Brevetoxin

Last updated

Brevetoxin (PbTx), or brevetoxins, are a suite of cyclic polyether compounds produced naturally by a species of dinoflagellate known as Karenia brevis . Brevetoxins are neurotoxins that bind to voltage-gated sodium channels in nerve cells, leading to disruption of normal neurological processes and causing the illness clinically described as neurotoxic shellfish poisoning (NSP). [1] Although brevetoxins are most well-studied in K. brevis, they are also found in other species of Karenia and at least one large fish kill has been traced to brevetoxins in Chattonella . [1]

Contents

Types of brevetoxins

Brevetoxins are grouped into two main types: brevetoxin A and brevetoxin B. They are further classified by what chemical substituent (R group) is attached at certain positions within the core molecule.

Brevetoxin A [2] Brevetoxin B [3]
chemical structure
Brevetoxin A Brevetoxin A.svg
Brevetoxin A
Brevetoxin B Brevetoxin B.svg
Brevetoxin B
subtypes
  • Brevetoxin-1 (PbTx-1) R = -CH2C(=CH2)CHO
  • Brevetoxin-7 (PbTx-7) R = -CH2C(=CH2)CH2OH
  • Brevetoxin-10 (PbTx-10) R = -CH2CH(-CH3)CH2OH
  • Brevetoxin-2 (PbTx-2) R = -CH2C(=CH2)CHO
  • Brevetoxin-3 (PbTx-3) R = -CH2C(=CH2)CH2OH
  • Brevetoxin-8 (PbTx-8) R = -CH2COCH2Cl
  • Brevetoxin-9 (PbTx-9) R = -CH2CH(CH3)CH2OH

Other Brevetoxins

Synthesis in the lab

Brevetoxin-B was synthesized in 1995 by K. C. Nicolaou and coworkers in 123 steps with 91% average yield (final yield ~9·10−6) [4] and in 2004 in a total of 90 steps with an average 93% yield for each step (0.14% overall). [3]

K. C. Nicolaou and coworkers reported their synthesis of Brevetoxin-1 in 1998. [5] In 2009, Michael Crimmins and co-workers reported their synthesis of Brevetoxin-1 as well. [6]

Biosynthesis

Proposed pathway for brevetoxin-B Proposed pathway for brevetoxin-B.png
Proposed pathway for brevetoxin-B

Brevetoxins share the common backbone structure of polyketides, but there are several methyl and oxygen groups that are not typical in traditional polyketide biosynthesis. Labelling studies using carbon-13 confirm that the biosynthesis of brevetoxins greatly deviates from the polyketide synthetic pathway. The proposed biosynthetic pathway for brevetoxin class compounds begins with traditional polyketide synthesis to create the carbon backbone, using carbon originating from acetate modified by the citric acid cycle. After the carbon backbone is synthesized, oxidation produces the necessary epoxides and the multi-ring system is closed. It is unclear if the methyl groups seen in BTX-B are added after cyclization or during the modification of the polyketide metabolites, but it is clear that methyl groups can originate from sources outside of acetate such as S-adenosylmethionine.

From labelling experiments of Brevetoxin-B (BTX-B), out of 50 carbons in the molecule, 16 carbon signals were enhanced by [1-C13] acetate, 30 signals were enhanced by [2-C13] acetate, and 4 carbon signals were enhanced by [methyl-C13] methionine. 14 intact acetate units were identified with a fifteenth two carbon unit with a weak possibility of being an acetate unit. Based on the oxygen locations in BTX-B, this molecule could not be produced using a traditional polyketide synthesis pathway.

Attention was turned to the citric acid cycle to solve the problem. Acetate can be used in the polyketide synthetic pathway or modified by the citric acid cycle. Intermediate products of this cycle can then be reintroduced to the polyketide synthetic pathway, resulting in the addition of atypical carbon units. Previous studies of the citric acid pathway revealed three and four carbon units that can potentially explain the atypical condensation and oxidation pattern seen in BTX-B. That being said, there is currently no explanation as to why this particular pattern is favored. [7]

Mechanisms of activity

The potent polyether brevetoxins produced by K. brevis activate voltage-sensitive sodium channels (VSSCs) by binding to site 5 on the alpha-subunit of VSSCs, which serve as key proteins in the structure of the cell membrane. [8] The binding of brevetoxin to VSSCs produces three key effects: a lowering of the activation potential required to activate and open the sodium channel, persistent activation of the channel and therefore repetitive firing of nerves, and the inability to reverse the prolonged open state. This leads to a number of health problems in both humans and animals. For instance, pulmonary receptors associated with ligand-gated epithelial Na+ channels and cathepsin inhibition in macrophages have been reported to be affected by brevetoxin exposure.

The uptake of brevetoxin into both humans and animals occurs primarily through inhalation and ingestion. [9] Dermal contact, such as through swimming in red tides, is a suspected method of uptake, although direct contact with the toxin in the water is not well studied. In the case of inhalation, aerosolized toxins carried onshore in sea spray can cause respiratory irritation that can escalate, in more extreme cases, to more severe airway constriction, an effect observed at pM concentrations. More significant are the cases of ingestion, whether by direct swallowing of seawater during blooms of K. brevis or digestion of contaminated filter-feeding animals. After feeding upon K. brevis, aquatic invertebrates and shellfish in particular can accumulate brevetoxins, resulting in neurotoxic shellfish poisoning (NSP). [10] In humans, the characteristic symptoms of NSP include Paresthesia (tingling), reversal of hot-cold temperature sensation, myalgia (muscle pain), vertigo, ataxia (loss of coordination), abdominal pain, nausea, diarrhea, headache, bradycardia (slow heart rate), dilated pupils and, as previously mentioned, respiratory distress. The bioaccumulation effect has been observed for this toxin in the food web, and it has been noted that this accumulation is not restricted to times when K. brevis is present.

Impacts of exposure on health and economy

Exposure

Brevetoxins in nature often occur from a phenomenon called red tide, where species of harmful algae such as Karenia brevis bloom, causing a red coloration of the water and potentially dangerous levels of brevetoxins. Brevetoxins in nature namely results in massive fish kills and the poisoning of marine mammals and other aquatic invertebrates, which in turn are a source of human health problems.

In marine mammals, a clear vector is difficult to identify due to confounding variables such as inability to confirm exposure and complicated pathological testing measures. One way to suggest a pathway into the marine mammal food web, is to examine what their primary food source is. A 2009 study examines a possible avenue of exposure though fish in cetaceans, mostly bottlenose dolphins, and sea grass in manatees. In this study, scientists also examine by what category they were exposed, by aerosols or ingestion, which is analyzed by measuring the levels of brevetoxin in the lungs versus in the stomach contents. They found that the majority of stomach contents in manatees were seagrass, and of those seagrass, the brevetoxin accumulation in the epiphytes was as high as 87%. In dolphins, the vector was more challenging to test for, because it was thought that fish die off before they can be eaten by larger animals, but this study also showed that fish can bioaccumulate brevetoxin and survive long enough to poison cetaceans. This is important because while a bloom might not be currently occurring, wildlife still could potentially die from exposure due to brevetoxin moving through the food web. [11] Another way of assessing a pathway for exposure is the location of lesions and hemorrhaging, for example lesions in the lungs from inhalation. [12]

Another study investigates differing concentrations of brevetoxin in different organs between avian, cetacean, and sirenian species, specifically a cormorant, bottlenose dolphin, and the Florida manatee. These organs include the liver, kidneys, brain, lungs, and stomach contents of all of these animals, and compared them to see where in the food web they were exposed, and to what extent. Manatees had the highest concentrations of brevetoxin in their livers, dolphins in their stomach contents, and cormorants in their brain and lungs. The kidney analysis showed that manatees and cormorants had equally high levels. Over all animals, the concentrations were highest in the liver, then kidneys, then lungs, and finally the brain, perhaps indicating a pathway for metabolizing brevetoxin. Dolphins in this study did not show much tissue damage compared to the other two, indicating that brevetoxin has a more profound lethal impact at lower concentrations.

Some symptoms of brevetoxicosis on the central nervous system include behavioral changes, muscular impairments, and disorientation. In manatees this is expressed in difficulty breathing difficulties, balance issues, and flexing of the back. In cormorants, they demonstrate difficulties flying. Another study showed that lemon sharks have similar issues with disorientation associated with brevetoxin exposure. [12] In addition to brevetoxicosis, manatees also have impaired immune system function, making them unable to fight off the exposure and more susceptible to other diseases. This happens due to decreased lymphocyte response to exposure and inflammation in the affected areas, this study was done on sublethal exposed manatees. [13]

The FWC marine mammal pathobiology lab collects and tests manatee carcasses for brevetoxin exposure. In 2015 alone, there were 170 positive carcasses and 107 suspected cases, resulting in a total of 277 manatees. [14] In 2004 there were 107 dolphin deaths in just two months around the Florida panhandle, due to brevetoxicosis. Both cormorants and manatees have been rehabbed for brevetoxicosis, but no dolphins have survived it. [12]

Public health and economy

The range and degree of human health effects seems to vary annually and temporally in coastal regions, depending on the red tide density as well as variation in toxicity differences among dinoflagellate strains and their subsequent consumers. [8] The Gulf of Mexico, and in particular the west coast of Florida, is the most heavily impacted by the adverse health and environmental effects of nearly annual K. brevis blooms. This region has suffered significant economic losses in local communities that rely on tourism and recreational fishing along with bad publicity over the years. Shellfish poisonings have been known about in Florida since the 1880s, although the cause was not identified as K. brevis until 1960.

The fishing industry loses around 18 million dollars annually due to brevetoxin exposure and the resulting fish kills. Also, around one million dollars has been spent annually on public health due to shellfish poisoning from 1987 to 1992. A major obstacle for these industries and public health is inability to contain a bloom, and it is undetectable in taste and smell, only chemically. One major concern for exposure is not just illness, but that brevetoxin can alter human DNA in lymphocytes, impacting immune function. [15]

The metabolism of brevetoxins in shellfish is particularly concerning, as certain derivatives have been shown to remain in the animal over extended periods of time. It has been shown that the main toxin produced by K. brevis, PbTx-2, is rapidly metabolized, resulting in the production of metabolites that endure in the animal's system for a significantly longer period of time. This stands in contrast to PbTx-3, which is typically eliminated from the shellfish in more or less its original form within a few weeks. [9]

Brevetoxin concentrations in seafood and the regulation of toxic substance monitoring in the animals is concerning. In Florida, only oysters and clams are monitored for NSP. Scallops are not monitored, although scallop-related NSP does not normally occur because in most cases, the muscle which does not accumulate brevetoxin to dangerous levels is consumed. Additionally, scallops are less tolerant to brevetoxins as compared to other bivalves and die off quickly after exposure to K. brevis red tides. However, smaller bivalves such as chione clams and coquinas can accumulate extremely high levels of brevetoxins and are not monitored, which could potentially impact both human and wildlife health in negative ways. According to evidence from Poli et al., whelks are implicated in an NSP event in 1996.

With respect to ichthyotoxicity, reports of massive fish kills have been reported in the Gulf of Mexico as far back as 1844. [9] Originally, fish bioassay-guided fractionation was used to isolate the toxins, but accumulation in or food-web transfer by fish has not been regarded as a threat. Steidinger hypothesized that the presence of brevetoxin found in dolphin mortalities and prey mortalities in 1987-1988 were in part due to brevetoxin transfer through fish. While dangerous levels of brevetoxins have not been found in the muscles of live fish to date, the internal organs of fish are highly susceptible to dangerous levels of toxicity and should not be eaten. It is conjectured that chronic low-level exposure to brevetoxin metabolites can occur through shellfish and fish, although the effects of this have not been studied in detail and remain largely unknown.

Nitrogen and phosphorus availability vs toxicity level

Nitrogen and phosphorus grow a K. brevis red tide. [16] Although K. brevis is initiated off shore, it will grow from nutrients (phosphorus and nitrogen) found on the shore. Along the southwest coast of Florida, when surface summer south winds blow phosphorus, nitrogen, green algae, and cyanobacteria into K. brevis that has come close to shore, there is a massive growth in the K. brevis red tide. The waves crashing break the cells open aerosolizing the subsequent brevetoxins which cause respiratory illnesses in humans. In 2018, MOTE Marine in Sarasota, FL updated their frequently asked questions to make it more clear that nutrients (nitrogen is a nutrient found in fertilizer) can grow K. brevis. [17]

Along the west coast of Florida, the early phase of K. brevis blooms are initiated by northerly winds, resulting in upwelling events that cause nutrients to rise towards the surface of the water and transport multiple Karenia cell species towards the shore. Here they concentrate and either continue to grow or are taken up by onshore winds that spread the cells over beaches and near shore communities. It has been shown that K. brevis blooms are limited by available nitrogen (N) or phosphorus (P), but until recently it was not clear what sources K. brevis was utilizing for these key developmental nutrients. The most likely proposition is some combination of the upwelling of subsurface nutrients, land runoff (agricultural and sugar plantations, cattle ranches, golf courses, theme parks, septic systems, etc.) N2-fixation, drainage from phosphate mines and atmospheric deposition provides the necessary support for the blooms.

In addition to the breaking of the cells by waves, K. brevis cells can die because N-limitation directly affects the growth potential of blooms and the toxicity of K. brevis cells that comprise them. When N-limitation is present, intracellular brevetoxin concentrations (fg/μm3) increased up to 2.5-fold in laboratory cultures, implying that during periods of N-limitation of algal growth, there is a higher chance of brevetoxin influx into the marine food web. [10] The toxin content per cell increases when algal growth becomes P-limited. Various field measurements collected in the Gulf of Mexico have shown that the brevetoxin content of K. brevis cells is between 1 and 68 pg/cell; however, Hardison et al. discovered that during periods of transient P- and N-limitation, there is a 2- to 5-fold increase in brevetoxins per mole of cell carbon or unit of cell volume. Hardison concluded that this data suggest that the exposure of marine ecosystems to significantly different toxin levels depends on the nutrient status of the K. brevis cells. While brevetoxins remain intracellular during early stages of bloom development, the triggering of apoptosis and cell lysis with age release the toxins into the surrounding waters, implying that greater P-limitation that results in more cell death ultimately elevates brevetoxin levels. These high levels may persist in a food chain long after a bloom has subsided due to brevetoxin's high affinity for adsorbing to biological surfaces like sea grass fronds, and thereby accumulating in consuming organisms. [18]

Overall, brevetoxins seem to increase under N- and P-limitation, however, the concentration of brevetoxins per cell under P-limitation has been reported to be roughly twice that under N-limitation. One major concern of this is that management of shellfish bed closures operating under the assumption that brevetoxin concentrations per cell do not vary may compromise public safety if a bloom became nutrient limited. [10]

See also

Related Research Articles

<span class="mw-page-title-main">Toxin</span> Naturally occurring organic poison

A toxin is a naturally occurring poison produced by metabolic activities of living cells or organisms. They occur especially as proteins, often conjugated. The term was first used by organic chemist Ludwig Brieger (1849–1919) and is derived from the word "toxic".

<span class="mw-page-title-main">Algal bloom</span> Spread of planktonic algae in water

An algal bloom or algae bloom is a rapid increase or accumulation in the population of algae in freshwater or marine water systems. It is often recognized by the discoloration in the water from the algae's pigments. The term algae encompasses many types of aquatic photosynthetic organisms, both macroscopic multicellular organisms like seaweed and microscopic unicellular organisms like cyanobacteria. Algal bloom commonly refers to the rapid growth of microscopic unicellular algae, not macroscopic algae. An example of a macroscopic algal bloom is a kelp forest.

<span class="mw-page-title-main">Domoic acid</span> Chemical compound

Domoic acid (DA) is a kainic acid-type neurotoxin that causes amnesic shellfish poisoning (ASP). It is produced by algae and accumulates in shellfish, sardines, and anchovies. When sea lions, otters, cetaceans, humans, and other predators eat contaminated animals, poisoning may result. Exposure to this compound affects the brain, causing seizures, and possibly death.

<span class="mw-page-title-main">Saxitoxin</span> Paralytic shellfish toxin

Saxitoxin (STX) is a potent neurotoxin and the best-known paralytic shellfish toxin. Ingestion of saxitoxin by humans, usually by consumption of shellfish contaminated by toxic algal blooms, is responsible for the illness known as paralytic shellfish poisoning (PSP).

Okadaic acid, C44H68O13, is a toxin produced by several species of dinoflagellates, and is known to accumulate in both marine sponges and shellfish. One of the primary causes of diarrhetic shellfish poisoning, okadaic acid is a potent inhibitor of specific protein phosphatases and is known to have a variety of negative effects on cells. A polyketide, polyether derivative of a C38 fatty acid, okadaic acid and other members of its family have shined light upon many biological processes both with respect to dinoflagellete polyketide synthesis as well as the role of protein phosphatases in cell growth.

<span class="mw-page-title-main">Paralytic shellfish poisoning</span> Syndrome of shellfish poisoning

Paralytic shellfish poisoning (PSP) is one of the four recognized syndromes of shellfish poisoning, which share some common features and are primarily associated with bivalve mollusks. These shellfish are filter feeders and accumulate neurotoxins, chiefly saxitoxin, produced by microscopic algae, such as dinoflagellates, diatoms, and cyanobacteria. Dinoflagellates of the genus Alexandrium are the most numerous and widespread saxitoxin producers and are responsible for PSP blooms in subarctic, temperate, and tropical locations. The majority of toxic blooms have been caused by the morphospecies Alexandrium catenella, Alexandrium tamarense, Gonyaulax catenella and Alexandrium fundyense, which together comprise the A. tamarense species complex. In Asia, PSP is mostly associated with the occurrence of the species Pyrodinium bahamense.

<span class="mw-page-title-main">Thin layers (oceanography)</span> Congregations of plankton

Thin layers are concentrated aggregations of phytoplankton and zooplankton in coastal and offshore waters that are vertically compressed to thicknesses ranging from several centimeters up to a few meters and are horizontally extensive, sometimes for kilometers. Generally, thin layers have three basic criteria: 1) they must be horizontally and temporally persistent; 2) they must not exceed a critical threshold of vertical thickness; and 3) they must exceed a critical threshold of maximum concentration. The precise values for critical thresholds of thin layers has been debated for a long time due to the vast diversity of plankton, instrumentation, and environmental conditions. Thin layers have distinct biological, chemical, optical, and acoustical signatures which are difficult to measure with traditional sampling techniques such as nets and bottles. However, there has been a surge in studies of thin layers within the past two decades due to major advances in technology and instrumentation. Phytoplankton are often measured by optical instruments that can detect fluorescence such as LIDAR, and zooplankton are often measured by acoustic instruments that can detect acoustic backscattering such as ABS. These extraordinary concentrations of plankton have important implications for many aspects of marine ecology, as well as for ocean optics and acoustics. Zooplankton thin layers are often found slightly under phytoplankton layers because many feed on them. Thin layers occur in a wide variety of ocean environments, including estuaries, coastal shelves, fjords, bays, and the open ocean, and they are often associated with some form of vertical structure in the water column, such as pycnoclines, and in zones of reduced flow.

<i>Karenia brevis</i> Species of dinoflagellate

Karenia brevis is a microscopic, single-celled, photosynthetic organism in the genus Karenia. It is a marine dinoflagellate commonly found in the waters of the Gulf of Mexico. It is the organism responsible for the "Florida red tides" that affect the Gulf coasts of Florida and Texas in the U.S., and nearby coasts of Mexico. K. brevis has been known to travel great lengths around the Florida peninsula and as far north as the Carolinas.

<i>Heterosigma akashiwo</i> Species of alga

Heterosigma akashiwo is a species of microscopic algae of the class Raphidophyceae. It is a swimming marine alga that episodically forms toxic surface aggregations known as harmful algal bloom. The species name akashiwo is from the Japanese for "red tide".

<span class="mw-page-title-main">Neurotoxic shellfish poisoning</span> Syndrome of shellfish poisoning

Neurotoxic shellfish poisoning (NSP) is caused by the consumption of brevetoxins, which are marine toxins produced by the dinoflagellate Karenia brevis. These toxins can produce a series of gastrointestinal and neurological effects. Outbreaks of NSP commonly take place following harmful algal bloom (HAB) events, commonly referred to as "Florida red tide". Algal blooms are a naturally-occurring phenomenon, however their frequency has been increasing in recent decades at least in-part due to human activities, climate changes, and the eutrophication of marine waters. HABs have been occurring for all of documented history, evidenced by the Native Americans' understanding of the dangers of shellfish consumption during periods of marine bioluminescence. Blooms have been noted to occur as far north as North Carolina and are commonly seen alongside the widespread death of fish and sea birds. In addition to the effects on human health, the economic impact of HAB-associated shellfish toxin outbreaks can have significant economic implications as well due to not only the associated healthcare costs, but the adverse impact on the commercial shellfish industry.

<span class="mw-page-title-main">Harmful algal bloom</span> Population explosion of organisms that can kill marine life

A harmful algal bloom (HAB), or excessive algae growth, is an algal bloom that causes negative impacts to other organisms by production of natural algae-produced toxins, water deoxygenation, mechanical damage to other organisms, or by other means. HABs are sometimes defined as only those algal blooms that produce toxins, and sometimes as any algal bloom that can result in severely lower oxygen levels in natural waters, killing organisms in marine or fresh waters. Blooms can last from a few days to many months. After the bloom dies, the microbes that decompose the dead algae use up more of the oxygen, generating a "dead zone" which can cause fish die-offs. When these zones cover a large area for an extended period of time, neither fish nor plants are able to survive. Harmful algal blooms in marine environments are often called "red tides".

<i>Karenia</i> (dinoflagellate) Genus of single-celled organisms

Karenia is a genus that consists of unicellular, photosynthetic, planktonic organisms found in marine environments. The genus currently consists of 12 described species. They are best known for their dense toxic algal blooms and red tides that cause considerable ecological and economical damage; some Karenia species cause severe animal mortality. One species, Karenia brevis, is known to cause respiratory distress and neurotoxic shellfish poisoning (NSP) in humans.

Phycotoxins are complex allelopathic chemicals produced by eukaryotic and prokaryotic algal secondary metabolic pathways. More simply, these are toxic chemicals synthesized by photosynthetic organisms. These metabolites are not harmful to the producer but may be toxic to either one or many members of the marine food web. This page focuses on phycotoxins produced by marine microalgae; however, freshwater algae and macroalgae are known phycotoxin producers and may exhibit analogous ecological dynamics. In the pelagic marine food web, phytoplankton are subjected to grazing by macro- and micro-zooplankton as well as competition for nutrients with other phytoplankton species. Marine bacteria try to obtain a share of organic carbon by maintaining symbiotic, parasitic, commensal, or predatory interactions with phytoplankton. Other bacteria will degrade dead phytoplankton or consume organic carbon released by viral lysis. The production of toxins is one strategy that phytoplankton use to deal with this broad range of predators, competitors, and parasites. Smetacek suggested that "planktonic evolution is ruled by protection and not competition. The many shapes of plankton reflect defense responses to specific attack systems". Indeed, phytoplankton retain an abundance of mechanical and chemical defense mechanisms including cell walls, spines, chain/colony formation, and toxic chemical production. These morphological and physiological features have been cited as evidence for strong predatory pressure in the marine environment. However, the importance of competition is also demonstrated by the production of phycotoxins that negatively impact other phytoplankton species. Flagellates are the principle producers of phycotoxins; however, there are known toxigenic diatoms, cyanobacteria, prymnesiophytes, and raphidophytes. Because many of these allelochemicals are large and energetically expensive to produce, they are synthesized in small quantities. However, phycotoxins are known to accumulate in other organisms and can reach high concentrations during algal blooms. Additionally, as biologically active metabolites, phycotoxins may produce ecological effects at low concentrations. These effects may be subtle, but have the potential to impact the biogeographic distributions of phytoplankton and bloom dynamics.

Euglenophycin is an ichthyotoxic compound isolated from Euglena sanguinea, a protist of the genus Euglena. It exhibits anticancer and herbicidal activity in vitro.

Karenia mikimotoi is a dinoflagellate species from the genus Karenia. Its first appearance was in Japan in 1935 and since then, it has appeared in other parts of the world such as the east coast of the United States, Norway, and the English Channel.

Dinotoxins are a group of toxins which are produced by flagellate, aquatic, unicellular protists called dinoflagellates. Dinotoxin was coined by Hardy and Wallace in 2012 as a general term for the variety of toxins produced by dinoflagellates. Dinoflagellates are an enormous group of marine life, with much diversity. With great diversity comes many different toxins, however, there are a few toxins that multiple species have in common.

<span class="mw-page-title-main">Antillatoxin</span> Chemical compound

Antillatoxin (ATX) is a potent lipopeptide neurotoxin produced by the marine cyanobacterium Lyngbya majuscula. ATX activates voltage-gated sodium channels, which can cause cell depolarisation, NMDA-receptor overactivity, excess calcium influx and neuronal necrosis.

<span class="mw-page-title-main">Mixotrophic dinoflagellate</span> Plankton

Dinoflagellates are eukaryotic plankton, existing in marine and freshwater environments. Previously, dinoflagellates had been grouped into two categories, phagotrophs and phototrophs. Mixotrophs, however include a combination of phagotrophy and phototrophy. Mixotrophic dinoflagellates are a sub-type of planktonic dinoflagellates and are part of the phylum Dinoflagellata. They are flagellated eukaryotes that combine photoautotrophy when light is available, and heterotrophy via phagocytosis. Dinoflagellates are one of the most diverse and numerous species of phytoplankton, second to diatoms.

Jan H. Landsberg is a biologist, researcher, and author. Her professional research interests in biology have particular focus on aquatic animal and environmental health.

Prymnesin-2 is an organic compound that is secreted by the haptophyte Prymnesium parvum. It belongs to the prymnesin family and has potent hemolytic and ichthyotoxic properties. In a purified form it appears as a pale yellow solid. P. parvum is responsible for red harmful algal blooms worldwide, causing massive fish killings. When these algal blooms occur, this compound poses a threat to the local fishing industry. This is especially true for brackish water, as the compound can reach critical concentrations more easily.

References

  1. 1 2 Watkins SM, Reich A, Fleming LE, Hammond R (2008). "Neurotoxic Shellfish Poisoning". Marine Drugs. 6 (3): 431–455. doi: 10.3390/md20080021 . PMC   2579735 . PMID   19005578.
  2. ↑ Nicolaou KC, Yang Z, Shi G, Gunzner JL, Agrios KA, Gärtner P (1998). "Total Synthesis of Brevetoxin A". Nature. 392 (6673): 264–269. Bibcode:1998Natur.392..264N. doi:10.1038/32623. PMID   9521320. S2CID   373710.
  3. 1 2 Matsuo G, Kawamura K, Hori N, Matsukura H, Nakata T (2004). "Total Synthesis of Brevetoxin-B". Journal of the American Chemical Society. 126 (44): 14374–14376. doi:10.1021/ja0449269. PMID   15521755.
  4. ↑ Nicolaou KC, Rutjes FP, Theodorakis EA, Tiebes J, Sato M, Untersteller E (1995). "Total Synthesis of Brevetoxin B. 3. Final Strategy and Completion". Journal of the American Chemical Society. 117 (41): 10252–10263. doi:10.1021/ja00146a010. hdl: 2066/26297 .
  5. ↑ Nicolaou KC, Yang Z, Shi GQ, Gunzner JL, Agrios KA, Gärtner P (1998). "Total Synthesis of Brevetoxin A". Nature. 392 (6673): 264–269. Bibcode:1998Natur.392..264N. doi:10.1038/32623. PMID   9521320. S2CID   373710.
  6. ↑ Crimmins MT, Zuccarello JL, Ellis JM, McDougall PJ, Haile PA, Parrish JD, Emmitte KA (2009). "Total Synthesis of Brevetoxin A". Organic Letters. 11 (2): 489–492. doi:10.1021/ol802710u. PMC   2640830 . PMID   19099481.
  7. ↑ Lee MS, Qin G, Nakanishi K, Zagorski MG (August 1989). "Biosynthetic studies of brevetoxins, potent neurotoxins produced by the dinoflagellate Gymnodinium breve". Journal of the American Chemical Society. 111 (16): 6234–41. doi:10.1021/ja00198a039.
  8. 1 2 Bourdelais AJ, Campbell S, Jacocks H, Naar J, Wright JL, Carsi J, Baden D (2004). "Brevenal Is a Natural Inhibitor of Brevetoxin Action in Sodium Channel Receptor Binding Assays". Cell Mol Neurobiol. 24 (4): 553–563. doi:10.1023/B:CEMN.0000023629.81595.09. PMC   2659878 . PMID   15233378.
  9. 1 2 3 Van Deventer M, Atwood K, Vargo GA, Flewelling LJ, Landsberg JH, Naar JP, Stanek D (2012). "Karenia brevis red tides and brevetoxin-contaminated fish: a high-risk factor for Florida's scavenging shorebirds?". Journal of the Botanica Marina. 55 (1): 31–37. doi:10.1515/bot.2011.122. S2CID   87230917.
  10. 1 2 3 Hardison DR, Sunda WG, Shea D, Litaker RW (2013). Lin S (ed.). "Increased Toxicity of Karenia brevis during Phosphate Limited Growth: Ecological and Evolutionary Implications". PLOS ONE. 8 (3): e58545. Bibcode:2013PLoSO...858545H. doi: 10.1371/journal.pone.0058545 . PMC   3595287 . PMID   23554901.
  11. ↑ Flewelling, Leanne J.; Naar, Jerome P.; Abbott, Jay P.; Baden, Daniel G.; Barros, Nélio B.; Bossart, Gregory D.; Bottein, Marie-Yasmine D.; Hammond, Daniel G.; Haubold, Elsa M. (2005-06-09). "Red tides and marine mammal mortalities". Nature. 435 (7043): 755–756. doi:10.1038/nature435755a. ISSN   0028-0836. PMC   2659475 . PMID   15944690.
  12. 1 2 3 Wittnich, Carin; Belanger, Mike; Sadchatheeswaran, Saachi (2012). "A comparison of published brevetoxin tissue levels in West Indian manatee, bottlenose dolphin and double-crested cormorants in southwest Florida" (PDF). Journal of Marine Animals and Their Ecology. 5 (1): 20–27. S2CID   54860841. Archived (PDF) from the original on 2024-02-12. Retrieved 2023-06-30.
  13. ↑ Walsh, Catherine J.; Butawan, Matthew; Yordy, Jennifer; Ball, Ray; Flewelling, Leanne; de Wit, Martine; Bonde, Robert K. (2015-04-01). "Sublethal red tide toxin exposure in free-ranging manatees (Trichechus manatus) affects the immune system through reduced lymphocyte proliferation responses, inflammation, and oxidative stress". Aquatic Toxicology. 161: 73–84. Bibcode:2015AqTox.161...73W. doi:10.1016/j.aquatox.2015.01.019. ISSN   0166-445X. PMID   25678466.
  14. ↑ "Red Tide". Florida Fish And Wildlife Conservation Commission. Archived from the original on 2019-07-23. Retrieved 2019-07-23.
  15. ↑ Sayer, Andrew; Hu, Qing; Bourdelais, Andrea J.; Baden, Daniel G.; Gibson, James E. (2005-11-01). "The effect of brevenal on brevetoxin-induced DNA damage in human lymphocytes". Archives of Toxicology. 79 (11): 683–688. doi:10.1007/s00204-005-0676-2. ISSN   1432-0738. PMC   2561221 . PMID   15986201.
  16. ↑ "What forms of nutrients can Karenia brevis use to grow and bloom?". myfwc.com. Retrieved 2018-09-15.
  17. ↑ "Florida Red Tide FAQs". mote.org. Archived from the original on 2018-09-15. Retrieved 2018-09-15.
  18. ↑ Hardison DR, Sunda WG, Shea D, Litaker RW (2013). Lin S (ed.). "Increased Toxicity of Karenia brevis during Phosphate Limited Growth: Ecological and Evolutionary Implpications". PLOS ONE. 8 (3): e58545. Bibcode:2013PLoSO...858545H. doi: 10.1371/journal.pone.0058545 . PMC   3595287 . PMID   23554901.
This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.