Impact of Cyanobacteria Toxins

Impact of gruesome-green algae ToxinsIntroduction blue-green algae, or besides known as blue-green algae is wizard of the bacteria phylum. It was classified as blue-green algae be go it resembles eukaryotic green algae. Cyanobacteria be photosynthetic prokaryotes which start out the talent to synthesize chlorophyll a. Chlorophyll a primarily absorbs most red and blue light, which aloneow blue-green algae to obtain energy. This energy was then used to synthesize carbohydrate from carbon dioxide and pissing. Water is used as electron donor during the photosynthesis influence and produces oxygen as a byproduct. Thus, the ability of cyanobacteria down the stairswent the process of photosynthesis trioing to the evolution of oxygen as they play an important lineament in increasing the amount of oxygen in Earth. Besides, cyanobacteria in any carapace called blue-green algae because of its ability to bounce the phycobilin paint (phycocyanin). Phycocyanin is an accessory pigment where it works in conjunction with chlorophyll a. Phycocyanin pigment is the one that stool bluish colour to cyanobacteria. According to Dittmann and Wiegand (2006), the lyses of a cyanophyte bloom head ups to stop of noble amounts of blue pigmented. However, the colour sewer degrade under chink of laid-back exposure to light and heat (Jespersen et al., 2005).Because cyanobacteria argon prokaryote, it is ordinaryly small and uni prison cellular. Usually individual cyanobacteria ar round, oval, globular or string-like in shape. However, cyanobacteria often growth in colonies and, thus atomic number 18 large and advantageously to view. These colonies atomic number 18 built of m any layers and can form filaments, sheets or even hallow ball depend on its species and environmental condition. Cyanobacteria begin been classified into five groups based on their morphologies. in that respect argon chrooccales (I), pleurocapsales (II), oscillatoriales (III), nostacal es (IV) and stigonematales (V). Group l is unicellular cyanobacteria that divide by binary fusion or budding, piece of music group II is unicellular form that divide by multiple fission. Then, group III is ropy colonies that reproduce by trichome breakage (Henson, 2002). However, only groups IV and V are supported by phylogenetic studies and make up the heterocystous cyanobacteria. They arrive the ability to fix Nitrogen such as genera of Anabaena, Nostoc, and etc.Cyanobacteria are extremely successful organism that can adapt in any condition depend on its species. The fossil record shows their existence since 3.5 one thousand million years ago and it are palliate around. According to Hitzfeld et al. (2000), the cyanobacteria inhabitants set forth from hot springs to temporary frozen ponds in Antarctica. Cyanobacteria are gravitational constant negative that has cell jetty made up of pepti weenielycan and lipopolysaccharide layers that surrounded by gelatinous and mucilagi nous sheath. The presence of the gelatinous sheath whitethorn sponsor in survival of cyanobacteria during extreme conditions and desiccation (Duy et al., 2000). Cyanobacteria for the most part free-base in brackish, fresh peeing, rivers, lakes, ponds and some reservoirs. They normally live in such condition to feel access of piddle and sunlight, as they do the photosynthesis process. The high accumulation of cyanobacteria is collect to nutritious enrichment (eutrophication). The eutrophication is the process of irrigate bodies gets the wasted of nutrient and this promotes extremely growth of cyanobacteria. This nutrient may come from umpteen sources, such as fertilizers applied to agriculture, erosion of soil containing nutrients and etc. The repletion of nutrient mavin to massive population of cyanobacteria, include the blooms, scums, and mats and biofilms (Codd et al., 2005). The existence of cyanobacteria bloom can reduce dissolved oxygen in water and may cause othe r(a) aquatic organisms died. Alperdoorn et al. (2007) suggest that complex fundamental interaction of high c one timentration of nutrients, sunlight, warm temperature, turbidity, pH, conductivity, salinity, carbon availability and slow-flowing stagnant water are snarly in production of blooms. Besides, the bloom of cyanobacteria is think with toxins judgment of dismissald.Purpose of studyThe purpose of study is to analyze the type of toxins produced by bloom of cyanobacterial. Growth of cyanobacteria bloom is favored by nutrient enrichment. The increase of mass population of cyanobacteria will lead to high amount of toxin produced. Then, relate how these toxins act in order to affect tender and animals health.Objectives of studyProduction and mode of action of cyanobacteriaOccurrence of cyanobacterial toxins in affects creation and animals -example caseRoutes of exposureDiseases in Humans and Animals expiry further workProduction and mode of action of cyanobacteria toxinsProp erties of cyanobacterial toxins on that point are around 150 genera with about 2000 species of cyanobacteria has been recognized, as according to the current t axoneomy. However, out of them, only 40 genera collect been place to produce toxins (Hitzfeld et al., 2000). The toxins produced by bloom of cyanobacteria are some prison names called cyanotoxins. The genera that way out toxins from cyanobacteria bloom are include Microcystis, Anabaena, Anabaenopsis, Plankthothrix, Aphanizomenon, Cylindrospermopsis, Raphidiopsis and Nodularia (Codd et al., 2005). Cyanotoxins are classified into deuce grouped, where one is based on their modes of toxin affect the animals cells or cell system, and the other one is based on their chemic composition and dust mental synthesis (Codd et al.,1999). The set-back grouped are divided into quatern types, which are hepatotoxins, neurotoxins, cytotoxin and irritant toxins (Codd et al., 2005). However, the endorsement grouped is classify into three different chemic structure which are cyclic peptides, alkaloids and lipopolysaccharides (LPS) (Sivonen Jones 1999). The production of cyanotoxin are highly uncertain depends on time and an individual bloom itself. Besides, the arrangement of the genes and their expression under certain environmental condition as well as contribute in released the toxins.Hepatotoxins-cyclic peptidesHepatotoxins class has the chemical structure of cyclic peptides. These kinds of toxins are released by bloom of cyanobacteria that ranging from freshwater to oceans. Among the common hepatotoxins produced are mycrocystins and nodularins. Microcystin is first found in the early 1980 and isolated from Microcystis aeruginosa. Thus, the toxins were named as microcystin (Sivonen Jones 1999). Then, it was determine that microcystins also have been produced from the genera of Anabaena, Microcystis, Planktothrix, Nostoc and Anabaenopsis (Hitzfeld et al., 2000). Differ from microcystins, where nodularins o nly produced by the genera of Nodularia and were call as nodularins after its producer, Nodularia spumigena (Falconer 1998). twain are widespread cyanotoxins because the presence of atom smasher vesicle that provides buoyancy. Gas vesicles enable them to float up or discharge in order to get sunlight and reach the site of nutrient-rich layers (Dittmann Wiegand 2006). complete of nutrient and sunlight enable the cyanobacteria to undergo the photosynthesis process and lead to excess growth. Therefore, the cyanotoxins of microcystins and nodularins could be produce enormously and can disturb the ecosystemsMicrocystins are difference from nodularins based on their chemical structure of cyclic peptides. The chemical structures of microcystins have been identified as cyclic heptapeptides, while nodularins has chemical structure of cyclic pentapeptides (Codd et al., 1999). cyclic heptapeptides refer to microcystins that contain seven peptide-linked amino venomouss. There are five c ommon amino acids and another two L-amino acids are varied (Park et al., 1993). The five common amino acids are D-erythro--methylaspartic acid, D-alanine, N-methyldehydroalanine, D-glutamate and Adda-3-amino-9-methoxy-2, 6, 8-trimethyl- 10-phenyldeca-4, 6-dienoic acid. The variable L amino acids are located at position 2 and 4. The variable of L amino acids increased the variations in microcsytins structure and so farther on that point are about 70 geomorphologic variables have been identified (Codd et al., 2005). Besides that, demethylation of D-erythro--methylaspartic acid and N-methyldehydroalanine amino acids also give variation in microcystin structure. In contrast, only about 6 variant of nodularins structure have been recognized (Codd et al. 1999).Both microcystins and nodularins only release from cyanobacteria bloom once it was lyses. These toxins are potent inhibitors of eukaryotic protein phosphotases activity (Park et al., 1993). According to Codd et al, (2005), this in hibition can change the membrane integrity and causing tumor production and coloured damage. colorful is the briny targeting organ in this action of toxins.Neurotoxin-alkaloidsNeurotoxins contain the chemical structure of alkaloids. Alkaloids are chemical compound that contains any basic atomic number 7 atoms and produced by cyanobacteria. It cause deadly that act on nerve cell ( neuron).So far, three known families of neurotoxins are anatoxin-a, anatoxin-a(S) and saxitoxins. Anatoxin-a acts by mimic acetylcholine, while anatoxin-a(S) inhibit acetylcholinesterase. Next, saxitoxins which relatively associated with paralytic shellfish poisons (PSP) are works by block the sodium channels. These toxins have been reported found broadly speaking in realm of North America, Europe and Australia (Sivonen Jones 1999). Devlin et al. (1977), identified anatoxins-a as a thirdhand amine 2-acetyl-9-azabicyclo (4-2-1)non-2-ene. Anatoxin-a is usually released by Anabaena flos-aquae, Anabaena spp, Anabaena planktonica, Oscillatoria, Aphanizomenon and Cylindrospermum (Sivonen and Jones, 1999). This toxins cause symptoms such as fasciculation, gasping and convulsion, when transmission system occurred in animals (Mazur et al., 2003). In contrast, Anatoxin-a(S) is guanidine methyl phosphate ester and produced by Anabaena flos-aquae and Anabaena lemmermannii (Codd et al., 2005). However, its structure allay has not been recognized. Sanitoxins are group of carbonate alkaloids and about 20 of structural variations has been recognized (Codd et al., 2005). Sanitoxins are produced by species of Anabaena, Aphanizomenon, Cylindrospermopsis, Lyngbya, Planktothrix and Trichodesmium (Carmichael et al., 2001)Cytotoxin-alkaloidsCylindrospermopsin is the example of cytotoxin released and has been found in tropic and subtropical water such as in lakes, rivers and water fork out reservoir (Falconer 1998). According to Hitzfeld et al (2000) and Codd et al (1999), cylindrospermopsin cou ld also be categorized as hepatotoxins because it affects colorful damage. However, Codd et al (2005) and Falconer (1998) have categorized it under cytotoxin class because its action as an inhibitor of protein synthesis. This inhibition cause damage to interweave that rapidly synthesize protein such as pituitary gland, epithelia including gut lining, the pancreas, lymphoid tissue and the prostate gland, as well as the kidneys and colored (Falconer 1998). This toxin is also genotoxic, which can cause loss of chromosome and break of DNA strand (Humpage et al 2000). Cylindrospermopsin is a cyclic guanidine alkaloid and has been isolated mainly from cylindrospermopsis raciborskii and also from Aphanizomenon ovalisporum, Umezakia natans, Aphanizomenon flosaquae and Raphidiopsis curvata (Falconer and Humpage, 2006). spine toxinsIrritant toxins are usually related with skin irritant (dermatoxin). Aplysiatoxin and lyngbyatoxin is alkaloid structure and some(prenominal) are the most toxi ns that cause skin discomfort. Aplysiatoxin is produced by genera of Lyngbya, Oscillatoria and Schizothrix whereas Lyngbyatoxin is produced by Lyngbya (Codd et al 1999). Aplysiatoxin also is potent tumour promoters and Lyngbyatoxin also caused implike verbal and GI inflammation (Sivonen and Jones, 1999). LPS endotoxin released by cyanobacteria is less potent than released by bacteria, such as Salmonella (Codd et al 1999). LPS is localized at outer membrane wall of cyanobacteria and contain lipid A that liable for much of perniciousness of cyanobacteria. LPS endotoxin in cyanobacteria is produced by Microcystis, Oscillatoria and Anabaena (Codd et al 1999). The signs and symptoms of this toxin are fever, rigors, headache, nausea, mild amnesia and diarrhea (Stewart et al., 2006). According to Codd et al (2005), it may contribute to inflammatory and gastrointestinal incidents.ToxinChemical structureProducer GeneraPrimary target organHepatotoxinsMicrocystinsCyclic heptapeptidesMi crocystis, Anabaena, Planktothrix, Nostoc AnabaenopsisLiverNodularinsCyclic pentaptidesNodulariaLiverNeurotoxinsAnatoxin-aAlkaloidsAnabaena, Oscillatoria and Aphanizomenon, Cylindrospermum MicrocystisNerve synapseAnatoxin-a(s)AlkaloidsAnabaenaNerve synapseSaxitoxinsAlkaloidsAphanizomenon, Anabaena, Lyngbya CylindrospermopsisNerve axonCytotoxinsCylindrospermosinCyclic guanidine alkaloidsCylindrospermopsis, Aphanizomenon, Umezakia RhapidiopsisTissue damage include liver and kidneyIrritant toxinsLyngbyatoxinAlkaloidsLyngbyaSkin, GI tractAplysiatoxinAlkaloidsLyngbya, Oscillatoria SchizothrixSkinEndotoxinsLPSMicrocystis, Oscillatoria AnabaenaPotential irritant affect any overt tissuesTable 1 Updated from Codd et al. (1999) and Sivonen Jones (1999). This shows the summaries of general features of cyanotoxins.Occurrence of cyanobacterial toxinsThe cases of cyanotoxins affect creation and animals have been reported occurred throughout the world. This include part of Europe (such as Belgium, France, Ger many another(prenominal) a(prenominal), UK, etc), America (at least 27 states), Middle East and Asia (such as Bangladesh, Saudi-Arabian Arabia, Thailand), Australasia (such as Australia, New Zealand), Africa (Botswana, Morocco) and also Marine Atlantic Ocean (Baltic Sea, Caribbean sea) and Antarctica (McMurdo scratch Shelf) (Codd et al., 2005). From the case reported, cyanatoxins affect animals, include wild and domestic mammals, birds, amphibians and fish, while forgivings cases ranging from groovy to chronic (Hitzfeld et al., 2000).The first case of cyanotoxins occurred in animals was the death of cows, sheep, dogs, horses and pigs. This took located in Lake Alexandrina, Australia in 1878. The death of these animals was delinquent to drink the water that contains a scum of Nodularia spumigena (Francis, 1878) . After this case, numerous cases have been reported and most commonly involved death of farm animals after drink the contaminate water with cy anobacterial bloom (Hitzfeld et al., 2000). For example, in 1991 the death of sheep has been recorded in near River, Australia. This death occurred after drink from a farm dam contaminated with saxitoxins, released by Anabaena circinalis (Goodman et al., 1999). Besides, the cases of dog deaths after go in, or eating, cyanobacteria also occurred. In 1992, death of dogs at Loch Insh, Scotland happened after swimming was collectible to release of Anatoxin-a by Oscillatoria sp. into the water (Edwards et al., 1992).Among the earliest reported cases involving acute effect in man was a series of town along the Ohio River, US in 1931. It start when the water of a side branch of the river develop a cyanobacteria bloom because of low rainfall. This water was then washed into the main river and caused a series of gastroenteritis once it moves downstream (Tisdale 1931). However, the toxins caused this outbreak is undiagnosed and the organism that released this toxins was unspecified. The n, another case involving the same pathologic, (gastroenteritis) was reported in Harare, Zimbabwe in 1966. This time Microcystis aeruginosa was the one that has been identified trustworthy in this case, but the toxins released was still not known (Hitzfeld et al., 2000). Children living in this area developed gastroenteritis each year as they use the water reservoir which contains a natural bloom of Microcystis (Zilberg 1966).The case of chronic effects in humans may be collapse due to short exposure to toxins (Goodman et al., 1999). The relative incidence in China, 1995 due to microcystins have lead to chronic of liver injury, hepatocellular carcinoma. This is un puzzleatic cancer of the liver and most are secondary to hepatitis B tarnishion. From the case analyzed, cyanobacteria are abundant in surface waters of federation east China, where the incidence of hepatocellular carcinoma is highest. Thus, it has been concluded that microcystins in the drinking water are responsib le for the increased of liver cancer (Falconer 1998).Compare to all cyanotoxins, cyclic peptides (mostly microcystins) has high risk because of their potential to develop diseases in long term time, even when exposed to low concentration of cyanotoxins. This was confirmed after examined all the cases reported, where the major injury is hepatotoxicosis, cause liver damage. In contrast, neurotoxin mostly shows acute effect in mammals (Goddman et al., 1999).Routes of exposureThere are many ways where humans and animals can be exposed to cyanotoxins. From the cases reported, animals usually infected by cyanotoxins orally via drinking contaminated water. For instance, the case reported of cattle deaths in Alpine Lakes, Switzerland (1974-1994). The cattle died because of liver damage after drinking the water which contains bloom of cyanobacteria (Hitzfeld et al., 2000). Besides, human can get transmittal of cyanotoxins during the recreational activity involving direct clutch with water such as swimming, canoeing and paddling (Apeldoorn et al., 2007). In 1989, UK, some of army recruits showed symptoms of infected by cyanotoxins after swimming and canoes training in water with dense bloom of Mocrocystis. The signs of symptoms were vomiting, diarrhea, blistering of the lips, unspeakable throat and central abdominal pain (Turner et al., 1990). The person that worked in the area of water such as boatmen and environmental scientists are also easily to get transmittal. According to Dittmann and Wiegand (2006), the consumption of blue green algae containing intellectual nourishment and dietary supplements, such as pills or capsules, also can lead to gain the toxicity of cyanobacteria.According to Codd et al (1999), there are four routes of exposure where human can get infection of cyanotoxins (Table 2). The first one is via oral routes, taken by ingestion during recreational activity, drinking water, sustenance and dietary supplements that contain dried cyanotoxins. The oral route has caused the outbreak of many diseased, such as gastroenteritis and hepatoenteritis after drinking water (Codd et al 1999). Infection by pulmonary route occurs either by inhalation of cyanobacteria bloom during recreational activity or work practices in industrial spray water (Codd et al., 1999). Next, dermal route is associated with skin or mucosal affair the contaminated water. This can lead to skin irritation and hypersensitised reaction. Lastly, hemodialysis route can occurred via water used in haemodialysis treatment. Among the cases of this route, is the case of major fatal incident at haemodialysis clinic in Caruaru, brazil nut. This case happened in 1996, where the patients with dialysis treatment were treated with water from local reservoir. All patients experienced symptoms of nausea, vomiting, muscle weakness and painful hepatomegaly. Then, these patients developed acute liver failure and acute neurotoxicity signs. From all the treated patients, 60 ha ve been recorded as dead. Microcystins released by Aphanizomenon and Oscillatoria have been recognized as the toxins that responsible for this death (Codd et al., 1999).Exposure route Exposure mediumOral (ingestion) drinking water, recreational water, food (shellfish, finfish if toxin if toxin accumulationhas occurred during production), dietary supplements (pills, capsules) if contains driedcyanobacterial cells with toxins. pneumonic(inhalation, aspiration) water aerosols, spray during recreation, work, showeringDermal water during recreation, work, showering(skin, mucosal contact)Haemodialysis water used for haemodialysisTable 2 Taken from Codd et al., 2005. This figure summaries the human exposure route and exposure medium for cyanotoxins.Diseases in Animals and HumansHepatoenteritis Liver damageHepatoenteritis is described as hepatitis-like illness, where associated with liver problem. This diseased can infect both human and animals. The outbreak of hepatoenteritis disease was reported in 1979 and occurred in Palm Island of the Queensland, Australia. Thus, this case also name as Palm Island conundrum Disease because the water drinking is supply from Palm Island reservoir (Ohtani et al., 1992). probe have shown that the reservoir contain the bloom of Cylindrospermopsis raciborskii. This species released cylindrospermopsin and responsible for developed of severe hepatoenteritis among the 140 children and 10 adults. The common symptoms of this disease are malaise, anorexia, vomiting, painful liver enlargement, dehydration and bloody diarrhea. This toxin is very water soluble and infect into body by oral route via drinking water. According to Falconer and Humpage (2006), the implement of action for cylindrospermopsin is relatively slow. It work by inhibit protein synthesis at ribosome during the peptide chain elongation step. Besides, the toxins also released CYP450 oxidation that work to inhibit the glutathione synthesis. Both inhibitions caused major cha nges in liver, particularly hepatocytes. First, accumulation of ribosomes in the cytoplasm of hepatocytes and followed by membrane proliferation. Next, the accumulation of lipid in the central portion of liverwort lobules and all this lead to severe liver necrosis (Duy et al., 2000). Kidney, lung, heart, spleen and thymus also major power be affects.The toxins of microcystins are majorly involved in liver damage. Most of microcystins types are hydrophilic and thus, not able to penetrate craniate cell membrane. It only can uptake into cell membrane via transporter. at a time the microcystins are uptake by mammals, it is transport into the blood from the ileum via bile acid type transporter, that present in hepatocytes (Apeldoorn et al 2007). As a result, the present of microcystins is higher in liver due to active uptake by hepatocytes. Once in spite of appearance the hepatocytes, microcystins act as potent inhibitor of eukaryotic protein phosphatases 1 and 2A. These inhibitions cause changes in cytoskeletal proteins, and thus results in deformation of hepatocytes. The liver may undergo changes in term of a disruption of hepatocytes structure due to damage of cytoskeleton, loss of sinusoidal structure, increased in liver cant over because of intrahepatic haemorrhage, heart failure and death.GastroenteritisGastroenteritis is inflammation of the gastrointestinal tract, where involved stomach and intestine. This diseased can be cause by infection from cyanobacteria bloom of Microcystis sp and Anabaena sp. Acording to Hitzfeld et al (2000), the cases of gastroenteritis that have been recorded due to cyanobacteria bloom were occured in Ohio River, US (1931), Harare, Zimbabwe (1966) and Itaparica Dam, Brazil (1993). However, the toxins that responsible for this diseased still remain unknown because lack of available toxin analysis order and knowledge of candidate toxins at the time (Codd et al., 1999).Recently, there is case where LPS endotoxin is responsible for gastroenteritis incidents (Codd et al., 2005). Gastroenteritis is categorized under acute effect and mostly results in diarrhea. Besides, the symptoms shows are nausea and vomiting, loss of appetite, fever, headaches and abnormal pain.Respiratory problemNeurotoxins effects can lead to progressive paralysis and death because of respiratory failure. The case of livestock death in Europe and the US have been reported due to anatoxin-a, released from the genera of Oscillatoria, Aphanizomenon and Anabaena (Falconer, 1998). Anatoxin-a acts as a potent postsynaptic depolarizing neuromuscular block up agent, where it binds to neuronal nicotinic acetylcholine receptors of neuromuscular junction (Goodman et al., 1999) .This cause postsynaptic sodium channel of neuron is remain open and lead to continuous stimulation of sodium ion inflow and continuously generates action potential. Consequently, the muscle contraction is over react and might be followed by fatigue and respiratory failure (Dittmann and Wiegand, 2006). This toxin can cause rapidly death depending on the species and amount of toxin ingested. The clinical sign of this infection are muscle fasciculation, decreased movement, abdominal breathing, cyanosis, and death by respiratory failure. Saxitoxins are another type of neurotoxins that can infect both human and animals. As bring up before, the case of Darling River in Australia (1990-1991) involved the deaths of sheep and cattle due to saxitoxins. Then, in human, saxitoxins have been the cause of paralytic shellfish inebriety (PSP). Saxitoxins acts as a blocking agent of sodium channel in nerve axons. In mammals, this induces muscle paralyzed (respiratory muscle) and can follow by death due to respiratory failure (Apeldoorn et al., 2007).Skin irritation and allergicLyngbya majuscula is one of the cyanobacteria that released aplysiatoxin and lyngbyatoxin. These toxins act as potent skin tumour promoters. Both toxins, especially aplysiatoxin, cause skin i rritation after contact with bloom of Lyngbya majuscula. Swimmers of Hawaii and Okinawa got acute dermatitis (causing itch), erythematous wheals and desquamation after contact with Lyngbya majuscule (Codd et al., 1999). Besides, symptoms have included rashes, blisters, allergic reaction, asthma, conjunctivitis, and eye irritation.ConclusionThe increment of cyanobacterial bloom tends to be favored by nutrient enrichment (eutrophication). Therefore, plenty nutrients will provide extremely growth of cyanobacteria bloom and thus, lead to high production of cyanotoxins once it is lyses. The most clearly study of toxins is microcystins due to widespread of its production among the cyanobacteria blooms. Besides, their existences that usually can be found in lakes, rivers and water supply reservoirs also lead to increased the feel to affect humans and animals health compare to the other toxins. As mention above, there are four routes where infection of cyanotoxins could occurs, which are by oral route, dermal route, pulmonary route and lastly via haemodialysis route. Once the toxins get inside humans and animals, they will start reacts and disturb the system inside the body according to its modes of actions. Therefore, it leads to outbreak of many diseased such as hepatoenteritis, gastroenteritis, respiratory problem and skin irritation and allergic.However, till now there are some mechanism of toxins that still not understood, such as lyngbyatoxins (Goodman et al., 1999).Then, further work also need to be done in order to solve the cases of unknown toxic affect humans and animals that have been recorded. For example, the case of the outbreak of gastroenteritis diseased occurred in Ohio River, US (1931), Harare, Zimbabwe (1966) and Itaparica, Dam, Brazil (1993), where no authentic toxins have been identified (Hitzfeld et al., 2000). All the features of cyanobacterial cell include their type of the toxins released and their mode of action is needed to understand cl early, in order to monitor and control their growth from continuously affect humans and animals. 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