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Selective Drug Delivery Using Targeted Enzymes For Prodrug Activation
Published in Siegfried Matzku, Rolf A. Stahel, Antibodies in Diagnosis and Therapy, 2019
Nathan O. Siemers, Peter D. Senter
The strategy of using targeted enzymes for the generation of cytotoxic agents has been extended to include more conventional anticancer drugs (reviewed in Senter et al., 1993; Jungheim et al., 1994; Bagshawe et al., 1994). Table 1 summarizes the enzyme/prodrug combinations that have been reported. Prodrug forms of important anticancer agents such as doxorubicin, etoposide, methotrexate, 5-fluorouracil, melphalan, and paclitaxel have been described. In addition, the feasibility of using prodrugs of agents that have either failed or would likely fail in the clinic due to systemic toxicity is evident from studies utilizing prodrugs of agents such as palytoxin, potent alkylating agents (phenol and phenylenediamine mustards), and cyanide. In principle, this delivery strategy should broaden the scope of drugs that can be used clinically, since drug release takes place in a site-selective manner.
Palytoxin
Published in Dongyou Liu, Handbook of Foodborne Diseases, 2018
Jiri Patocka, Qinghua Wu, Kamil Kuca
Palytoxin (PLTX) is a lethal, heat-stable marine toxin [1], which was first isolated in 1971 in Hawaii from the seaweed-like coral, Limu-make-o-Hana (Seaweed of Death from Hana), polyps of the genus Palythoa [2]. Later identified as Palythoa toxica, a zoanthid of the tropical areas of the Pacific Ocean [3], this organism has been shown to produce a marine polyalcohol toxin (i.e., PLTX) with a very large and complex chemical structure including both lipophilic and hydrophilic moieties. PLTX and its analogues have been implicated in toxic events in humans following ingestion, dermal exposure, or inhalation of vapors, and in animals following various routes of administration [4]. Moreover, PLTX and its analogues exert their potent biological activity by altering normal ion homeostasis in excitable and nonexcitable tissues [5,6]. The toxin depolarizes mammalian cells by causing cation conductance with relatively low ion selectivity [7].
Clinical Toxicology of Ciguatera Poisoning
Published in Jürg Meier, Julian White, Handbook of: Clinical Toxicology of Animal Venoms and Poisons, 2017
Philippe Glaziou, Mireille Chinain, Anne-Marie Legrand
Neurotoxic and paralytic shellfish poisoning should be considered for differential diagnosis as these two diseases have a lot of clinical similarities with ciguatera fish poisoning79. However, the dinoflagellates responsible for these entities are most common in waters in latitudes above 30° north and below 30° south, whereas the ciguatera organisms are essentially confined to latitudes between 35° north and 35° south95. Also, fish poisoning induced by tetrodotoxin or palytoxin should be considered for differential diagnosis in some areas of the South Pacific (New Caledonia).
Outbreak of Haff disease caused by consumption of crayfish (Procambarus clarkii) in nanjing, China
Published in Clinical Toxicology, 2019
Baofu Guo, Guoxiang Xie, Xiaocheng Li, Yun Jiang, Di Jin, Yonglin Zhou, Yue Dai, Shiqi Zhen, Guiju Sun
While the etiology of rhabdomyolysis in Haff disease is unknown, it is considered to be caused by an unidentified, heat-stable toxin, which is similar to cyanotoxins or palytoxin [7,8,17,19,20]. An investigation via a mouse model indicated that the hazardous substance causing crayfish-induced rhabdomyolysis was not an allergen or palytoxin [21]. No microcystins were found in our laboratory analyses, and the exact etiology remains unconfirmed. In Chen’s study, some mice which were administered with gills, intestines, and glands (GIG) obtained from cooked crayfish appeared to show rhabdomyolysis symptoms. The majority of cases we reported have eaten the contents of crayfish’s head and removed crayfish’s gut during cooking or eating process, and the case-control study revealed that eating crayfish head and intestine might be related to increased disease risk, which suggests that the toxin inducing the rhabdomyolysis might be present in the head part of the crayfish.
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.