Biochemical studies on paralytic shellfish poisons.
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Simultaneous presence of paralytic and diarrheic shellfish poisoning toxins in Mytilus chilensis samples collected in the Chiloe Island, Austral Chilean fjords.
The study shown here provides the first indisputable evidence that shellfish can be contaminated with Paralytic Shellfish Poisoning (PSP) and Diarrheic Shellfish Poisoning (DSP) toxins during the summer season in the Southern Chilean fjords. Quantitative analysis of the simultaneous presence of PSP and DSP toxins in Mytilus chilensis samples collected in the Chiloe Island are shown. The High Performance Liquid Chromatography (HPLC) analysis with pre-column derivatization method for DSP toxins and the post-column derivatization methods for PSP toxins, both with fluorescent on-line detections, showed that both type of toxins were concentrated by the filter bivalve Mytilus chilensis in amounts above the international safe limits. The phytoplankton analysis showed the presence of both Alexandrium catenella and Dinophysis acuta in the water column. The data shows stratification of the toxic dinoflagellates in the water column, since the lowest amount of both DSP and PSP toxins were measured in the superficial and deeper levels of the water column. Moreover, the highest toxicities of both types of toxins were shown by the shellfish samples collected at a depth of 6 meters with 190 nanograms of DTX-1 / gram of digestive gland and 709.8 microg of PSP toxins / 100 grams of mussel meat.
Animals↗
Shellfish poisons.
In our ongoing search for bioactive metabolites from marine organisms, novel shellfish poisons have been isolated. Pinnatoxins, which are amphoteric polyether compounds, were purified from the Okinawan bivalve Pinna muricata. Pinnatoxins show acute toxicity against mice and activate Ca2+ channels. Two novel alkaloids, pinnamine and pinnaic acid, were also obtained from P. muricata. Pinnaic acid inhibits cytosolic phospholipase (cPLA2). Pteriatoxins, which are pinnatoxin analogs, were isolated from the Okinawan bivalve Pteria penguin. A nanomole-order structure determination of pteriatoxins was achieved by the detailed analysis of 2D-NMR and ESI-TOF MS/MS. This review covers the isolation, structure determination, bioactivity, synthesis, and biogenesis of these shellfish poisons and related compounds.
Animals↗
Evidence of paralytic shellfish poisoning toxin in milkfish in South Taiwan.
Natural phytoplankton blooms of the dinoflagellate Alexandrium minutum, milkfish (Chanos chanos) exposed to natural blooms, sediment and mangrove crab (Scylla serrata) were analysed for paralytic shellfish poisoning toxins by high-performance liquid chromatography. The toxin profiles of milkfish and mangrove crab were similar to that of A. minutum collected from blooming fishponds. In a laboratory A. minutum-blooming environment, the stomach and intestine of milkfish accumulated paralytic shellfish poisoning toxins during the exposure period. The non-visceral tissues were non-toxic. However, milkfish lost their entire body burden of toxin on the first day of transferring to a toxic algae-free environment. The result shows that milkfish concentrate paralytic shellfish poisoning toxins in digestive organs and did not retain toxins.
Animals↗
A rapid detection method for paralytic shellfish poisoning toxins by cell bioassay.
We report here a rapid detection method for paralytic shellfish poisoning (PSP) toxins using a cultured neuroblastoma cell line, modified from the bioassay system previously established by Manger et al. [Manger, R.L., Leja, L.S., Lee, S.Y., Hungerford, J.M., Kirkpatrick, M.A., Yasumoto, T., Wekell, M.M., 2003. Detection of paralytic shellfish poison by rapid cell bioassay: antagonism of voltage-gated sodium channel active toxins in vitro. J. AOAC Int. 86 (3), 540-543]. In the present study, we made two major modifications to the previous method. The first is the use of maitotoxin, a marine toxin of ciguatera fish poisoning, which enables the incubation period to be reduced to 6 h when applied to the microplate 15 min prior to the end of the incubation. The second is the use of WST-8, a dehydrogenase detecting water-soluble tetrazolium salt for determining the target cell viability, which permits the omission of a washing step and simplifies the counting process. In addition, we attempted to reduce the required materials as much as possible. Thus, our modified method should be useful for screening the PSP-toxins from shellfish.
Animals↗
Cell bioassay for paralytic shellfish poisoning (PSP): comparison with postcolumn derivatization liquid chromatographic analysis and application to the monitoring of PSP in shellfish.
We performed a neuroblastoma cell (Neuro2a) culture assay modified slightly from a method reported previously to provide a simple and sensitive evaluation of paralytic shellfish poisoning (PSP) toxicity in shellfish. The cell bioassay was just as sensitive for C-toxins as for gonyautoxins. The sensitivity of our cell bioassay was 4 times that of the current standard mouse bioassay. Using the cell bioassay, we evaluated PSP toxicity in 361 shellfish samples collected from Mikawa Bay and Ise Bay, Aichi Prefecture, Japan, from April 1999-March 2002. The results were compared with those obtained in a postcolumn derivatization liquid chromatographic analysis. PSP toxins were detected in 236/361 samples by both assays, and there was a fairly good correlation (r = 0.9001, n = 236, p < 0.001) between the results from the two assays. We applied this cell bioassay when short-necked clams in the bay turned poisonous in 2001. The chronological changes in PSP toxicity in the short-necked clams were analyzed and compared with those of the cell density of poisonous plankton (Alexandrium tamarense) occurring in the bay. The PSP toxicity in shellfish peaked 2 weeks after the cell density reached a maximum. We recommend using the cell bioassay for routine monitoring of PSP toxicity in shellfish living in natural marine environments.
Animals↗
Measurements of paralytic shellfish poisons. A review of biological and chemical procedures.
Paralytic shellfish poisons (PSP) are derivatives of a tetrahydropurine base, which includes saxitoxin, 1-hydroxy saxitoxin, and 11-hydroxy saxitoxin sulfate. These compounds are produced by Gonyaulax catenella and other dinoflagellate species, and the algal toxins (phycotoxins) contaminate shellfish during the filter-feeding process performed by the bivalve molluscs. Increased incidence of algal blooms and outbreaks of PSP food poisonings have been encountered in recent years, resulting in a demand for closely monitoring of shellfish for these toxins. The existing biological and chemical procedures for analysis are reviewed. The mouse bioassay is commonly used in routine analysis, but is nonspecific. Several of the chemical procedures are specific and more sensitive than the mouse bioassay. The disadvantage, however, seems to be that not all known PSP compounds can be quantitiatively measured by any single chemical procedure.
Animals↗
Ecological analysis of digestive cancer mortality related to contamination by diarrhetic shellfish poisoning toxins along the coasts of France.
Shellfish consumers are exposed to the risk of diarrhea from, among other contaminants, algae that produce diarrhetic shellfish poisoning (DSP) toxins, such as Dinophysis spp. These illnesses have been effectively prevented since 1984, when a phycotoxin monitoring network was set up along the coasts of France. There is nonetheless concern that residual levels of okadaic acid, a known tumor promoter that is the main toxin present in French coastal waters, might increase the risk of cancer among regular shellfish consumers. To test this hypothesis, we conducted an ecological study linking digestive cancer mortality rates with a proxy measure of contamination by DSP toxins in 59 coastal areas. Observed and expected numbers of deaths (using national rates as the reference) were computed by sex, cause of death, and area for two time periods: 1984-1988 and 1989-1993. The level of contamination in each area was estimated by the total number of weeks since monitoring began that production was shut down because of DSP toxin contamination. Using both Poisson regressions and test for trends of standardized mortality ratios across four exposure categories, we found some evidence of associations for several digestive cancer sites (esophagus, stomach, colon, liver, and total digestive cancers for men; stomach and pancreatic cancers for women). Among men, the only statistically significant result that remained after taking possible confounding by alcohol use into account involved colon cancer. The conclusions provided by this analysis are very tentative; they need to be reproduced and interpreted in the light of additional information on the potential long-term effects of DSP toxins. In the absence of human data, they provide some indication of a possible association between exposure to DSP toxins and digestive cancers.
Adult↗
Transmission of the paralytic shellfish poisoning toxins, from dinoflagellate to gastropod.
Purple clams, Hiatula diphos Linnaeus, are filter-feeding bivalves and maculated ivory shells. Babylonia areolata Link are carnivorous gastropods. Both shellfishes are popular seafood delicacies among the Taiwanese. Hiatula diphos were forced to contain gonyautoxins (GTXs) in this research by feeding them with cells of Alexandrium minutum Halim, a toxic dinoflagellate species responsible for the paralytic shellfish poisonings in Taiwan. The intoxicated purple clams of known toxicity and toxin composition were fed to B. areolata to observe the transmission and transformation of GTXs among this shellfish. It was found that the toxin composition in bivalve and gastropod were similar to that in dinoflagellate. Our data provide evidence for food-chain transmission of paralytic shellfish poisoning toxins, from dinoflagellate to gastropod through a filter-feeding bivalve. The transmitted GTX-I. -II. -III and -IV of A. minutum could only be found in the viscera of these shellfish. There was a notable degradation of GTX-I in the ivory shell that resulted in a decrease in toxicity while the total amount of toxins was accumulatively increasing.
Animals↗
Paralytic shellfish poisoning: a potential public health problem.
Paralytic shellfish poisoning (PSP) is a serious illness in which neurological symptoms predominate. Recovery is usually complete and uncomplicated, but in severe cases there may be respiratory paralysis and death. Most cases follow consumption of bivalve molluscs that have filter-fed on toxic marine microalgae (phytoplankton). Microalgae capable of causing the intoxication have been recorded in all States of Australia, and major toxic blooms have occurred in Tasmania, Victoria and South Australia.
Adult↗
Integrated enzyme-linked immunosorbent assay screening system for amnesic, neurotoxic, diarrhetic, and paralytic shellfish poisoning toxins found in New Zealand.
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.
Amnesia↗
Paralytic shellfish poisons produced by the freshwater cyanobacterium Aphanizomenon flos-aquae NH-5.
A single filament clonal isolate of Aphanizomenon flos-aquae was made from a water bloom sample taken at a small pond near Durham, New Hampshire, in 1980. When batch cultured the strain was toxic to mice and had an i.p. LD50 of about 5.0 mg/kg. Using an extraction procedure originally designed for paralytic shellfish poisons and other neurotoxins of freshwater cyanobacteria, a purification method was developed. The procedure involved acidified water/ethanol extraction of the cells followed by ultrafiltration, gel filtration, use of C18 cartridges to remove pigments, ion-exchange and high performance liquid chromatography using u.v. detection at 220 or 240 nm. Thin-layer chromatography and high performance liquid chromatography results indicate that Aphanizomenon flos-aquae NH-5 may produce paralytic shellfish poisons, mainly neo-saxitoxin and saxitoxin. Three labile toxins were also detected which were not similar to any of the known paralytic shellfish poisons.
Animals↗
Paralytic shellfish poisoning: clinical and electrophysiological observations.
In paralytic shellfish poisoning a mollusc contaminated with a toxin (saxitoxin) causes a potentially lethal disease, clinically characterised by gastrointestinal and neurological symptoms, of which possible respiratory depression is the most serious. The toxin acts by blocking the sodium channels. We report 9 Portuguese patients with this disease. The mollusc was identified as Mytilus edulis, contaminated with the dinoflagellate Gymnodinium catenatum, and the toxin saxitoxin. Our patients had a benign clinical course with cerebellar ataxia as the most severe neurological impairment. Eight out of 9 patients had neurophysiological investigations, the largest number so far reported. Motor and sensory conduction velocities and amplitudes were normal. The proximal conduction times, as assessed by F waves, showed delayed conduction and decreased frequency, which returned to normal in few weeks. The somatosensory evoked potentials confirmed normal peripheral and central sensory conduction. The rich vascular supply at root level of the sodium channels of the proximal motor nerves may explain the greater vulnerability to toxin damage. The typically transient and quickly reversible nerve dysfunction caused by ion channel blockade is reported.
Adult↗
Use of two-dimensional gel electrophoresis to differentiate morphospecies of Alexandrium minutum, a paralytic shellfish poisoning toxin-producing dinoflagellate of harmful algal blooms.
Contamination of shellfish with paralytic shellfish poisoning toxins (PST) produced by toxic harmful algal blooms (HABs) have been negatively affecting the shellfish and aquaculture industries worldwide. Therefore, accurate and early identification of toxic phytoplankton species is crucial in HABs surveillance programs that allow fish-farmers to take appropriate preventive measures in shellfish harvesting and other aquaculture activities to overcome the negative impacts of HABs on human health. The identification of toxic dinoflagellates present in the water is currently a time-consuming operation since it requires skillful taxonomists and toxicologists equipped with optical and scanning electron microscopes as well as sophisticated equipment, for example, high-performance liquid chromotography-fluorescence detection. In this paper, a two-dimensional gel electrophoresis (2-DE)-based proteomic approach was applied to discriminate between toxic and nontoxic strains of Alexandrium minutum. Variation in morphological features between toxic and nontoxic strains was minimal and not significant. Also, variation in 2-DE protein patterns within either toxic or nontoxic strains was low, but pronounced differences were detected between toxic and nontoxic strains. The most notable differences between these strains were several abundant proteins with pIs ranging from 4.8 to 5.3 and apparent molecular masses between 17.5 and 21.5 kDa. Groups of proteins, namely NT1, NT2, NT3, and NT4, were consistently found in all nontoxic strains, while T1 and T2 were prominent in the toxic strains. These specific protein spots characteristic for toxic and nontoxic strains remained clearly distinguishable irrespective of the various growth conditions tested. Therefore, they have the potential to serve as "taxonomic markers" to distinguish toxic and nontoxic strains within A. minutum. Initial studies revealed that the expression pattern of T1 was tightly correlated to toxin biosynthesis in the examined alga and may be used to serve as a potential toxin indicator.
Amino Acid Sequence↗
Accumulation of paralytic shellfish poisoning toxins in the edible shore crab Telmessus acutidens.
Several shellfishes including the crab Telmessus acutidens and its prey bivalve Mytilus galloprovincialis were collected at Onahama in Japan to investigate the accumulation of paralytic shellfish poisoning (PSP) toxins during the blooming season of toxic dinoflagellates. The toxicity of the viscera of T. acutidens collected in 1999 was 30.0 and 80.0 MU/g, and that of M. galloprovincialis was 9.6 MU/g by mouse bioassay. PSP toxins in the crab viscera were identified by HPLC-FLD and ESI-MS, so this is the first observation of PSP toxins in T. acutidens. Carbamate toxins (GTX1-4, and STX) were the major component in the crab as well as in the mussels, and accounted for over 60% on a molar basis. However, the ratio of the N1-OH toxin to N1-H toxin of the crabs were largely different from that of the mussels, and a reductive conversion of the toxins in T. acutidens is concluded as the probable cause. In 2000, PSP toxins were also detected in both crabs and mussels, though the contents were very low compared with the levels observed in 1999. The difference in the toxin abundance suggests that the toxin content in the crab was affected by those of the prey.
Animals↗
An outbreak of diarrhoeic shellfish poisoning in Antwerp, Belgium.
In Antwerp, Belgium, 403 cases of diarrhoeic shellfish poisoning were reported after consumption of blue mussels. Symptoms included diarrhoea, vomiting, abdominal pain, and nausea. The analysis of faecal specimens from patients allowed diagnosis exclusions for bacteria and viruses. Mouse-assays revealed the presence of biotoxins specific of dinoflagellates, which were identified and quantified by LC-MS. The mussels were imported from Denmark, and were part of a batch presenting high concentrations of okadaic acid above the regulatory limits.
Adolescent↗
Molecular evidence for plastid robbery (Kleptoplastidy) in Dinophysis, a dinoflagellate causing diarrhetic shellfish poisoning.
The dinoflagellate genus Dinophysis contains species known to cause diarrhetic shellfish poisoning. Although most photosynthetic dinoflagellates have plastids with peridinin, photosynthetic Dinophysis species have cryptophyte-like plastids containing phycobilin rather than peridinin. We sequenced nuclear- and plastid-encoded SSU rDNA from three photosynthetic species of Dinophysis for phylogenetic analyses. In the tree of nuclear SSU rDNA, Dinophysis was a monophyletic group nested with peridinin-containing dinoflagellates. However, in the tree of plastid SSU rDNA, the Dinophysis plastid lineage was within the radiation of cryptophytes and was closely related to Geminigera cryophila. These analyses indicate that an ancestor of Dinophysis, which may have originally possessed peridinin-type plastid and lost it subsequently, adopted a new plastid from a cryptophyte. Unlike dinoflagellates with fully integrated plastids, the Dinophysis plastid SSU rDNA sequences were identical among the three species examined, while there were species-specific base substitutions in their nuclear SSU rDNA sequences. Queries of the DNA database showed that the plastid SSU rDNA sequence of Dinophysis is almost identical to that of an environmental DNA clone of a <10 pm sized plankter, possibly a cryptophyte and a likely source of the Dinophysis plastid. The present findings suggest that these Dinophysis species engulfed and temporarily retained plastids from a cryptophyte.
Animals↗
Resistance of nerves from certain toxic crabs to paralytic shellfish poison and tetrodotoxin.
The inhibitory effect of paralytic shellfish poison and tetrodotoxin on nerves from toxic and nontoxic crabs was examined. The toxins at concentrations of 10(-3) - 10(-4) M partially or completely inhibited the action potential of nerves isolated from the legs of toxic crab species (Zosimus aeneus, Atergatis floridus and Platypodia granulosa), but had no effect at 10(-6) M, the concentration at which the action potential of nerves from a nontoxic crab (Plagusia dentipes) was inhibited completely. A xanthid crab Daira perlata was intermediate in respect to the resistance to toxins. These results agree with the previous results obtained by i.p. administration of both toxins into those crabs.
Action Potentials↗