Cyanotoxin
Cyanotoxins are toxins produced by cyanobacteria (also known as blue-green algae). Cyanobacteria are found almost everywhere, but particularly in lakes and in the ocean where, under high concentration of phosphorus conditions, they reproduce exponentially to form blooms. Blooming cyanobacteria can produce cyanotoxins in such concentrations that they can poison and even kill animals and humans. Cyanotoxins can also accumulate in other animals such as fish and shellfish, and cause poisonings such as shellfish poisoning.
Some of the most powerful natural poisons known are cyanotoxins. They include potent
The first published report that blue-green algae or cyanobacteria could have lethal effects appeared in Nature in 1878. George Francis described the algal bloom he observed in the estuary of the Murray River in Australia, as "a thick scum like green oil paint, some two to six inches thick." Wildlife which drank the water died rapidly and terribly.[4] Most reported incidents of poisoning by microalgal toxins have occurred in freshwater environments, and they are becoming more common and widespread. For example, thousands of ducks and geese died drinking contaminated water in the midwestern United States.[5] In 2010, for the first time, marine mammals were reported to have died from ingesting cyanotoxins.[6]
Background
Cyanobacteria are considered the most primitive groups of
A range of toxic
It has been assumed that cyanotoxins play an important role in
Cyanotoxins are produced by
Cyanobacteria are found almost everywhere; in oceans, lakes and rivers as well as on land. They flourish in Arctic and Antarctic lakes,[22] hotsprings[23] and wastewater treatment plants.[24] They even inhabit the fur of polar bears, to which they impart a greenish tinge.[25] Cyanobacteria produce potent toxins, but they also produce helpful bioactive compounds, including substances with antitumour, antiviral, anticancer, antibiotic and antifungal activity, UV protectants and specific inhibitors of enzymes.[26][27]
Harmful algal blooms
Cyanotoxins are often implicated in what are commonly called
While some of these blooms are harmless, others fall into the category of harmful algal blooms, or HABs. HABs can contain toxins or pathogens which result in fish kill and can also be fatal to humans.[29] In marine environments, HABs are mostly caused by dinoflagellates,[30] though species of other algae taxa can also cause HABs (diatoms, flagellates, haptophytes and raphidophytes).[31] Marine dinoflagellate species are often toxic, but freshwater species are not known to be toxic. Neither are diatoms known to be toxic, at least to humans.[32]
In freshwater ecosystems, algal blooms are most commonly caused by high levels of nutrients (eutrophication). The blooms can look like foam, scum or mats or like paint floating on the surface of the water, but they are not always visible. Nor are the blooms always green; they can be blue, and some cyanobacteria species are coloured brownish-red. The water can smell bad when the cyanobacteria in the bloom die.[29]
Strong cyanobacterial blooms reduce visibility to one or two centimetres. Species which are not reliant on sight (such as cyanobacteria themselves) survive, but species which need to see to find food and partners are compromised. During the day blooming cyanobacteria saturate the water with oxygen. At night respiring aquatic organisms can deplete the oxygen to the point where sensitive species, such as certain fish, die. This is more likely to happen near the sea floor or a thermocline. Water acidity also cycles daily during a bloom, with the pH reaching 9 or more during the day and dropping to low values at night, further stressing the ecosystem. In addition, many cyanobacteria species produce potent cyanotoxins which concentrate during a bloom to the point where they become lethal to nearby aquatic organisms and any other animals in direct contact with the bloom, including birds, livestock, domestic animals and sometimes humans.[32]
In 1991 a harmful cyanobacterial bloom affected 1,000 km of the Darling-Barwon River in Australia[33] at an economic cost of $10M AUD.[34]
Chemical structure
Cyanotoxins usually target the nervous system (
Structure | Cyanotoxin | Primary target organ in mammals | Cyanobacteria genera |
---|---|---|---|
Cyclic peptides | Microcystins | Liver | Microcystis, Anabaena, Planktothrix (Oscillatoria), Nostoc, Hapalosiphon, Anabaenopsis |
Nodularins | Liver | Nodularia | |
Alkaloids | Anatoxin-a | Nerve synapse | Anabaena, Planktothrix (Oscillatoria), Aphanizomenon |
Guanitoxin | Nerve synapse | Anabaena | |
Cylindrospermopsins | Liver | Cylindrospermopsis, Aphanizomenon, Umezakia | |
Lyngbyatoxin-a | Skin, gastro-intestinal tract | Lyngbya | |
Saxitoxin | Nerve synapse | Anabaena, Aphanizomenon, Lyngbya, Cylindrospermopsis | |
Aetokthonotoxin | white matter of the brain; toxicity to mammals not yet confirmed | Aetokthonos | |
Lipopolysaccharides | Potential irritant; affects any exposed tissue | All | |
Polyketides | Aplysiatoxins | Skin | Lyngbya, Schizothrix, Planktothrix (Oscillatoria) |
Amino Acid | BMAA
|
Nervous system | All |
Most cyanotoxins have a number of variants (
Cyclic peptides
A
Microcystins
As with other cyanotoxins, microcystins were named after the first organism discovered to produce them, Microcystis aeruginosa. However it was later found other cyanobacterial genera also produced them.[35] There are about 60 known variants of microcystin, and several of these can be produced during a bloom. The most reported variant is microcystin-LR, possibly because the earliest commercially available chemical standard analysis was for microcystin-LR.[35]
Blooms containing microcystin are a problem worldwide in freshwater ecosystems.
Nodularins
The first nodularin variant to be identified was
Globally, the most common toxins present in cyanobacterial blooms in fresh and brackish waters are the cyclic peptide toxins of the nodularin family. Like the microcystin family (above), nodularins are potent hepatotoxins and can cause serious damage to the liver. They present health risks for wild and domestic animals as well as humans, and in many areas pose major challenges for the provision of safe drinking water.[27]
Alkaloids
Anatoxin-a
Investigations into anatoxin-a, also known as "Very Fast Death Factor", began in 1961 following the deaths of cows that drank from a lake containing an algal bloom in Saskatchewan, Canada.[40][41] The toxin is produced by at least four different genera of cyanobacteria and has been reported in North America, Europe, Africa, Asia, and New Zealand.[42]
Toxic effects from anatoxin-a progress very rapidly because it acts directly on the nerve cells (
External videos | |
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Very Fast Death Factor University of Nottingham |
The toxin was called the Very Fast Death Factor because it induced tremors, paralysis and death within a few minutes when injected into the body cavity of mice. In 1977, the structure of VFDF was determined as a secondary, bicyclic amine alkaloid, and it was renamed anatoxin-a.[45][46] Structurally, it is similar to cocaine.[47] There is continued interest in anatoxin-a because of the dangers it presents to recreational and drinking waters, and because it is a particularly useful molecule for investigating acetylcholine receptors in the nervous system.[48] The deadliness of the toxin means that it has a high military potential as a toxin weapon.[3]
Cylindrospermopsins
Cylindrospermopsin (abbreviated to CYN or CYL) was first discovered after an outbreak of a mystery disease on Palm Island in Australia.[49] The outbreak was traced back to a bloom of Cylindrospermopsis raciborskii in the local drinking water supply, and the toxin was subsequently identified. Analysis of the toxin led to a proposed chemical structure in 1992, which was revised after synthesis was achieved in 2000. Several variants of cylindrospermopsin, both toxic and non-toxic, have been isolated or synthesised.[50]
Cylindrospermopsin is
Saxitoxins
Saxitoxin has been used in molecular biology to establish the function of the
Aetokthonotoxin
Vacuolar myelinopathy is characterized by widespread vacuolization of the myelinated axons (intramyelinic edema) in the white matter of the brain and spinal cord. Clinical signs of the intoxication include the severe loss of motor functions and sight. Affected birds fly into objects, lack coordination in swimming, flying and walking, develop tremors of the head and lose their responsiveness. As the toxin has been shown to bioaccumulate, there is concern that it might also be a threat to human health.[58] However, toxicity to mammals has yet to be confirmed experimentally.
Lipopolysaccharides
Lipopolysaccharides are present in all cyanobacteria. Though not as potent as other cyanotoxins, some researchers have claimed that all lipopolysaccharides in cyanobacteria can irritate the skin, while other researchers doubt the toxic effects are that generalized.[61]
Amino acids
BMAA
The non-proteinogenic amino acid
Gallery
Other cyanotoxins:
-
Guanitoxin
-
Aplysiatoxin
See also
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External links
- Cyanosite - A Webserver for Cyanobacterial Research, Purdue University.
- Dangers of toxic algae Environment Canterbury Updated 31 October 2009. Retrieved 23 January 2011.