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At least 523 records · Page 29Linked to original sources
PubMed2003

Studies of the biosynthesis of DTX-5a and DTX-5b by the dinoflagellate Prorocentrum maculosum: regiospecificity of the putative Baeyer-Villigerase and insertion of a single amino acid in a polyketide chain.

The biosynthetic origins of the diarrhetic shellfish poisoning toxins DTX-5a and DTX-5b have been elucidated by supplementing cultures of the producing organism Prorocentrum maculosum with stable isotope labeled precursors and determining the incorporation patterns by 13C NMR spectroscopy. The amino acid residue in the sulfated side chain is found to originate from glycine, and oxygen insertion in the chain is shown to occur after polyketide formation.

Amino Acids↗
PubMed2003

Sulfonyl-stabilized oxiranyllithium-based approach to polycyclic ethers. Convergent synthesis of the ABCDEF-ring system of yessotoxin and adriatoxin.

Convergent synthesis of the ABCDEF-ring system of yessotoxin and adriatoxin, marine polycyclic ether toxins causative of diarrheic shellfish poisoning, has been accomplished. The A-ring fragment was constructed by coupling of an appropriately functionalized sulfonyl-stabilized oxiranyl anion and a triflate prepared from an erythritol derivative. An iterative protocol of the oxiranyl anion strategy was also applied for the construction of the DEF-ring fragment. The triflate derivatives of the A-ring and the DEF-ring fragments were connected with lithium acetylide. The resulting acetylene derivative was further transformed into the hexacyclic ABCDEF fragment via oxidation of the acetylene unit to 1,2-diketone, double methyl acetal formation, and reductive etherification.

Ethers↗
PubMed1998

Identification and Characterization of Pectenotoxin (PTX) 4 and PTX7 as Spiroketal Stereoisomers of Two Previously Reported Pectenotoxins.

Pectenotoxins (PTXs) isolated from the scallop Patinopecten yessoensis were shown to be involved in an episode of diarrhetic shellfish poisoning (DSP). A total of eight analogues (PTX1-PTX7 and PTX10) have been isolated to date, and the structures of four of these analogues (PTX1, PTX2, PTX3, and PTX6) have already been elucidated. Here, we report the characterization of PTX4 and PTX7 as 7-epi-PTX1 and 7-epi-PTX6, respectively, on the basis of NMR data and an acid-catalyzed chemical interconversion. The structures of two new artifacts, PTX8 and PTX9, produced following this treatment are also reported.

Journal Article↗
PubMed2005

Glycoyessotoxin a, a new yessotoxin derivative from cultures of Protoceratium reticulatum.

The dinoflagellate Protoceratium reticulatum produces toxins of the yessotoxin group currently included in the diarrhetic shellfish poisoning class. In this paper we report on the isolation and structural elucidation of a 32-arabinoside of yessotoxin, G-YTXA (2), obtained from laboratory cultures of P. reticulatum (strain GG1AM) that possesses a pentose unit, beta-arabinofuranose, as a side chain.

Animals↗
PubMed1996

Isolation and structure of prorocentrolide B, a fast-acting toxin from Prorocentrum maculosum.

A new toxin, prorocentrolide B (1), has been isolated following bioassay-guided fractionation of a BuOH extract of the tropical dinoflagellate, Prorocentrum maculosum Faust. This compound produces a rapid toxic response in the mouse bioassay, a type of activity not accounted for by other diarrhetic shellfish poisoning toxins produced by P. maculosum. The structure 1 was established by NMR and MS and is similar to prorocentrolide (2), a toxin from a strain of Prorocentrum lima. NMR data and the modeling program ConGen have been used to establish the relative stereochemistry of some individual ether ring systems and the hexahydroisoquinoline ring.

Animals↗
PubMed2003

Three novel hydroxybenzoate saxitoxin analogues isolated from the dinoflagellate Gymnodinium catenatum.

In a recent survey of paralytic shellfish poisoning (PSP) toxins in Gymnodinium catenatum Graham extracts, using LC with postcolumn oxidation and fluorescence detection, three novel saxitoxin analogues were revealed in isolates from several locations, including Australian waters. We have named them as G. catenatum toxins, GC1 (1), GC2 (2), and GC3 (3). The compounds were isolated from a culture of the Australian strain by LC-MS-guided fractionation employing a C18-silica column and hydrophilic interaction chromatography. The unusual structures of these novel compounds were characterized by low- and high-resolution MS, MS/MS, and NMR spectroscopy. GC3 (3) was found to be the 4-hydroxybenzoate ester derivative of decarbamoylsaxitoxin, while GC1 (1) and GC2 (2) are the epimeric 11-hydroxysulfate derivatives of GC3 (3).

Animals↗
PubMed2004

Effects of Azaspiracids 2 and 3 on intracellular cAMP, [Ca2+], and pH.

Azaspiracids (AZs) are a new group of phycotoxins discovered in the Ireland coast that includes the isolated analogues: AZ-1, AZ-2, AZ-3, AZ-4, and AZ-5 and the recently described AZ-6-11. Toxic episodes of AZs show gastrointestinal illness as in diarrhetic shellfish poisoning, but neurotoxic symptoms are also observed in a mouse bioassay. Despite their great importance in human health, so far, its mechanism of action is largely unknown. In this report, we present the first data of AZ-2 and AZ-3 effects on intracellular cyclic adenosine monophosphate (cAMP), intracellular calcium ([Ca(2+)](i)), and cytosolic pH levels (pH(i)) in freshly human lymphocytes. The variations of cAMP, calcium, and pH were determined by fluorescence digital imaging microscopy using recombinant fluorescein- and rhodamine-labeled protein kinase A, Fura2-AM, and 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein acetoxymethyl ester, respectively. Our experiments show that both analogues, AZ-2 and AZ-3, clearly increase cytosolic cAMP levels of human lymphocytes. In calcium studies, we found that only if cells are initially in a calcium-free medium, AZ-2 increases the intracellular calcium concentration with two components: Ca(2+) release from internal stores and Ca(2+) influx from extracellular medium. AZ-2 sensitive Ca(2+) stores seem to be different from the thapsigargin sensitive one. AZ-2-induced Ca(2+) influx is mediated through Ni(2+) and SKF96365 blockable channels, and it is additive with Tg-induced Ca(2+) influx. Surprisingly, AZ-3 does not empty intracellular stores but also increases cytosolic calcium levels. This AZ-3-induced Ca(2+) influx is mediated through Ni(2+) blockable channels, and it is not additive with Tg-induced Ca(2+) influx. In addition, AZ-3 slightly alkalinizes cytosol. In accordance with cAMP studies, we found that adenylyl cyclase (AC) modulation inhibits AZ-2- and AZ-3-evoked Ca(2+) increase and AZ-3-induced pH(i) rise. Thus, both analogues seem to involve an AC pathway, although its effects on [Ca(2+)](i) and pH(i) are quite different.

Calcium↗
PubMed2004

Brevenal is a natural inhibitor of brevetoxin action in sodium channel receptor binding assays.

1. Florida red tides produce profound neurotoxicity that is evidenced by massive fish kills, neurotoxic shellfish poisoning, and respiratory distress. Red tides vary in potency, potency that is not totally governed by toxin concentration. The purpose of the study was to understand the variable potency of red tides by evaluating the potential for other natural pharmacological agents which could modulate or otherwise reduce the potency of these lethal environmental events. 2. A synaptosome binding preparation with 3-fold higher specific brevetoxin binding was developed to detect small changes in toxin binding in the presence of potential antagonists. Rodent brain labeled in vitro with tritiated brevetoxin shows high specific binding in the cerebellum as evidenced by autoradiography. Synaptosome binding assays employing cerebellum-derived synaptosomes illustrate 3-fold increased specific binding. 3. A new polyether natural product from Florida's red tide dinoflagellate Karenia brevis, has been isolated and characterized. Brevenal, as the nontoxic natural product is known, competes with tritiated brevetoxin for site 5 associated with the voltage-sensitive sodium channel (VSSC). Brevenal displacement of specific brevetoxin binding is purely competitive in nature. 4. Brevenal, obtained from either laboratory cultures or field collections during a red tide, protects fish from the neurotoxic effects of brevetoxin exposure. 5. Brevenal may serve as a model compound for the development of therapeutics to prevent or reverse intoxication in red tide exposures.

Animals↗
PubMedDate not supplied

An endogenous annual clock in the toxic marine dinoflagellate Gonyaulax tamarensis.

Blooms of the toxic dinoflagellate Gonyaulax tamarensis (synonyms Protogonyaulax tamarensis and Alexandrium tamarense) cause outbreaks of paralytic shellfish poisoning (PSP) in coastal waters throughout the world. In the Gulf of Maine, episodes occur between April and November, a seasonality due in part to life-cycle alternations between motile, vegetative cells and resting cysts which overwinter in bottom sediments. Newly formed cysts have a mandatory 2-6 month dormancy period during which germination is not possible, but once mature, the resting state will continue if temperatures are unfavourable or oxygen is unavailable. We now report another factor controlling germination of cysts of G. tamarensis from deep coastal waters--an endogenous annual clock that can override an otherwise favourable environment for germination. Similar annual variability in germination has not been observed for cysts of this species from shallow estuaries. These results represent the first conclusive demonstration of an endogenous circannual rhythm in a marine plant. They are evolutionarily and ecologically significant because an endogenous annual clock can lead to the release of motile cells into deep and relatively invariant bottom waters at those times when temperature and light at the surface are suitable for growth. In shallow waters where seasonal variability is large and extends to bottom sediments, a strategy similar to that of the seeds of terrestrial plants would be more appropriate, namely a direct coupling between germination and the external environment.

Biological Clocks↗
PubMed1989

Effects of the tumour promoter okadaic acid on intracellular protein phosphorylation and metabolism.

Okadaic acid is a polyether derivative of 38-carbon fatty acid, and is implicated as the causative agent of diarrhetic shellfish poisoning. It is a potent tumour promoter that is not an activator of protein kinase C, but is a powerful inhibitor of protein phosphatases-1 and -2A (PP1 and PP2A) in vitro. We report here that okadaic acid rapidly stimulates protein phosphorylation in intact cells, and behaves like a specific protein phosphatase inhibitor in a variety of metabolic processes. Our results indicate that PP1 and PP2A are the dominant protein phosphatases acting on a wide range of phosphoproteins in vivo. We also find that okadaic acid mimics the effect of insulin on glucose transport in adipocytes, which suggests that this process is stimulated by a serine/threonine phosphorylation event.

Acetyl-CoA Carboxylase↗
PubMed2005

Sodium channel mutation leading to saxitoxin resistance in clams increases risk of PSP.

Bivalve molluscs, the primary vectors of paralytic shellfish poisoning (PSP) in humans, show marked inter-species variation in their capacity to accumulate PSP toxins (PSTs) which has a neural basis. PSTs cause human fatalities by blocking sodium conductance in nerve fibres. Here we identify a molecular basis for inter-population variation in PSP resistance within a species, consistent with genetic adaptation to PSTs. Softshell clams (Mya arenaria) from areas exposed to 'red tides' are more resistant to PSTs, as demonstrated by whole-nerve assays, and accumulate toxins at greater rates than sensitive clams from unexposed areas. PSTs lead to selective mortality of sensitive clams. Resistance is caused by natural mutation of a single amino acid residue, which causes a 1,000-fold decrease in affinity at the saxitoxin-binding site in the sodium channel pore of resistant, but not sensitive, clams. Thus PSTs might act as potent natural selection agents, leading to greater toxin resistance in clam populations and increased risk of PSP in humans. Furthermore, global expansion of PSP to previously unaffected coastal areas might result in long-term changes to communities and ecosystems.

Amino Acid Sequence↗
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

Glucose uptake in enterocytes: a test for molecular targets of okadaic acid.

The main diarrheic shellfish poisoning (DSP) toxin is okadaic acid (OA). Although OA is a protein phosphatase 1 and 2A inhibitor less is known about the involvement of the toxin in diarrhea. The initial statement was that OA, by altering the phosphorylation state of proteins, might modify glucose uptake and consequently ionic and water reabsorption across the small intestine. This report presents studies of glucose transport in isolated rabbit enterocytes by using a fluorescent derivative of D-glucose. The dye allowed examining the relation between the toxic effect of OA and cellular mechanisms involved in glucose transport. The central findings are: (i) OA potentiates decrease on glucose uptake due to protein kinase A (PKA) inhibitors such as H89; and (ii) the increase of sugar uptake induced by the protein kinase C (PKC) inhibitor chelerythrine is enhanced by OA. Importance of this work is justified by the need to determine molecular targets of diarrheic toxins in intestinal cells.

4-Chloro-7-nitrobenzofurazan↗
PubMed2005

Illnesses caused by marine toxins.

Marine toxins are produced by algae or bacteria and are concentrated in contaminated seafood. Substantial increases in seafood consumption in recent years, together with globalization of the seafood trade, have increased potential exposure to these agents. Marine toxins produce neurological, gastrointestinal, and cardiovascular syndromes, some of which result in high mortality and long-term morbidity. Routine clinical diagnostic tests are not available for these toxins; diagnosis is based on clinical presentation and a history of eating seafood in the preceding 24 h. There is no antidote for any of the marine toxins, and supportive care is the mainstay of treatment. In particular, paralytic shellfish poisoning and puffer fish poisoning can cause death within hours after consuming the toxins and may require immediate intensive care. Rapid notification of public health authorities is essential, because timely investigation may identify the source of contaminated seafood and prevent additional illnesses. Extensive environmental monitoring and sometimes seasonal quarantine of a harvest are employed to reduce the risk of exposure.

Animals↗