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PubMed2003

Phylogeography of the invasive cyanobacterium Cylindrospermopsis raciborskii.

Cylindrospermopsis raciborskii is a planktonic freshwater cyanobacterium that has become increasingly prevalent in tropical and temperate water bodies world-wide. This species is of concern from a water-quality perspective because of its known ability to produce toxins that can affect the health of humans and other animals. This study investigates genetic variation between strains of C. raciborskii isolated from freshwater rivers and reservoirs in Australia, Brazil, Germany, Hungary, Portugal and the USA. Strains were first characterized by analysis of their 16S rRNA gene nucleotide sequences and were found to have a sequence divergence of 99.1%. A phylogenetic tree, constructed using the 16S rRNA gene sequences showed that strains grouped into Australian, European and North/South American phylotypes. To investigate further the observed separation of strains into geographically distinct groups, we applied a cyanobacterium-specific short tandem repeat sequence technique, HIP1. An electrophoretic comparison of the HIP1 polymerase chain reaction products showed clear distinctions between the C. raciborskii strains. A phylogenetic tree, based on the repeat element banding patterns, also revealed three distinct groups of C. raciborskii strains. The first group consisted of strains from the USA and Brazil; the second comprised European strains from Germany, Hungary and Portugal; and the third were strains from Australia. In general, between-country variation was greater than within-country variation, indicating that this fingerprinting technique can successfully distinguish C. raciborskii strains taken from different global locations. The relationship between toxicity and the observed HIP1 polymerase chain reaction fingerprint profiles was less clear, although it is interesting to note that of the strains analysed in this study, only Australian strains are known to produce cylindrospermopsin and only Brazilian strains have been reported to produce paralytic shellfish poisoning toxins.

Alkaloids↗
PubMed2001

Crystal structure of the tumor-promoter okadaic acid bound to protein phosphatase-1.

Protein phosphatase-1 (PP1) plays a key role in dephosphorylation in numerous biological processes such as glycogen metabolism, cell cycle regulation, smooth muscle contraction, and protein synthesis. Microorganisms produce a variety of inhibitors of PP1, which include the microcystin class of inhibitors and okadaic acid, the latter being the major cause of diarrhetic shellfish poisoning and a powerful tumor promoter. We have determined the crystal structure of the molecular complex of okadaic acid bound to PP1 to a resolution of 1.9 A. This structure reveals that the acid binds in a hydrophobic groove adjacent to the active site of the protein and interacts with basic residues within the active site. Okadaic acid exhibits a cyclic structure, which is maintained via an intramolecular hydrogen bond. This is reminiscent of other macrocyclic protein phosphatase inhibitors. The inhibitor-bound enzyme shows very little conformational change when compared with two other PP1 structures, except in the inhibitor-sensitive beta12-beta13 loop region. The selectivity of okadaic acid for protein phosphatases-1 and -2A but not PP-2B (calcineurin) may be reassessed in light of this study.

Carcinogens↗
PubMed1999

Use of immunoaffinity columns for clean-up of diarrhetic toxins (okadaic acid and dinophysistoxins) extracts from shellfish prior to their analysis by HPLC/fluorimetry.

Diarrhetic Shellfish Poisoning (DSP) is a severe gastro-intestinal disease caused by consumption of seafood contaminated by microalgal toxins, mainly okadaic acid (OA) and structurally related toxins, dinophysistoxins (DTXs). Regulatory monitoring is generally based on rodent bioassays which, however, present some technical and ethical disadvantages. The most promising technique of analysis of these toxins involves an HPLC separation with spectrofluorimetric detection after derivatization of the toxins with a fluorescent reagent. The lack of specificity of the extraction procedure (liquid-liquid partition), and the presence of interfering compounds in the matrix, does not allow the determination and the quantification of low amounts of toxins in seafood. In this paper, the authors report the development and the characterization of immunoaffinity columns (IAC), which were elaborated using anti-okadaic acid monoclonal antibodies, for a specific retention of the OA group of toxins. The coupling yield and the stability of these columns were investigated as well as their capacity to remove interfering compounds. Cross-reactivity was observed between the antibodies and the DTX-1 and the DTX-2, allowing the detection of the different toxins in a single analysis. Different spiked (1 microgram OA/g) or naturally-contaminated (mussel digestive gland: 2 micrograms OA/g; algae: 165 micrograms OA/g) matrices were tested. The recovery for OA varied from 55 to 95% according to the matrices. The IAC purification was then included as a step of a global [IAC/HPLC/spectrofluorimetric detection] method and the performance of the method was evaluated. Estimations of the linearity and the accuracy (percentages of the presumptive response for OA in the range +101% to +114%) were satisfactory in accordance with the method validation criteria.

Animals↗
PubMed1986

Evaluation of chicken embryo, brine shrimp, and bacterial bioassays for saxitoxin.

The chicken embryo, brine shrimp (Artemia salina) and selected bacteria (Staphylococcus epidermidis, Micrococcus flavus, and Bacillus subtilis) were evaluated as alternative test systems for the determination of paralytic shellfish poisoning toxicity (saxitoxin). Dose levels ranging from 0.045 to 0.3 microgram were administered to the developing embryo through the air cell at either 0 or 96 h following incubation. Embryos dosed 96 h after incubation were the most sensitive, with 100% mortality at the 0.11-microgram dose level 24 h following exposure. Embryo mortality was 42% at to 0.3-microgram dose level when the toxin was administered at 0 h. Some embryonic malformations were observed in the 0-h treatment group. Brine-shrimp larvae were sensitive to saxitoxin at a dose level of 5 micrograms. A dose response based on mortality was apparent only 48 h after dosing. Limited growth inhibition was observed with the bacteria tested at concentrations between 0.0035 and 0.35 microgram and 0.35 microgram/well.

Animals↗
PubMed2003

Aneugenic potential of okadaic acid revealed by the micronucleus assay combined with the FISH technique in CHO-K1 cells.

Okadaic acid (OA) is a major toxin involved in diarrhetic shellfish poisoning in humans and has been shown to be both a potent tumor promoter in rodent skin and stomach and an inhibitor of serine/threonine protein phosphatases, specifically PP1 and PP2A. The research on the genotoxic potential of OA amounts to only a few studies, which give conflicting results. In order to evaluate the ability of OA to induce DNA damage, the cytokinesis-block micronucleus assay was performed in the CHO-K1 cell line. A statistically significant induction of micronuclei without strong cytotoxicity was obtained after a 24 h treatment with 20 (approximately 5-fold) and 30 nM (approximately 10-fold) OA. Then, in order to discriminate between a clastogenic or aneugenic effect of OA, the micronucleus assay was carried out in combination with fluorescence in situ hybridization (FISH) using a (TTAGGG)(n) DNA probe for centromere detection. FISH analysis showed that OA mainly induced centromere-positive micronuclei (68.9% induction with 20 nM OA and 77.0% with 30 nM). Therefore, OA can be considered aneugenic. Using the same assay, biotransformation of OA was studied after a 4 h treatment with and without metabolic activation. The results show that reactive metabolites of OA were generated with a significant increase in genotoxic potential. The relationship between the different components involved in the mitotic process and OA inhibition of protein phosphatase is also discussed.

Aneugens↗
PubMed1988

Diarrhetic shellfish toxin, dinophysistoxin-1, is a potent tumor promoter on mouse skin.

Dinophysistoxin-1, 35-methylokadaic acid, is a causative agent of diarrhetic shellfish poisoning. The biological activities and tumor-promoting activity of dinophysistoxin-1 were studied together with those of okadaic acid and 7-O-palmitoyl okadaic acid. Dinophysistoxin-1 is a skin irritant and induces ornithine decarboxylase in mouse skin with the same potency as okadaic acid. 7-O-Palmitoyl okadaic acid induced a lower activity than the other compounds. Dinophysistoxin-1 inhibited the specific [3H]okadaic acid binding to a particulate fraction of mouse epidermis. The binding affinities of dinophysistoxin-1 and okadaic acid to a particulate fraction were almost the same. Dinophysistoxin-1 showed a tumor-promoting activity as strong as that of okadaic acid in a two-stage carcinogenesis experiment on mouse skin. The percentages of tumor-bearing mice in the groups treated with 100 micrograms of 7,12-dimethylbenz[a]anthracene (DMBA) followed by 5 micrograms of dinophysistoxin-1, twice a week, and with DMBA followed by 5 micrograms of okadaic acid twice a week were 86.7% and 80.0% in week 30, respectively. The average number of tumors per mouse was 4.6 in the former group and 3.9 in the latter. Dinophysistoxin-1 and okadaic acid act on cells through different pathways from the 12-O-tetradecanoylphorbol-13-acetate-type tumor promoters.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1988

Seasonal, geographic and individual variation of okadaic acid content in cultivated mussels in Sweden.

In Western Europe the dinoflagellate toxin, okadaic acid (OA) has been the main cause of diarrheic shellfish poisoning (DSP). Chemical determination of OA in mussels by homogenization of the hepatopancreas, extraction, purification, reaction with 9-anthryldiazomethane (ADAM), HPLC-separation, and fluorometric quantification has been used for weekly monitoring of mussel growing farms and to control harvested mussels. Within a week, substantial rises (from 0.41 to 5.4 micrograms OA/g hepatopancreas) as well as great reductions (from 7.2 to 1.8 micrograms/g hepatopancreas) were recorded. The rapid rise implies that weekly sampling is not sufficient to ensure that mussels are free from toxic levels of OA. The rapid decrease reveals that efficient toxin clearance mechanisms exist in the mussels. Substantial OA clearance occurs also at low temperatures (1.4-3 degrees C). Within a mussel growing site the OA concentrations could differ considerably between adjacent mussels (0.63 and 4.2 micrograms OA/g hepatop.) and even more between mussels grown at different depths along the same rope (0.63 and 10 micrograms OA/g hepatop.). These data emphasize the importance of sampling in studies on DST in mussels. Great differences between the different mussel growing sites were also observed. These data have been discussed with respect to the spread of the toxin by the sea, and the possibilities of reducing the exposure of the mussels to the toxic algae.

Animals↗
PubMed2000

Molecular phylogeny of Anabaena circinalis and its identification in environmental samples by PCR.

Although the cyanobacterium Anabaena circinalis occurs worldwide, Australian isolates are believed to exclusively possess the saxitoxin group neurotoxins (paralytic shellfish poisons). Identification of A. circinalis in a mixed population is complicated due to limited morphological differences between Anabaena species. Sequence analysis of the DNA-dependent RNA polymerase (rpoC1) gene from 24 Anabaena isolates, including 12 designated A. circinalis, permitted a phylogenetic analysis to be performed. In addition, an A. circinalis-specific PCR was developed and tested successfully on environmental samples.

Anabaena↗
PubMed2003

Effect of associated bacteria on the growth and toxicity of Alexandrium catenella.

Saprophytic bacteria in cultures of the marine dinoflagellate Alexandrium catenella were removed to assess their effect on growth and paralytic shellfish poisoning toxin production of this dinoflagellate. The actual axenic status was demonstrated by the lack of observable bacteria both immediately after treatment and following extended incubation in the absence of antibiotics. Bacteria were measured by counting CFU and also by epifluorescence microscopy and PCR amplification of bacterial 16S-23S spacer ribosomal DNA to detect noncultivable bacteria. Removal of bacteria did not have any effect on the growth of the dinoflagellate except for the inhibition of A. catenella disintegration after reaching the stationary phase. Toxicity was determined in dinoflagellate cell extracts by different methods: high-performance liquid chromatography (HPLC); an electrophysiological test called the Electrotest, which measures the inhibition of saxitoxin-sensitive Na(+) channels expressed in a cell line; and a mouse bioassay, which measures the toxic effect on the whole mammal neuromuscular system. A lower toxicity of the dinoflagellates in axenic culture was observed by these three methods, though the difference was significant only by the mouse bioassay and HPLC methods. Altogether the results indicate that axenic cultures of A. catenella are able to produce toxin, though the total toxicity is probably diminished to about one-fifth of that in nonaxenic cultures.

Animals↗
PubMed1996

Microalgal metabolites: a new perspective.

Occurrence of secondary metabolites in microalgae (protoctista) is discussed with respect to the phylogenic or taxonomic relationships of organisms. Biosynthetic mechanisms of certain metabolites such as paralytic shellfish poisoning toxins and polyether toxins are also discussed, and genetic aspects of the secondary metabolite production as well.

Classification↗
PubMed1996

Calcium is permeable through a maitotoxin-activated nonselective cation channel in mouse L cells.

The shellfish poison maitotoxin causes the irreversible opening of nonselective cation channels in mouse L cell fibroblasts, consistent with the action of this toxin in other cell types and the previously demonstrated existence of 28-pS voltage-insensitive nonselected cation channels that are activated by platelet-derived growth factor in these cells. Toxin-induced opening of these nonselective cation channels led to increases of intracellular calcium and secondary activation of calcium-activated potassium channel. These effects were completely dependent on influx of extracellular calcium, supporting the conclusion that the maitotoxin-activated nonselective cation channels are permeable to calcium as well as to sodium and potassium. The implication of this finding is that calcium signaling through this channel underlies its links into the growth factor response.

Animals↗
PubMed1996

Transplacental passage of [3H]-okadaic acid in pregnant mice measured by radioactivity and high-performance liquid chromatography.

Okadaic acid (OA) is the main toxin produced by dinoflagellates, which can accumulate in the hepatopancreas of mussels and cause diarrhoetic shellfish poisoning in consumers. This toxin is also a tumour promoter and a specific potent inhibitor of protein phosphatases 1 and 2A. The results in this study show for the first time that this marine toxin is able to cross the transplacental barrier. Foetal tissue contains more okadaic acid than the liver or kidney: 5.60% compared to 1.90 and 2.55% respectively as measured by HPLC and fluorescent detection after derivatization with 9-Anthryldiazomethane (ADAM). In view of its adverse effects, okadaic acid might impair foetal development and promote tumours in neonates.

Animals↗
PubMed2001

Effect of a short-term in vitro exposure to the marine toxin domoic acid on viability, tumor necrosis factor-alpha, matrix metalloproteinase-9 and superoxide anion release by rat neonatal microglia.

BACKGROUND: The excitatory amino acid domoic acid, a glutamate and kainic acid analog, is the causative agent of amnesic shellfish poisoning in humans. No studies to our knowledge have investigated the potential contribution to short-term neurotoxicity of the brain microglia, a cell type that constitutes circa 10% of the total glial population in the brain. We tested the hypothesis that a short-term in vitro exposure to domoic acid, might lead to the activation of rat neonatal microglia and the concomitant release of the putative neurotoxic mediators tumor necrosis factor-alpha (TNF-alpha), matrix metalloproteinases-2 and-9 (MMP-2 and -9) and superoxide anion (O2-). RESULTS: In vitro, domoic acid [10 microM-1 mM] was significantly neurotoxic to primary cerebellar granule neurons. Although neonatal rat microglia expressed ionotropic glutamate GluR4 receptors, exposure during 6 hours to domoic acid [10 microM-1 mM] had no significant effect on viability. By four hours, LPS (10 ng/mL) stimulated an increase in TNF-alpha mRNA and a 2,233 % increase in TNF-alpha protein In contrast, domoic acid (1 mM) induced a slight rise in TNF-alpha expression and a 53 % increase (p < 0.01) of immunoreactive TNF-alpha protein. Furthermore, though less potent than LPS, a 4-hour treatment with domoic acid (1 mM) yielded a 757% (p < 0.01) increase in MMP-9 release, but had no effect on MMP-2. Finally, while PMA (phorbol 12-myristate 13-acetate) stimulated O2- generation was elevated in 6 hour LPS-primed microglia, a similar pretreatment with domoic acid (1 mM) did not prime O2- release. CONCLUSIONS: To our knowledge this is the first experimental evidence that domoic acid, at in vitro concentrations that are toxic to neuronal cells, can trigger a release of statistically significant amounts of TNF-alpha and MMP-9 by brain microglia. These observations are of considerable pathophysiological significance because domoic acid activates rat microglia several days after in vivo administration.

Animals↗
PubMed1999

Variations in the distribution of okadaic acid in organs and biological fluids of mice related to diarrhoeic syndrome.

Okadaic acid (OA) is the main toxin produced by dinoflagellates which can accumulate in the hepatopancreas of mussels and cause diarrhetic shellfish poisoning in consumers. This toxin is also a tumour promoter and a specific potent inhibitor of protein phosphatases 1 and 2A. No specific target organ is known for this toxin. This study concerns the distribution of [3H]OA in organs and biological fluids of Swiss mice having received a single dose per os of AO (50 microg/kg). The determination of the toxin extracted from mouse organs 24 h after administration of [3H]OA and derivatised with 9-anthryldiazomethane (ADAM) before HPLC and fluorescent detection showed the highest concentration in intestinal tissue and stomach. This distribution was even more pronounced in intestinal tissue, when animal were given per os 90 microg/kg which induced diarrhoea. The high concentrations of [3H]OA in intestinal tissues and contents 24 h after administration demonstrates a slow elimination of OA. When the dose of OA was increased from 50-90 microg/kg, the concentrations of the toxin in the intestinal content and faeces increased proportionally. A good correlation was found between an increase of OA in the intestinal tissue and the diarrhoea in animals given 90 microg/kg orally. Moreover OA was present in liver and bile and in all organs including skin and also fluids. Altogether these results confirmed an enterohepatic circulation of OA as previously shown. These data also revealed that in acute OA intoxication the concentration of the toxin in the intestinal tissues reaches cytotoxic concentrations in accordance with the diarrhoea which is the main symptom of OA poisoning.

Animals↗
PubMed1999

[Actin depolymerizing action by marine toxin, pectenotoxin-2].

Pectenotoxin-2 (PCTX-2), which is one of Diarrhetic Shellfish Poisoning (DSP), is a family of cyclic polyether macrolide toxin isolated from scallop Patinopecten yessoensis. Although PCTX-2 has a potent cytotoxic activities against several cancer cell lines, the biochemical activity of PCTX-2 has not been determined yet. To clarify the biochemical activity of PCTX-2 is the aime in this study. PCTX-2 inhibited the contractions elicited by 72.7 mM KCl or 1 microM phenyrephrine in a concentration dependent manner in the isolated rat aorta. In A10 cells, actin stressfiber in center but not in periphery of the cell was disrupted by PCTX-2 without any visible shape change. By monitoring fluorescent intensity of pyrenyl-actin, PCTX-2 was found to inhibit the velocity and the degree of actin polymerization in a concentration dependent manner. In addition, PCTX-2 decreased viscosity of F-actin measured with falling ball viscometry. Stoichiometric analysis indicated that PCTX-2 forms 1:4 complex with G-actin. These results suggest that PCTX-2 is a potent natural actin depolymerizing compound with unique mode of action.

Actins↗
PubMedDate not supplied

Determination of domoic acid in Japanese mussels by enzyme immunoassay.

Ten samples of commercial blue mussels (Mytilus edulis) from Japan were analyzed for domoic acid by an indirect competitive enzyme immunoassay (idc-EIA) based on an anti-domoic acid monoclonal antibody. Domoic acid was found in all samples at low concentrations (0.11-1.81 ng/g mussel tissue). The presence of domoic acid was confirmed by liquid chromatography coupled with immunoaffinity chromatography using an anti-domoic acid monoclonal antibody as ligand. To our knowledge, this is the first reported detection of domoic acid, a causative agent of amnesic shellfish poisoning, in Japanese mussels.

Animals↗