Husain K, Pant SC, Raza SK, Singh R, Das Gupta S. 1995. Most of the effects of sarin, including the acute cholinergic syndrome, are thought to be mediated by the excess ACh at the synapse.Electrophysiologic experiments have indicated that sarin (in picomolar concentrations) can interact with one subtype of ACh receptors, the muscarinic ACh receptors (Rocha et al., 1998; Chebabo et al., 1999). However, validation of such an approach, using components of gross EEG recordings, may not be plausible because of the large number of ionotropic channels represented. It was synthesized in 1937 in Germany in a quest for improved insecticides (Somani, 1992). 1996. Organophosphorous-induced delayed neuropathy. Fidder et al. Effect of atropine and the oxime HI-6 on low-level sarin-induced alteration of performance of rats in a T-maze.

Solubilities of cyclosarin in water are 3.7 g GF per 100 g and 5.1 g GF per 100 g at 20 and 0 °C, respectively. Nagao M, Takatori T, Matsuda Y, Nakajima M, Iwase H, Iwadate K. 1997.

Minami M, Hui DM, Katsumata M, Inagaki H, Boulet CA. 1986. Yamasaki Y, Sakamoto K, Watada H, Kajimoto Y, Hori M. 1997. 1. The acute toxicity of sarin in marmosets (Duncan EJ, Conley JD, Grychowski KD, Conley SA, Lundy PM, Hamilton MG, Sawyer TW. Gordon J, Inns R, Johnson M, Leadbeater L, Maidment M, Upshall D, Cooper G, Rickard R. 1983. Long-term effects of low-level sarin inhalation exposure on the spatial memory of rats in a T-maze. Exposure to sarin or cyclosarin can be fatal within minutes to hours. The intermediate syndrome has been reported in humans after exposure to malathion and diazinon (Gallo and Lawryk, 1991).Another type of toxicity caused by a few OP compounds is a progressive, irreversible delayed neuropathy termed organophosphate-induced delayed neuropathy (OPIDN). Haley RW, Billecke S, La Du BN. In: Krieger RI, ed. It isfound in humans in the brain and the blood. Although most Gulf War veterans resumed their normal activities, many soon began reporting a variety of nonexplained health problems that they attributed to their participation in the Gulf War, including chronic fatigue, muscle and joint pain, loss of concentration, forgetfulness, headache, and rash. Recovery of AChE function occurs only with synthesis of new enzyme. Noort D, Hulst AG, Platenburg DH, Polhuijs M, Benschop HP. Cyclosarin or GF (cyclohexyl methylphosphonofluoridate) is an extremely toxic substance used as a chemical weapon. Organophosphorous compounds. Brain cytokine concentrations (interleukin (IL)-1β, IL-6, and tumor necrosis factor-α) were affected by both sarin treatment and heat stress; this is consistent with evidence of immunosuppression seen in other experiments (decreased anti-sheep RBC antibody forming cell response and suppression of T cell response) (Kalra et al., 2002).Receptor density was measured for the M1, M2, and M3 subtypes of muscarinic receptors (Henderson et al., 2002). Rocha ES, Chebabo SR, Santos MD, Aracava Y, Albuquerque EX. Anticholinesterase intoxication in man and its treatment.

Hoskins B, Fernando JC, Dulaney MD, Lim DK, Liu DD, Watanabe HK, Ho IK. M1 receptors were decreased in a dose-dependent manner. Clinical and electrophysiological study of intermediate syndrome in patients with organophosphorous poisoning. Those effects, however, did not appear to be associated with detectable behavioral changes or clinically-relevant effects.As discussed previously, exposure to some organophosphates produces a delayed neurotoxic syndrome known as organophosphate-induced delayed neuropathy. A recent study in rats (Abu-Qare and Abou-Donia, 2001) showed that concurrent exposure to sarin and pyridostigmine bromide produced biomarkers of oxidative stress (3-nitrotyrosine and 8-hydroxy-2′-deoxyguanosine in rats), raising the possibility that some effects in rats could be mediated by oxidative stress.Not all exposed people show all signs, and signs can vary with the OP compound, dose, route of exposure, and species.

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