Organophosphorus Compounds: An Overview

Inhibition of neurite outgrowth in differentiating mouse N2a neuroblastoma cells by phenyl saligenin phosphate: Effects on MAP kinase (ERK 1/2) activation, neurofilament heavy chain phosphorylation and neuropathy target esterase activity

“…Since PSP is an analogue of one of the main neuropathic metabolites of TOCP [37], the observed inhibition of neurite outgrowth is in good agreement with our previous work, in which the neuropathic effect of TOCP in vitro was enhanced by metabolic activation with NADPH activated rat liver microsomes [20]. It is also consistent with the findings from in vivo studies of the pathogenesis of OPIDN, in which PSP and other metabolites of TOCP are more effective than TOCP in the induction of OPIDN [1,2,20,21,23,32]. The fact that the longer (i.e.…”

“…Certain organophosphate compounds (OPs) are capable of inducing a delayed neurodegenerative condition in central and peripheral nervous system of man, birds and livestock [1][2][3][4][5][6]. This condition, which may arise up to 3 weeks after exposure to neuropathic OPs, is known as organophosphate-induced delayed neuropathy (OPIDN).…”

Review of the Toxicology of Chlorpyrifos With an Emphasis on Human Exposure and Neurodevelopment

“…Of particular importance is the desulfuration to chlorpyrifos-oxon since this metabolite must be formed to express potent anticholinesterase activity; chlorpyrifos by itself is unable to inhibit AChE to any significant extent (Chambers, 1992). The main route of inactivation of the oxon is by hydrolysis to form 3,5,6-trichloro-2-pyridinol (TCPy).…”

Delayed Neurologic and Behavioral Effects of Subtoxic Doses of Cholinesterase Inhibitors

“…Possible exposure to sarin may have occurred after explosions of ammunition dumps with consequent air contamination at Khamisiyah, Iraq (McCauley et al, 2001). The effects of low-level repeated exposure to OP nerve agents, not associated with acute clinical signs or symptoms, have attracted less attention than the well known effects of acute intoxication with these agents (Sidell, 1974;Ecobichon and Joy, 1982;Chambers, 1992). Behavioral and electroencephalographic alterations in workers exposed to low levels (not associated with acute intoxication) of nerve agents have been reported (Burchfield and Duffy, 1982;Ecobichon and Joy, 1982).…”