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Insecticides
Published in Frank A. Barile, Barile’s Clinical Toxicology, 2019
Decontamination, airway stabilization, and activated charcoal are important initial supportive measures for OP intoxication. Washing dermal areas with a mild soap, removal of contaminated clothes, and rinsing the eyes are necessary for dermal or ocular exposure. Atropine and the oxime cholinesterase reactivators follow as specific OP antidotes.
Ciguatera: A Treating Physician's Perspective on a Global Illness
Published in Dongyou Liu, Handbook of Foodborne Diseases, 2018
Ritchie C. Shoemaker, James C. Ryan
Symptoms in the Morris paper were quite different from those reported by Bagnis in distribution and number. No symptom questionnaire was used, just emergency room (ER)–recorded symptoms. It remains unsupported to presume that an ER would be a reliable setting for complete recording of more than 25 health symptoms. Patients had diarrhea (91%), vomiting (70%), or abdominal pain (39%). Fatigue was seen in 70%, itching 60%, pain/weakness in lower extremities 60%, paresthesias 33%, and metallic taste 27%. Treatment was supportive; back then some thought that there was value of use of a cholinesterase reactivator, pralidoxime. That therapy is no longer used. No fish flesh testing is reported.
Cholinesterase inhibitor pesticides
Published in Bev-Lorraine True, Robert H. Dreisbach, Dreisbach’s HANDBOOK of POISONING, 2001
Bev-Lorraine True, Robert H. Dreisbach
Antidote: Atropine – In the presence of symptoms give atropine sulfate, 2 mg intramuscularly, and repeat every 3–8 min until signs of parasympathetic toxicity are controlled: eyelid and tongue tremors, miosis, salivation, sweating, slow pulse, muscular fasciculations, respiratory difficulty, pulmonary edema, heart block. Repeat dose of 2 mg of atropine frequently to maintain control of symptoms. As much as 12 mg of atropine has been given safely in the first 2 h. Interruption of atropine therapy may be rapidly followed by fatal pulmonary edema or respiratory failure.Cholinesterase reactivator – Do not use in the presence of carbaryl intoxication. Use only with maximum atropine administration. Give pralidoxime (Protopam, pyridine-2-aldoxime methochloride, 2-PAM), 1 g in aqueous solution, intravenously and slowly. Repeat after 30 min if respiration does not improve. This dose may be repeated twice within each period of 24 h. Obidoxim (Toxogonin) is available in some countries and is used similarly.
Polyethyleneglycol-serine nanoparticles as a novel antidote for organophosphate poisoning: synthesis, characterization, in vitro and in vivo studies
Published in Drug and Chemical Toxicology, 2023
Pedram Ebrahimnejad, Ali Davoodi, Hamid Irannejad, Javad Akhtari, Hamidreza Mohammadi
In this research, the binding study of the PEG-NPs with DZ was evaluated and our findings showed that a connection between the PEG-NPs and DZ can occur (Figure 4). This is not only has toxicological importance but also confirms that is one of the vital pathways in which this NP can reduce DZ toxicity. In our in vitro studies, we found that PEG-NPs can reactivate the human BChE and AChE enzymes attached to the DZ (Figures 5 and 6). Therefore, it was found that our synthesized NPs can be effective in reducing the toxicity of DZ. The study proposes that the new treatment will serve as a cholinesterase reactivator and/or DZ sequestration molecule. In this study, we demonstrated that engineered PEG-NPs with high biomimetic surface properties could be applied to separate the binding between DZ and endogenous BChE and AChE, thereby reducing the severity of DZ poisoning. According to the beneficial effects of PEG-NPs in brain AChE reactivation, it can be considered as a hypothesis that the PEG-NPs may cross the blood–brain barrier (BBB) and via this pathway exert their beneficial effects and reduce the toxicity induced by DZ in the brain nervous system (CNS), which requires further studies in the future. According to reactivation of ChE enzymes by PEG-NPs, we suggest that this NP has a nucleophilic property and according to this point, by attacking to the DZ compound can liberate the DZ from the inhibited enzyme site.
Pyridinium-2-carbaldoximes with quinolinium carboxamide moiety are simultaneous reactivators of acetylcholinesterase and butyrylcholinesterase inhibited by nerve agent surrogates
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2021
Hyun Myung Lee, Rudolf Andrys, Jakub Jonczyk, Kyuneun Kim, Avinash G. Vishakantegowda, David Malinak, Adam Skarka, Monika Schmidt, Michaela Vaskova, Kamil Latka, Marek Bajda, Young-Sik Jung, Barbara Malawska, Kamil Musilek
The OP intoxication can be treated by cholinesterase antidotes. They are usually composed of parasympatholytic agent (e.g. atropine and avizafone), cholinesterase reactivator (e.g. pralidoxime 1, obidoxime 2, and asoxime 3; Figure 1), and anticonvulsant (e.g. diazepam)4. The symptomatic treatment is mediated by parasympatholytics and anticonvulsants. However, the causal treatment is done by cholinesterase reactivator with oxime moiety. The oxime functional group is able to transform into nucleophilic oximate anion under physiological pH 7.4 and split the OP moiety from AChE active site via formation of phosphylated oxime that is further degraded or excreted5. This way, OP is detoxified and AChE function is restored.
Coptidis Rhizoma: a comprehensive review of its traditional uses, botany, phytochemistry, pharmacology and toxicology
Published in Pharmaceutical Biology, 2019
Jin Wang, Lin Wang, Guan-Hua Lou, Hai-Rong Zeng, Ju Hu, Qin-Wan Huang, Wei Peng, Xiang-Bo Yang
CR has been banned in Singapore in recent decades because of the suggestion that berberine aggravated jaundice and kernicterus in neonates with glucose-6-phosphate dehydrogenase deficiency (Wong 1980). In 2012, researchers found no organ toxicity or electrolyte imbalance in 20 patients administered with CR at a daily dose of 3 g for 1055 patient-days (Linn et al. 2012). In 2016, the ban of Chinese herbal medicines rich in berberine was officially lifted. Nevertheless, toxicity cannot be ignored. An acute toxicity study showed that the oral medial lethal dose (LD50) of the fibrous roots of CR was greater than 7000 mg/kg body weight in Kunming mice. A sub-chronic toxicity study showed that the no-observed-adverse effect level (NOAEL) was 1.88 g/kg body weight in rats, whereas 3.76 g/kg body weight resulted in liver and lung damage. An Ames test, a mouse micronucleus test, and a mouse sperm abnormality test provided negative results (Ning et al. 2015). The median acute oral lethal dose of the CRE was 2.95 g/kg in mice; however, the alkaloid-rich extract was much more toxic than the total extract of CR (Ma et al. 2010). In another study, the LD50 values of four alkaloids (berberine, coptisine, palmatine and epiberberine) were determined as 713.57, 852.12, 1533.68 and 1360 mg/kg, respectively. Likewise, the cytotoxicity of berberine was the highest and that of palmatine was the lowest toward HepG2 and 3T3-L1 cells. In a subchronic toxicity study, no mortality or morbidity was observed (Yi et al. 2013). To determine the NOAEL and the toxicity of CR, rats received repeated oral administration of CR for 13 weeks. No mortality or remarkable clinical signs were observed during this 13-week study. The NOAEL of CR was determined as 667 mg/kg/day for male rats and 2000 mg/kg/day for female rats (Lee et al. 2014). Oral berberine has caused respiratory failure, extrapyramidal system reactions, severe arrhythmia, liver function injury and even death in clinics in China (Li et al. 2008), which as believed to caused by its inhibitory effect on the human eag-related gene (hERG) potassium channel and induction of mitochondrial dysfunction (Pereira et al. 2008; Schramm et al. 2011). Furthermore, the authors reported that an AChE inhibitor significantly increased the acute toxicity of the CRE, whereas a cholinesterase reactivator significantly decreased the acute toxicity. Therefore, the authors suggested that the acute toxicity of the oral CR extract was related to AChE inhibition (Ma et al. 2011) Taking these findings together, we concluded that the toxic constituents of CR were the alkaloids, mainly berberine. However, the toxic mechanism of the CR alkaloids may be complicated and remains to be determined. The currently recommended doses of CR alkaloids and CR consumption are relatively safe (Ho et al. 2014). In fact, CR is seldom used alone in clinics; instead, it is usually prescribed with other medicines that could reduce its toxic effect.