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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.

Phytoplankton are photosynthetic microorganisms in aquatic environments that produce many bioactive substances. However, some of them are toxic to aquatic organisms via filter-feeding and are even poisonous to humans through the food chain. Human poisoning from these substances and their serious long-term consequences have resulted in several health threats, including cancer, skin disorders, and other diseases, which have been frequently documented. Seafood poisoning disorders triggered by phytoplankton toxins include paralytic shellfish poisoning (PSP), neurotoxic shellfish poisoning (NSP), amnesic shellfish poisoning (ASP), diarrheic shellfish poisoning (DSP), ciguatera fish poisoning (CFP), and azaspiracid shellfish poisoning (AZP). Accordingly, identifying harmful shellfish poisoning and toxin-producing species and their detrimental effects is urgently required. Although the harmful effects of these toxins are well documented, their possible modes of action are insufficiently understood in terms of clinical symptoms. In this review, we summarize the current state of knowledge regarding phytoplankton toxins and their detrimental consequences, including tumor-promoting activity. The structure, source, and clinical symptoms caused by these toxins, as well as their molecular mechanisms of action on voltage-gated ion channels, are briefly discussed. Moreover, the possible stress-associated reactive oxygen species (ROS)-related modes of action are summarized. Finally, we describe the toxic effects of phytoplankton toxins and discuss future research in the field of stress-associated ROS-related toxicity. Moreover, these toxins can also be used in different pharmacological prospects and can be established as a potent pharmacophore in the near future.

Although lipophilic shellfish toxins (LSTs) pose a significant threat to the health of seafood consumers, their systematic investigation and risk assessment remain scarce. The goals of this study were as follows: (1) analyze LST levels in commercially available shellfish in Zhejiang province, China, and determine factors influencing LST distribution; (2) assess the acute dietary risk of exposure to LSTs for local consumers during the red tide period; (3) explore potential health risks of LSTs in humans; and (4) study the acute risks of simultaneous dietary exposure to LSTs and paralytic shellfish toxins (PSTs). A total of 546 shellfish samples were collected. LSTs were detected in 89 samples (16.3%) at concentrations below the regulatory limits. Mussels were the main shellfish species contaminated with LSTs. Spatial variations were observed in the yessotoxin group. Acute exposure to LSTs based on multiple scenarios was low. The minimum tolerable exposure durations for LSTs calculated using the mean and the 95th percentile of consumption data were 19.7 and 4.9 years, respectively. Our findings showed that Zhejiang province residents are at a low risk of combined exposure to LSTs and PSTs; however, the risk may be higher for children under 6 years of age in the extreme scenario.

The more frequent occurrence of marine harmful algal blooms (HABs) and recent problems with newly-described toxins in Puget Sound have increased the risk for illness and have negatively impacted sustainable access to shellfish in Washington State. Marine toxins that affect safe shellfish harvest because of their impact on human health are the saxitoxins that cause paralytic shellfish poisoning (PSP), domoic acid that causes amnesic shellfish poisoning (ASP), diarrhetic shellfish toxins that cause diarrhetic shellfish poisoning (DSP) and the recent measurement of azaspiracids, known to cause azaspiracid poisoning (AZP), at low concentrations in Puget Sound shellfish. The flagellate, Heterosigma akashiwo, impacts the health and harvestability of aquacultured and wild salmon in Puget Sound. The more recently described flagellates that cause the illness or death of cultivated and wild shellfish, include Protoceratium reticulatum, known to produce yessotoxins, Akashiwo sanguinea and Phaeocystis globosa. This increased incidence of HABs, especially dinoflagellate HABs that are expected in increase with enhanced stratification linked to climate change, has necessitated the partnership of state regulatory programs with SoundToxins, the research, monitoring and early warning program for HABs in Puget Sound, that allows shellfish growers, Native tribes, environmental learning centers and citizens, to be the “eyes on the coast”. This partnership enables safe harvest of wholesome seafood for consumption in the region and helps to describe unusual events that impact the health of oceans, wildlife and humans.

Diarrheic shellfish toxins (DSTs), especially okadaic acid (OA) and its related compounds, are lipophilic marine biotoxins mainly synthesized by dinoflagellates of the genera Dinophysis and Prorocentrum. These compounds bioaccumulate in filter-feeding shellfish like mussels and clams, posing a considerable public health risk due to their strong gastrointestinal effects when contaminated seafood is consumed. This review offers a thorough overview of the current understanding of OA-group toxins with a focus on the molecular mechanisms of toxicity, including cytoskeletal disruption, apoptosis, inflammation, oxidative stress, and mitochondrial dysfunction. Additionally, their ecological impacts on aquatic organisms and patterns of bioaccumulation are explored. Recent advances in detection methods and regulatory frameworks are discussed, highlighting the necessity for robust monitoring systems to safeguard seafood safety. Enhanced knowledge of the toxicity, distribution, and fate of DSP (diarrheic shellfish poisoning) is essential for improving risk assessment and managing marine biotoxins. Despite methodological advances, gaps remain regarding chronic exposure and species-specific detoxification pathways.

Paralytic shellfish poisoning toxins (PSPTs) are a class of neurotoxins most known for causing illness from consuming contaminated shellfish. These toxins are also present in freshwater systems with the concern that they contaminate drinking and recreational waters. This review provides (1) a complete list of the 84+ known PSPTs and important chemical features; (2) a complete list of all environmental freshwater PSPT detections; (3) an outline of the certified PSPT methods and their inherent weaknesses; and (4) a discussion of PSPT toxicology, the weaknesses in existing data, and existing freshwater regulatory limits. We show ample evidence of production of freshwater PSPTs by cyanobacteria worldwide, but data and method uncertainties limit a proper risk assessment. One impediment is the poor understanding of freshwater PSPT profiles and lack of commercially available standards needed to identify and quantify freshwater PSPTs. Further constraints are the limitations of toxicological data derived from human and animal model exposures. Unassessed mouse toxicity data from 1978 allowed us to calculate and propose toxicity equivalency factors (TEF) for 11-hydroxysaxitoxin (11-OH STX; M2) and 11-OH dcSTX (dcM2). TEFs for the 11-OH STX epimers were calculated to be 0.4 and 0.6 for 11α-OH STX (M2α) and 11β-OH STX (M2β), while we estimate that TEFs for 11α-OH dcSTX (dcM2α) and 11β-OH dcSTX (dcM2β) congeners would be 0.16 and 0.23, respectively. Future needs for freshwater PSPTs include increasing the number of reference materials for environmental detection and toxicity evaluation, developing a better understanding of PSPT profiles and important environmental drivers, incorporating safety factors into exposure guidelines, and evaluating the accuracy of the established no-observed-adverse-effect level.

Paralytic shellfish poisoning (PSP) occurs when shellfish contaminated with saxitoxin or equivalent paralytic shellfish toxins (PSTs) are ingested. In British Columbia, Canada, documented poisonings are increasing in frequency based on 62 investigations identified from 1941–2020. Two PSP investigations were reported between 1941 and 1960 compared to 31 since 2001 (p < 0.0001) coincident with rising global temperatures (r2 = 0.76, p < 0.006). The majority of PSP investigations (71%) and cases (69%) were linked to self-harvested shellfish. Far more investigations involved harvests by indigenous communities (24%) than by commercial and recreational groups. Single-case-exposure investigations increased by more than 3.5 times in the decade 2011–2020 compared to previous periods. Clams (47%); mussels (26%); oysters (14%); scallops (6%); and, in more recent years, crabs (4%) were linked to illnesses. To guide understanding of self-harvesting consumption risks, we recommend collecting data to determine when PST-producing algae are present in high concentrations, improving the quality of data in online shellfish harvest maps to include dates of last testing; biotoxin testing results; and a description of bivalve species tested. Over reliance on toxin results in biomonitored species may not address actual consumption risks for unmonitored species harvested from the same area. We further recommend introducing phytoplankton monitoring in remote indigenous communities where self-harvesting is common and toxin testing is unavailable, as well as continuing participatory education about biotoxin risks in seafoods.

Paralytic shellfish toxins (PSTs) are the major neurotoxic contaminants of edible bivalves in Japan. Tetrodotoxin (TTX) was recently detected in bivalve shellfish around the world, drawing widespread attention. In Japan, high levels of TTX were reported in the digestive gland of the scallop, Patinopecten yessoensis, in 1993; however, no new data have emerged since then. In this study, we simultaneously analyzed PSTs and TTX in scallops cultured in a bay of east Japan using hydrophilic interaction chromatography (HILIC)-MS/MS. These scallops were temporally collected from April to December 2017. The highest concentration of PSTs (182 µmol/kg, total congeners) in the hepatopancreas was detected in samples collected on May 23, lined to the cell density of the dinoflagellate, Alexandrium tamarense, in seawater around the scallops, whereas the highest concentration of TTX (421 nmol/kg) was detected in samples collected on August 22. Contrary to the previous report, temporal variation of the PSTs and TTX concentrations did not coincide. The highest concentration of TTX in the entire edible tissues was 7.3 µg/kg (23 nmol/kg) in samples obtained on August 22, which was lower than the European Food Safety Authority (EFSA)-proposed threshold, 44 µg TTX equivalents/kg shellfish meat. In addition, 12β-deoxygonyautoxin 3 was firstly identified in scallops.

Phytotoxins produced by marine microalgae, such as paralytic shellfish toxins (PSTs), can accumulate in bivalve molluscs, representing a human health concern due to the life-threatening symptoms they cause. To avoid the commercialization of contaminated bivalves, monitoring programs were established in the EU. The purpose of this work is the implementation of a PST transforming enzyme—carbamoylase—in an impedimetric test for rapid simultaneous detection of several carbamate and N-sulfocarbamoyl PSTs. Carbamoylase hydrolyses carbamate and sulfocarbamoyl toxins, which may account for up to 90% of bivalve toxicity related to PSTs. Conformational changes of carbamoylase accompanying enzymatic reactions were probed by Fourier transform mid-infrared spectroscopy (FT-MIR) and electrochemical impedance spectroscopy (EIS). Furthermore, a combination of EIS with a metal electrode and a carbamoylase-based assay was employed to harness changes in the enzyme conformation and adsorption on the electrode surface during the enzymatic reaction as an analytical signal. After optimization of the working conditions, the developed impedimetric e-tongue could quantify N-sulfocarbamoyl toxins with a detection limit of 0.1 µM. The developed e-tongue allows the detection of these toxins at concentration levels observed in bivalves with PST toxicity close to the regulatory limit. The quantification of a sum of N-sulfocarbamoyl PSTs in naturally contaminated mussel extracts using the developed impedimetric e-tongue has been demonstrated.

In 2011, a Diarrhetic Shellfish Poisoning (DSP) outbreak occurred in British Columbia (BC), Canada that was associated with cooked mussel consumption. This is the first reported DSP outbreak in BC. Investigation of ill individuals, traceback of product and laboratory testing for toxins were used in this investigation. Sixty-two illnesses were reported. Public health and food safety investigation identified a common food source and harvest area. Public health and regulatory agencies took actions to recall product and notify the public. Shellfish monitoring program changes were implemented after the outbreak. Improved response and understanding of toxin production will improve management of future DSP outbreaks.