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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 main source of neurotoxic shellfish poisoning or brevetoxin is Karenia brevis (a dinoflagellate). Its mechanism of action is at the site 5 of voltage-gated sodium channels. The toxicity appears from fifteen minutes to three hours after the use of neurotoxic shellfish. Neurotoxic shellfish poisoning can likewise be contracted by means of inhalation [17, 41, 62].
Brevetoxin
Published in Dongyou Liu, Handbook of Foodborne Diseases, 2018
Constituting a group of neurotoxic compounds produced by dinoflagellate Karenia brevis, brevetoxin binds to voltage-gated sodium channels in nerve cells and disrupts normal neurological processes, leading to NSP in humans, massive fish kills, and mortalities in seabirds. While Karenia-associated NSP outbreaks have only been recorded in the Gulf of Mexico and the coast of New Zealand to date, there is a possibility that they may venture into other parts of the world, with the introduction of K. brevis and increasing frequency of algal blooms.
Biology and Distribution of Poisonous Marine Animals
Published in Jürg Meier, Julian White, Handbook of: Clinical Toxicology of Animal Venoms and Poisons, 2017
Toxic algal blooms especially have occurred in alarming proportions in recent years6. A red tide which was previously restricted to the Gulf coast of Florida spread northward to North Carolina causing dramatic losses in the shellfish industry in 1987/88. The toxin involved is brevetoxin. An outbreak of a hitherto unknown shellfish poisoning hit Prince Edward Island, Canada, 1987. For the first time domoic acid was found to be involved causing brain damage (amnesic shellfish poisoning). The toxin was traced to a bloom of diatoms, Nitzschia pungens, a species, which has a worldwide distribution and which is generally considered to be nontoxic. In 1991 domoic acid was also found on the coast of California killing pelicans which had eaten anchovies. Shellfish and crabs contained high levels of this toxin. Paralytic shellfish poisoning occurred also on the Pacific coast of Guatemala killing 26 people11.
Immunotoxins and nanobody-based immunotoxins: review and update
Published in Journal of Drug Targeting, 2021
Mohammad Reza Khirehgesh, Jafar Sharifi, Fatemeh Safari, Bahman Akbari
ITs are new tools for cancer therapy that consists of two functional components: targeting and cytotoxic moieties. In ITs design, the binding domain of the protein toxin, responsible for binding to a specific receptor, replaces with a targeting moiety, usually mAbs [17]. Therefore, non-protein toxins such as Brevetoxin B [11,25–27] and Aflatoxins [28,29] did not use in ITs construction. Up to now, four generations of ITs produced via four different approaches. The first generation of IT has been developed by attaching the native toxin to full-length mAbs through chemical methods. The ITs had some problems such as low specificity and stability, heterogeneity, reactivity to normal cells, and immunogenicity. Due to these problems, the second generation of IT has been developed. In this generation, the modified toxin, without the natural binding domain, chemically bonded to full-length mAbs. Although the specificity increased, other problems remained [11,30,31]. Third-generation produced by recombinant DNA technology. In this generation, the truncated toxins, without the natural receptor-binding domain, linked to antibody fragments by the peptide linker that led to developing recombinant ITs (RITs) [32,33]. For immunogenicity reduction of RITs, fourth-generation was developed using humanised or fully human formats of antibodies and endogenous proteins of human origin [34,35]. Numerous clinical trials and the US Food and Drug Administration (FDA) approvals indicate the promising IT landscape in cancer treatment (Table 1).
Nature and applications of scorpion venom: an overview
Published in Toxin Reviews, 2020
Saadia Tobassum, Hafiz Muhammad Tahir, Muhammad Arshad, Muhammad Tariq Zahid, Shaukat Ali, Muhammad Mohsin Ahsan
Toxins interact with VGSCs in two ways. It either results in a blockage of pore when the neurotoxin physically obstructs the pore and inhibits the conductance of sodium ions, or in a modification of the gating, that altered the voltage-dependence and gating kinetics of the ion channels. Toxins that interact with the site 1 use first mechanism. For example, tetrodotoxin (TTX) and sexitoxin (STX) are pore blockers of site 1. Grayanotoxin and batrachotoxin are site 2 toxins which prevent inactivation and therefore, channel remain persistently active (Stevens et al. 2011). Scorpion α-toxins and sea anemone toxins bind to site 3 and inhibit the inactivation (Possani et al. 2000). Scorpion β-toxins and spider β-toxins are site 4 toxins which shift the activation toward hyperpolarized state (Shichor et al. 2002). Site 5 toxins like ciguatoxins and brevetoxins display a real effect upon binding with VGSC, for example, inhibition of activation and the hyperpolarizing shift of voltage-dependence activation. Finally, δ-conotoxins interact with site 6 and produce similar outcomes as the site 3 neurotoxins by inhibiting inactivation (Figure 3) (Stevens et al. 2011).
Thioredoxin reductase inhibitors: updated patent review (2017-present)
Published in Expert Opinion on Therapeutic Patents, 2021
Evgeny Chupakhin, Mikhail Krasavin
The Rein group from Florida International University discovered that brevetoxin-2 (27) possessed inhibitory activity toward TrxR (IC50 25 μM). Moreover, it was demonstrated that this activity is due to a unique, selective binding C-terminal redox center of the enzyme [98].