservoir in the duodenum, and thus may be an effective stimulant of the gut maturation in suckling mammals (Zacharko-Siembida et al. 2014). Raw red kidney bean (RRKB) causes bacterial overgrowth of the small intestine due to the lectin phytohaemagglutinin (PHA) (Andrews et al. 1974, Banwell et al. 1983, Ramadass et al. 2010).
9.Grayanotoxins (Honey intoxication):
Grayanotoxins are a group of closely related toxins found in rhododendrons and other plants of the family Ericaceae. They can be found in honey made from their nectar and cause a very rare poisonous reaction called grayanotoxin poisoning, honey intoxication, or rhododendron poisoning (Demircan et al. 2009). Grayanotoxin I is also known asandromedotoxin, acetylandromedol, rhodotoxin and asebotoxin; the systematic chemical name is: grayanotaxane-3,5,6,10,14,16-hexol 14-acetate (Rahway 1983).
Its chemical structure has been fully elucidated as a diterpene, a polyhydroxylated cyclic hydrocarbon with a 5/7/6/5 ring structure that does not contain nitrogen (Tallent et al. 1957). More than 25 grayanotoxin isoforms have been isolated from Rhododendron (Qiang et al. 2011). Grayanotoxin 1 present in Rhododendron simsii (Poon 2008), has been reported from a case in Hong Kong while in the honey from Grouse Mountain, BC and Canada, which causes a similar type of poisoning, only grayanotoxins 2 and 3 were found (Yavuz et al. 1991). Currently, grayanotoxin 1 and 3 are thought to be the principal toxic isomers (Gunduz et al. 2008, Wong et al. 2002, Yavuz et al. 1991, Scott et al. 1971).
Plants contain numerous compounds that, when beneficial to humans, are categorized as ââmedicinalââ and when harmful they are termed ââpoisonousââ. Secondary products derived from plants, such as honey, can contain a number of chemical compounds that, depending on their concentration and application, can also be considered medicinal or poisonous (Viuda-Martos et al. 2008).
Clinical signs begin between several hours and one day following ingestion of the plant (Casteel and Wagstaff 1989). The observed signs are depression, severe drooling, vomiting, abdominal pain, tachycardia, dyspnea, weakness, muscle tremors, moaning, ataxia, recumbency, and opisthotonos (Armien et al.1995, Pereira et al. 2008). Gross lesions are nonspecifi c, and serous bleeding in the intestines, and aspiration pneumonia in two animals (Casteel and Wagstaff 1989, Armien et al.1995) were observed. It causes a sharp burning sensation in the throat and is thus also referred to as bitter honey (Gunduz et al. 2006).
Spontaneous poisoning cases generally occur in the winter, when the plant is green and when other forages have dried up and are depleted. Accidental poisoning occurs when prunings or clippings are discarded within reach of animals (Casteel and Wagstaff 1989). Poisoning in humans has been associated with the consumption of “mad honey”, or honey containing grayanotoxin; Labrador tea; cigarettes; and various decoctions used in alternative medicine (Jansen et al. 2012).
The voltage-gated sodium channels of the neurons are most likely a prominent target of grayanotoxins. In animal studies, Onat et al. found that injecting a small dose equivalent to 50 mg of honey intracerebroventricularly in anaesthetized albino rats caused marked bradycardia and respiratory depression (Onat et al. 1991). Kim et al. reported grayanotoxin intoxication in three patients who ingested either blossom leaves or medicinal preparations made from Rhododendron species (Kim et al. 2000). Children that eat the plants are also at risk. A 9-year-old boy from Korea consumed about ten Rhododendron schlippenbachii flowers and, besides the common signs of grayanotoxin intoxication, presented with impaired consciousness and delirium 26 h later. All symptoms resolved completely after a further 17 h (Kim et al. 2008).
Naturally occurring toxins are harmful for human beings some of them were described in above. Shellfish poisoning occurs after ingestion of organisms contaminated by infectious agents or concentrated toxins. Toxins concentrated in the flesh of shellfish can produce syndromes that include paralytic shellfish poisoning, amnesic shellfish poisoning, diarrheic shellfish poisoning, and neurologic shellfish poisoning. Altogether, seafood toxins are responsible for about 4% of foodborne outbreaks. Grayanotoxins are present in many members of the Ericaceae plant family. Medicinal use of grayanotoxin is not well understood and care should be taken when consuming grayanotoxin containing herbal preparation. Finally concluded that naturally occurring toxins such as Ciguatera poisoning, Shellfish toxins (PSP, DSP, NSP, ASP, AZP), Scombroid toxin, Tetrodotoxin (Pufferfish), Mushroom toxins, Aflatoxins, Pyrrolizidine alkaloids, Phytohaemogglutinin (Red kidney bean poisoning), Grayanotoxin (Honey intoxication) are harmful for human health and causes various diseases in humans, before taking above please aware and take care about its disease causing effects.
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