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Medical Countermeasures for Intoxication by Botulinum Neurotoxin
Published in Brian J. Lukey, James A. Romano, Salem Harry, Chemical Warfare Agents, 2019
Michael Adler, Ajay K. Singh, Nizamettin Gul, Frank J. Lebeda
In control mouse hemidiaphragm preparations, the scorpion toxins produced small increases in twitch tension but more substantial increases when they were co-applied with 3,4-DAP. However, they were ineffective in BoNT/A-intoxicated muscles when added after tensions were reduced by >30% at any concentration tested (10–100 nM). Although the scorpion toxins examined were ineffective against BoNT, the availability of a large pool of K+ channel toxins in scorpion venom suggests that a more thorough investigation of the toxin components would be profitable (Gao et al., 2013).
Clinical Toxicology of Scorpion Stings
Published in Jürg Meier, Julian White, Handbook of: Clinical Toxicology of Animal Venoms and Poisons, 2017
Manuel Dehesa-davila, Alejandro C. Alagon, Lourival D. Possani
In the past, some attempts have been made to prepare a possible immunogen for vaccination of experimental animals73. A toxic fraction of the venom from Centruroides noxius was detoxified with glutaraldehyde and was shown to produce neutralizing antibodies in rabbits. Purified antibodies protected mice against the lethal effect of the toxic fraction (number II from Sephadex G-50 gel filtration)73. Detoxification of scorpion toxins by acetylation was also reported for pure toxins of Androctonus australis and Buthus occitanus tunetanus by Delori et al74. These authors conclude that the use of fraction II from Sephadex G-50 is the most suitable substrate for obtaining a potent acetylated anatoxin that is capable of producing neutralizing antibodies against several venoms of African scorpions. A more recent review on this subject is also available75. Heneine et af76. showed that iodination of fraction T2 from the venom of Tityus serrulatus abolishes its lethal capacity, without changing its immunological properties.
Overview of Ion Channels, Antiepileptic Drugs, and Seizures
Published in Carl L. Faingold, Gerhard H. Fromm, Drugs for Control of Epilepsy:, 2019
Voltage-gated Na+ channels are widespread in excitable cells in multicellular animals. The constitution of the Na+ channel in most cells is fundamentally similar with some variations (see Figure 6 in Chapter 4 by Evans18). The sodium channel from mammalian brain consists of three subunits, alpha (260-kDa), beta-1 (36-kDa) and beta-2 (33-kDa), and those from other sites and species have some differences in the smaller subunits.6 The alpha subunit contains the binding site for tetrodotoxin, which is a widely used experimental sodium channel blocking agent, and this subunit is thought to contain most if not all the functional domains of the Na+ channel. Evidence for the existence of sodium channel subtypes has been observed during development based on quantitative differences in response to neurotoxins, and more selective neurotoxins have been discovered that can differentially affect Na+ channels in different tissues.18 Some differences in Na+ channel parameters have been noted among different structures within the brain.2 Recent work with selective toxins has led to the elucidation of several distinct receptor sites on the Na+ channel.19 Sodium channels are sensitive to several classes of drugs. Guanidinium toxins block permeation, while veratridine alkaloids produce prolonged activation. Alpha scorpion toxins inhibit inactivation, beta scorpion toxins shift activation, and the brevetoxins prolong activation by acting at discrete sites.6 Local anesthetics have long been known to exert their actions in large part through blocking Na+ channels.3 Immunologie and site-directed mutagenesis techniques, along with patch clamp recording, are being utilized to determine the role of specific structural elements of the Na+ channel that subserve specific functions of this channel type.20,21
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
Physiological effects of scorpion sting vary widely from inflammation or local pain to severe complications (Chgoury et al. 2011; 2015; Pucca et al. 2015) such as pulmonary edema, nervous disorder, and cardiogenic shock (Quintero-Hernández et al. 2013; Maghsoodi et al. 2015). Scorpion toxins cause massive release of neurotransmitter such as catecholamines which generates a cascade of events that can progress to heart failure, pulmonary edema, arterial hypotension or hypertension, arrhythmia, tachycardia or bradycardia, unconsciousness, and death (Isbister and Bawaskar 2014). The cytotoxin from H. lepturus causes psychological problems (Mental disorders, Anxiety, Depression, Schizophrenia, etc.) necrotic ulcers, cutaneous necrosis, hemoglubinuria, renal failure, ankylosis of the joints, fatal hemolysis, hematuria and even death (Rahmani and Jalali 2012; Shahi et al. 2015). Scorpion venom is linked to dysfunctions of the immune system by recruiting inflammatory cells, leukocytes, platelet activating factor, adhesion molecules, immunoglobulins, and cytokines (Petricevich 2004).
Assessment of the relationship between the amount of scorpion venom in the central nervous system and the severity of scorpion envenomation in rats
Published in Toxin Reviews, 2021
Mehdi Ait Laaradia, Sara Oufquir, Moulay Abdelmonaim El Hidan, Fatimazahra Marhoume, Jawad Laadraoui, Kenza Bezza, Zineb El Gabbas, Rachida Aboufatima, Ali Boumezzough, Abderrahman Chait
Previous studies have shown that systemic manifestations observed after severe scorpion envenomation were reproduced after central administration of low doses of scorpion venom (e.g. lung edema and cardiac arrhythmias) (Mesquita et al. 2002, 2003). Therefore, this work provides additional evidence of the possible implication of the CNS in severe scorpion envenomation. In fact, Microinjected rats with B. lienhardi venom have manifested symptoms accounting for respiratory and cardio-vascular systems impairments. Thus, we report focal necrosis of the heart tissue and lungs congestion manifested by hemorrhage, alveolar air space enlargement and focal rupture of the alveolar structure. Additionally, as a consequence of myocardial and pulmonary damages, an increment in levels of plasmatic LDH and CPK enzymes was also observed. Support of our finding is provided by previous studies, indeed, El Hidan et al. (2016) and Fatani et al. (2000), had shown necrosis of the heart tissue and lungs hemorrhage after ICV injection of scorpion venom. Moreover, other investigations have demonstrated that centrally injected scorpion toxins induce an increment in heart rate and heart arrhythmia (Mesquita et al. 2003, Guidine et al. 2008, 2009). Moreover, some research groups have observed macroscopic and microscopic evidence of renal lesions in rodents after central administration of scorpion venoms (Fatani 2010, El Hidan et al. 2016). In our study, we report a parenchymatous tubular degeneration, predominantly of the distal tubules, manifested by epithelial swelling. Additionally, we observed an increase in the level of some renal function markers, such as urea and creatinine in venom centrally injected rats.