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PubMed1998

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↗

PubMed2002

kappa-Carrageenan gel as agent to sequester paralytic shellfish poison.

The action of k-carrageenan gel to sequester paralytic shellfish poison (PSP) was tested and characterized. When an extract from a Philippine strain of Pyrodinium bahamense var. compressum was used as PSP solution, the PSP-sequestering property of kappa-carrageenan gel was found to be dependent on gel surface area, interaction time, and polysaccharide concentration. The interaction was also found to be affected by high concentrations of monovalent cations. The characteristics of kappa-carrageenan as a PSP-sequestering agent all point to cation exchange as its mechanism of action. It is also proposed that the polysaccharide gel can be utilized as an agent to alleviate PSP intoxication.

Journal Article↗

PubMed1994

Development of a capillary electrophoresis method for the characterization of enzymatic products arising from the carbamoylase digestion of paralytic shellfish poisoning toxins.

A sample stacking procedure is presented for the capillary electrophoretic (CE) separation of paralytic shellfish poisoning (PSP) toxins dissolved in high ionic strength buffers. The application of such a stacking procedure prior to the zone electrophoretic separation is demonstrated for the analysis of decarbamoyl toxins arising from the digestion of PSP toxins by an hydrolytic enzyme from little neck clams (Protothaca staminea). Improvements in separation efficiency facilitated identification and quantitation of substrates and enzymatic products present in the digest using CE. The separation conditions developed were found to be entirely compatible with electrospray mass spectrometry, which permitted the analysis of PSP toxins and their decarbamoyl derivatives present in the low micromolar range in crude enzyme digests. The products released during the enzymatic digestion were identified using CE combined with tandem mass spectrometry.

Animals↗

PubMed1983

The occurrence of paralytic shellfish toxins in two species of xanthid crab from Suva barrier reef, Fiji Islands.

Five species of crabs commonly occurring on Suva barrier reef, Fiji Islands, were tested for the presence of paralytic shellfish toxins. All 35 specimens of Atergatis floridus and all 18 specimens of Zosimus aeneus tested were lethal to mice, whilst none of 12 specimens of Carpilius maculatus, 8 of C. convexus and 10 of Eriphia sebana tested were lethal. A. floridus contained saxitoxin (55--60%), neosaxitoxin (35--40%), gonyautoxin-II (less than 5%) and a new toxin previously found in a toxic dinoflagellate, Pyrodinium bahamense var. compressa, and tentatively coded PBT (1%). Z. aeneus contained the same components, with additional trace amounts of gonyautoxin-I and III, but neosaxitoxin was the major component in this species. Comparison with the results of testing Okinawan specimens of Z. aeneus, A. floridus and Platipodia granulosa suggests that the toxin profile is specific to species.

Animals↗

PubMed1989

Paralytic shellfish toxins in bivalves which are not associated with dinoflagellates.

Paralytic shellfish toxins (PSP toxins) were detected in the freshwater bivalve Corbicula sandai collected from Lake Biwa, Shiga Prefecture, Japan, and marine mussel Septifer virgatus from Mutsu Bay where known causative dinoflagellates and their cysts have never been observed. The toxin profile of C. sandai and S. virgatus was considerably different from suspected causative organisms Aphanizomenon flos-aquae and Protogonyaulax spp., respectively. The causative organism(s) responsible for PSP toxins in these waters is at present unknown.

Animals↗

PubMed1989

Toxicity and paralytic shellfish toxin profiles of the xanthid crabs, Lophozozymus pictor and Zosimus aeneus, collected from some Australian coral reefs.

Purification of toxic aqueous extracts from the xanthid crabs Zosimus aeneus and Lophozozymus pictor, collected from Australian waters, yielded paralytic shelfish toxins, including saxitoxin (STX), neosaxitoxin (neoSTX) and gonyautoxins 1, 2 and 4 (GTX1,2,4). No more than two paralytic shellfish toxins were found in any of the purified extracts from any specimen. Four specimens of Z. aeneus and one specimen of L. pictor each contained more toxic material than the suggested human oral lethal dose. The moult of a specimen of L. pictor was toxic, which may indicate a route in crabs for toxin removal.

Animals↗

PubMed1991

Diarrhetic shellfish toxins: improvement of sample clean-up for HPLC determination.

Okadaic acid and dinophysistoxin-1, the principal toxic components in diarrhetic shellfish poisoning, may be detected by high-performance liquid chromatography and fluorometric measurement as 9-anthrylmethyl esters. However, "greasy" samples may occur and the fluorescent reagent 9-anthryldiazomethane may decompose during storage, resulting in impurities that may seriously interfere with quantitative determination. Ultrasonic treatment of the samples during derivatization with 9-anthryldiazomethane was found to improve reproducibility. This may result from increased access to reactive sites on toxins by 9-anthryldiazomethane due to disruption of micelles formed by toxins and other partly hydrophobic compounds. A procedure for cleaning the derivatized samples, using a 0.1 g silica cartridge column and different eluent compositions from that reported by LEE et al. (1987), was found to facilitate chromatogram interpretation. Deoxycholic acid, a commercial available bile acid, was found to be an acceptable internal standard. The 9-anthrylmethyl esters of okadaic acid, dinophysistoxin-1 and deoxycholic acid, were stable at 4 degrees C for at least seven days when stored dry or in methanol.

Animals↗

PubMed1995

Bioaccumulation of paralytic shellfish poisoning (PSP) toxins from the cyanobacterium Anabaena circinalis by the freshwater mussel Alathyria condola.

The Australian freshwater mussel Alathyria condola accumulated high levels of paralytic shellfish poisoning (PSP) toxins when fed the neurotoxic cyanobacterium Anabaena circinalis, shown recently to contain high concentrations of C-toxins and gonyautoxins. Significant accumulation (>80 mu g/100 g of mussel flesh) was detected following 2-3 exposure to water containing 2 x 105 cells/ml A. circinalis. Only trace accumulation of PSP toxins was demonstrated over long-term (5 week) exposure at low concentration (c. 104 cells/ml). The relative abundance of C-toxins, gonyautoxins and saxitoxins in mussels generally matched the toxin profiles of the dietary A. circinalis, although there were differences in the GTX2/3 and C1/2 ratios with time, and an increase in abundance of decarbamoylgonyautoxins. Analysis of mussel tissues after 7 days, exposure to A. circinalis revealed that 96% of the toxins were accumulated in the viscera. As in marine waters, the bioaccumulation of PSP toxins in freshwater mussels may pose a health risk to humans and animals, especially in areas where seasonally decreasing water levels expose mussel beds to surface scums of toxic cyanobacteria.

Anabaena↗

PubMed1992

Ecology and prevention of a shellfish-associated hepatitis A epidemic in Shanghai, China.

During a shellfish-borne hepatitis A outbreak in Shanghai during the first quarter of 1988, 300,000 cases were reported in two months. Using cell culture and experimental infection of marmosets, hepatitis A virus (HAV) was isolated from clams collected from the market and the sea bed during the epidemic. A dose-response curve correlating the quantity of clams consumed to the attack rate of hepatitis A was well documented. The occurrence of the epidemic was associated with a good harvest of clams in a new area, serious pollution of this area with sewage and importation of the clams in large quantities into Shanghai where most young adults were susceptible. Clams can apparently be decontaminated by using a continuous water flow. In this way, HAV titres can be reduced by 90% in one day and by 99.9% in two weeks. An attenuated live HAV vaccine which has been developed in China has been shown to be safe and immunogenic and may be used for prevention of such epidemics in the future.

Adolescent↗

PubMed1992

An evaluation of the mouse bioassay applied to extracts of 'diarrhoetic' shellfish toxins.

The standard mouse bioassay, used to assess 'diarrhoetic shellfish poison' (DSP), is based on intraperitoneal administration of toxic mussel extracts, and monitoring of survival time within a 24-hr period. Toxic effects on mice were examined for extracts of mussel samples from two different regions of south Norway known to possess toxins of specific properties. Both samples revealed an exponential pattern in the dose-response relationship. Whereas the time lag from injection to death was linearly dependent on mouse weight, the effect of weight also increased with decreased sample toxicity. When tested with doses adjusted for weight, a marked individual variation was found within all size groups of mice. The results imply that, regarding prohibition limits for distribution and sale of mussels, a certain degree of variation with regard to time should be accepted in the testing of parallel samples. On the basis of the results, a revised method for the determination of toxicity by mouse bioassay is proposed for DSP testing. The method is based on administration to two mice of size-adjusted doses of extracts, followed by a 4-hr surveillance period and a 1-hr upper limit of acceptable time variation between parallel samples. The method shows advantages regarding savings of time and money, in precision in determination of toxicity level, as well as curtailed exposure to toxin and reduced suffering of laboratory animals.

Animals↗

PubMed1988

Occurrence and distribution of D-cysteinolic acid in fish and shellfish.

1. An unknown compound which is very similar to taurine was detected in the extract of sardine Sardinops melanosticta. 2. It was identified as D-cysteinolic acid: 2-amino-3-hydroxy-1-propanesulfonic acid from instrumental analysis. 3. This may be the first report in which the occurrence of D-cysteinolic acid in fish has been demonstrated. 4. Of 14 species of fish and shellfish examined, the presence of this compound was confirmed in 7 species.

Animals↗

PubMed1994

A comparison of methods for diarrhoeic shellfish poison detection.

Samples of diarrhoeic shellfish poison (DSP) mussels from several parts of the Italian Adriatic coastline were extracted and tested according to a number of different methods presently available, i.e. Yasumoto's mouse biotest, Kat's biotest, the ELISA test and the HPLC method. Results were compared for toxic levels detected in each sample. While a common qualitative result (toxic/non-toxic) was given by all the methods, no clear quantitative agreement was found. The differences between methods and consequent lack of agreement in results are discussed.

Animals↗

PubMed2004

Accumulation and depuration of cyanobacterial paralytic shellfish toxins by the freshwater mussel Anodonta cygnea.

The increasing frequency by which the production of paralytic shellfish toxins (PST) by freshwater bloom-forming cyanobacteria is being noticed world-wide raises the possibility of PST bioaccumulation by freshwater mussels. This study evaluates PST accumulation and depuration by the freshwater mussel Anodonta cygnea exposed over a 14-day period to high densities (mean = 1.4 x 10(9) cells1(-1), S.D. = 0.29 x 10(9) cellsl(-1)) of the toxic cyanobacterium Aphanizomenon issatschenkoi (corresponding to a mean toxin concentration of 25.5 nmol PSTl(-1), S.D. = 9.9 nmol PSTl(-1)). Mussels were subsequently detoxified either by starvation or by feeding on the non-toxic green-algae Ankistodesmus falcatus. Filter feeding activity and toxin uptake by the mussels were followed by cell counting and toxin analysis in water samples taken before and after each daily water renewal. The accumulation and depuration of PST as well as the anatomical distribution of toxins were monitored throughout the experiment by HPLC analysis of mussel extracts. Mussels fed the toxic cyanobacterium removed on average 65.3% of cells and 40.36% of total PST daily provided. Daily rates of cell clearance (% of initial) were negatively correlated with the amounts of PST daily provided (but not with the amount of cells). This suggests a negative effect of toxins on the feeding behaviour of mussels. Small amounts of toxins could be detected in the mussels after the second day of exposure, reaching a maximum of 26 microg PST100 g(-1) by day 7. The viscera contained the greatest proportion of toxins (78%) at the start of the toxification. However, increasing amounts of PST were found in the remaining tissues (gills, mantle and foot) over time. Toxins detected in the mussel extracts were the same provided in the dietary A. issatschenkoi. Nevertheless, mussels showed a higher proportion of saxitoxin and decarbomoylsaxitoxin and a lower proportion of gonyautoxin-5 than the fed cyanobacterium. Similar depuration efficiencies were observed among starved individuals (6.9% day(-1)) and those fed with A. falcatus (8.2% day(-1)) indicating that both treatments had comparable effects on toxin metabolism. Mussels showed a typical S shaped depuration kinetics curve consisting of a first short period of slow toxin decay followed by a rapid loss and a subsequent slower release of toxins. Trace to undetectable levels of PST were found in mussels after the 14-day depurating period. Although freshwater mussels are not widely consumed by humans, their capacity to accumulate PST points to the risk of PST propagation through the food chain of freshwater ecosystems via filter-feeding mussels.

Analysis of Variance↗

PubMed2006

The uptake, distribution and elimination of paralytic shellfish toxins in mussels and fish exposed to toxic dinoflagellates.

We exposed green-lipped mussels Perna viridis and black sea breams Acanthopagrus schlegeli to toxic dinoflagellates Alexandrium fundyense to evaluate the accumulation, distribution, transformation, and elimination of paralytic shellfish toxins (PSTs) in a controlled environmental condition. The mussels were fed A. fundyense for 7 days followed by 3 weeks of depuration, and the fish were fed toxic clams (pre-exposed to the dinoflagellates) for 5 days followed by 2 weeks of depuration. The toxin content and the compartmental distribution of PSTs were monitored throughout the experiments by high-performance liquid chromatography with post-column fluorescence derivatization (HPLC-FLD). This is the first report to assess the biokinetics of PSTs in marine fish under dietary exposure. The hepatopancreas in the mussels and the viscera in the fish accumulated most of the PSTs. Differential elimination of each toxin was observed in the mussels. The C2 toxins were eliminated rapidly in all organs; except in hepatopancreas, the more potent toxins such as GTX4, were eliminated slower during the depuration period. The relative proportions of various PSTs in the mussels changed over time, suggesting toxin-specific uptake and elimination rates, or biotransformation preferences between toxins. In the fish, the ratio of C1/C2 was 3.0 times (p<0.01) higher when compared to the clam tissues, indicating that conversion from C2 to C1 might have occurred when the toxin was transferred from the clams to the fish. In summary, species differences in uptake, distribution and elimination of PSTs were observed between mussels and fish, and this may influence trophic transfer of algal toxins in marine organisms.

Animals↗

PubMed2004

Yessotoxin, a shellfish biotoxin, is a potent inducer of the permeability transition in isolated mitochondria and intact cells.

The diarrhetic poisoning by bivalve molluscs, diarrhetic shellfish poisoning, is due to consumption of mussels containing biotoxins produced by some Dinoflagellate species. Toxic effects of yessotoxin (YTX) include morphological alterations of mitochondria from heart and liver but the biochemical basis for these alterations is completely unknown. This paper demonstrates that YTX is a very powerful compound that opens the permeability transition pore (PTP) of the inner mitochondrial membrane of rat liver mitochondria at nanomolar concentrations. The effect requires the presence of a permissive level of calcium, by itself incapable of opening the pore. The direct effect of YTX on PTP is further confirmed by the inhibition exerted by cyclosporin A (CsA) that is known as a powerful inhibitor of PTP opening. Moreover, YTX induces membrane depolarization as shown by the quenching of tetramethylrhodamine methyl ester (TMRM), also prevented by the addition of CsA. YTX caused PTP opening in Morris Hepatoma 1C1 cells, as shown by the occurrence of CsA-sensitive depolarization within minutes of the addition of submicromolar concentrations of the toxin. These results provide a biochemical basis for the mitochondrial alterations observed in the course of intoxication with YTX, offering the first clue into the pathogenesis of diseases caused by YTX, and providing a novel tool to study the PTP in situ.

Animals↗

PubMed2004

Quantitation of paralytic shellfish toxins using mouse brain synaptoneurosomes.

A membrane potential assay based on synaptoneurosomes prepared from mouse brain was evaluated further for its utility in estimating saxitoxin and related bioactives. Saxitoxin concentrations quantitated in mussel extracts by the synaptoneurosomal technique correlated well with spiked concentrations in these samples (r2 = 0.995; slope=1.048). Other experiments found that the synaptoneurosomal assay can detect saxitoxin-like bioactives in zooplankton samples and the concentrations measured were consistent with preliminary estimations of saxitoxin equivalents using the [3H] saxitoxin receptor binding technique. Veratrine, a mixture of alkaloids that activate sodium channels, had similar potential as a substitute for veratridine in the synaptoneurosomal assay. The results provide additional evidence that the mouse brain synaptoneurosomal membrane potential assay has excellent capability for quantitation of saxitoxin-like activity in shellfish tissues and may also be applied to zooplankton samples.

Animals↗

PubMed2006

Trophic transfer of paralytic shellfish toxins from clams (Ruditapes philippinarum) to gastropods (Nassarius festivus).

A local strain of the dinoflagellate Alexandrium tamarense (ATCI01), which predominantly produces C2 toxin, was fed to the clams (Ruditapes philippinarum) under laboratory conditions. Concentrations of paralytic shellfish toxins (PSTs) in the dosed clams were determined by High Performance Liquid Chromatographic (HPLC) analyses, and the clams were homogenized and then fed to the gastropods (Nassarius festivus). In the toxin accumulation phase, which lasted for 42 days, concentrations of PSTs increased in the snails gradually, reaching a maximum of 1.10 nmole g(-1) at the end of the exposure period. The toxin content of the homogenized clams (food) was 13.18 nmole g(-1), which was about 12-fold higher than the PST content in the snails. Between day 43 and day 82, the snails were fed with non-toxic clams, and this period represented the depuration phase. Accumulation and depuration rates of PSTs in the snails, N. festivus, were determined by fitting the experimental data to user-defined parameters program using a one-compartment model. Two different modeling approaches were used to derive the accumulation and depuration rates. The first approach is to derive both values from the data for the toxin uptake. The second approach is to derive depuration rate from the depuration data and then to derive uptake rate, allowing for toxin depuration, from the data for toxin uptake. The first approach yielded more consistent results for the toxin concentration at the end of the uptake period, when compared with the experimental data. The toxin uptake and depuration rates were 1.64 (pmole of toxin into snail per day) per (nmole g(-1) of toxin in food) and 0.06+/-0.02 day(-1) (mean+/-SE), respectively. The toxin profiles of snails were similar to the clams, but different from the algae. Besides C toxins (C1 and C2), dcGTX2 and dcGTX3 were also detected in both clams and snails. The beta:alpha epimer ratio gradually decreased during trophic transfer and approached a ratio of 1:3 (26.4 mol%:73.6 mol% at day 42) in the snails, near the end of the accumulation period.

Bivalvia↗

PubMed2004

Analysis of paralytic shellfish poisoning toxin congeners by a sodium channel receptor binding assay.

This study was carried out to characterize the detection and quantitation of several paralytic shellfish poisoning (PSP) toxin congeners using a receptor binding assay (RBA). This involved competitive binding of the toxin congeners against tritium-labeled STX for receptor sites on rat brain sodium channels. Competitive binding curves were described by a four-parameter logistic equation. Half-saturation values (EC(50)) ranged from 4.38 nM for STX to 142 nM for GTX5. Receptor binding affinity was in the order STX>GTX1/4>neoSTX>GTX2/3>dcSTX>GTX5, and this was similar to the order of mouse toxicity of these congeners. Predicted toxin concentrations from observed STXeq values and EC(50) ratios relative to STX were within 20% or better of the actual concentrations used in the assay. In contrast predicted toxin concentrations using mouse toxicity ratios relative to STX did not provide a good match to actual concentrations, except for GTX1/4. This study has shown that the rat brain sodium channel RBA will provide a reliable integration of total toxicity of various PSP toxin congeners present in a sample.

Animals↗