PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Shellfish Poisoning”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 217 records · Page 12Linked to original sources
PubMed1997

A simple procedure for sulfation and 35S radiolabelling of paralytic shellfish poisoning (PSP) gonyautoxins.

A method is described to sulfate PSP toxins at various positions in the molecule and to prepare 35S labelled compounds using H2(35)SO4 in the presence of dicyclohexylcarbodiimide (DCC). The 11-sulfates of saxitoxin and neosaxitoxin, known as gonyautoxins, are often the most abundant of the PSP toxins in algae and contaminated shellfish. Receptor site binding and antibody assays based on these analogues should, therefore, better reflect toxicity than those in which saxitoxin is used. Although the specific activity of 35S-gonyautoxins is lower than that of commercially available 3H-saxitoxin, the label is strongly bound and is not lost through proton exchange with water as occurs with tritiated saxitoxin. The labelling procedure is rapid, inexpensive and can be done on a small scale. Sulfate can be removed from the 11-position of GTX's in methanolic-HCl and from the 21-position by mild acid hydrolysis and H2(35)SO4 added in 5-10-fold excess. Addition or exchange occurs rapidly on mixing DCC in dimethylformamide with dry toxin and sulfate. Reaction conditions were optimized and reaction products identified by capillary electrophoresis, autoradiography and ionspray mass spectrometry. Together with methods for selective removal of sulfate, the sulfation reaction provides an additional way to prepare some of the naturally occurring derivatives of saxitoxin, many of which are sulfates.

Animals↗
PubMed2003

[Neurological manifestations of fish, mollusk and shellfish poisoning].

Sea-food poisoning is observed in several areas of the world. Intoxication results from ingestion of fresh fish, mollusks, or shellfish contaminated by toxins produced by microorganisms (dinoflagellates). Neurological manifestations are sometimes associated with signs and may be life-threatening. We describe here the principle toxins, their geographic distribution, clinical manifestations, therapeutic management, and possible prevention measures.

Adult↗
PubMed2005

New targets in diarrhetic shellfish poisoning control.

The toxic profile of dinoflagellates varies even among identical species, raising an interesting question about the mechanism of toxin regulation and production. In consequence, it also poses a considerable problem in their control methods. In this paper, we report on the isolation and structural elucidation of several new ester derivatives of okadaic acid (OA) from artificial cultures of the genus Prorocentrum. These new compounds enlarge the range of target molecules that must be considered in the monitoring programs.

Animals↗
PubMed1996

Study on neurotoxic shellfish poisoning involving the oyster, Crassostrea gigas, in New Zealand.

Lipid-soluble polyether marine toxins were isolated from 80% methanol extract of oysters, Crassostrea gigas, harvested in 1993 at Tiki Road, Coromandel Peninsula, New Zealand, by chromatography on columns of LH-20 and ODS (C18), followed by reversed-phase high-performance liquid chromatography. They were identified as known brevetoxins, PbTx-2 and 3. PbTx-3 was also isolated from oysters collected at Rangaunu Harbour in February 1994 and June 1995, followed by the above procedures.

Animals↗
PubMed2006

Detection of the marine toxin okadaic acid in mussels during a diarrhetic shellfish poisoning (DSP) episode in Thermaikos Gulf, Greece, using biological, chemical and immunological methods.

An approach involving chemical and biological techniques was taken for the detection and quantification of the marine toxin okadaic acid (OA) in mussels from Thermaikos Gulf, Greece, during a 4-month DSP episode that occurred in 2002. Samples were analyzed using the mouse bioassay, high performance liquid chromatography (HPLC) with fluorimetric detection and an enzyme-linked immunosorbent assay (ELISA). Okadaic acid was quantifiable at three different sites of Thermaikos Gulf reaching a maximum concentration of 36 microg/g hepatopancreas. High correlation was revealed between results derived from HPLC and ELISA (R2=0.998), while 91% consistency between HPLC and the mouse bioassay results was observed.

Animals↗
PubMedDate not supplied

A study of ten toxins associated with paralytic shellfish poison using prechromatographic oxidation and liquid chromatography with fluorescence detection.

Ten paralytic shellfish toxins [saxitoxin, neosaxitoxin, B-1, B-2, gonyautoxin 1, 2, and 3 (i.e., GTX-1, GTX-2, and GTX-3), C-1, C-2, and C-3] were oxidized at room temperature under mildly basic conditions with hydrogen peroxide or periodic acid. The products were then analyzed by liquid chromatography (LC). The N-1-hydroxylated toxins (neosaxitoxin, B-2, GTX-1, and C-3) formed fluorescent products after periodate oxidation at ca pH 8.7, but did not form fluorescent derivatives with peroxide oxidation. The non-N-1-hydroxylated toxins (saxitoxin, B-1, GTX-2, GTX-3, C-1, and C-2) formed highly fluorescent derivatives with both peroxide and periodate oxidations. Individual toxins produced mainly single fluorescent peaks by reverse-phase LC. However, all GTX toxins eluted with the same retention time. Also, C-1 and C-2 eluted together, as did neosaxitoxin and B-2. The non-N-1-hydroxylated toxins could be detected in quantities as low as 20-50 pg/injection, while the N-1-hydroxy analogues could be detected at levels as low as 100-500 pg/injection. UV absorption and fluorescence emission spectra were similar for the oxidation products of all toxins examined (max. 333 +/- 2 nm absorption, 389 +/- 4 nm fluorescence emission).

Animals↗