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At least 343 records · Page 19Linked to original sources
PubMed2005

Collapse of mitochondrial membrane potential and caspases activation are early events in okadaic acid-treated Caco-2 cells.

Diarrhetic Shellfish Poisoning (DSP) results from the consumption of shellfish contaminated with okadaic acid (OA) or one of the dinophysistoxins (DTX). It has been reported that this toxin induces apoptosis in several cell models, but the molecular events involved in this process have not been clarified. In this report we studied intracellular signals induced by OA in Caco-2 cells: mitochondrial membrane potential, F-actin depolymerization, caspases activation, cell proliferation and cell membrane integrity. Results indicate that caspases-8 and -9 increased their activity after 30 min of OA treatment according to their role as initiator caspases. In contrast, activation of the downstream caspase-3 is a later event in the execution phase of apoptosis. Mitochondrial membrane potential changes are detected at 30 min of OA exposure indicating that this is an early response in the apoptotic cascade. F-actin depolymerization occurs after 24h of incubation with OA and this effect is significant at low doses of the toxin. LDH is released into the culture medium, although there is not PI uptake, indicative of a significant cell death in addition to apoptosis. Moreover, OA led to a dose- and time-dependent decrease in cellular proliferation.

Actins↗
PubMed1996

Dinophysistoxin-2: the predominant diarrhoetic shellfish toxin in Ireland.

Diarrhoetic shellfish poisoning (DSP) in Europe is due mainly to the presence of the dinoflagellate toxin, okadaic acid (OA). However, analysis of cultivated mussels (Mytilus edulis) from southwest Ireland revealed that an isomer of OA, dinophysistoxin-2, was the major toxin present during DSP episodes. Using fluorimetric HPLC, following derivatisation with 9-anthryldiazomethane, both OA and DTX-2 were found in shellfish during a prolonged toxic episode in 1991. However, examination of similar mussel cultivation locations in 1994 showed that DTX-2 was even more predominant. During this DSP period, OA levels were less than 0.7 microgram/g, whereas maximum DTX-2 levels of 6.3 micrograms/g hepatopancreas were recorded. This toxicity in shellfish occurred soon after high cell counts of Dinophysis acuta were observed. As well as large seasonal variability in toxin levels in rope cultured mussels, substantial variations were also observed, both horizontally and vertically, within the water column.

Animals↗
PubMed1994

A competitive enzyme-linked immunoassay for domoic acid determination in human body fluids.

A polyclonal antiserum was raised in mice against domoic acid. Two of three immunogens consisted of domoic acid coupled to ovalbumin (OVA) and keyhole limpet haemocyanin at molar ratios of 47:1 and 44:1, respectively using a carbodiimide reaction. Titres of both antisera exceeded 1/35,000 against domoic acid coupled to the non-relevant carrier. Domoic acid was also conjugated to bovine serum albumin at a molar ratio of 30:1 using N-hydroxysuccinimidyl-4-azidobenzoate, a photoreactive compound. This immunogen, however, produced no measurable serum titres against domoic acid. The antiserum produced against the OVA conjugate displayed the highest affinity for free domoic acid in competitive enzyme-linked immunosorbent assay (ELISA). Furthermore, this antiserum preparation did not significantly cross-react with glutamic acid, aspartic acid, the structural analogue kainic acid, or the paralytic shellfish toxin, saxitoxin. The competitive ELISA was used to quantify domoic acid concentrations in human body fluids spiked with pure domoate. The lower limits of accurate domoic acid determinations in competitive ELISA were 0.2 micrograms/ml in urine, 0.25 micrograms/ml in plasma and 10 micrograms/ml in milk. It was concluded that the competitive ELISA described herein could be used to quantitate directly the concentration of domoic acid in the body fluids of individuals with amnesic shellfish poisoning.

Animals↗
PubMed1996

Occurrence of paralytic toxin in Taiwanese crab Atergatopsis germaini.

Paralytic toxicity was detected by paralytic shellfish poison bioassay for all 17 specimens of the xanthid crab A. germaini collected from northern Taiwan in November 1993. The average toxicity of crab specimens was 3809 +/- 2591 mouse units (mean +/- S.D.). The toxin was partially purified from ethanolic extract of the crab by ultrafiltration and Bio-Gel P-2 column chromatography. Electrophoresis, TLC, HPLC, ultraviolet spectrum and GC-MS analyses indicated that the crab toxin was composed of gonyautoxin 3 (50%), neosaxitoxin and saxitoxin (7%), a novel paralytic shellfish poison-like toxin (40%) and tetrodotoxin (3%).

Animals↗
PubMed1993

[Poisoning by the consumption of shellfish contaminated with paralytic venom in the XII Region, Chile. Anatomopathological study].

The necropsy findings of ten subjects died as a consequence of paralytic shellfish intoxication are presented. These deaths occurred between march 1991 and january 1992, affected to seamen and occurred within 72 hours of contaminated shellfish ingestion. Necropsies were performed within 24 hours of death. The most outstanding necropsy findings were the presence of pink lividities, mydriasis and isocoria, airway obstruction with gastric contents, severe brain, lung liver and spleen swelling and edema, and digestive and respiratory mucosal congestion and friability. The toxicological study of urine, gastric content and organ samples revealed the presence of shellfish paralytic poison.

Adolescent↗
PubMed2001

Domoic acid accumulation in French shellfish in relation to toxic species of Pseudo-nitzschia multiseries and P. pseudodelicatissima.

Within the French phytoplankton monitoring network (REPHY), domoic acid (DA), the toxin responsible for amnesic shellfish poisoning, was first detected in samples collected in 1998. Toxin analysis by the official method [liquid chromatography with diode array detection (LC/DAD)] was performed when Pseudo-nitzschia cell concentration was greater than 1.0 x 10(5) cells/l. LC/DAD results obtained in 1999 and 2000 showed increased DA accumulation in bivalves sampled at different sites along French coasts. The toxin maximum in 1999 was 3.2 microg DA/g of whole tissue, whereas the levels in 2000 (53 microg) were above the sanitary threshold (20 microg DA/g tissue). Phytoplankton samples collected during blooms were observed by both light and scanning electron microscopy (SEM). Identification of phytoplankton species by SEM analyses confirmed the presence of two known DA-producing species, P. pseudodelicatissima and P. multiseries. LC/DAD results for a mass culture of P. multiseries indicated that this species was involved in DA accumulation in French shellfish.

Animals↗
PubMedDate not supplied

Development of a protein phosphatase-based assay for the detection of phosphatase inhibitors in crude whole cell and animal extracts.

Diarrhetic shellfish poisoning (DSP) is a serious and globally widespread phytoplankton-related seafood illness. Although DSP is rarely life-threatening, it causes incapacitating diarrhea and vomiting with no known medical treatments. In addition, phytoplankton producing DSP toxins have been identified in temperate coastal waters worldwide, and their numbers may be increasing as a result of coastal eutrophication. The toxic effects of the major DSP toxins, okadaic acid and dinophysistoxin-1 (35-methylokadaic acid), appear to originate from their inhibitory activity against a family of structurally related serine/threonine protein phosphatases (PSPases). In particular, the inhibition of essential PSPases (e.g. PP1 and PP2A) has catastrophic consequences in most eukaryonic cells. Exploiting the potent inhibitory property of the DSP toxins, we have developed an enzyme-based assay (PP2A assay) capable of detecting both okadaic acid and dinophysistoxin-1 in nanogram amounts. The assay employs purified PP2A, which has an extremely high affinity for both DSP toxins. This provides the PP2A assay with a level of sensitivity comparable to, or surpassing, that of most monoclonal antibody probes. To evaluate the PP2A assay as a means of detecting contaminated shellfish, a series of spike recovery experiments was conducted. The findings from these studies suggest that the PP2A assay has the potential for development into a rapid and relatively simple method for detecting PSPase inhibitors in crude extracts produced from shellfish.

Animal Population Groups↗
PubMed1998

[Algal toxins, inhibitors of serine/threonine phosphatases].

Under certain environmental conditions, marine and freshwater phytoplankton may produce phycotoxins inhibitors of serine/thréonine protein phosphatases 1, 2A and 3. In the marine environment, dinoflagellates produce fatty polyethers: okadaic acid and its derivatives, the dinophysistoxins, which accumulate in shellfish and can cause diarrhetic shellfish poisoning (DSP) when ingested. In freshwater, the toxins are microcystins and nodularin, 7 or 5 amino acid cyclic peptides and are hepatotoxic. These toxins have caused massive poisoning of wild animals or domestic livestock and now are a health threat for humans through use of drinking and recreation water. Moreover, all these toxins are potent tumor promoters but belong to a new class, different from the TPA class, because they do not act on Protein Kinase C. Although the mutagenicity Ames test responds negatively, several results show their genotoxic potential, and therefore they are a health hazard through chronic exposition to low doses. Finally, okadaic acid, through its easy penetration in all cellular types can be used as a tool to study mechanisms involved in protein phosphorylation/dephosphorylation processes.

Animals↗
PubMed2003

Spatial and temporal evolution of PSP toxins along the Atlantic shore of Morocco.

A monitoring program for bivalve molluscs contaminated by algal toxins was established in 1992 at different stations along the Atlantic Moroccan shore. The presence of toxicity in bivalve molluscs commercially exploited was tested fortnightly using the mouse bioassay method. Results obtained from this surveillance indicate paralytic shellfish poisoning is responsible for bivalve molluscs contamination along the Atlantic coastline of Morocco. Toxin profile was established by automated pre-column HPLC/FLD in selected contaminated tissues. The study of individual toxins in mussel during a bloom in the northern Atlantic coastline in 1994 showed a very complex profile, typical to that obtained with cultures of the toxigenic dinoflagellate Gymnodinium catenatum isolated from the Iberian region. However, toxin composition of mussels and marine beans from later blooms in the southern Atlantic coastline in 1999 showed a strong resemblance with that of Alexandrium minutum, due to dominance of gonyautoxins 1/4. A minor contamination by G. catenatum due to the presence of decarbamoyl-saxitoxin is hypothesized.

Animals↗
PubMed2001

Non-selective retention of PSP toxins by the mussel Mytilus galloprovincialis fed with the toxic dinoflagellate Alexandrium tamarense.

Mussels, Mytilus galloprovincialis, were contaminated by paralytic shellfish poisoning (PSP) toxins by being fed with the toxic dinoflagellate Alexandrium tamarense. Temporal variations in the toxin content and the profile of mussels during the feeding experiment were monitored by high-performance liquid chromatography (HPLC). The toxin profile of mussels was compared with that of A. tamarense to clarify the mechanism of uptake of toxins in mussels. The prominent toxins in mussels and A. tamarense were N-sulfocarbamoyl toxins (C1,2) and carbamate toxins, gonyautoxin-1,4 (GTX1,4). The toxin profiles of both mussels and A. tamarense were almost constant throughout the experimental period. There were no remarkable differences in the toxin proportion between mussel and A. tamarense. These results indicate that mussels do not selectively accumulate particular toxins.

Animals↗
PubMed2003

[Effects of marine bacteria on the growth and toxin production of red-tide algae under different pH and salinities].

The effects of strain S10 isolated from sediments of Xiamen Western Sea Area on the growth and paralytic shellfish poison (PSP) production of Alexandrium tamarense at different pH and salinities were studied. The results showed that the alga grew well at pH 6-8 and at salinity of 20-34. The toxicity of A. tamarense varied markedly at different pH and salinities: it decreased with increasing pH, while increased with salinity and reached its peak value at the salinity of 30, and then declined. The strain S10 inhibited the growth and the PSP production of A. tamarense at different pH and salinities. It had the best inhibitory function on the growth of A. tamarense at pH 7 and salinity of 34. The best inhibitory function on the PSP production of A. tamarense was at pH 7, but this inhibitory function was not related to salinity.

Bacteria↗
PubMed2005

Morphology, toxin composition and pigment content of Prorocentrum lima strains isolated from a coastal lagoon in southern UK.

Prorocentrum lima was isolated from the coastal Fleet lagoon, Dorset, UK in 2000 and a number of clonal cultures established. These were analyzed for okadaic acid (OA), dinophysistoxin-1 (DTX-1), DTX-2, DTX-4 and diol esters by liquid chromatography coupled to mass spectrometry. OA concentrations varied from 0.4 to 17.1pg OAcell(-1) and DTX-1 from 0.4 to 11.3pg DTX-1cell(-1); DTX-2 was not detected in these isolates. OA and DTX-1 were detected in the culture media, as a result of toxin excretion. DTX-4 and a selection of DTX-4 diol esters were identified using selected ion monitoring, although not all strains produced these compounds. Cell size and number of marginal and valve pores of each strain were observed using scanning electron microscopy. OA and DTX-1 concentrations, pigment content and changes in nitrate and phosphate concentrations in the culture media were followed during growth of one strain of P. lima in batch culture. Diarrhetic shellfish poisoning (DSP) toxins have been previously detected in shellfish cultivated in the Fleet lagoon, but in the absence of any Dinophysis sp. cells. The identification of toxic P. lima strains from the Fleet suggests that this dinoflagellate is the most probable source of occasional DSP detected in the lagoon.

Animals↗
PubMed1994

Comparative study of the stability of saxitoxin and neosaxitoxin in acidic solutions and lyophilized samples.

Paralytic shellfish poison (PSP) has historically been a problem for the shellfish industry. In order to prevent the marketing of contaminated seafood products, governments have implemented monitoring programs where standards of toxins are necessary. The stability of these standard toxins is very important. In this paper we analysed the stability of saxitoxin (STX) and neosaxitoxin in acidic solution and lyophilized samples. Individual toxins were determined in each sample using a high-performance liquid chromatographic procedure employing post-column oxidation of the toxins to form fluorescent derivatives. Our results demonstrate that STX is very stable in solution samples and could be adopted as a reference standard. This toxin can be kept in dilute acidic solutions for 18 months without loss of potency. However, neosaxitoxin is unstable, possibly due to transformation to other toxins.

Animals↗
PubMed2001

Isolation and structural determination of DTX-6, a new okadaic acid derivative.

Diarrhetic shellfish poisoning is an illness caused by toxins accumulated in shellfish and produced by dinoflagellates, mainly of the Dinophysis and Prorocentrum genera. This paper reports the isolation and spectroscopic structural elucidation of a new compound, DTX-6 (2), an ester derivative of okadaic acid (OA) (1), isolated from an artificial culture of strain PLV2 of Prorocentrum lima.

Animals↗
PubMed1975

Lack of secondary intoxification by red tide poison in the American lobster Homarus americanus.

Lobsters are able to feed on shellfish which are toxic with PSP (paralytic shellfish poisoning from Gonyaulax tamarensis) with no apparent harm to themselves, and no measurable assimilation of the poison into their tissues. Lobsters consumed food containing in excess of 1000 mug PSP. There was no impairment of respiration (oxygen consumption) measurable two to three hours after feeding, and no PSP measured in the meat of the claws and tail 48 to 120 hours after feeding. The only PSP was in the guts and contents which were measured 48 hours after feeding began.

Aging↗
PubMed2002

Confirmation of brevetoxin metabolism in the Eastern oyster (Crassostrea virginica) by controlled exposures to pure toxins and to Karenia brevis cultures.

Previously, we analyzed Eastern oysters (Crassostrea virginica) naturally exposed to a Karenia brevis red tide and found that brevetoxins (PbTx) are rapidly accumulated and metabolized. Several metabolites were isolated and later identified, including a cysteine-PbTx conjugate (MH(+): m/z 1018) and its sulfoxide product (m/z 1034). In the present study, we confirm and extend those findings by examining PbTx metabolism and elimination in oysters exposed to pure toxins (PbTx-2 and -3) under controlled conditions. Waterborne PbTx-3 was rapidly accumulated, but not metabolized, in the oyster and was largely eliminated within 2 weeks after exposure. In contrast, PbTx-2 was accumulated and rapidly metabolized. Metabolites of PbTx-2 included the reduction product PbTx-3 (m/z 897), and the cysteine conjugates (m/z 1018 and 1034) isolated previously from the field samples. Levels of the metabolite PbTx-3 in PbTx-2-exposed oysters were highest immediately after exposure and declined at a rate similar to parent PbTx-3 in PbTx-3-exposed oysters. Cysteine-PbTx persisted for 8 weeks after exposure. The same metabolites were confirmed in oysters exposed to laboratory cultures of K. brevis. PbTx metabolites contribute to neurotoxic shellfish poisoning (NSP) and should be included in analytical protocols for monitoring shellfish toxicity after a K. brevis red tide event.

Animals↗
PubMed2005

Metabolic transformation of dinophysistoxin-3 into dinophysistoxin-1 causes human intoxication by consumption of O-acyl-derivatives dinophysistoxins contaminated shellfish.

This paper describes for the first time a massive intoxication episode due to consumption of shellfish contaminated with 7-O-acyl-derivative dinophysistoxin-1, named Dinophysistoxin-3 (DTX-3). 7-O-acyl-derivative dinophysistoxin-1, a compound recently described in the literature, was found in shellfish samples collected in the Chilean Patagonia fjords. This compound does not inhibit Protein Phosphatases and also does not elicit the symptoms described for Diarrheic Shellfish Poisoning (DSP). The data showed here, give evidence of metabolic transformation of 7-O-acyl-derivative dinophysistoxin-1 (DTX-3) into Dinophysistoxin-1 (DTX-1, Methyl-Okadaic acid) in intoxicated patients. This metabolic transformation is responsible for the diarrheic symptoms and the intoxication syndrome showed by patients that consumed contaminated shellfish, which showed only the presence of 7-O-acyl-derivative dinophysistoxin-1. Patients fecal bacterial analysis for the presence of enteropathogens was negative and the mouse bioassay for DSP, performed as described for regulatory testing, was also negative. The HPLC-FLD and HPLC-MS analysis showed only the presence of DTX-3 as the only compound associated to DSP toxins in the contaminated shellfish samples. No other DSP toxins were found in the shellfish sample extracts. However, the patient fecal samples showed DTX-1 as the only DSP toxins detected in fecal. Moreover, the patient fecal samples did not show DTX-3. Since 7-O-acyl-derivative dinophysistoxin-1 (DTX-3) was the only compound associated to DSP toxins detected in the shellfish samples, an explanation for the diarrheic symptoms in the intoxicated patients would be the metabolic transformation of DTX-3 into DTX-1. This transformation should occur in the stomach of the poisoned patients after consuming 7-O-acyl-derivatives dinophysistoxin-1 (DTX-3) contaminated bivalves.

Abdominal Pain↗