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Marine Biotoxins: Symptoms and Monitoring Programs
Published in Hafiz Ansar Rasul Suleria, Megh R. Goyal, Health Benefits of Secondary Phytocompounds from Plant and Marine Sources, 2021
Huma Bader Ul Ain, Farhan Saeed, Hafiza Sidra Yaseen, Tabussam Tufail, Hafiz Ansar Rasul Suleria
The paralytic shellfish poisoning poison saxitoxin is not damaged by cooking, solidifying, or smoking and is imperceptible by sight or smell, so that identification of paralytic shellfish poisoning toxin is compulsory before the shellfish arrive the consumers [62]. During the period of April to October, blossoming of Alexandrium happens each year, particularly along the New England States, Alaska, California, and Washington. When the poison levels surpass 80 mcg/g in the United States, the closing of those territories is ordered due to possibility of high risk [41]. The best strategy for counteractive action of paralytic shellfish poisoning is to abstain from eating shellfish amid red tide poisonous alert, a significant number of which are declared by federal and state governments, particularly in the Americas, Scandinavia, and Western Europe (Figure 9.1).
Saxitoxin and Related Paralytic Shellfish Toxins
Published in Dongyou Liu, Handbook of Foodborne Diseases, 2018
Leanne Andrea Pearson, Brett Anthony Neilan
Saxitoxin and other PSTs exhibit their neurotoxicity by inhibiting the flow of Na+ ions through voltage-gated sodium channels, thereby restricting signal transmission between neurons. This biological activity disrupts the generation of action potentials in nerve and muscle cells in the peripheral nervous system, leading to paralysis and sensory disturbances. Saxitoxin has also been shown to bind calcium and potassium channels, neuronal nitric oxide synthase, STX metabolizing enzymes, and transferrin-like proteins, although with reduced affinity compared to sodium channels.27
Pufferfish Poisoning
Published in Ramasamy Santhanam, Biology and Ecology of Toxic Pufferfish, 2017
Description of Saxitoxin Pufferfish Poisoning (SPFP): SPFP is a similar illness, expect that bioaccumulation occurs in pufferfish (rather than shellfish) through food chain. From January 2002 to May 2004, 28 puffer fish poisoning (PFP) cases in Florida, New Jersey, Virginia and New York were associated with the pufferfish (Sphoeroides spp.) harvested from the Indian River Lagoon (IRL), Florida, USA. Saxitoxin and two of its derivatives were found to be the active toxins, with the dinoflagellate P bahamense identified as the source. This lead to the characterization of the food poisoning syndrome as saxitoxin pufferfish poisoning (SPFP) to distinguish it from pufferfish poisoning (PFP), which is traditionally associated with tetrodotoxin. These findings led to a permanent ban on pufferfish harvesting along the east coast of Florida along with the establishment of a monitoring program to determine the distribution and concentrations of PSTs in various pufferfish species. This monitoring program found that STX concentrations from pufferfish tissue averaged greater than 20-times the action limit for shellfish, with maximum values exceeding 200-times the action limit (Cusick and Sayler, 2013). Small-sized brackish water and freshwater pufferfish have also occasionally caused food poisoning incidents, including fatal cases in Asian countries such as Thai, Bangladesh, and Cambodia, though the causative toxin is PSP bearing saxitoxin in freshwater species (Noguchi and Arakawa, 2008).
Human poisonings by neurotoxic phycotoxins related to the consumption of shellfish: study of cases registered by the French Poison Control Centres from 2012 to 2019
Published in Clinical Toxicology, 2022
Sandra Sinno-Tellier, Eric Abadie, Luc de Haro, Nathalie Paret, Jérôme Langrand, Gaël Le Roux, Magali Labadie, David Boels, Juliette Bloch, Nicolas Delcourt
Some species of phytoplankton (microscopic microalgae) produce toxins called phycotoxins that can accumulate in live bivalve shellfish. These shellfish filter large amounts of water as they feed. Neither cooking nor freezing destroys these toxins. Most of them cause digestive symptoms (diarrheic toxins), while others can cause serious and even fatal neurological effects of rapid onset [1–3]. This is the case of the paralytic toxins produced by algae of the genus Alexandrium, in particular saxitoxin and its derivatives. Amnesic toxins, like domoic acid, produced by algae of the genus Pseudo-nitzschia, as well as toxins that have emerged more recently in Europe (pinnatoxins, brevetoxins, etc.) can also cause poisoning. Concentrations of paralytic toxins, including saxitoxin and domoic acid in seafood products, are regulated [4]. When the thresholds are exceeded, the local authorities temporarily close the shellfish production areas on the advice of the health authorities, and/or withdraw the contaminated batches from the market, in order to protect consumers from poisoning.
A case of fatal paralytic shellfish poisoning in Alaska
Published in Clinical Toxicology, 2022
Courtney Temple, Adrienne Hughes
Paralytic shellfish poisoning is reported worldwide but fatalities are extremely uncommon. This is the first fatal case of PSP in Alaska in over a decade [3]. The specimens contained concentrations of SXT and congeners that were 140 times the FDA limit for human consumption (<80mcg/100 mg). Large harmful algae blooms (HAB) of Alexandrium spp. cysts and cells have been confirmed in the Aleutian Islands since 2017 and have been migrating northward as a result of warming air temperatures and reduced Arctic sea ice [4]. These species are responsible for the production of unprecedented concentrations of saxitoxin in filter-feeding shellfish [5]. Reports from the 2020 Alaska Harmful Bloom Network as well as the Alaska Ocean Observing System have confirmed the presence of an HAB producing paralytic shellfish toxins (PST) expressed as weekly totals of SXT concentrations specifically in Unalaska harvested Blue Mussels. These concentrations peaked at >7000 mcg/100g tissue in 2020 the same week of the patient’s presentation [6]. The bloom was later confirmed to contain Alexandrium catenella [7]. Elevated concentrations of PSTs result in large-scale public health outreach campaigns including massive beach closures and harvesting bans for public safety [8]. Remote and resource-limited areas require special considerations where prompt identification and intervention are critical for adequate management.
Uncovering the proteome response of murine neuroblastoma cells against low-dose exposure to saxitoxin
Published in Toxicology Mechanisms and Methods, 2018
Xiao Chen, Ye Sun, Haiyan Huang, Wei Liu, Panpan Hu, Xinfeng Huang, Fei Zou, Jianjun Liu
The current limit for saxitoxin intake set in 1930s according to toxicity measured by mouse bioassays (Sommer and Meyer 1937) is 0.8 mg saxitoxin equivalent per kg of bivalve mussels. Based on the result of a 500-individual study of the adverse effect of saxitoxin (Alexander et al. 2009), European Food Safety Authority (EFSA) suggested a lower dose of saxitoxin at 0.42 mg saxitoxin equivalent per kg of bivalve mussels (when a 60 kg adult taking 100 g of bivalve mussels) as the acute reference dose of saxitoxin (Alexander et al. 2008). The reduction in value raised the concern of the toxicity of low-dose saxitoxin exposure. Studies on various cellular and animal model claimed that the low-dose exposure of saxitoxin (at nanomolar range) could lead to morphological changes (O’Neill et al. 2017), fragmentations of DNA (Melegari et al. 2015), enhances of lipid peroxidation (da Silva et al. 2011; Melegari et al. 2012), production of reactive oxygen species (Abi-Khalil et al. 2017), cytotoxicity (da Silva et al. 2014) and developmental toxicity (Oberemm et al. 1999). While a review (O’Neill et al. 2016) enumerated the cellular and animal evidence of toxicity of low-dose saxitoxin exposure, the neurotoxicity and molecular mechanism of saxitoxin need to be assessed in a definitive mammalian neuron model.