Sarin neuropathy induced

The protein kinase C (PKC) signaling pathway has been associated with modulation of A-methyl-D-aspartate (NMDA) receptor activity, motor behavior, learning, and memory, all of which are severely impaired in intoxication with sarin and similar OPs. There was a reduction in the immunoreactivity levels of betall-PKC and Zeta-PKC in the frontal cortex (up to 24 h), and in the striatum (up to 5 days) post-sarin exposure, in contrast to the increase in the immunoreactivity of both enzymes in the hippocampus or thalamus, following a IxLDso exposure to sarin. These observations suggest a role for both conventional and atypical PKC isozymes in OP-induced neuropathy in the rat and further support their role in cell death (Bloch-Shilderman et al., 2005). 

No review of subacute, subchronic, or chronic toxicity of chemical warfare nerve agents would be complete without discussion of the significant paper by Munro et al. that reviewed both animal and human studies of the nerve agents tabun (GA), sarin (GB), and VX. These studies included subacute, subchronic, and chronic toxicity studies in animals. Special attention was paid to the phenomenon of Organophosphorus-Induced Delayed Neuropathy (OPIDN). Reproductive toxicity and carcinogenicity tests were reviewed as well as in vitro studies of mutagenicity. Munro et al. s findings can be summarized as follows ... 

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