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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
Toxins are poisonous substances produced by microorganisms and others. Toxins act as primary factors for pathogenicity. There are about 220 known bacterial toxins 40% of which are harmful to humans by damaging the Eukaryotic cell membrane. Based on toxins, there are various classes of toxins, such as [11, 47]: Cytotoxins (cells);Dermatotoxins (skin cells);Enterotoxins (enteric system);Hemotoxins (blood cells);Hepatotoxins (liver tissue);Neurotoxins (nerve tissue).
Clinical Toxicology of Snakebite in North America
Published in Jürg Meier, Julian White, Handbook of: Clinical Toxicology of Animal Venoms and Poisons, 2017
Richard C. Dart, Hernan F. Gomez
The venom gland in all crotalids is located in the upper jaw area posterior to the eye. This gland is surrounded by striated muscle which enables the snake to inject large doses of venom19. Crotalid venom is a complex mixture of proteins which have enzymatic activities that can cause local tissue injury, systemic vascular damage, hemolysis, fibrinolysis, and neuromuscular dysfunction, resulting in a combination of local and systemic effects. These proteins include: transaminase, hyaluronidase, phospholipase, phosphodiesterase, cholinesterase, and endonucleases (Table 3). Venom proteins range in molecular weight from less than 6,000 to over 100,00020. The peptides in snake venom appear to bind to multiple receptor sites in their prey21. Because there are multiple sites of action, it is prudent not to label or treat a poisoning as a “neurotoxin”, “hemotoxin” or “cardiotoxin”.1 Collectively, crotalid snake venom components affect almost every organ system. In crotalid envenomations, the most deleterious effects are seen in the cardiovascular, hematologic, respiratory and nervous systems.
Pesticides and Chronic Diseases
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 4, 2017
William J. Rea, Kalpana D. Patel
The toxic action of these pesticides is to interfere with axonal transmission of nerve impulses, thus disrupting the proper activation of NS function, particularly in the central nervous system (CNS).15 The sensitivity pathway appears to involve both the CNS and autonomic nervous systems. There are indications that some DDT and DDE, for example, serve to change the electrophysiology and alter enzymatic properties of nerve cell membranes. Chlorinated pesticides also induce mixed-function oxidases and protein and lipid synthesis, with changes in hepatic enzymes. They are cleared from the body by oxidative dehalogenation as well as peptide, glucuronic, and sulfur conjugation. Frequently, these systems become overloaded, resulting in chemical sensitivity. The degree of toxicity and sensitivity appears to be a function of the extent of chlorination on the molecule. However, other factors enter into their adverse effects. Toxicity clearly varies with different formulas. Some organochlorines can damage the liver and kidneys, and can also be hemotoxic agents. Many have now been designated as mutagens and carcinogens.16 Photolysis can produce compounds of greater toxicity than the original pesticides as can exposure to nonionizing radiation (Smith, C. W. 1989, personal communication). Chemical breakdown in the body can produce more toxic intermediates, such as the case of chlordane breaking down to heptachlor epoxide. Organochlorine pesticides can have a severe impact on immune and nonimmune systems (Chemicaly Sensitivity, Vol. I).
Snakebite-associated thrombotic microangiopathy: a spotlight on pharmaceutical interventions
Published in Expert Review of Clinical Pharmacology, 2023
Tina Noutsos, Geoffrey K Isbister
Snake venoms cause death and disability via multiple different and potentially fatal clinical toxin syndromes, one of which is venom-induced consumption coagulopathy (VICC). There are a broad range of different clinical toxin syndromes, including neurotoxicity, myotoxicity, cardiotoxicity, and hemotoxicity [4]. Particular syndromes are associated with specific snake genera and species, dependent on the composition of the respective snake’s venom. Hemotoxins cause coagulopathy, and there are a diverse variety of these hemotoxins from multiple snake groups. Circulating blood clotting factors are the most common targets of snake venom hemotoxins [5–8]. Hemotoxic venoms are broadly categorized by their mechanism of action as either procoagulant (with an activating effect on clotting factor/s leading to activation of the clotting cascade) or anticoagulant (inhibitory effect on clotting factor/s) [9]. Procoagulant toxins lead to activation of the clotting cascade and VICC [8]. VICC is the most common form of coagulopathy in snakebite [10,11]. The major complication of VICC is bleeding, which can be fatal [6].
Haemostatic bioactivity of novel Schizonepetae Spica Carbonisata-derived carbon dots via platelet counts elevation
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2018
Ziwei Sun, Fang Lu, Jinjun Cheng, Meiling Zhang, Yue Zhang, Wei Xiong, Yan Zhao, Huihua Qu
In order to study the haemostatic bioactivity of novel Schizonepetae Spica Carbonisata-derived CDs (SSC-CDs), we used the innovative Deinagkistrodon acutus (D. acutus) venom model as well as the classical haemorrhagic animal model. The venom of D. acutus is a potent haemotoxin that is strongly haemorrhagic [31,32]. The haemotoxin can destroy the normal coagulation mechanism and result in the massive consumption of coagulation factors and platelets (PLTs) [33–38]. In addition, haemostasis is a unique system, including the endothelial cells, PLTs, coagulation and fibrinolytic systems interactions [39]. Among which, PLTs are essential for primary haemostasis and repair of the endothelium [40,41]. Interestingly, some studies indicated that the PLT count may have a negative correlation with the amount of venom envenomation in victims [35,38]. Hence, in studying the haemostatic bioactivity of SSC-CDs, PLT can not only serve as a functional indicator but also a pharmacodynamic indicator.
How can monoclonal antibodies be harnessed against neglected tropical diseases and other infectious diseases?
Published in Expert Opinion on Drug Discovery, 2019
Firstly, there is no incubation period for amplification of the disease-causing agent, as the entire dose of venom is injected instantaneously. There may, however, be a delay in pathogenesis, if the venom toxins are systemically-acting and need to leave the bite/sting site to exert their toxic actions (e.g. neurotoxins and hemotoxins), known as the depot effect. This has the implication that intervention is exceptionally urgently needed, and that envenomings must be treated as critical emergencies. Secondly, the toxin loads from envenomings by larger venomous animals are delivered immediately and can be pharmacologically enormous. As an example, larger snakes can deliver up to 2.5 g (dry weight) of venom toxins with molecular weights of 5–100 kDa. This has the implication that exceptionally high amounts of antitoxin (up to 15+ gram dry weight antibody protein) may be needed for successful treatment [84]. This further has the consequence that the cost of manufacture has a high impact on what therapeutic modalities are economically feasible, as most animal envenomings occur in poor communities in the rural tropics [17,85,86]. Thirdly, animal venoms are highly complex, comprising tens to hundreds of different toxins. This has the implication that mixtures of antitoxins are likely to be needed against most envenomings, and that antivenom developers should carefully consider which venom components are medically important to neutralize, and which are not, to minimize the complexity of the therapeutic intervention [87–89]. Fourthly, envenomings are not infectious and therefore only carry a risk to the envenomed victim. This has the implication that the utility of vaccination is limited, if at all existent, as there is no benefit of herd immunity and no risk of uncontrollable epidemic outbreaks. Finally, animals evolve significantly slower than microorganisms and viruses. This has the fortunate implication that mutations in medically relevant toxins and the development of resistance against treatment are unlikely to occur for thousands of years.