Disease relevance of DTX2

• In bivalve mollusks from the Portuguese coast contaminated by diarrhetic shellfish poisoning (DSP), most of the parent toxins, okadaic acid (OA) or dinophysistoxin-2 (DTX2), are found esterified, and toxicity assessment is only performed after an alkaline hydrolysis step to recover the parent molecules in their free form [1].

High impact information on DTX2

• T Cells Develop Normally in the Absence of both Deltex1 and Deltex2 [2].
• A rapid and simple method for confirmation of the diarrhetic shellfish poisons (DSP): okadaic acid (OA), dinophysistoxin-1 (DTX-1) and dinophysistoxin-2 (DTX-2) using fluorescence detection following derivatization with 9-chloromethylanthracene, has been established as an alternate to LC/MS [3].
• We have used cerebellar primary cultures to investigate the effects of the DSP toxin dinophysistoxin-2 (DTX-2) on central nervous system neurons and glial cells [4].
• DTX-2-induced neurodegeneration required long exposures (at least 20 h), involved DNA fragmentation and condensation and fragmentation of chromatin, typical hallmarks of apoptosis, and required the synthesis of new proteins [4].
• Exposure to DTX-2 produced neurotoxicity at concentrations starting at 2.5 nM, characterized first by disintegration of neurites and later by cell death [4].

Biological context of DTX2

• Base hydrolysis of DTX3 toxins gave free OA and DTX2, which were determined following ADAM derivatization [5].
• In mussels esterified OA did not surpass 50% of the total OA found in edible parts, while DTX2 esterification rates were usually much lower [6].
• Flow-injection analysis-mass spectrometry (FIA-MS) with an atmospheric pressure ionization (API) and an ionspray (ISP) interface showed a mass spectrum dominated by the protonated molecule, [M+H]+, at m/z 805 for DTX-2B, thus indicating that this new toxin has the same mol.wt as okadaic acid and DTX-2 [7].
• The rare diarrhoeic shellfish poisoning (DSP) toxin, dinophysistoxin-2 (DTX-2), which is an okadaic acid (OA) isomer, has been isolated from a marine phytoplankton biomass that consisted mainly of Dinophysis acuta [8].

Anatomical context of DTX2

• DTX-2 (< or = 6.1 micrograms/g hepatopancreas) and DTX-2B (< or = 0.08 micrograms/hepatopancreas) were unique to Irish shellfish [9].
• Morphology and viability of glial cells remained unaffected up to at least 15 nM DTX-2 [4].

Associations of DTX2 with chemical compounds

• Hexane-soluble derivatives of okadaic acid (OA) and dinophysistoxin-2 (DTX-2) were found [10].
• An enzymic mechanism for the conversion of OA and DTX-2 seems to be implicated in some kind of detoxification process because the percentage of esters increases with the toxin amount ingested by the bivalve and there is some degree of selectivity as DTX-2 seems more difficult to acylate [10].
• Fluorimetric LC analyses of the extracts of bulk phytoplankton samples using derivatisation with 9-anthryldiazomethane (ADAM) showed a complex toxin profile, with peaks corresponding to OA and dinophysistoxin-2 (DTX-2) as well as a third unidentified compound [11].
• Using 1-bromoacetylpyrene (BAP), as a precolumn derivatisation reagent, the diarrhetic shellfish toxins, okadaic acid (OA), dinophysistoxin-1 (DTX-1) and DTX-2, were determined by HPLC with fluorimetric detection [12].

Other interactions of DTX2

• To develop a multiple reaction monitoring (MRM) method, fragmentation studies were performed to determine the optimum precursor-product ion combinations: OA (803/255), DTX2 (803/255), DTX1 (817/255), PTX2SAs (875/137) and PTX2 (857/137) [13].
• However, the OA/DTX2 ratio in the DTX3 conjugated form was different, with OA being the most abundant in all cases [5].

Analytical, diagnostic and therapeutic context of DTX2

• Results were confirmed by liquid chromatography/mass spectrometry analyses, and in most of the samples, free DTX2 was the most abundant toxin [5].
• Previous analyses of okadaic acid (OA) and related toxins in these two species by HPLC revealed significant amounts of OA and DTX2 in D. acuta, but only trace amounts of OA in D. caudata cells, and led to the erroneous conclusion that the contribution of the latter species to autumn LST events was negligible [14].

References