Anticholinesterase insecticide

Galal EE, Latif MA, Kandil A, et al. 1975. The percutaneous cardiac toxicokinesis of anticholinesterase insecticides. J Drug Res 7 29-43. 

Galal EE, Samaan HA, Nour El Dien S, et al. 1977. Studies on the acute and subchronic toxicities of some commonly used anticholinesterase insecticides in rats. J Drug Res Eg t 1-17. 

Grob D, Garlick WL, Harvey AM. 1950. The toxic effects in man of the anticholinesterase insecticide parathion (p-nitrophenyl diethylthionophosphate). Johns Hopkins Med J 87 106-129. 

Gupta RC, Goad JT, Kadel WL. 1996. Distribution and responses of brain biomarkers to anticholinesterase insecticides exposure. FASEB J 10 A690. 

Wiemeyer, S.N. and D.W. Sparling. 1991. Acute toxicity of four anticholinesterase insecticides to American kestrels, eastern screech-owls and northern bobwhites. Environ. Toxicol. Chem. 10 1139-1148. 

Hill, E.F. and M.B. Camardese. 1984. Toxicity of anticholinesterase insecticides to birds technical grade versus granular formulations. Ecotoxicol. Environ. Safety 8 551-563. 

Brodeur J, DuBois KP. 1963. Comparison of acute toxicity of anticholinesterase insecticides to weanling and adult male rats. In Proceedings of the Society for Experimental Biology and Medicine, Vol. 114. New York, NY Academic Press, 509-511. 

Stevens JT, Greene FE. 1974. Alteration of hepatic microsomal metabolism of male mice by certain - anticholinesterase insecticides. Bull Environ Contam Toxicol 11 538-544. 

Stevens JT, Greene FE, Stitzel RE, et al. 1973. Effects of anticholinesterase insecticides on mouse and rat liver microsomal mixed function oxidase. In Deichmann W.B., Ed. Pesticides and the environment A continuing controversy. Proceedings of the 8th Inter-American Conference on Toxicology and Occupational Medicine, University of Miami School of Medicine, 489-501. 

Stevens JT, Stitzel K, McPhillips JJ. 1972a. Effects of anticholinesterase insecticides on hepatic microsomal metabolism. J Pharmacol ExpTher 181 576-583. 

Weizman Z, Sofer S. 1992. Acute pancreatitis in children with anticholinesterase insecticide intoxication. Pediatrics 90(2) 204-206. 

J.C. Fernando, K.R. Rogers, N.A. Anis, J.J. Valdes, R.G. Thompson, A.T. Eldefrawi andM.E. Eldefrawi, Rapid detection of anticholinesterase insecticides by a reusable light addressable potentiometric biosensor, J. Agrie. Food Chem., 41(3) (1993) 511-516. 

Recalling that parathion was developed as an insecticide by aayer in 1944 and that the Geigy Company were developing the carbamate anticholinesterases for this purpose in the late 1940s, we see that the 1950s were entered with (including toxaphene) no less than four new classes of chlorinated insecticides and two new classes of anticholinesterase insecticides - a truly unique situation ... 

Thompson, C.M., Richardson, R.J. (2004). Anticholinesterase insecticides. In Pesticide Toxicology and Lnternational Regulation (Current Toxicology Series) (T.C. Marrs, B. Ballantyne, eds), pp. 89-127. John Wiley Sons, Chichester. 

Anticholinesterase insecticides may produce life-threatening respiratory distress and paralysis by all routes of exposure and may be treated with symptomatic care, atropine, and pralidoxime. 

Poisoning and drug overdose with acetaminophen, anticholinesterase insecticides, calcium channel blockers, iron, and tricyclic antidepressants are the focus of the remainder of this chapter because they represent commonly encountered poisonings for which pharmacotherapy is indicated. These agents also were chosen because they represent common examples with different mechanisms of toxicity, and they illustrate the application of general treatment approaches as well as ... 

The clinical manifestations of anticholinesterase insecticide poisoning include any or all of the following pinpoint pupils, excessive lacrimation, excessive salivation, bronchorrhea, bron-chospasm and expiratory wheezes, hyperperistalsis producing abdominal cramps and diarrhea, bradycardia, excessive sweating, fas-ciculations and weakness of skeletal muscles, paralysis of skeletal muscles (particularly those involved with respiration), convulsions, and coma. Symptoms of anticholinesterase poisoning and their response to antidotal therapy depend on the action of excessive acetylcholinesterase at different receptor types (Table 10-11). 

The time of onset and severity of symptoms depend on the route of exposure, potency of the agent, and total dose received (see below). Toxic signs and symptoms develop most rapidly after inhalation or intravenous injection and slowest after skin contact. Anticholinesterase insecticides are absorbed through the skin, lungs, conjunctivae, and gastrointestinal tract. Severe symptoms can occur from absorption by any route. Within 6 hours, most patients are symptomatic, and without treatment, death may occur within 24 hours. Death typically is caused by respiratory failure owing to the combination of pulmonary and cardiovascular effects (Fig. 10-4). Poisoning may be complicated by aspiration pneumonia, urinary tract infections, and sepsis. ... 

Anticholinesterase insecticides phosphorylate the active site of cholinesterase in all parts of the body. Inhibition of this enzyme leads to accumulation of acetylcholine at affected receptors and results in widespread toxicity. Acetylcholine is the neurohormone responsible for physiologic transmission of nerve impulses from preganglionic and postganglionic neurons of the cholinergic (parasympathetic) nervous system, preganglionic adrenergic (sympathetic) neurons, the neuromuscular junction in skeletal muscles, and multiple nerve endings in the central nervous system (Fig. 10-5). 

Anticholinesterase insecticides include organophosphate and carbamate insecticides. These insecticides are currently in widespread... 

Anticholinesterase insecticides are among the most poisonous substances commonly used for pest control and are a frequent source of serious poisoning in children and adults in rural and urban settings. The 2003 AAPCC-TESS report documented 11,332 nonfatal exposures and 19 deaths from anticholinesterase insecticides alone or in combination with other pesticides, with 31% of the exposures in children younger than 6 years of age. ... 

Some references indicate that prahdoxime should be avoided in the treatment of carbamate (another type of anticholinesterase insecticide) poisoning because of reports of worsened toxicity in animals. Prahdoxime may be considered when exposure to carbamates is not known but an anticholinesterase is suspected based on symptoms or when respiratory paralysis due to nicotinic effects is not managed sufficiently by mechanical ventilation. 

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