Цианобактериялардың токсиндері және олардың қауіптері

Toxin produced by cyanobacteria

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 neurotoxins, hepatotoxins, cytotoxins, and endotoxins. Despite the similarity in name, they are unrelated to cyanides. Exposure to cyanobacteria can result in gastro intestinal and hayfever symptoms or pruritic skin rashes. Exposure to the cyanobacteria neurotoxin BMAA may be an environmental cause of neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS), Parkinson's disease, and Alzheimer's disease. There is also an interest in the military potential of biological neurotoxins such as cyanotoxins, which "have gained increasing significance as potential candidates for weaponization." 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. 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. In 2010, for the first time, marine mammals were reported to have died from ingesting cyanotoxins. and possibly appeared on the Earth about 3.5 billion years ago. They are ubiquitous in nature and thrive in a variety of ecological niches ranging from desert to hot springs and ice cold water. Most cyanobacteria are an immense source of several secondary natural products with applications in the food, pharmaceuticals, cosmetics, agriculture, and energy sectors. Moreover, some species of cyanobacteria grow vigorously and form a dominant microflora in terms of their biomass and productivity in specific ecosystems. Bloom formations due to excessive growth of certain cyanobacteria followed by the production of toxic compounds have been reported in many eutrophic to hypertrophic lakes, ponds, and rivers throughout the world. Cyanotoxins may also take part in chemical signalling. and usually indicates any of a number of colours in the blue/green range of the spectrum. Cyanobacteria are commonly referred to as blue green algae. Traditionally they were thought of as a form of algae, and were introduced as such in older textbooks. However modern sources tend to regard this as outdated; they are now considered to be more closely related to bacteria, and the term for true algae is restricted to eukaryotic organisms. Like true algae, cyanobacteria are photosynthetic and contain photosynthetic pigments, which is why they are usually green or blue. Cyanobacteria are found almost everywhere; in oceans, lakes and rivers as well as on land. They flourish in Arctic and Antarctic lakes, hotsprings and wastewater treatment plants. They even inhabit the fur of polar bears, to which they impart a greenish tinge. 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.]] Cyanotoxins are often implicated in what are commonly called red tides or harmful algal blooms. Lakes and oceans contain many single celled organisms called phytoplankton. Under certain conditions, particularly when nutrient concentrations are high, these organisms reproduce exponentially. The resulting dense swarm of phytoplankton is called an algal bloom; these can cover hundreds of square kilometres and can be easily seen in satellite images. Individual phytoplankton rarely live more than a few days, but blooms can last weeks. 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. though species of other algae taxa can also cause HABs (diatoms, flagellates, haptophytes and raphidophytes). 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. In 1991 a harmful cyanobacterial bloom affected 1,000 km of the Darling Barwon River in Australia at an economic cost of $10M AUD.

Cyanotoxins usually target the nervous system (neurotoxins), the liver (hepatotoxins) or the skin (dermatoxins).

A peptide is a short polymer of amino acids linked by peptide bonds. They have the same chemical structure as proteins, except they are shorter. In a cyclic peptide, the ends link to form a stable circular chain. In mammals this stability makes them resistant to the process of digestion and they can bioaccumulate in the liver. Of all the cyanotoxins, the cyclic peptides are of most concern to human health. The microcystins and nodularins poison the liver, and exposure to high doses can cause death. Exposure to low doses in drinking water over a long period of time may promote liver and other tumours. Blooms containing microcystin are a problem worldwide in freshwater ecosystems. Microcystins are cyclic peptides and can be very toxic for plants and animals including humans. They bioaccumulate in the liver of fish, in the hepatopancreas of mussels, and in zooplankton. They are hepatotoxic and can cause serious damage to the liver in humans.

The first nodularin variant to be identified was nodularin R, produced by the cyanobacterium Nodularia spumigena. This cyanobacterium blooms in water bodies throughout the world. In the Baltic Sea, marine blooms of Nodularia spumigena are among some of the largest cyanobacterial mass events in the world. (Parts of nine industrialized countries drain into the Baltic Sea, which has little water exchange with the North Sea and Atlantic Ocean. It is consequently one of the more polluted bodies of water in the world (nutrient rich, from the perspective of cyanobacteria).) 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.

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. 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. Toxic effects from anatoxin a progress very rapidly because it acts directly on the nerve cells (neurons) as a neurotoxin. The progressive symptoms of anatoxin a exposure are loss of coordination, twitching, convulsions and rapid death by respiratory paralysis. The nerve tissues which communicate with muscles contain a receptor called the nicotinic acetylcholine receptor. Stimulation of these receptors causes a muscular contraction. The anatoxin a molecule is shaped so it fits this receptor, and in this way it mimics the natural neurotransmitter normally used by the receptor, acetylcholine. Once it has triggered a contraction, anatoxin a does not allow the neurons to return to their resting state, because it is not degraded by cholinesterase which normally performs this function. As a result, the muscle cells contract permanently, the communication between the brain and the muscles is disrupted and breathing stops. 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. Structurally, it is similar to cocaine. 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. The deadliness of the toxin means that it has a high military potential as a toxin weapon. 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. Cylindrospermopsin is toxic to liver and kidney tissue and is thought to inhibit protein synthesis and to covalently modify DNA and/or RNA. There is concern about the way cylindrospermopsin bioaccumulates in freshwater organisms. Toxic blooms of genera which produce cylindrospermopsin are most commonly found in tropical, subtropical and arid zone water bodies, and have recently been found in Australia, Europe, Israel, Japan and the USA. Puffer fish and some marine dinoflagellates also produce saxitoxin. Saxitoxins bioaccumulate in shellfish and certain finfish. Ingestion of saxitoxin, usually through shellfish contaminated by toxic algal blooms, can result in paralytic shellfish poisoning. Saxitoxin was originally isolated and described by the United States military, who assigned it the chemical weapon designation "TZ". Saxitoxin is listed in schedule 1 of the Chemical Weapons Convention. According to the book Spycraft, U 2 spyplane pilots were provided with needles containing saxitoxin to be used for suicide in the event escape was impossible.

Aetokthonotoxin (abbreviated to AETX) was discovered in 2021 as the cyanobacterial neurotoxin causing vacuolar myelinopathy (VM). As the biosynthesis of aetokthonotoxin depends on the availability of bromide in freshwater systems and requires an interplay between the toxin producing cyanobacterium Aetokthonos hydrillicola and the host plant it epiphytically grows on (most importantly hydrilla), it took > 25 years to discover aetokthonotoxin as the VM inducing toxin after the disease has first been diagnosed in bald eagles in 1994. The toxin cascades through the food chain: Among other animals, it affects fish and waterfowl such as coots or ducks which feed on hydrilla colonized with the cyanobacterium. Aetokthonotoxin is transmitted to raptors, such as the bald eagle, that prey on these affected animals. 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.

The non proteinogenic amino acid beta Methylamino L alanine (BMAA) is ubiquitously produced by cyanobacteria in marine, freshwater, brackish, and terrestrial environments. The exact mechanisms of BMAA toxicity on neuron cells is being investigated. Research suggests both acute and chronic mechanisms of toxicity. BMAA is being investigated as a potential environmental risk factor for neurodegenerative diseases, including ALS, Parkinson's disease and Alzheimer's disease.