Song_2012_Chem.Biol.Interact_200_114

A few organophosphorus compounds (OPs) can cause toxic neuropathy known as organophosphorus ester-induced delayed neuropathy (OPIDN). Although the incidents of OPIDN have been documented for over a century, its molecular mechanisms underlying the axonopathy are still unclear. Recently, increasing evidences suggest that proteases are closely associated with OPIDN. Herein, we have summarized the roles of calcium-dependent cysteine proteases (calpains) in OPIDN. The activation of calpains should be an early molecular event during the onset and development of OPIDN. However, the understanding of the mechanism underlying the disruption of Ca(2+) homeostasis and the activation of calpain by neurotoxic OPs is still limited. Therefore, a better understanding of molecular mechanisms that can prevent the disturbance in cellular Ca(2+) homeostasis can facilitate to establish the novel therapeutic strategies for OPIDN.