Brevetoxin Poisoning

Blocks action potentials in nerves by preventing sodium flow, reducing nerve conduction 

Abdomen - pain Bowel movements - diarrhea Breathing - diff, acute (acute dyspnea) [1] Breath sounds - wheezes [ 1 ] 

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Symptoms of Brevetoxins Poisoning Human Exposure to Neurotoxic Shellfish Poisoning... 

Templeton, C.B., Poli, M. A., and Leclaire, R.D. 1988. Antibodies to prevent the effects of brevetoxin poisoning in conscious rats. Abstract. Gov Rep Announce Index 88, 155. 

Arsine poisoning Brevetoxin poisoning BZ poisoning Campylobacteriosis Chickenpox Cholera... 

This chapter deals with single crystal x-ray diffraction as a tool to study marine natural product structures. A brief introduction to the technique is given, and the structure determination of PbTX-1 (brevetoxin A), the most potent of the neurotoxic shellfish poisons produced by Ptychodiscus brevis in the Gulf of Mexico, is presented as an example. The absolute configuration of the brevetoxins is established via the single crystal x-ray diffraction analysis of a chiral 1,2-dioxolane derivative of PbTX-2 (brevetoxin B). 

The toxicological consequences of P. brevis red tides are mass mortality of fishes exposed to the red tide toxic shellfish which, if consumed, result in human neurotoxic shellfish poisoning and an irritating aerosol which results from contact with P. brevis cell particles entrapped in seaspray. In all cases, the threshhold levels for intoxication are in the picomolar to nanomolar concentration ranges, implying a specific locus or loci of action for brevetoxins (reviewed in 6). 

Microalgae produce many potent natural products in the form of complex polycyclic polyethers, a type of polyketide. The ladder-like polyether brevetoxin B (Fig. 1.8a) (Lin et al. 1981) is representative of a host of such toxins, which include cigua-toxin (Scheuer et al. 1967), yessotoxin (Murata et al. 1987), maitotoxin (Murata et al. 1993), gambieric acids (Murata et al. 1992), and azaspiracid (Satake et al. 1998). Brevetoxin B, one of the causitive agents of red tide poisoning, can be isolated from... 

The toxins responsible for DSP include a series of polyether molecules (including okadaic acid and six derivatives of dinophysistoxin), four pecteno-toxins (polyether lactones), and yessotoxins (including two sulfate esters that resemble brevetoxins) (Murata, 1982 Murata, 1987 Tachibana et al., 1981 Yasumoto, 1989). Diarrhetic shellfish poisons are produced primarily by dinoflagellates from the genera Dinophysis, although Prorocentrum lima also produces both okadaic acid and dinophysistoxin-1 (Heredia-Tapia et al., 2002). 

Nozawa, A., Tsuji, K. and Ishida, H., 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, 1, 91, 2003. 

The cockle, Austrovenus stutchburyi from New Zealand contained brevetoxin Bi (225) [230] and the greenshell mussel, Pema canaliculus contained brevetoxin B3 (226) [231]. A further brevetoxin analogue, brevetoxin B2 (227) was isolated from the hepatopancreas of P. canaliculus [232], while the major toxin in neurological shellfish poisoning (NSP) associated with P. canaliculus was identified as brevetoxin B4 (228) [233]. 

Neurotoxic Shellfish Poisoning (NSP) is caused by a red-tide producer that was first identified in 1880 from Florida, with earlier historical references. It causes sickness in humans lasting several days. NSP is not fatal to humans however, it is known to kill fish, invertebrates, seabirds, and marine mammals (e.g., manatees). It is caused by the brevetoxin family (brevetoxin + 10 related compounds produced by the dinoflagellate Karenia brevis a.k.a. Gymnodinium breve. The main contamination problems include oysters, clams, and other filter feeders of the Gulf of Mexico and southeast Atlantic, including North Carolina. 

After the 1992-93 outbreak of neurotoxic shellfish poisoning (NSP) in New Zealand, several metabolites of brevetoxins were isolated from seafood . NSP is a term applied to an illness resulting from the ingestion of shellfish exposed to blooms of dinoflagellate K. brevis < 1965MI111, 1991MI471>. 

How can this scattered taxonomic occurrence of the picrotoxanes be explained Many of the apparent chemical convergences in animal toxins have been explained as toxins received via the food chain e.g. brevetoxin, pederin, saxitoxin, tetrodo-toxin, and the toxins of the arrow-poison frogs). This may explain the occurrence of picrotoxanes in both parasitic animals and plants, but further research will be necessary for a better understanding of this phenomenon. 

Ishida, H., Nozawa, A., Nukaya, H., Rhodes, L., McNabb, P, Holland, PT, Tsuji, K. 2004a. 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, 701-712. 

Morohashi, A., Satake, M., Naoki, H., Kasper, H.F., Oshima, Y, Yasumoto, T. 1999. Brevetoxin B4 isolated from greenshell mussels Pema canaliculus, the major toxin involved in neurotoxic shellfish poisoning in New Zealand. Natural Toxins 7, 45 8. 

Poli, M.A., Musser, S.M., Dickey, R.W., Eilers, P.P., and Hall, S. 2000. Neurotoxic shellfish poisoning and brevetoxin metabolites a case study from Elorida. Toxicon 38, 981-993. 

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