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Perna Viridis has become a common dish in daily life. Consumption of Perna Viridis, which is contaminated with diarrhetic shellfish poisoning (DSP) toxins can cause food poisoning in humans. Therefore, there is an urgent need for a rapid and accurate method to identify Perna Viridis contaminated with DSP toxins. In this study, a non-destructive method based on near-infrared spectroscopy (NIS) is proposed to detect DSP toxin-laden Perna Viridis. Spectral data of Perna Viridis were collected in the range of 950–1700 nm for DSP toxin-laden and non-laden (non-DSP) samples. The second derivative (D2) spectral preprocessing method was used to reduce the influence of noise and light scattering. A support vector machine (SVM) model based on Bayesian optimization (BO-SVM) was constructed as a classifier for the detection of the DSP toxin-laden Perna Viridis. The average accuracy for the D2-BO-SVM classifier in detecting DSP toxin-laden Perna Viridis in 50 random tests reached 99.97%. The recognition performance of the D2-BO-SVM model was analyzed to solve the problems of different ratios of training and test datasets, small sample datasets, and unbalanced class datasets in practical applications. The experimental results show that the D2-BO-SVM model was found to be superior to BO-SVM, D2-Standard SVM, and Standard SVM. These results suggest that the combination of NIS and artificial intelligence models has great potential for the detection of the DSP toxin-laden Perna Viridis. This study provides a new method for detecting the quality and safety of shellfish, which is of great practical importance for ensuring the safety of shellfish for consumers.

The successful cultivation of Dinophysis norvegica Claparède & Lachmann, 1859, isolated from Japanese coastal waters, is presented in this study, which also includes an examination of its toxin content and production for the first time. Maintaining the strains at a high abundance (>2000 cells per mL−1) for more than 20 months was achieved by feeding them with the ciliate Mesodinium rubrum Lohmann, 1908, along with the addition of the cryptophyte Teleaulax amphioxeia (W.Conrad) D.R.A.Hill, 1992. Toxin production was examined using seven established strains. At the end of the one-month incubation period, the total amounts of pectenotoxin-2 (PTX2) and dinophysistoxin-1 (DTX1) ranged between 132.0 and 375.0 ng per mL−1 (n = 7), and 0.7 and 3.6 ng per mL−1 (n = 3), respectively. Furthermore, only one strain was found to contain a trace level of okadaic acid (OA). Similarly, the cell quota of pectenotoxin-2 (PTX2) and dinophysistoxin-1 (DTX1) ranged from 60.6 to 152.4 pg per cell−1 (n = 7) and 0.5 to 1.2 pg per cell−1 (n = 3), respectively. The results of this study indicate that toxin production in this species is subject to variation depending on the strain. According to the growth experiment, D. norvegica exhibited a long lag phase, as suggested by the slow growth observed during the first 12 days. In the growth experiment, D. norvegica grew very slowly for the first 12 days, suggesting they had a long lag phase. However, after that, they grew exponentially, with a maximum growth rate of 0.56 divisions per day (during Days 24–27), reaching a maximum concentration of 3000 cells per mL−1 at the end of the incubation (Day 36). In the toxin production study, the concentration of DTX1 and PTX2 increased following their vegetative growth, but the toxin production still increased exponentially on Day 36 (1.3 ng per mL−1 and 154.7 ng per mL−1 of DTX1 and PTX2, respectively). The concentration of OA remained below detectable levels (≤0.010 ng per mL−1) during the 36-day incubation period, with the exception of Day 6. This study presents new information on the toxin production and content of D. norvegica, as well as insights into the maintenance and culturing of this species.

Blooms of the dinoflagellate Dinophysis acuminata occur every year in an important mussel cultivation area in Port Underwood, Marlborough Sounds, New Zealand. Annual maximum cell numbers range from 1500–75,000 cells L−1 and over 25 years of weekly monitoring the D. acuminata bloom has never failed to exhibit peaks in abundance at some time between spring and autumn. During winter (June–August) the dinoflagellate is often undetectable, or at low levels (≤100 cells L−1), and the risk of diarrhetic shellfish poisoning (DSP)-toxin contamination over this period is negligible. Bloom occurrence may be coupled to the abundance of D. acuminata prey (Mesodinium sp.) but the mechanism by which it maintains its long-term residence in this hydrologically dynamic environment is unknown. The toxin profile of D. acuminata is dominated by pectenotoxin-2 (PTX-2) and dinophysistoxin-1 (DTX-1), but the cellular toxin content is low. It is rare that free DTX-1 is detected in mussels as this is invariably exclusively present as fatty acid-esters. In only five out of >2500 mussel samples over 16 years have the levels of total DTX-1 marginally exceeded the regulated level of 0.16 mg kg−1. It is also rare that free PTX-2 is detected in mussels, as it is generally only present in its hydrolysed non-toxic PTX-2 seco acid form. The D. acuminata alert level of 1000 cells L−1 is often exceeded without DTX-1 residues increasing appreciably, and this level is considered too conservative.

Okadaic acids (OAs) are causative agents of diarrhetic shellfish poisoning, produced by the dinoflagellates Dinophysis spp. and Prorocentrum spp. Microcystins (MCs) are cyclic heptapeptide hepatotoxins produced by some cyanobacteria genera, including Microcystis spp. Traditionally, toxicity detection and quantification of these natural toxins were performed using a mouse bioassay (MBA); however, this is no longer widely employed owing to its lack of accuracy, sensitivity, and with regard to animal welfare. Therefore, alternative toxicity analyses have been developed based on MCs’ and OAs’ specific inhibition of protein phosphatase 2A (PP2A), using p-nitrophenylphosphate (p-NPP) as a substrate. The assay is simple, inexpensive, ready for use on site, and can be applied to several samples at once. For OA detection, this assay method is appropriate for widespread application as a substitute for MBA, as evidenced by its alignment with the oral toxicity of MBA. In this review, we summarize the structure and function of PP2A, the inhibitory activities of OAs and MCs against PP2A, and the practical applications of the PP2A assay, with the aim of improving understanding of the PP2A assay as an OAs and MCs detection and quantification method, as well as its suitability for screening before confirmatory chemical analysis.

The dinoflagellate Dinophysis spp. is responsible for diarrhetic shellfish poisoning (DSP). In the bivalves exposed to the toxic bloom of the dinoflagellate, dinophysistoxin 3 (DTX3), the 7-OH acylated form of either okadaic acid (OA) or DTX1, is produced. We demonstrated in vitro acylation of OA with palmitoyl CoA in the presence of protein extract from the digestive gland, but not other tissues of the bivalve Mizuhopecten yessoensis. The yield of 7-O-palmitoyl OA reached its maximum within 2 h, was the highest at 37 °C followed by 28 °C, 16 °C and 4 °C and was the highest at pH 8 in comparison with the yields at pH 6 and pH 4. The transformation also proceeded when the protein extract was prepared from the bivalves Corbicula japonica and Crassostrea gigas. The OA binding protein OABP2 identified in the sponge Halichondria okadai was not detected in the bivalve M. yessoensis, the bivalve Mytilus galloprovincialis and the ascidian Halocynthia roretzi, though they are known to accumulate diarrhetic shellfish poisoning toxins. Since DTX3 does not bind to protein phosphatases 1 and 2A, the physiological target for OA and DTXs in mammalian cells, the acylation of DSP toxins would be related to a detoxification mechanism for the bivalve species.

Okadaic acid (OA) and dinophysistoxins-1 and -2 (DTX1, DTX2), the toxins responsible for incidents of diarrhetic shellfish poisoning (DSP), can occur as complex mixtures of ester derivatives in both plankton and shellfish. Alkaline hydrolysis is usually employed to release parent OA/DTX toxins, and analyses are conducted before and after hydrolysis to determine the concentrations of nonesterified and esterified toxins. Recent research has shown that other toxins, including pectenotoxins and spirolides, can also exist as esters in shellfish, but these toxins cannot survive alkaline hydrolysis. A promising alternative approach is enzymatic hydrolysis. In this study, two enzymatic methods were developed for the hydrolysis of 7-O-acyl esters, “DTX3,” and the carboxylate esters of OA, “diol-esters.” Porcine pancreatic lipase induced complete conversion of DTX3 to OA and DTXs within one hour for reference solutions. The presence of mussel tissue matrix reduced the rate of hydrolysis, but an optimized lipase concentration resulted in greater than 95% conversion within four hours. OA-diol-ester was hydrolyzed by porcine liver esterase and was completely converted to OA in less than 30 min, even in the presence of mussel tissue matrix. Esters and OA/DTX toxins were all monitored by LC-MS. Further experiments with pectenotoxin esters indicated that enzymatic hydrolysis could also be applied to esters of other toxins. Enzymatic hydrolysis has excellent potential as an alternative to the conventional alkaline hydrolysis procedure used in the preparation of shellfish samples for the analysis of toxins.

Presents a set of practical recommendations for ensuring the safety of the seafood supply. Provides an overview of the topic, covering seafood consumption patterns, where and how seafood contamination occurs, and the efffectiveness of regulation, sources of contamination such as microbes, natural toxins, and chemical pollutants and their effects on human health. Also evaluates methods used for risk assessment of chemical contamination and inspection sampling

Massive phytoplankton proliferation, and the consequent release of toxic metabolites, can be responsible for seafood poisoning outbreaks: filter-feeding mollusks, such as shellfish, mussels, oysters or clams, can accumulate these toxins throughout the food chain and present a threat for consumers’ health. Particular environmental and climatic conditions favor this natural phenomenon, called harmful algal blooms (HABs); the phytoplankton species mostly involved in these toxic events are dinoflagellates or diatoms belonging to the genera Alexandrium, Gymnodinium, Dinophysis, and Pseudo-nitzschia. Substantial economic losses ensue after HABs occurrence: the sectors mainly affected include commercial fisheries, tourism, recreational activities, and public health monitoring and management. A wide range of symptoms, from digestive to nervous, are associated to human intoxication by biotoxins, characterizing different and specific syndromes, called paralytic shellfish poisoning, amnesic shellfish poisoning, diarrhetic shellfish poisoning, and neurotoxic shellfish poisoning. This review provides a complete and updated survey of phycotoxins usually found in marine invertebrate organisms and their relevant properties, gathering information about the origin, the species where they were found, as well as their mechanism of action and main effects on humans.

Recently, Park et al. (2006) succeeded in cultivating the toxic dinoflagellate Dinophysis acuminata and maintaining them by feeding the ciliate Myrionecta rubra grown with a cryptophyte Teleaulax sp. After this report, the present study is the second report of propagation of a Dinophysis species (Dinophysis caudata) under laboratory conditions and describes the maintenance of several clonal strains kept at high abundance (5,000 cells/mL) for a relatively long period (4 months) when fed on M. rubra with the addition of Teleaulax amphioxeia. We confirmed that D. caudata swam actively around its ciliate prey and inserted its peduncle (feeding tube) into the ciliate. Thereafter, the prey became immobile and rounded. Dinophysis caudata actively ingested the cytoplasm of the prey through the peduncle. Dinophysis caudata grew at a growth rate of 1.03 divisions/day when supplied with M. rubra as prey, reaching a maximum concentration of ca. 5,000 cells/well (810 microL) during a 9 day growth experiment. In contrast, a culture of D. caudata was not able to be established in the absence of the ciliate or when provided with T. amphioxeia only, suggesting that D. caudata can not directly utilize T. amphioxeia as prey.

Exposure to toxigenic harmful algal blooms (HABs) can result in widely recognized acute poisoning in humans. The five most commonly recognized HAB-related illnesses are diarrhetic shellfish poisoning (DSP), paralytic shellfish poisoning (PSP), amnesic shellfish poisoning (ASP), neurotoxic shellfish poisoning (NSP), and ciguatera poisoning (CP). Despite being caused by exposure to various toxins or toxin analogs, these clinical syndromes share numerous similarities. Humans are exposed to these toxins mainly through the consumption of fish and shellfish, which serve as the main biological vectors. However, the risk of human diseases linked to toxigenic HABs is on the rise, corresponding to a dramatic increase in the occurrence, frequency, and intensity of toxigenic HABs in coastal regions worldwide. Although a growing body of studies have focused on the toxicological assessment of HAB-related species and their toxins on aquatic organisms, the organization of this information is lacking. Consequently, a comprehensive review of the adverse effects of HAB-associated species and their toxins on those organisms could deepen our understanding of the mechanisms behind their toxic effects, which is crucial to minimizing the risks of toxigenic HABs to human and public health. To this end, this paper summarizes the effects of the five most common HAB toxins on fish, shellfish, and humans and discusses the possible mechanisms.