Biology and Distribution of Poisonous Marine Animals
Jürg Meier, Julian White in 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.
Brevetoxin
Dongyou Liu in 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.
Marine Biotoxins: Symptoms and Monitoring Programs
Hafiz Ansar Rasul Suleria, Megh R. Goyal in Health Benefits of Secondary Phytocompounds from Plant and Marine Sources, 2021
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].
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).
Haff disease complicated by acute lung injury after crayfish consumption: a case report
Published in Clinical Toxicology, 2018
The toxin that may be responsible for Haff disease has not yet been identified. All patients with Haff disease report a history of eating cooked fish or crayfish within 24 h before symptom onset [2–4]. The toxin appears to be heat-stable and accumulates in the implicated food. The United States Food and Drug Administration has assayed and excluded several known toxins in Haff disease-implicated food items including heavy metals, pesticides, herbicides, ciguatoxin, saxitoxin, brevetoxin, tetrodotoxin, palytoxin, domoic acid, and okadaic acid [3,5]. Currently, the diagnosis of Haff disease is mainly based on clinical manifestations, a history of freshwater fish consumption within 24 h before the onset of symptoms, and the levels of muscle necrosis markers, particularly myoglobin and CK [4]. In the present case, his condition was complicated by shortness of breath and decreased blood oxygen saturation as a result of exudates and atelectasis in a portion of the lower lobes, and a small amount of pleural effusion bilaterally. Although aspiration during vomiting was possible, the patient remained conscious during this time and there was no clinical suspicion of aspiration. Thus, we consider the patient to have had severe Haff disease complicated by acute lung injury after crayfish consumption.
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].
Related Knowledge Centers
- Acetylation
- Bioaccumulation
- Cathepsin
- Ciguatoxin
- Domoic Acid
- Epoxide
- Sodium Channel
- Neurotoxic Shellfish Poisoning
- Hydroxy Group
- S-Adenosyl Methionine