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PubMed2004

Comparative concentrations of brevetoxins PbTx-2, PbTx-3, BTX-B1 and BTX-B5 in cockle, Austrovenus stutchburyi, greenshell mussel, Perna canaliculus, and Pacific oyster, Crassostrea gigas, involved neurotoxic shellfish poisoning in New Zealand.

Previously, we found brevetoxins PbTx-3, BTX-B5 and BTX-B1 in cockle, Austrovenus (A.) stutchburyi, PbTx-2, PbTx-3 and BTX-B1 in Pacific oyster, Crassostrea (C.) gigas and PbTx-3 and BTX-B1 in greenshell mussel, Perna (P.) canaliculus following outbreak of neurotoxic shellfish poisoning (NSP) in New Zealand by isolation and/or liquid chromatography coupled with tandem mass spectrometry (LC-MS/MS). In this study, procedures for quantitative determination of PbTx-2 and BTX-B5 were developed and those for PbTx-3 and BTX-B1 were further examined by LC-MS/MS. In mass spectrometry with an electrospray ionization interface operating in the positive or negative ion mode, the protonated ions [M+H]+ of PbTx-2 (m/z 895), [M+H]+ of PbTx-3 (m/z 897), [M-H]- of BTX-B5 (m/z 909), and [M-Na]- of BTX-B1 (m/z 1016) were generated abundantly, when 0.1% formic acid-acetonitrile was used as the mobile phase for column chromatography. The product ions of m/z 877, 725, 111 and 80 from PbTx-2, PbTx-3, BTX-B5 and BTX-B1 were identified, respectively, allowing unambiguous confirmation of these toxins by selective reaction monitoring LC-MS/MS analysis. High levels of PbTx-3 and BTX-B5 were detected in C. gigas, of PbTx-3, BTX-B1 and BTX-B5 in A. stutchburyi, and of PbTx-2, PbTx-3 and BTX-B5 in P. canaliculus by this LC-MS/MS method.

Animals↗

PubMed1990

Paralytic shellfish poisoning: a case report and serial electrophysiologic observations.

We report serial electrophysiologic observations in a patient with acute bulbar and respiratory paralysis following ingestion of saxitoxin-contaminated clams. Prolonged distal motor and sensory latencies, slowed conduction velocities, and moderately diminished amplitudes were present at the outset. All values returned to normal over 5 days. These findings, the result of incomplete sodium channel blockade, distinguish paralytic shellfish poisoning from most other acute paralytic illnesses.

Animals↗

PubMed2004

Paralytic shellfish poisoning: post-mortem analysis of tissue and body fluid samples from human victims in the Patagonia fjords.

In July 5, 2002 fishermen working in harvesting sea urchin (Loxechinus albus) in the Patagonia Chilean fjords were intoxicated by consumption of filter-feeder bivalve Aulacomya ater. After the ingestion of 7-9 ribbed mussel, two fishermen died 3-4 h after shellfish consumption. The forensic examination in both victims did not show pathological abnormalities with the exception of the lungs conditions, crackling to the touch, pulmonary congestion and edema. The toxic mussel sample showed a toxicity measured by mouse bioassay of 8575 microg of STX (saxitoxin) equivalent by 100 g of shellfish meat. Using post-column derivatization HPLC method with fluorescent on line detection was possible to measure mass amount of each paralytic shellfish poisoning (PSP) toxin yielding individual toxin concentrations. These PSP toxins were identified in the gastric content, body fluids (urine, bile and cerebrospinal fluid) and tissue samples (liver, kidney, lung, stomach, spleen, heart, brain, adrenal glands, pancreas and thyroids glands). The toxin profiles of each body fluid and tissue samples and the amount of each PSP toxin detected are reported. The PSP toxins found in the gastric content, were STX and the gonyautoxins (GTX4, GTX1, GTX5, GTX3 and GTX2) which showed to be the major amount of PSP toxins found in the victims biological samples. The PSP toxin composition in urine and bile showed as major PSP toxins neoSaxitoxin (neoSTX) and GTX4/GTX1 epimers, both STX analogues with an hydroxyl group (-OH) in the N(1) of the tetrahydropurine nucleus. The neoSTX was not present in the gastric content sample, indicating that the oxidation of N(1) in the STX tetrahydropurine nucleus resulted neoSTX, in a similar way that GTX3/GTX2 epimers were transformed in GTX4/GTX1 epimers. Beside this metabolic transformation, also the hydrolysis of carbamoyl group from STX to form its decarbomoyl analogue decarbamoylsaxitoxin was detected in liver, kidney and lung. These two findings show that PSP toxins went under metabolic transformation during the 3-4 h of human intoxication period, in which PSP toxins showed enzymatic oxidation of N(1) in the tetrahydropurine nucleus, producing neoSTX and GTX4/GTX1 epimers starting from STX and GTX3/GTX2 epimers, respectively. This study conclude, that PSP toxins are metabolically transformed by humans and that they are removed from the body by excretion in the urine and feces like any other xenobiotic compound.

Animals↗

PubMed2002

Fate of paralytic shellfish poisoning toxins in purple clam Hiatula rostrata, in outdoor culture and laboratory culture.

Purple clams (Hiatula rostrata Lighttoot) accumulate paralytic shellfish poisoning (PSP) toxins produced by a toxic strain of the dinoflagellate Alexandriun minutum Halim. The results confirm the data of our previous study concerning the muscle and siphon that were not showing a gradual rise in toxicity when shellfish accumulated more A. minutum. However, muscle and siphon are intermittently toxic both in exposure and depuration period in laboratory cultured purple clams. PSP toxins were detected in outdoor cultured purple clams, whereas no A. minutum were found in the culture pond during most of the survey time. The outdoor cultured purple clams need longer time to decrease toxicity to allowable levels than laboratory cultured purple clams. It was shown that laboratory data may not predict times over which pond-cultured purple clams may prove toxic to consumers.

Adaptation, Physiological↗

PubMed1992

Cross-reacting antigens in the butter clam (Saxidoma giganteus) and their relationship to total paralytic shellfish poison toxicity.

A specific protein with an apparent mol. wt of 23,000 was identified in foot homogenate derived from paralytic shellfish poisoning (PSP) contaminated butter clams and was found to cross-react with crab-saxitoxin-induced protein (SIP) antiserum. Antiserum, once cross-absorbed against non-toxic shellfish material, was incubated with tissue homogenate derived from 52 butter clams with varying total PSP toxicities in a prototype ELISA. A significant (r = 0.83; P less than 0.001) correlation existed between soluble clam antigen content in foot homogenate and total PSP toxicity; the latter measured by the mouse lethality bioassay. From the ELISA results, a soluble antigen threshold of 0.1% total protein was successfully used to distinguish between PSP toxic and non-toxic butter clams. It is proposed that this type of screening assay could be used in conjunction with the standard mouse bioassay to increase PSP monitoring and potentially reduce unnecessary animal testing.

Animals↗

PubMed2004

The effect of temperature on growth and production of paralytic shellfish poisoning toxins by the cyanobacterium Cylindrospermopsis raciborskii C10.

Cylindrospermopsis raciborskii is a cyanobacterium which produces either cylindrospermopsine or paralytic shellfish poisoning (PSP) toxins. We studied the effect of temperature on growth and production of PSP toxins by C. raciborskii C10, isolated from a freshwater reservoir in Brazil. We analyzed the extracellular and intracellular content of PSP toxins at two different temperatures: 19 and 25 degrees C. C. raciborskii C10 produces STX, GTX2, and GTX3 at both temperatures. dcSTX was also detected at 25 degrees C in the intracellular extracts obtained at the end of the stationary phase. The growth achieved at 25 degrees C and estimated by optical density at 700 nm was three times greater than at 19 degrees C. However, no significant differences were observed in the content of PSP toxins in either the cells or the extracellular media. The kinetics of accumulation of PSP toxins within the cells rather than in the media suggests an active PSP toxins-export process that is not related to cell lysis. The extracellular accumulation of PSP toxins at 19 degrees C suggested a biotransformation of STX to the epimers GTX2 and GTX3. The stability of the PSP toxins produced by C. raciborskii C10 was high enough for them to remain active in the media after 30 days (at 25 degrees C) or after 50 days (at 19 degrees C).

Animals↗

PubMed1997

Development and preliminary validation of a microtiter plate-based receptor binding assay for paralytic shellfish poisoning toxins.

More than 20 countries have either established or proposed regulatory limits for one or more of the paralytic shellfish poisoning (PSP) toxins as they occur in seafood products. PSP toxin levels are generally estimated using the standard AOAC mouse bioassay, yet because of various limitations of this method [e.g. high variability (+/-20%), low sensitivity, limited sample throughput and use of live animals], there remains a need for alternative testing protocols. A sensitive and selective, high capacity assay was developed for the PSP toxins which exploits the highly specific interaction of these toxins with their biological receptor (i.e. voltage-dependent sodium channel) and is thus based on functional activity. This receptor binding assay provides a radioactive endpoint, and is performed in a microtiter filter plate format with results determined by standard liquid scintillation counting within 24 hr. The Ki for the assay is 3.66 +/- 0.86 nM saxitoxin, with a limit of detection of c. 5 ng saxitoxin/ml in a sample extract. Good quantitative agreement of the assay with both mouse bioassay and high-performance liquid chromatographic analysis of crude extracts of contaminated shellfish, as well as PSP toxin-producing algae, was observed. Our findings indicate that the receptor binding assay has a strong predictive value for toxicity determined by mouse bioassay, and that this approach warrants consideration as a rapid, reliable and cost-effective alternative to live animal testing for detection and estimation of PSP-related toxicity in seafood and toxic algae.

Animals↗

PubMed1991

Clinical and epidemiological features of neurotoxic shellfish poisoning in North Carolina.

BACKGROUND: In October 1987, a red tide due to P. brevis affected the North Carolina coast for the first time. The purpose of our study was to describe the clinical and epidemiological features of neurotoxic shellfish poisoning (NSP), an illness caused by eating shellfish contaminated with the neurotoxins of P. brevis. METHODS: Active surveillance was established for cases of NSP. A descriptive study of the NSP cases was then completed. RESULTS: Forty-eight persons, who had eaten oysters at 20 meals, met the case definition. A variety of gastrointestinal tract and neurological symptoms were reported. The illnesses were generally mild and of short duration, and there were no deaths. Forty-one (85 percent) affected persons lived in five communities located within a 70-kilometer area along the coast. Cases occurred from October 27 to December 9; 27 (56 percent) of the cases occurred before the first closure of affected shellfish waters on November 2. There was a significant increase in the illness attack rate with an increase in the number of oysters eaten. CONCLUSIONS: Routine monitoring of coastal waters for P. brevis is needed to facilitate earlier recognition of red tides, closure of affected areas, and education of the public before substantial exposure to contaminated shellfish occurs.

Adolescent↗

PubMed2005

Assessment of the quantitative determination of paralytic shellfish poisoning toxins by pre-column derivatization and elimination of interfering compounds by solid-phase extraction.

Monitoring programmes for paralytic shellfish poisoning toxins in bivalve molluscs still rely heavily on the use of mouse bioassays (MBA) for consumer protection. A high-performance liquid chromatography (HPLC) methodology (Lawrence method) was implemented in 1996 in the Portuguese monitoring programme as a complementary means of analysis. Comparison between MBA and HPLC was done at the time only by a qualitative approach due to the scarce number of positive samples tested. More quantitative data were obtained recently when studying toxin profiles in Moroccan shellfish, and the correlation found between these two methodologies is reported here for the first time. Two different matrices were studied: blue mussel and the giant cockle Acanthocardia tuberculatum. A good linear correlation was obtained for both matrices. However, a second-degree polynomial best fitted the data at both low and high extremes of toxicity. According to the HPLC quantitative results, 13% of false-negatives could be obtained by MBA due to an underestimation of toxicity near the limit of detection of the MBA. Difficulties on relying solely on HPLC for consumer protection have been aroused with uncommon matrices, such as imported clams or crustaceans, due to the presence of high concentrations of interfering compounds. The solid-phase extraction step of the Lawrence method was implemented to eliminate an unknown compound that could be mistaken for saxitoxin, and an 80% reduction of another common unknown compound eluting close to decarbamoylsaxitoxin. The implementation of the HPLC methodology achieved so far allows a high degree of consumer protection without the need to resource to animal sacrifice.

Animals↗

PubMedDate not supplied

Proficiency testing of eight French laboratories in using the AOAC mouse bioassay for paralytic shellfish poisoning: interlaboratory collaborative study.

In an interlaboratory study, 8 French laboratories were tested for their proficiency in using the AOAC mouse bioassay for paralytic shellfish poisoning (PSP). Each laboratory received 1 saxitoxin (STX) standard solution, 1 STX acidified water solution for determination of the titer, 1 noncontaminated shellfish sample, 1 naturally contaminated shellfish sample, and 2 shellfish samples spiked, respectively, at low (152.8 microg STX/100 g meat) and moderate (334.7 microg STX/100 g meat) levels. All samples were analyzed in duplicate. Mean recoveries were 35.1% for the low level and 46.6% for the moderate level. Relative standard deviations (RSD) for within-laboratory variations (repeatability) ranged from 5.4 to 9.8%; RSD for between-laboratory variations (reproducibility) varied from 7.8 to 39.6%, depending on STX level. On the basis of overall performance, all 8 participating laboratories were proficient in their use of the AOAC mouse bioassay.

Animals↗

PubMed1994

Comparison of mouse bioassay, HPLC and enzyme immunoassay methods for determining diarrhetic shellfish poisoning toxins in mussels.

Mussel specimens (Mytilus galloprovincialis) collected from two different areas of the Adriatic Sea were analysed for diarrhoetic shellfish poisoning (DSP) toxin by three methods: mouse bioassay, the DSP Check enzyme immunoassay kit, and high-performance liquid chromatography (HPLC). The results obtained confirm that Yasumoto's mouse bioassay, capable of detecting all the components of the DSP group, is still necessary to determine the wholesomeness of the product. The ELISA method has not always given quantitatively reliable results. The HPLC method is advantageous in terms of sensitivity, accuracy, specificity and rapidity. However, its application is limited so far to the determination of okadaic acid in mussels.

Animals↗

PubMed2005

Diarrhetic shellfish poisoning toxin esters in Danish blue mussels and surf clams.

Until recently, little focus was given to the presence of diarrhetic shellfish poisoning (DSP) toxin esters in seafood products. However, during the last few years, the occurrence of a high percentage of esters of the total amount of DSP toxins present in some seafood products has been observed. Samples of Danish surf clams (Spisola spp.) and blue mussels (Mytilus edulis) from 1999-2004 were analysed by liquid chromatography coupled with tandem mass spectrometry (LC/MS/MS) for the presence of DSP toxin esters. The samples contained only okadaic acid and esters of okadaic acid. The level of total okadaic acid equivalents ranged from 224 to 2516 microg kg-1 in surf clams. The percentage of okadaic acid esters of the total okadaic acid equivalents ranged from 83 to 98%, mean 95%. The level of total okadaic acid equivalents ranged from 43 to 1631 microg kg-1 in blue mussels. The percentage of okadaic acid esters of the total okadaic acid equivalents ranged from 21 to 86%, mean 59%. The probability of a high percentage of okadaic acid esters seems to increase with higher amounts of total okadaic acid equivalents in the bivalves. The large prevalence of DSP toxin esters are of particular importance because of the increased use of chemical methods instead of mouse bioassay for the detection of DSP toxicity.

Animals↗

PubMed1983

Separation of tetrodotoxin and paralytic shellfish poisons by high-performance liquid chromatography with a fluorometric detection using o-phthalaldehyde.

Tetrodotoxin (TTX) and a variety of paralytic shellfish poisons (PSPs) were extracted from toxic specimens of puffer and scallop, and quantitated by high-performance liquid chromatography with a fluorometric detection using o-phthalaldehyde. Fluorescence spectra for the TTX- and PSP-fluorophors in 0.05 M borate buffer (pH 10) showed maxima at 453 nm with 332-nm excitation. The fluorescence intensity per nM of TTX was found to be 3 and those of PSP to be 4-12. This fluorometric technique may be useful for the simultaneous quantitation of TTX and PSP in small volumes of toxin extracts.

Animals↗

PubMed2005

Determination of paralytic shellfish poisoning toxins in cultured microalgae by high-performance liquid chromatography with fluorescence detection.

A novel method for the determination of paralytic shellfish poisoning (PSP) toxins using high-performance liquid chromatography with fluorescence detection was developed. The fluorescent derivates of neosaxitoxin (neoSTX), saxitoxin (STX), gonyautoxins 1 and 4 (GTX1+4), and gonyautoxins 2 and 3 (GTX2+3) were separated on a muBondapak NH2 column (300 mm x 3.9 mm, 10 microm) using water and acetate buffer (pH 6.5) as the mobile phase (1.00 mL min(-1)) in gradient mode with fluorescence detection at 390 nm (excitation at 330 nm). The linear ranges of neoSTX, STX, GTX1+4 and GTX2+3 were 3.31-331, 0.952-95.2, 3.78-378 and 0.124-12.4 ng mL(-1), respectively. The detection limits of neoSTX, STX, GTX1+4 and GTX2+3 were 1.10, 0.32, 1.26 and 0.041 ng mL(-1), respectively. The method was successfully applied to the determination of PSP toxins in microalgae. The recoveries ranged from 88+/-2% to 107+/-4% and the relative standard deviations were 0.16% to 4.4%. The procedure is also environmentally friendly because no organic solvent is used in the mobile phase.

Amides↗

PubMed2004

Comparison of paralytic shellfish poisoning toxin between carnivorous crabs (Telmessus acutidens and Charybdis japonica) and their prey mussel (Mytilus galloprovincialis) in an inshore food chain.

Paralytic shellfish poisoning toxin in two shore crab species, Telmessus acutidens and Charybdis japonica, were compared with the toxin in the prey mussel Mytilus galloprovincialis and causative dinoflagellates Alexandrium tamarense, all having been collected at Onahama, Fukushima Prefecture, in the northern part of Japan. When the toxicities were detected in mussels by mouse bioassays, 73.7% of the sampled T. acutidens were toxic in the hepatopancreas. T. acutidens has been found to become toxic for three years, therefore, it can be concluded that the crab commonly and repeatedly accumulate the toxins via the food chain at Onahama. C. japonica was also expected to be a possible vector species, because small quantities of the toxins were detected in eight specimens of the crab by HPLC analysis. By the comparison of the toxin profiles in the dinoflagellates, mussels and the crab T. acutidens, reductive conversions of GTX1 and GTX4 were observed when the toxins passed through the three species in the food chain. But increases of STX and neoSTX by further reductive process were not observed in the crab. The absence of the STX group toxins in the crab suggests that the crab eliminates the toxin before such reductive process occur.

Animals↗

PubMed2005

Application of solid phase microextraction in the determination of paralytic shellfish poisoning toxins.

A SPME-HPLC-post-column fluorescent derivatization method for the direct determination of saxitoxin (STX), the most potent paralytic shellfish poisoning (PSP) toxin, in water has been developed. Commercially available SPME devices with 50 microm Carbowax templated resin (CW/TPR) coating was found to be able to pre-concentrate STX from aqueous media. A special pre-conditioning treatment of soaking the SPME coating in 0.1 M NaOH solution significantly improved the extraction efficiency. The optimal pH for the SPME process is 8.1 and the equilibration time is 40 min. The partition coefficient, K, of the distribution of STX between the SPME coating and the aqueous media was measured to be 2.99 +/- 0.04 x 10(3). Extracted toxin on the SPME stationary phase was difficult to be desorbed by the HPLC mobile phase under dynamic desorption mode. A static ion-pairing desorption technique using a desorption solvent mixture of 20 mM sodium 1-heptanesulfonate in 30% aqueous acetonitrile acidified with 50 mM sulfuric acid was developed to overcome this problem. The method detection limit and repeatability achieved by this SPME-HPLC method were 0.11 ng ml(-1) and 3.7%, respectively, with a sample volume of just 5 ml of water. This analytical method is adequate for the monitoring of the PSP toxin in fresh/drinking waters. However, serious interference was observed when this technique was applied to saline water samples. This is probably due to competition of sodium ions with the cationic STX for absorption into the SPME stationary phase.

Food Contamination↗

PubMed2005

Accumulation and depuration rates of paralytic shellfish poisoning toxins in the shore crab Telmessus acutidens by feeding toxic mussels under laboratory controlled conditions.

Accumulation and depuration rates of paralytic shellfish poisoning toxins (PSP) in the crab Telmessus acutidens were investigated by feeding toxic and non-toxic mussels under laboratory controlled conditions. The crab accumulated toxins in the hepatopancreas in proportion to the amount of toxic mussels they ingested, and the toxicity in the crab hepatopancreas became 3.2 fold of that in the prey mussels after 20 days of feeding. During depuration, a fast reduction of the total toxicity was observed in the crab, and the retention rate of the toxicity after 5 days depuration with feeding of non-toxic mussels was 45.8+/-18.7%. The reduction of the toxicity was moderated in the later period of depuration, and the retention rates of the total toxicity after 10 and 20 days were 54.1+/-29.8% and 14.5+/-9.0%, respectively. The toxin profiles in the crab and mussel were investigated by high performance liquid chromatography, and reductive conversions of the toxins were observed when the toxins were transferred from the mussel to the crab. Consequently, high concentrations of GTX2 and GTX3, and STX that were not detected in the prey mussels, were found in the crab.

Animals↗

PubMedDate not supplied

Zinc from oyster tissue as causative factor in mouse deaths in official bioassay for paralytic shellfish poison.

Toxicity (extreme weakness, body temperature drop, cyanosis, some slow deaths) in test mice, upon intraperitoneal injection of standard-method paralytic shellfish poison (PSP) extracts of some PSP-free oysters, is consistent with the relatively high levels of zinc in these extracts. As a rough guideline, the threshold for a toxic response corresponds to a drained tissue zinc level of over 900 micrograms/g. The identification of zinc as the substance responsible has been supported by inducing toxicity in control extracts by spiking with nontoxic levels of zinc, and by eliminating toxicity from toxic extracts by chemical removal (precipitation, ion exchange) of metals.

Animals↗