Journal articles: 'Neurotoxic Shellfish Poisoning'

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Watkins, Sharon M. "Neurotoxic Shellfish Poisoning." Marine Drugs 6, no. 3 (September 2008): 430–55. http://dx.doi.org/10.3390/md20080021.

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Watkins, Sharon, Andrew Reich, Lora Fleming, and Roberta Hammond. "Neurotoxic Shellfish Poisoning." Marine Drugs 6, no. 3 (July 12, 2008): 431–55. http://dx.doi.org/10.3390/md6030431.

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Abraham, Ann, Steven M. Plakas, Leanne J. Flewelling, Kathleen R. El Said, Edward L. E. Jester, Hudson R. Granade, Kevin D. White, and Robert W. Dickey. "Biomarkers of Neurotoxic Shellfish Poisoning." Toxicon 52, no. 2 (August 2008): 237–45. http://dx.doi.org/10.1016/j.toxicon.2008.04.175.

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Martín, R., T. García, B. Sanz, and P. E. Hernández. "Biotoxinas marinas: intoxicaciones por el consumo de moluscos bivalvos/Seafood toxins: poisoning by bivalve consumption." Food Science and Technology International 2, no. 1 (February 1996): 13–22. http://dx.doi.org/10.1177/108201329600200102.

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Seafood toxins are becoming increasingly important as etiologic agents of foodborne diseases around the world. This is partly because of greater awareness of the potential problems of the paralytic shellfish poisoning (PSP), neurotoxic shellfish poisoning (NSP), diarrheic shellfish poisoning (DSP) and more recently, a new type of seafood toxicity, called amnesic shellfish poisoning (ASP). This review describes the molluskan shellfish and biotoxins implicated, the development of standardized methods for detecting and quantifying these toxins, the importance of the economic loss resulting from their presence and the establishment of regular chemical monitoring for marine toxins.

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Garthwaite, Ian, Kathryn M. Ross, Christopher O. Miles, Lyn R. Briggs, Neale R. Towers, Teresa Borrell, and Phil Busby. "Integrated Enzyme-Linked Immunosorbent Assay Screening System for Amnesic, Neurotoxic, Diarrhetic, and Paralytic Shellfish Poisoning Toxins Found in New Zealand." Journal of AOAC INTERNATIONAL 84, no. 5 (September 1, 2001): 1643–48. http://dx.doi.org/10.1093/jaoac/84.5.1643.

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Abstract Enzyme-linked immunosorbent assays (ELISAs) were developed for amnesic, neurotoxic, and diarrhetic shellfish poisoning (ASP, NSP, and DSP) toxins and for yessotoxin. These assays, along with a commercially available paralytic shellfish poisoning (PSP) ELISA, were used to test the feasibility of an ELISA-based screening system. It was concluded that such a system to identify suspect shellfish samples, for subsequent analysis by methods approved by international regulatory authorities, is feasible. The assays had sufficient sensitivity and can be used on simple shellfish extracts. Alcohol extraction gave good recovery of all toxin groups. The ease of ELISAs permits the ready expansion of the system to screen for other toxins, as new ELISAs become available.

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Lefebvre, Kathi A., Betsy Jean Yakes, Elizabeth Frame, Preston Kendrick, Sara Shum, Nina Isoherranen, Bridget E. Ferriss, et al. "Discovery of a Potential Human Serum Biomarker for Chronic Seafood Toxin Exposure Using an SPR Biosensor." Toxins 11, no. 5 (May 23, 2019): 293. http://dx.doi.org/10.3390/toxins11050293.

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Domoic acid (DA)-producing harmful algal blooms (HABs) have been present at unprecedented geographic extent and duration in recent years causing an increase in contamination of seafood by this common environmental neurotoxin. The toxin is responsible for the neurotoxic illness, amnesic shellfish poisoning (ASP), that is characterized by gastro-intestinal distress, seizures, memory loss, and death. Established seafood safety regulatory limits of 20 μg DA/g shellfish have been relatively successful at protecting human seafood consumers from short-term high-level exposures and episodes of acute ASP. Significant concerns, however, remain regarding the potential impact of repetitive low-level or chronic DA exposure for which there are no protections. Here, we report the novel discovery of a DA-specific antibody in the serum of chronically-exposed tribal shellfish harvesters from a region where DA is commonly detected at low levels in razor clams year-round. The toxin was also detected in tribal shellfish consumers’ urine samples confirming systemic DA exposure via consumption of legally-harvested razor clams. The presence of a DA-specific antibody in the serum of human shellfish consumers confirms long-term chronic DA exposure and may be useful as a diagnostic biomarker in a clinical setting. Adverse effects of chronic low-level DA exposure have been previously documented in laboratory animal studies and tribal razor clam consumers, underscoring the potential clinical impact of such a diagnostic biomarker for protecting human health. The discovery of this type of antibody response to chronic DA exposure has broader implications for other environmental neurotoxins of concern.

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Morris, P. D., D. S. Campbell, T. J. Taylor, and J. I. Freeman. "Clinical and epidemiological features of neurotoxic shellfish poisoning in North Carolina." American Journal of Public Health 81, no. 4 (April 1991): 471–74. http://dx.doi.org/10.2105/ajph.81.4.471.

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Poli, Mark A., Steven M. Musser, Robert W. Dickey, Paul P. Eilers, and Sherwood Hall. "Neurotoxic shellfish poisoning and brevetoxin metabolites: a case study from Florida." Toxicon 38, no. 7 (July 2000): 981–93. http://dx.doi.org/10.1016/s0041-0101(99)00191-9.

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Cuypers, Eva, Angel Yanagihara, Jon D. Rainier, and Jan Tytgat. "TRPV1 as a key determinant in ciguatera and neurotoxic shellfish poisoning." Biochemical and Biophysical Research Communications 361, no. 1 (September 2007): 214–17. http://dx.doi.org/10.1016/j.bbrc.2007.07.009.

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Truman, Penelope, David J. Stirling, Peter Northcote, Robin J. Lake, Catherine Seamer, and Donald J. Hannah. "Determination of Brevetoxins in Shellfish by the Neuroblastoma Assay." Journal of AOAC INTERNATIONAL 85, no. 5 (September 1, 2002): 1057–63. http://dx.doi.org/10.1093/jaoac/85.5.1057.

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Abstract A neuroblastoma assay for determination of brevetoxins in shellfish was developed together with a method for sample cleanup that allows separation of brevetoxins from most of the components that cause matrix interference in the assay. This improved assay method was applied to a range of shellfish samples with different characteristics. Extracts of naturally contaminated and nontoxic shellfish together with extracts spiked with known amounts of toxin were tested. The results demonstrated that brevetoxins could be reliably detected in shellfish extracts at concentrations below the regulatory limit. Brevetoxin activity was detected in 15 of 23 samples from 5 separate toxicity incidents in which shellfish tested positive in the neurotoxic shellfish poisoning (NSP) mouse bioassay. Twelve of these positive NSP results came from 2 toxicity incidents. Yessotoxin was the major contributor to toxicity in 2 other incidents, although some samples contained both yessotoxin and brevetoxin. The sample from the remaining incident contained an unidentified toxin bioactivity, together with gymnodimine. In contrast to earlier versions of the neuroblastoma assay, gymnodimine was not detected by this modified method.

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Bienfang, P. K., S. V. DeFelice, E. A. Laws, L. E. Brand, R. R. Bidigare, S. Christensen, H. Trapido-Rosenthal, et al. "Prominent Human Health Impacts from Several Marine Microbes: History, Ecology, and Public Health Implications." International Journal of Microbiology 2011 (2011): 1–15. http://dx.doi.org/10.1155/2011/152815.

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This paper overviews several examples of important public health impacts by marine microbes and directs readers to the extensive literature germane to these maladies. These examples include three types of dinoflagellates (Gambierdiscusspp.,Karenia brevis, andAlexandrium fundyense), BMAA-producing cyanobacteria, and infectious microbes. The dinoflagellates are responsible for ciguatera fish poisoning, neurotoxic shellfish poisoning, and paralytic shellfish poisoning, respectively, that have plagued coastal populations over time. Research interest on the potential for marine cyanobacteria to contribute BMAA into human food supplies has been derived by BMAA's discovery in cycad seeds and subsequent implication as the putative cause of amyotrophic lateral sclerosis/parkinsonism dementia complex among the Chamorro people of Guam. Recent UPLC/MS analyses indicate that recent reports that BMAA is prolifically distributed among marine cyanobacteria at high concentrations may be due to analyte misidentification in the analytical protocols being applied for BMAA. Common infectious microbes (including enterovirus, norovirus,Salmonella,Campylobacter,Shigella,Staphylococcus aureus,Cryptosporidium, andGiardia) cause gastrointestinal and skin-related illness. These microbes can be introduced from external human and animal sources, or they can be indigenous to the marine environment.

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Kumar-Roiné, Shilpa, Mariko Matsui, Serge Pauillac, and Dominique Laurent. "Ciguatera fish poisoning and other seafood intoxication syndromes: A revisit and a review of the existing treatments employed in ciguatera fish poisoning." South Pacific Journal of Natural and Applied Sciences 28, no. 1 (2010): 1. http://dx.doi.org/10.1071/sp10001.

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Ciguatera fish poisoning (CFP) is acquired through consumption of tropical reef fishes, contaminated with potent neurotoxins, ciguatoxins (CTXs), produced by benthic dinoflagellate of the Gambierdiscus genus. Both spatially and temporally unpredictable, a tainted fish is impossible to differentiate from an untainted one by appearance, taste, texture or odour. Given the predominance of reef fish in the diet of insular countries, the risk of CFP is ever-present. In the Pacific where the incidence of CFP is the highest, the consequences on public health and socio-economy can be extremely severe. Multidisciplinary in nature, the present review revisits the phenomenon of CFP, covering certain of its aspects, notably the etiology, toxicology, ecotoxicology, pharmacology, pathology and the treatments administrated. These aspects of CFP have been reviewed in relation to other poisoning syndromes: tetrodotoxin poisoning and other dinoflagellates- or diatoms-associated intoxications such as paralytic (PSP), diarrhetic (DSP), neurotoxic (NSP), amnesic (ASP) and azaspiracid shellfish poisoning (AZP) and palytoxin poisoning. Based on case reports and bibliographic accounts, a list inventorying the western medicines prescribed to patients suffering from CFP has been established. Within the last two decades, several of the herbal remedies have been evaluated for their efficiencies in in vivo and in a number of in vitro tests, which have also been reviewed herein.

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Abraham, Ann, Leanne J. Flewelling, Kathleen R. El Said, William Odom, Stephen P. Geiger, April A. Granholm, Jennifer T. Jackson, and Dean Bodager. "An occurrence of neurotoxic shellfish poisoning by consumption of gastropods contaminated with brevetoxins." Toxicon 191 (February 2021): 9–17. http://dx.doi.org/10.1016/j.toxicon.2020.12.010.

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Arnich, Nathalie, Eric Abadie, Zouher Amzil, Marie-Yasmine Dechraoui Bottein, Katia Comte, Estelle Chaix, Nicolas Delcourt, et al. "Guidance Level for Brevetoxins in French Shellfish." Marine Drugs 19, no. 9 (September 15, 2021): 520. http://dx.doi.org/10.3390/md19090520.

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Brevetoxins (BTXs) are marine biotoxins responsible for neurotoxic shellfish poisoning (NSP) after ingestion of contaminated shellfish. NSP is characterized by neurological, gastrointestinal and/or cardiovascular symptoms. The main known producer of BTXs is the dinoflagellate Karenia brevis, but other microalgae are also suspected to synthesize BTX-like compounds. BTXs are currently not regulated in France and in Europe. In November 2018, they have been detected for the first time in France in mussels from a lagoon in the Corsica Island (Mediterranean Sea), as part of the network for monitoring the emergence of marine biotoxins in shellfish. To prevent health risks associated with the consumption of shellfish contaminated with BTXs in France, a working group was set up by the French Agency for Food, Environmental and Occupational Health & Safety (Anses). One of the aims of this working group was to propose a guidance level for the presence of BTXs in shellfish. Toxicological data were too limited to derive an acute oral reference dose (ARfD). Based on human case reports, we identified two lowest-observed-adverse-effect levels (LOAELs). A guidance level of 180 µg BTX-3 eq./kg shellfish meat is proposed, considering a protective default portion size of 400 g shellfish meat.

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Baden, Daniel G., Rosemary Melinek, Veronique Sechet, Vera L. Trainer, Duane R. Schultz, Kathleen S. Rein, Carmelo R. Tomas, Jesus Delgado, and Lauren Hale. "Modified Immunoassays for Polyether Toxins: Implications of Biological Matrixes, Metabolic States, and Epitope Recognition." Journal of AOAC INTERNATIONAL 78, no. 2 (March 1, 1995): 499–507. http://dx.doi.org/10.1093/jaoac/78.2.499.

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Abstract Polyether marine toxins are responsible for the seafood intoxication phenomena known as neurotoxic shellfish poisoning (due to brevetoxins), ciguatera (due to ciguatoxin), and diarrheic shellfish poisoning (due to okadaic acid). Using traditional techniques of hapten (pure toxin) conjugation to protein to create complete antigen, animal immunization and antibody isolation, and specific antibody subpopulation purification, discriminating antibodies have been isolated that detect brevetoxins and ciguatoxin, but not okadaic acid, in a dose-dependent fashion. Using microorganic chemistry and purified toxins, a unique set of tools has been created for the study of polyether ladder toxin accumulation; depuration; and specific site localization in tissues, food sources, and clinical samples. Developed test protocols can detect toxin in dinoflagellate cells, in extracts from food sources, in seawater and culture media, and in human serum samples. Enzyme-linked immunosorbent assay protocols developed for eventual collaborative testing have been successful in limited applications within the laboratory (correlation coefficient of 0.92 excluding 2 outliers), and alternative formats are being developed to optimize the basic test for use in research laboratories, regulatory laboratories, and field inspections.

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McNabb, Paul S., Andrew I. Selwood, Roel van Ginkel, Michael Boundy, and Patrick T. Holland. "Determination of Brevetoxins in Shellfish by LC/MS/MS: Single-Laboratory Validation." Journal of AOAC INTERNATIONAL 95, no. 4 (July 1, 2012): 1097–105. http://dx.doi.org/10.5740/jaoacint.11-272.

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Abstract A single-laboratory validation is reported for an LC/MS/MS quantification of six brevetoxins in four matrixes (GreenshellTM mussel, eastern oyster, hard clam, and Pacific oyster). Recovery and precision data were collected from seven analytical batches using shellfish flesh at 0.05 mg/kg. Method recoveries and within-laboratory reproducibility ranged from 73 to 112%, with an RSD between 14 and 18% for brevetoxin-3, brevetoxin B5, brevetoxin B2, and S-desoxy brevetoxin B2. The recovery and within-laboratory reproducibility for brevetoxin-2 was 61%, with an RSD of 27%. Brevetoxin B1 gave an RSD of 12%, but no reference material was available and this toxin was only recorded in a hard clam sample naturally contaminated with brevetoxins. One naturally contaminated sample of each shellfish matrix, with brevetoxin levels ranging from 0.012 to 9.9 mg/kg, was tested in multiple batches, and the RSDs were similar to those for fortified samples at 0.05 mg/kg. Comparisons with limited data for the neurotoxic shellfish poisoning mouse bioassay for four naturally contaminated shellfish samples showed that the regulatory action limit of 0.8 mg/kg is conservative with respect to the bioassay regulatory limit of 20 mouse units/100 g.

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Murata, Kazuya, and Takeshi Yasumoto. "Chemiluminescent Receptor Binding Assay for Ciguatoxins and Brevetoxins Using Acridinium Brevetoxin-B2." Toxins 11, no. 10 (October 9, 2019): 580. http://dx.doi.org/10.3390/toxins11100580.

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Ciguatera is the term for poisoning resulting from eating fish from tropical or subtropical regions. The causative toxins collectively named ciguatoxins (CTXs) widely differ in structures depending on their geographic origins, which range from the Pacific Ocean and the Indian Ocean to the Caribbean Sea. Neurotoxic shellfish poisoning (NSP) is caused by the ingestion of bivalve shellfish contaminated with brevetoxins (BTXs). Structurally, both CTXs and BTXs consist of fused ether rings aligned in a ladder shape. Pharmacologically, they bind at the same site (site-5) of voltage-gated sodium channels. However, the great structural diversity and the rare availability of reference toxins hinder LC-MS and ELISA methods, which operate on structure-based recognition. In this study, we prepared a chemiluminescent ligand, acridinium BTXB2 (ABTX), and tested its suitability for use in competitive binding assays to detect CTXs and BTXs. The affinity of ABTX to the rat brain synaptosome estimated by Ki (1.66 pM) was approximately two-fold higher than that of PbTx-3 (BTX3). In addition, the equilibrium dissociation constant (KD) was 0.84 nM, the maximum number of binding was 6.76 pmol toxin/mg protein, and the detection limit was 1.4 amol. The assays performed on samples spiked with CTX3C or BTXB4 (N-palmitoylBTXB2) at 0.2–1.0 ng CTX/g fish flesh, and 200–800 ng BTXB4/g shellfish showed a linear relationship between the theoretical and observed toxin amounts.

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Reich, Andrew, Rebecca Lazensky, Jeremy Faris, Lora E. Fleming, Barbara Kirkpatrick, Sharon Watkins, Steve Ullmann, Kate Kohler, and Porter Hoagland. "Assessing the impact of shellfish harvesting area closures on neurotoxic shellfish poisoning (NSP) incidence during red tide (Karenia brevis) blooms." Harmful Algae 43 (March 2015): 13–19. http://dx.doi.org/10.1016/j.hal.2014.12.003.

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Robin, R. S., Vishnu Vardhan Kanuri, Pradipta R. Muduli, Rajani K. Mishra, M. Jaikumar, P. Karthikeyan, C. Suresh Kumar, and C. Saravana Kumar. "Dinoflagellate Bloom of Karenia mikimotoi along the Southeast Arabian Sea, Bordering Western India." Journal of Ecosystems 2013 (June 2, 2013): 1–11. http://dx.doi.org/10.1155/2013/463720.

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A harmful algal bloom (HAB) occurred along the southeast Arabian Sea, bordering Western India, during September to November 2004. This bloom was unique in the region in terms of its large spatial extent, and the trend was weakened towards November. Mass mortality of fish, emanation of noxious odour, and respiratory problems among the children on the coastal stretch were noticed. The phytoplankton species Gymnodiniium, class Dinophyceae bloom accounted for 98% of the standing crop. The bloom Karenia mikimotoi showed a maximum density of 19.37×104 cells L−1 and 18.94×104 cells L−1 at nearshore and offshore, respectively. The remotely sensed chlorophyll a (Chl a) data from seaWiFS, sea surface temperature (SST) from advanced very high resolution radiometer (AVHRR), rainfall from tropical rainfall measuring Mission (TRMM), and Sea winds from QuickSCAT reflected the bloom due to Karenia mikimotoi, suggesting the advection process at the coastal waters. The release of toxins specifically the neurotoxic shellfish poisoning (NSP) and azaspiracid shellfish poisoning (AZP) from the bloom was assessed by chemical and mouse bioassay of the extract from mussel Perna indica, showing negative results. These indicate that asphyxiation and abnormal mucus secreted by the K. mikimotoi led to clogging of gills that accentuated the mass fish kills.

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Ballot, Andreas, Jutta Fastner, and Claudia Wiedner. "Paralytic Shellfish Poisoning Toxin-Producing Cyanobacterium Aphanizomenon gracile in Northeast Germany." Applied and Environmental Microbiology 76, no. 4 (January 4, 2010): 1173–80. http://dx.doi.org/10.1128/aem.02285-09.

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ABSTRACT Neurotoxic paralytic shellfish poisoning (PSP) toxins, anatoxin-a (ATX), and hepatotoxic cylindrospermopsin (CYN) have been detected in several lakes in northeast Germany during the last 2 decades. They are produced worldwide by members of the nostocalean genera Anabaena, Cylindrospermopsis, and Aphanizomenon. Although no additional sources of PSP toxins and ATX have been identified in German water bodies to date, the observed CYN concentrations cannot be produced solely by Aphanizomenon flos-aquae, the only known CYN producer in Germany. Therefore, we attempted to identify PSP toxin, ATX, and CYN producers by isolating and characterizing 92 Anabaena, Aphanizomenon, and Anabaenopsis strains from five lakes in northeast Germany. In a polyphasic approach, all strains were morphologically and phylogenetically classified and then tested for PSP toxins, ATX, and CYN by liquid chromatography-tandem mass spectrometry (LC-MS/MS) and enzyme-linked immunosorbent assay (ELISA) and screened for the presence of PSP toxin- and CYN-encoding gene fragments. As demonstrated by ELISA and LC-MS, 14 Aphanizomenon gracile strains from Lakes Melang and Scharmützel produced four PSP toxin variants (gonyautoxin 5 [GTX5], decarbamoylsaxitoxin [dcSTX], saxitoxin [STX], and neosaxitoxin [NEO]). GTX5 was the most prevalent PSP toxin variant among the seven strains from Lake Scharmützel, and NEO was the most prevalent among the seven strains from Lake Melang. The sxtA gene, which is part of the saxitoxin gene cluster, was found in the 14 PSP toxin-producing A. gracile strains and in 11 non-PSP toxin-producing Aphanizomenon issatschenkoi, A. flos-aquae, Anabaena planktonica, and Anabaenopsis elenkinii strains. ATX and CYN were not detected in any of the isolated strains. This study is the first confirming the role of A. gracile as a PSP toxin producer in German water bodies.

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Poli, Mark A., Victor R. Rivera, Dwayne D. Neal, Daniel G. Baden, Shawn A. Messer, Steven M. Plakas, Robert W. Dickey, et al. "An Electrochemiluminescence-Based Competitive Displacement Immunoassay for the Type-2 Brevetoxins in Oyster Extracts." Journal of AOAC INTERNATIONAL 90, no. 1 (January 1, 2007): 173–78. http://dx.doi.org/10.1093/jaoac/90.1.173.

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Abstract A new competitive electrochemiluminescence-based immunoassay for the type-2 brevetoxins in oyster extracts was developed. The assay was verified by spiking known amounts of PbTx-3 into 80 methanol extracts of Gulf Coast oysters. We also provide preliminary data demonstrating that 100 acetone extracts, aqueous homogenates, and the clinical matrixes urine and serum can also be analyzed without significant matrix interferences. The assay offers the advantages of speed (≃ 2h analysis time); simplicity (only 2 additions, one incubation period, and no wash steps before analysis); low limit of quantitation (conservatively, 50 pg/mL 1 ng/g tissue equivalents); and a stable, nonradioactive label. Due to the variety of brevetoxin metabolites present and the lack of certified reference standards for liquid chromatographymass spectrometry confirmation, a true validation of brevetoxins in shellfish extracts is not possible at this time. However, our assay correlated well with another brevetoxin immunoassay currently in use in the United States. We believe this assay could be useful as a regulatory screening tool and could support pharmacokinetic studies in animals and clinical evaluation of neurotoxic shellfish poisoning victims.

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Wolny, Jennifer L., Paula S. Scott, Jacob Tustison, and Christopher R. Brooks. "Monitoring the 2007 Florida east coast Karenia brevis (Dinophyceae) red tide and neurotoxic shellfish poisoning (NSP) event." ALGAE 30, no. 1 (March 15, 2015): 49–58. http://dx.doi.org/10.4490/algae.2015.30.1.049.

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Morohashi, Akio, Masayuki Satake, Hideo Naoki, Heinrich F. Kaspar, Yasukatsu Oshima, and Takeshi Yasumoto. "Brevetoxin B4 isolated from greenshell musselsPerna canaliculus, the major toxin involved in neurotoxic shellfish poisoning in New Zealand." Natural Toxins 7, no. 2 (March 1999): 45–48. http://dx.doi.org/10.1002/(sici)1522-7189(199903/04)7:2<45::aid-nt34>3.0.co;2-h.

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Flewelling, Leanne J., Alina A. Corcoran, April A. Granholm, Noel Y. Takeuchi, Rebecca V. Van Hoeck, and Meredith L. Zahara. "Validation and Assessment of an Enzyme-Linked Immunosorbent Assay (Elisa) for Use in Monitoring and Managing Neurotoxic Shellfish Poisoning." Journal of Shellfish Research 39, no. 2 (August 26, 2020): 491. http://dx.doi.org/10.2983/035.039.0230.

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Barbaro, Elena, Roberta Zangrando, Carlo Barbante, and Andrea Gambaro. "Fast and Sensitive Method for Determination of Domoic Acid in Mussel Tissue." Scientific World Journal 2016 (2016): 1–6. http://dx.doi.org/10.1155/2016/8404092.

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Domoic acid (DA), a neurotoxic amino acid produced by diatoms, is the main cause of amnesic shellfish poisoning (ASP). In this work, we propose a very simple and fast analytical method to determine DA in mussel tissue. The method consists of two consecutive extractions and requires no purification steps, due to a reduction of the extraction of the interfering species and the application of very sensitive and selective HILIC-MS/MS method. The procedural method was validated through the estimation of trueness, extract yield, precision, detection, and quantification limits of analytical method. The sample preparation was also evaluated through qualitative and quantitative evaluations of the matrix effect. These evaluations were conducted both on the DA-free matrix spiked with known DA concentration and on the reference certified material (RCM). We developed a very selective LC-MS/MS method with a very low value of method detection limit (9 ng g−1) without cleanup steps.

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Konoki, Keiichi, Daniel G. Baden, Todd Scheuer, and William A. Catterall. "Molecular Determinants of Brevetoxin Binding to Voltage-Gated Sodium Channels." Toxins 11, no. 9 (September 3, 2019): 513. http://dx.doi.org/10.3390/toxins11090513.

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Brevetoxins are produced by dinoflagellates such as Karenia brevis in warm-water red tides and cause neurotoxic shellfish poisoning. They bind to voltage-gated sodium channels at neurotoxin receptor 5, making the channels more active by shifting the voltage-dependence of activation to more negative potentials and by slowing the inactivation process. Previous work using photoaffinity labeling identified binding to the IS6 and IVS5 transmembrane segments of the channel α subunit. We used alanine-scanning mutagenesis to identify molecular determinants for brevetoxin binding in these regions as well as adjacent regions IVS5-SS1 and IVS6. Most of the mutant channels containing single alanine substitutions expressed functional protein in tsA-201 cells and bound to the radioligand [42-3H]-PbTx3. Binding affinity for the great majority of mutant channels was indistinguishable from wild type. However, transmembrane segments IS6, IVS5 and IVS6 each contained 2 to 4 amino acid positions where alanine substitution resulted in a 2–3-fold reduction in brevetoxin affinity, and additional mutations caused a similar increase in brevetoxin affinity. These findings are consistent with a model in which brevetoxin binds to a protein cleft comprising transmembrane segments IS6, IVS5 and IVS6 and makes multiple distributed interactions with these α helices. Determination of brevetoxin affinity for Nav1.2, Nav1.4 and Nav1.5 channels showed that Nav1.5 channels had a characteristic 5-fold reduction in affinity for brevetoxin relative to the other channel isoforms, suggesting the interaction with sodium channels is specific despite the distributed binding determinants.

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Pierre, Ophélie, Maxime Fouchard, Nelig Le Goux, Paul Buscaglia, Raphaël Leschiera, Richard J. Lewis, Olivier Mignen, Joachim W. Fluhr, Laurent Misery, and Raphaële Le Garrec. "Pacific-Ciguatoxin-2 and Brevetoxin-1 Induce the Sensitization of Sensory Receptors Mediating Pain and Pruritus in Sensory Neurons." Marine Drugs 19, no. 7 (July 6, 2021): 387. http://dx.doi.org/10.3390/md19070387.

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Ciguatera fish poisoning (CFP) and neurotoxic shellfish poisoning syndromes are induced by the consumption of seafood contaminated by ciguatoxins and brevetoxins. Both toxins cause sensory symptoms such as paresthesia, cold dysesthesia and painful disorders. An intense pruritus, which may become chronic, occurs also in CFP. No curative treatment is available and the pathophysiology is not fully elucidated. Here we conducted single-cell calcium video-imaging experiments in sensory neurons from newborn rats to study in vitro the ability of Pacific-ciguatoxin-2 (P-CTX-2) and brevetoxin-1 (PbTx-1) to sensitize receptors and ion channels, (i.e., to increase the percentage of responding cells and/or the response amplitude to their pharmacological agonists). In addition, we studied the neurotrophin release in sensory neurons co-cultured with keratinocytes after exposure to P-CTX-2. Our results show that P-CTX-2 induced the sensitization of TRPA1, TRPV4, PAR2, MrgprC, MrgprA and TTX-r NaV channels in sensory neurons. P-CTX-2 increased the release of nerve growth factor and brain-derived neurotrophic factor in the co-culture supernatant, suggesting that those neurotrophins could contribute to the sensitization of the aforementioned receptors and channels. Our results suggest the potential role of sensitization of sensory receptors/ion channels in the induction or persistence of sensory disturbances in CFP syndrome.

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Garneau, Marie-Ève, Astrid Schnetzer, Peter D. Countway, Adriane C. Jones, Erica L. Seubert, and David A. Caron. "Examination of the Seasonal Dynamics of the Toxic Dinoflagellate Alexandrium catenella at Redondo Beach, California, by Quantitative PCR." Applied and Environmental Microbiology 77, no. 21 (September 16, 2011): 7669–80. http://dx.doi.org/10.1128/aem.06174-11.

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ABSTRACTThe presence of neurotoxic species within the genusAlexandriumalong the U.S. coastline has raised concern of potential poisoning through the consumption of contaminated seafood. Paralytic shellfish toxins (PSTs) detected in shellfish provide evidence that these harmful events have increased in frequency and severity along the California coast during the past 25 years, but the timing and location of these occurrences have been highly variable. We conducted a 4-year survey in King Harbor, CA, to investigate the seasonal dynamics ofAlexandrium catenellaand the presence of a particulate saxitoxin (STX), the parent compound of the PSTs. A quantitative PCR (qPCR) assay was developed for quantifyingA. catenellain environmental microbial assemblages. This approach allowed for the detection of abundances as low as 12 cells liter−1, 2 orders of magnitude below threshold abundances that can impact food webs.A. catenellawas found repeatedly during the study, particularly in spring, when cells were detected in 38% of the samples (27 to 5,680 cells liter−1). This peak in cell abundances was observed in 2006 and corresponded to a particulate STX concentration of 12 ng liter−1, whereas the maximum STX concentration of 26 ng liter−1occurred in April 2008. Total cell abundances and toxin levels varied strongly throughout each year, butA. catenellawas less abundant during summer, fall, and winter, when only 2 to 11% of the samples yielded positive qPCR results. The qPCR method developed here provides a useful tool for investigating the ecology ofA. catenellaat subbloom and bloom abundances.

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Morohashi, Akio, Masayuki Satake, Kazuya Murata, Hideo Naoki, Heinrich F. Kaspar, and Takeshi Yasumoto. "Brevetoxin B3, a new brevetoxin analog isolated from the greenshell mussel perna canaliculus involved in neurotoxic shellfish poisoning in new zealand." Tetrahedron Letters 36, no. 49 (December 1995): 8995–98. http://dx.doi.org/10.1016/0040-4039(95)01969-o.

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McCall, Jennifer R., Henry M. Jacocks, Susan C. Niven, Mark A. Poli, Daniel G. Baden, and Andrea J. Bourdelais. "Development and Utilization of a Fluorescence-Based Receptor-Binding Assay for the Site 5 Voltage-Sensitive Sodium Channel Ligands Brevetoxin and Ciguatoxin." Journal of AOAC INTERNATIONAL 97, no. 2 (March 1, 2014): 307–15. http://dx.doi.org/10.5740/jaoacint.sgemccall.

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Abstract Brevetoxins are a family of ladder-frame polyether toxins produced during blooms of the marine dinoflagellate Karenia brevis. Consumption of fish exposed to K. brevis blooms can lead to the development of neurotoxic shellfish poisoning. The toxic effects of brevetoxins are due to activation of voltage-sensitive sodium channels (VSSCs) in cell membranes. Binding of toxins has historically been measured using a radioligand competition assay that is fraught with difficulty. In thisstudy, we developed a novel fluorescence-based binding assay for the brevetoxin receptor. Several fluorophores were conjugated to polyether brevetoxin-2 andused as the labeled ligand. Brevetoxin analogs were able to compete for binding with the fluorescent ligands. This assay was qualified against the standard radioligand receptor assay for the brevetoxin receptor. Furthermore, the fluorescence-based assay was used to determine relative concentrations of toxins inraw extracts of K. brevis culture, and to determine ciguatoxin affinity to site 5 of VSSCs. The fluorescence-based assay was quicker, safer, and far less expensive. As such, this assay can beused to replace the current radioligand assay and will be a vital tool for future experiments examining the binding affinity of various ligands for site 5 on sodium channels.

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MOROHASHI, A., M. SATAKE, K. MURATA, H. NAOKI, H. F. KASPAR, and T. YASUMOTO. "ChemInform Abstract: Brevetoxin B3, a New Brevetoxin Analogue Isolated from the Greenshell Mussel Perna canaliculus Involved in Neurotoxic Shellfish Poisoning in New Zealand." ChemInform 27, no. 13 (August 12, 2010): no. http://dx.doi.org/10.1002/chin.199613274.

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Pierre, Ophélie, Maxime Fouchard, Paul Buscaglia, Nelig Le Goux, Raphaël Leschiera, Olivier Mignen, Joachim W. Fluhr, Laurent Misery, and Raphaële Le Garrec. "Calcium Increase and Substance P Release Induced by the Neurotoxin Brevetoxin-1 in Sensory Neurons: Involvement of PAR2 Activation through Both Cathepsin S and Canonical Signaling." Cells 9, no. 12 (December 17, 2020): 2704. http://dx.doi.org/10.3390/cells9122704.

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Red tides involving Karenia brevis expose humans to brevetoxins (PbTxs). Oral exposition triggers neurotoxic shellfish poisoning, whereas inhalation induces a respiratory syndrome and sensory disturbances. No curative treatment is available and the pathophysiology is not fully elucidated. Protease-activated receptor 2 (PAR2), cathepsin S (Cat-S) and substance P (SP) release are crucial mediators of the sensory effects of ciguatoxins (CTXs) which are PbTx analogs. This work explored the role of PAR2 and Cat-S in PbTx-1-induced sensory effects and deciphered the signaling pathway involved. We performed calcium imaging, PAR2 immunolocalization and SP release experiments in monocultured sensory neurons or co-cultured with keratinocytes treated with PbTx-1 or P-CTX-2. We demonstrated that PbTx-1-induced calcium increase and SP release involved Cat-S, PAR2 and transient receptor potential vanilloid 4 (TRPV4). The PbTx-1-induced signaling pathway included protein kinase A (PKA) and TRPV4, which are compatible with the PAR2 biased signaling induced by Cat-S. Internalization of PAR2 and protein kinase C (PKC), inositol triphosphate receptor and TRPV4 activation evoked by PbTx-1 are compatible with the PAR2 canonical signaling. Our results suggest that PbTx-1-induced sensory disturbances involve the PAR2-TRPV4 pathway. We identified PAR2, Cat-S, PKA, and PKC that are involved in TRPV4 sensitization induced by PbTx-1 in sensory neurons.

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Pérez-Morales, A., and C. J. Band-Schmidt. "BREVETOXINAS EN LAS COSTAS DE MÉXICO: EFECTOS POTENCIALES EN LA SALUD PÚBLICA." CICIMAR Oceánides 26, no. 2 (December 4, 2011): 59. http://dx.doi.org/10.37543/oceanides.v26i2.103.

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Las brevetoxinas provocan la intoxicación neurotóxica por mariscos. Las rutas principales son por ingesta e inhalación con efectos adversos en la salud. A nivel celular las brevetoxinas activan los canales de sodio sensibles al voltaje, permitiendo la entrada de iones de sodio y despolarizando la membrana nerviosa. Diversas especies de microalgas producen estas toxinas, principalmente dinoflagelados del género Karenia, así como rafidofíceas de los géneros Chattonella, Fibrocapsa y Heterosigma. El objetivo de este manuscrito es describir las brevetoxinas, los organismos que las producen, sus mecanismos de acción, los efectos que tienen en la salud pública y las áreas geográficas donde se ha detectado la presencia de especies productoras de brevetoxinas en costas mexicanas. Brevetoxins off the coasts of Mexico: potential effects on public health Brevetoxins cause neurotoxic shellfish poisoning. The main routes are ingestion and inhalation with adverse health effects. At the cellular level brevetoxins activate the voltage-sensitive sodium channels allowing the entry of sodium ions that depolarize the nerve membrane. Different species of microalgae produce these toxins, mainly dinoflagellates of the genus Karenia, and raphidophyceans of the genera Chattonella, Fibrocapsa, and Heterosigma. The aim of this manuscript is to describe the brevetoxins, the organisms that produce them, their mechanisms of action, and the effects on public health and geographic areas where it has detected the presence of brevetoxin-producing species in Mexican coasts.

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Nozawa, Akira, Kuniro Tsuji, and Hitoshi Ishida. "Implication of brevetoxin B1 and PbTx-3 in neurotoxic shellfish poisoning in New Zealand by isolation and quantitative determination with liquid chromatography-tandem mass spectrometry." Toxicon 42, no. 1 (July 2003): 91–103. http://dx.doi.org/10.1016/s0041-0101(03)00123-5.

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Smith, Zacharias J., Douglas E. Conroe, Kimberly L. Schulz, and Gregory L. Boyer. "Limnological Differences in a Two-Basin Lake Help to Explain the Occurrence of Anatoxin-a, Paralytic Shellfish Poisoning Toxins, and Microcystins." Toxins 12, no. 9 (August 30, 2020): 559. http://dx.doi.org/10.3390/toxins12090559.

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Chautauqua Lake, New York, is a two-basin lake with a deeper, cooler, and less nutrient-rich Northern Basin, and a warmer, shallower, nutrient-replete Southern Basin. The lake is populated by a complex mixture of cyanobacteria, with toxigenic strains that produce microcystins, anatoxins, and paralytic shellfish poisoning toxins (PSTs). Samples collected from 24 sites were analyzed for these three toxin classes over four years spanning 2014–2017. Concentrations of the three toxin groups varied widely both within and between years. During the study, the mean and median concentrations of microcystins, anatoxin-a, and PSTs were 91 and 4.0 μg/L, 0.62 and 0.33 μg/L, and 32 and 16 μg/L, respectively. Dihydro-anatoxin was only detected once in Chautauqua Lake, while homo-anatoxin was never detected. The Northern Basin had larger basin-wide higher biomass blooms with higher concentrations of toxins relative to the more eutrophied Southern Basin, however blooms in the North Basin were infrequent. Chlorophyll concentrations and toxins in the two basins were correlated with different sets of environmental and physical parameters, suggesting that implementing controls to reduce toxin loads may require applications focused on more than reductions in cyanobacterial bloom density (e.g., reduction of phosphorus inputs), and that lake limnological factors and morphology are important determinants in the selection of an appropriate management strategy. Chautauqua Lake is a drinking water source and is also heavily used for recreation. Drinking water from Chautauqua Lake is unlikely to be a significant source of exposure to cyanotoxins due to the location of the intakes in the deeper North Basin, where there were generally low concentrations of toxins in open water; however, toxin levels in many blooms exceeded the US Environmental Protection Agency’s recreational guidelines for exposure to cyanotoxins. Current cyanotoxin monitoring in Chautauqua Lake is focused on microcystins. However, the occurrence of blooms containing neurotoxic cyanotoxins in the absence of the microcystins indicates this restricted monitoring may not be sufficient when aiming to protect against exposure to cyanotoxins. The lake has a large number of tourist visitors; thus, special care should be taken to prevent recreational exposure within this group.

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Ishida, Hitoshi, Akira Nozawa, Haruo Nukaya, Lesley Rhodes, Paul McNabb, Patrick T. Holland, and Kuniro Tsuji. "Confirmation of brevetoxin metabolism in cockle, Austrovenus stutchburyi, and greenshell mussel, Perna canaliculus, associated with New Zealand neurotoxic shellfish poisoning, by controlled exposure to Karenia brevis culture." Toxicon 43, no. 6 (May 2004): 701–12. http://dx.doi.org/10.1016/j.toxicon.2004.03.002.

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Ishida, Hitoshi, Akira Nozawa, Haruo Nukaya, and Kuniro Tsuji. "Comparative concentrations of brevetoxins PbTx-2, PbTx-3, BTX-B1 and BTX-B5 in cockle, Austrovenus stutchburyi, greenshell mussel, Perna canaliculus, and Pacific oyster, Crassostrea gigas, involved neurotoxic shellfish poisoning in New Zealand." Toxicon 43, no. 7 (June 2004): 779–89. http://dx.doi.org/10.1016/j.toxicon.2004.03.007.

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Geraci, Joseph R., Donald M. Anderson, Ralph J. Timperi, David J. St. Aubin, Gregory A. Early, John H. Prescott, and Charles A. Mayo. "Humpback Whales (Megaptera novaeangliae) Fatally Poisoned by Dinoflagellate Toxin." Canadian Journal of Fisheries and Aquatic Sciences 46, no. 11 (November 1, 1989): 1895–98. http://dx.doi.org/10.1139/f89-238.

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During a 5–wk period beginning in late November, 1987, 14 humpback whales, Megaptera novaeangliae, died in Cape Cod Bay after eating Atlantic mackerel, Scomber scombrus, containing saxitoxin (STX), a dinoflagellate neurotoxin responsible for paralytic shellfish poisoning in humans. We propose a line of evidence to explain how whales, by virtue of their diving adaptations, may be particularly vulnerable to this systemic neurotoxin. Absence of STX in New England waters and shellfish during the episode suggests that the mackerel, representing the northern stock which spawns in the Gulf of St. Lawrence, accumulated the toxin there and delivered it to the Gulf of Maine and Cape Cod Bay in the fall of 1987. These findings challenge common perceptions of the manner in which planktonic toxins move through the food chain, and offer new insights into natural mortality and standings of marine mammals. It seems appropriate to search for STX and other phytotoxins when investigating marine mammal mortalities.

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Grattan, Lynn M., Laura Kaddis, J. Kate Tracy, and John Glenn Morris. "Long Term Memory Outcome of Repetitive, Low-Level Dietary Exposure to Domoic Acid in Native Americans." International Journal of Environmental Research and Public Health 18, no. 8 (April 9, 2021): 3955. http://dx.doi.org/10.3390/ijerph18083955.

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Domoic acid (DA) is a marine-based neurotoxin that, if ingested via tainted shellfish, is associated with Amnesic Shellfish Poisoning (ASP). These acute effects of elevated DA exposure in humans have been well described. In contrast, the long-term impacts of lower level, repetitive, presumably safe doses of DA (less than 20 ppm) are minimally known. Since Native Americans (NA) residing in coastal communities of the Pacific NW United States are particularly vulnerable to DA exposure, this study focuses on the long-term, 8-year memory outcome associated with their repeated dietary consumption of the neurotoxin. Measures of razor clam consumption, memory, clerical speed and accuracy, and depression were administered over eight years to 500 randomly selected adult NA men and women ages 18–64. Data were analyzed using GEE analyses taking into consideration the year of study, demographic factors, and instrumentation in examining the association between dietary exposure and outcomes. Findings indicated a significant but small decline in total recall memory within the context of otherwise stable clerical speed and accuracy and depression scores. There is reason to believe that a continuum of memory difficulties may be associated with DA exposure, rather than a unitary ASP syndrome.

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Chen, Si, Xiaojun Zhang, Zhongyong Yan, Yangyang Hu, and Yibo Lu. "Development and Application of Immunoaffinity Column Purification and Ultrahigh Performance Liquid Chromatography-Tandem Mass Spectrometry for Determination of Domoic Acid in Shellfish." Toxins 11, no. 2 (February 1, 2019): 83. http://dx.doi.org/10.3390/toxins11020083.

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Domoic acid (DA) is a neurotoxin associated with amnesic shellfish poisoning (ASP). Though LC coupled to tandem mass spectrometry (LC-MS/MS) has become the preferred method for DA determination, traditional sample pretreatment is still labor-intensive. In this study, a simple, efficient and selective method for LC-MS/MS analysis of DA in shellfish was established by optimizing clean-up procedures on a self-assembly immunoaffinity column (IAC). Shellfish was extracted with 75% methanol twice and diluted with phosphate buffered saline (PBS, 1:2). The mixture was purified on IAC as follows: preconditioned with PBS, loaded with sample, washed by 50% MeOH, and eluted with MeOH containing 2% ammonium hydroxide. Concentrated analyte was monitored by multiple reaction monitoring (MRM) using electrospray (ESI) positive ion mode throughout the LC gradient elution. Based on the post-extraction addition method, matrix effects for various shellfish matrices were found to be less than 8%. The developed method was fully validated by choosing mussel as the representative matrix. The method had a limit of detection (LOD) of 0.02 µg·g−1, showed excellent linear correlation in the range of 0.05–40 µg·g−1, and obtained ideal recoveries (91–94%), intra-day RSDs (6–8%) and inter-day RSDs (3–6%). The method was successfully applied to DA determination in 59 shellfish samples, with a detection rate of 10% and contaminated content of 0.1–14.9 µg·g−1.

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Dyhrman, Sonya T., Sheean T. Haley, Jerry A. Borchert, Bob Lona, Nicole Kollars, and Deana L. Erdner. "Parallel Analyses of Alexandrium catenella Cell Concentrations and Shellfish Toxicity in the Puget Sound." Applied and Environmental Microbiology 76, no. 14 (May 21, 2010): 4647–54. http://dx.doi.org/10.1128/aem.03095-09.

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ABSTRACT Alexandrium catenella is widespread in western North America and produces a suite of potent neurotoxins that cause paralytic shellfish poisoning (PSP) in humans and have deleterious impacts on public health and economic resources. There are seasonal PSP-related closures of recreational and commercial shellfisheries in the Puget Sound, but the factors that influence cell distribution, abundance, and relationship to paralytic shellfish toxins (PSTs) in this system are poorly described. Here, a quantitative PCR assay was used to detect A. catenella cells in parallel with state shellfish toxicity testing during the 2006 bloom season at 41 sites from April through October. Over 500,000 A. catenella cells liter−1 were detected at several stations, with two main pulses of cells driving cell distribution, one in June and the other in August. PSTs over the closure limit of 80 μg of PST 100 per g of shellfish tissue were detected at 26 of the 41 sites. Comparison of cell numbers and PST data shows that shellfish toxicity is preceded by an increase in A. catenella cells in 71% of cases. However, cells were also observed in the absence of PSTs in shellfish, highlighting the complex relationship between A. catenella and the resulting shellfish toxicity. These data provide important information on the dynamics of A. catenella cells in the Puget Sound and are a first step toward assessing the utility of plankton monitoring to augment shellfish toxicity testing in this system.

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Bates, S. S., C. J. Bird, A. S. W. de Freitas, R. Foxall, M. Gilgan, L. A. Hanic, G. R. Johnson, et al. "Pennate Diatom Nitzschia pungens as the Primary Source of Domoic Acid, a Toxin in Shellfish from Eastern Prince Edward Island, Canada." Canadian Journal of Fisheries and Aquatic Sciences 46, no. 7 (July 1, 1989): 1203–15. http://dx.doi.org/10.1139/f89-156.

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An outbreak of food poisoning in Canada during autumn 1987 was traced to cultured blue mussels (Mytilus edulis) from the Cardigan Bay region of eastern Prince Edward Island (P.E.I.). The toxin, identified as domoic acid, had not previously been found in any shellfish and this outbreak represents the first known occurrence of human poisoning by this neurotoxin. A plankton bloom at the time of the outbreak consisted almost entirely of the pennate diatom, Nitzschia pungens f. multiseries, and a positive correlation was found between the number of N. pungens cells and the concentration of domoic acid in the plankton. Nitzschia pungens f. multiseries isolated from Cardigan Bay produced domoic acid in culture at levels (1 to 20 pg∙cell−1) comparable with values estimated for N. pungens in the plankton samples. Isolates of several Cardigan Bay phytoplankton, including the closely related species Nitzschia seriata, failed to produce domoic acid. Other Nitzschia spp. and two Amphora coffeaeformis isolates also failed to produce domoic acid. We conclude that N. pungens was the major source of the domoic acid in toxic mussels in eastern P.E.I. The recurrence, in November 1988, of a monospecific bloom of N. pungens and the presence of domoic acid in plankton and mussels reinforced this conclusion.

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Yen, Tien-Jui, Marco Lolicato, Rhiannon Thomas-Tran, J. Du Bois, and Daniel L. Minor. "Structure of the saxiphilin:saxitoxin (STX) complex reveals a convergent molecular recognition strategy for paralytic toxins." Science Advances 5, no. 6 (June 2019): eaax2650. http://dx.doi.org/10.1126/sciadv.aax2650.

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Dinoflagelates and cyanobacteria produce saxitoxin (STX), a lethal bis-guanidinium neurotoxin causing paralytic shellfish poisoning. A number of metazoans have soluble STX-binding proteins that may prevent STX intoxication. However, their STX molecular recognition mechanisms remain unknown. Here, we present structures of saxiphilin (Sxph), a bullfrog high-affinity STX-binding protein, alone and bound to STX. The structures reveal a novel high-affinity STX-binding site built from a “proto-pocket” on a transferrin scaffold that also bears thyroglobulin domain protease inhibitor repeats. Comparison of Sxph and voltage-gated sodium channel STX-binding sites reveals a convergent toxin recognition strategy comprising a largely rigid binding site where acidic side chains and a cation-π interaction engage STX. These studies reveal molecular rules for STX recognition, outline how a toxin-binding site can be built on a naïve scaffold, and open a path to developing protein sensors for environmental STX monitoring and new biologics for STX intoxication mitigation.

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Su Nyun Pau, Suriyanti, Dzulhelmi Muhammad Nasir, and Gires Usup. "SCREENING OF TOXIC MARINE NITZSCHIA SPECIES (BACILLARIOPHYCEAE) IN MALAYSIA." Jurnal Kelautan: Indonesian Journal of Marine Science and Technology 10, no. 1 (May 1, 2017): 97. http://dx.doi.org/10.21107/jk.v10i1.2635.

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Amnesic Shellfish Poisoning (ASP) is a type of intoxication caused by the neurotoxin domoic acid (DA). The diatom genus Nitzschia is capable of producing this toxin. Screening for the presence of toxic Nitzschia spp. was carried out at various estuaries in Malaysia. Nitzschia-like cells were isolated and established into clonal cultures. Late stationary phase of cultures were harvested and tested for toxin production using HPLC. Toxin production and compound was verified by LC-MS. From the analyses, at least three cultures were detected with DA, while the rest of the cultures did not show detectable amounts of DA. The localities of the toxic species are Johor and Sabah. Here we conclude that toxic Nitzschia species are present in Malaysian water.Keywords: diatom, estuary, intoxication, safety, toxic

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Cirés, Samuel, Lars Wörmer, Andreas Ballot, Ramsy Agha, Claudia Wiedner, David Velázquez, María Cristina Casero, and Antonio Quesada. "Phylogeography of Cylindrospermopsin and Paralytic Shellfish Toxin-Producing Nostocales Cyanobacteria from Mediterranean Europe (Spain)." Applied and Environmental Microbiology 80, no. 4 (December 13, 2013): 1359–70. http://dx.doi.org/10.1128/aem.03002-13.

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ABSTRACTPlanktonicNostocalescyanobacteria represent a challenge for microbiological research because of the wide range of cyanotoxins that they synthesize and their invasive behavior, which is presumably enhanced by global warming. To gain insight into the phylogeography of potentially toxicNostocalesfrom Mediterranean Europe, 31 strains ofAnabaena(Anabaena crassa,A. lemmermannii,A. mendotae, andA. planctonica),Aphanizomenon(Aphanizomenon gracile,A. ovalisporum), andCylindrospermopsis raciborskiiwere isolated from 14 freshwater bodies in Spain and polyphasically analyzed for their phylogeography, cyanotoxin production, and the presence of cyanotoxin biosynthesis genes. The potent cytotoxin cylindrospermopsin (CYN) was produced by all 6Aphanizomenon ovalisporumstrains at high levels (5.7 to 9.1 μg CYN mg−1[dry weight]) with low variation between strains (1.5 to 3.9-fold) and a marked extracellular release (19 to 41% dissolved CYN) during exponential growth. Paralytic shellfish poisoning (PSP) neurotoxins (saxitoxin, neosaxitoxin, and decarbamoylsaxitoxin) were detected in 2Aphanizomenon gracilestrains, both containing thesxtAgene. This gene was also amplified in non-PSP toxin-producingAphanizomenon gracileandAphanizomenon ovalisporum. Phylogenetic analyses supported the species identification and confirmed the high similarity of SpanishAnabaenaandAphanizomenonstrains with other European strains. In contrast,Cylindrospermopsis raciborskiifrom Spain grouped together with American strains and was clearly separate from the rest of the European strains, raising questions about the current assumptions of the phylogeography and spreading routes ofC. raciborskii. The present study confirms that the nostocalean genusAphanizomenonis a major source of CYN and PSP toxins in Europe and demonstrates the presence of thesxtAgene in CYN-producingAphanizomenon ovalisporum.

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Finch, Sarah, Michael Boundy, and D. Harwood. "The Acute Toxicity of Tetrodotoxin and Tetrodotoxin–Saxitoxin Mixtures to Mice by Various Routes of Administration." Toxins 10, no. 11 (October 23, 2018): 423. http://dx.doi.org/10.3390/toxins10110423.

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Tetrodotoxin (TTX) is a potent neurotoxin associated with human poisonings through the consumption of pufferfish. More recently, TTX has been identified in bivalve molluscs from diverse geographical environments, including Europe, and is therefore recognised as an emerging threat to food safety. A recent scientific opinion of the EFSA Panel on Contaminants in the Food Chain recognised the need for further data on the acute oral toxicity of TTX and suggested that, since saxitoxin (STX) and TTX had similar modes of action, it was possible that their toxicities were additive so could perhaps be combined to yield one health-based guideline value. The present study determined the toxicity of TTX by various routes of administration. The testing of three different mixtures of STX and TTX and comparing the experimentally determined values to those predicted on the basis of additive toxicity demonstrated that the toxicities of STX and TTX are additive. This illustrates that it is appropriate to treat TTX as a member of the paralytic shellfish group of toxins. Since the toxicity of TTX was found to be the same as STX by feeding, a molar toxicity equivalence factor of 1.0 for TTX can be applied.

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Lonati, Davide, Azzurra Schicchi, Marta Crevani, Eleonora Buscaglia, Giulia Scaravaggi, Francesca Maida, Marco Cirronis, Valeria Margherita Petrolini, and Carlo Alessandro Locatelli. "Foodborne Botulism: Clinical Diagnosis and Medical Treatment." Toxins 12, no. 8 (August 7, 2020): 509. http://dx.doi.org/10.3390/toxins12080509.

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Botulinum neurotoxins (BoNTs) produced by Clostridia species are the most potent identified natural toxins. Classically, the toxic neurological syndrome is characterized by an (afebrile) acute symmetric descending flaccid paralysis. The most know typical clinical syndrome of botulism refers to the foodborne form. All different forms are characterized by the same symptoms, caused by toxin-induced neuromuscular paralysis. The diagnosis of botulism is essentially clinical, as well as the decision to apply the specific antidotal treatment. The role of the laboratory is mandatory to confirm the clinical suspicion in relation to regulatory agencies, to identify the BoNTs involved and the source of intoxication. The laboratory diagnosis of foodborne botulism is based on the detection of BoNTs in clinical specimens/food samples and the isolation of BoNT from stools. Foodborne botulism intoxication is often underdiagnosed; the initial symptoms can be confused with more common clinical conditions (i.e., stroke, myasthenia gravis, Guillain–Barré syndrome—Miller–Fisher variant, Eaton–Lambert syndrome, tick paralysis and shellfish or tetrodotoxin poisoning). The treatment includes procedures for decontamination, antidote administration and, when required, support of respiratory function; few differences are related to the different way of exposure.

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Oudra, B., M. El Andaloussi, S. Franca, P. Barros, R. Martins, K. Oufdou, B. Sbiyyaa, M. Loudiki, N. Mezrioui, and V. Vasconcelos. "Harmful cyanobacterial toxic blooms in waste stabilisation ponds." Water Science and Technology 42, no. 10-11 (November 1, 2000): 179–86. http://dx.doi.org/10.2166/wst.2000.0637.

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A coccoid picocyanobacterium Synechocystis sp. (0.6-2 μm of cell diameter) was found to be dominant during summer period in the experimental wastewater stabilisation pond of Marrakesh. The taxonomy of this isolated strain was confirmed by electron microscope study. The general patterns of ultrastructure and the mode of cell division resemble Chroococcales. The cyanobacterium strain was axenic and cultured on both inorganic Z8 and BG13 media. Mammalian toxicity was confirmed by mice bioassay. The major sympton of poisoning was severe diarrhoea. Histopathological study shows a slight hepatotoxicosis associated with a pronounced change in the intestinal mucosa which shows swelling and destruction of villi epithelium and shedding of enterocytes into the lumen. Although slow, these kinds of poisoning are comparable to those induced by okadiac acid intraperitoneal mice injection (diarrhetic shellfish poisoning “DSP” toxins). By using the enzyme-linked immunosorbent assay (ELISA), the amount ofhepatotoxins “microcystins” was determined. The result shows that Synechocystis can produce a small amount of total microcystine [an average of 15 μg−1 dry weight corresponding to 20 ng(109cell)−1]. These findings lead us to consider Synechocystis as both a potent neurotoxin and hepatotoxin producer. Because of the confirmed cyanobacterium toxicity, an eventual ecological implication should be considered. However, a toxic chronic test experiment on Daphnia was simultaneously carried out. Juvenile D. magna (less than 24 hours old), were fed three concentrations (104, 106, 108 cells / ml) of Synechocystis. A group of organisms fed with Chlorella vulgaris (3. 105 cells/ml) and another group without food, were studied as control treatments. Only animals cultured with 104 cells/ml of cyanobacterium survived at 80% until the end of the test (21 days). Reproduction and normal growth occurred in control treatments fed with Chlorella vulgaris and the group fed with the lowest concentration of Synechocystis. One-way ANOVA statistical analyses show significant differences in Daphnia survival and growth, between treatments with and without Synechocystis and between treatments with and without food. In terms of this study, there is evidence that toxic picocyanobacteria blooms occurring in wastewater stabilization ponds of Marrakesh, could have harmful repercussions on zooplanktonic, bacteria and other algae communities. Consequently, this will constitute a possible hindrance for sewage self-purification process and system treatment performance. In addition, the reuse of such treated wastewater effluent for irrigation will constitute an additional, potent, health hazard for animals and human's.

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Galluzzi, Luca, Antonella Penna, Elena Bertozzini, Magda Vila, Esther Garcés, and Mauro Magnani. "Development of a Real-Time PCR Assay for Rapid Detection and Quantification of Alexandrium minutum (a Dinoflagellate)." Applied and Environmental Microbiology 70, no. 2 (February 2004): 1199–206. http://dx.doi.org/10.1128/aem.70.2.1199-1206.2004.

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ABSTRACT The marine dinoflagellate genus Alexandrium includes a number of species which produce neurotoxins responsible for paralytic shellfish poisoning (PSP), which in humans may cause muscular paralysis, neurological symptoms, and, in extreme cases, death. A. minutum is the most widespread toxic PSP species in the western Mediterranean basin. The monitoring of coastal waters for the presence of harmful algae also normally involves microscopic examinations of phytoplankton populations. These procedures are time consuming and require a great deal of taxonomic experience, thus limiting the number of specimens that can be analyzed. Because of the genetic diversity of different genera and species, molecular tools may also help to detect the presence of target microorganisms in marine field samples. In this study, we developed a real-time PCR-based assay for rapid detection of all toxic species of the Alexandrium genus in both fixative-preserved environmental samples and cultures. Moreover, we developed a real-time quantitative PCR assay for the quantification of A. minutum cells in seawater samples. Alexandrium genus-specific primers were designed on the 5.8S rDNA region. Primer specificity was confirmed by using BLAST and by amplification of a representative sample of the DNA of other dinoflagellates and diatoms. Using a standard curve constructed with a plasmid containing the ITS1-5.8S-ITS2 A. minutum sequence and cultured A. minutum cells, we determined the absolute number of 5.8S rDNA copies per cell. Consequently, after quantification of 5.8S rDNA copies in samples containing A. minutum cells, we were also able to estimate the number of cells. Several fixed A. minutum bloom sea samples from Arenys Harbor (Catalan Coast, Spain) were analyzed using this method, and quantification results were compared with standard microscopy counting methods. The two methods gave comparable results, confirming that real-time PCR could be a valid, fast alternative procedure for the detection and quantification of target phytoplankton species during coastal water monitoring.

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SCHWARZ, M., K. JANDOVÁ, I. STRUK, D. MAREŠOVÁ, J. POKORNÝ, and V. RILJAK. "Low Dose Domoic Acid Influences Spontaneous Behavior in Adult Rats." Physiological Research, June 16, 2014, 369–76. http://dx.doi.org/10.33549/physiolres.932636.

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Domoic acid (DA) is a potent marine neurotoxine present in seafood. Intoxication by DA causes gastrointestinal symptoms like vomiting and diarrhoea and also the so-called amnesic shellfish poisoning (inflicting memory impairment and seizures). Since exposure to non-convulsive doses is relevant to the human health, we investigated the effect of low dose DA administration in adult Wistar rats. Rats were administered with DA at the dose 1.0 mg/kg and their behavior was monitored for one hour in three sessions. The first session started immediately after DA administration. The second and third session started one and two weeks later. After the third session, the histochemical analysis of the hippocampi of the animals was conducted (Fluoro-Jade B, bis-benzimide). DA increased time spent by locomotion and distance travelled in the second half of the first session and this effect was pronounced during the second and third session. Exploratory rearing was decreased by DA administration in the first half of the first session. DA influenced the grooming in biphasic manner (decrease followed by an increase of time spent by grooming). This biphasic trend was observed even two weeks after the DA administration. Histochemistry of DA treated rats did not confirm the presence of apoptotic bodies, Fluoro-Jade B positive cells were not found neither in CA1 nor CA3 area of the hippocampi. Our study revealed that a low dose of DA affect short and long-term the spontaneous behavior of rats without inducing neuronal damage.

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Journal articles on the topic 'Neurotoxic Shellfish Poisoning'

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