1983
DOI: 10.1007/bf00354767
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The delayed neuropathic effects of nerve agents and some other organophosphorus compounds

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1986
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Cited by 72 publications
(24 citation statements)
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“…26 The prevalence of chronic neurological complications in our cohort were similar to the chronic signs reported previously in animals exposed to either mustard gas or a nerve agent. 27 It is also interesting to note that 14% of exposed participants were suffering from repeated infections, eruptions of herpes zoster and mouth ulcers, as previous reports indicate that immuno-suppression and altered host-defence responses with depression of cell-mediated immunity have been reported in both animal and human studies following exposure to CWs. 13,28 There is no previous clear evidence linking CWs to teratogenic effects.…”
mentioning
confidence: 86%
“…26 The prevalence of chronic neurological complications in our cohort were similar to the chronic signs reported previously in animals exposed to either mustard gas or a nerve agent. 27 It is also interesting to note that 14% of exposed participants were suffering from repeated infections, eruptions of herpes zoster and mouth ulcers, as previous reports indicate that immuno-suppression and altered host-defence responses with depression of cell-mediated immunity have been reported in both animal and human studies following exposure to CWs. 13,28 There is no previous clear evidence linking CWs to teratogenic effects.…”
mentioning
confidence: 86%
“…Dendritic degeneration seen in this model of DFP-induced seizures is similar to neurodegeneration of pyramidal neurons in CA1 hippocampal area in mouse models of kainic acid (KA)-induced excitotoxicity (Zaja-Milatovic et al, 2008) and activated innate immunity (Milatovic et al, 2003 OPIDN has been attributable to inhibition of neuropathy target esterase (NTE), rather than AChE, as inhibition of AChE is not necessary for the development of OPIDN (Pope et al, 1993;Wu and Casida, 1996;Jamal, 1997). Hence, since nerve agents target AChE much more than NTE (Gordon et al, 1983), the degree to which OPIDN would emerge as a significant consequence of nerve agent exposure alone is questionable; rather, doses that could potentially lead to OPIDN would, as a practical matter, cause lethal acute anti-AChE effects first. As a practical matter, unlike many other OPs, VX has not been shown to induce OPIDN and is reported to be at least 1,000 times less effective than sarin in inhibiting NTE (Gordon et al, 1983).…”
Section: Organophosphate-induced Delayed Neuropathymentioning
confidence: 98%
“…Hence, since nerve agents target AChE much more than NTE (Gordon et al, 1983), the degree to which OPIDN would emerge as a significant consequence of nerve agent exposure alone is questionable; rather, doses that could potentially lead to OPIDN would, as a practical matter, cause lethal acute anti-AChE effects first. As a practical matter, unlike many other OPs, VX has not been shown to induce OPIDN and is reported to be at least 1,000 times less effective than sarin in inhibiting NTE (Gordon et al, 1983). However, several therapies, such as the anticonvulsant agent diazepam, that are used to minimize or prevent injury to the central nervous effects of nerve agents have less significant effects in the periphery; specifically, they have no effect on the targeting of NTE at peripheral sites.…”
Section: Organophosphate-induced Delayed Neuropathymentioning
confidence: 98%
“…OPinduced delayed neuropathy (OPIDN) is unlikely to occur except at doses greatly exceeding the median lethal dose (LD50) (13,80,(89)(90)(91) (1,80). These agents have been used by terrorists on civilian populations in Japan, and there was an accidental release of VX in a remote area of the United States.…”
Section: Ch2-ch2-ci S Ch2-ch2-cimentioning
confidence: 99%