Mechanism of allyl chloride-induced cytoskeletal injury to nerve cells.

K Xie, K Sun, S Gao, L Zhang, M Zhang

Index: Chin. Med. J. 111(6) , 556-9, (1998)

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Abstract

To dissect the molecular mechanism of toxic neuropathy induced by allyl chloride (AC).Fluorescence molecular probe (Fura-2/AM), electron probe X-ray microprobe analysis (EPMA) and biochemical methods were used to determine the concentrations of cytosolic free Ca2+, the contents of intracellular Ca2+ percentage, Ca(2+)-free calmodulin (CaM), the activity of Ca2+/CaM-dependent protein kinase II (Ca2+/CaM-PK II), and cytoskeletal protein synthesis in chicken embryo brain cells induced by AC.The contents of Ca2+ percentage, the concentrations of cytosolic free Ca2+, and the activities of Ca2+/CaM-PK II in the cells were increased significantly as AC was added (P < 0.01). However, the content of Ca(2+)-free CaM and the synthesis of cytoskeletal proteins were markedly decreased (P < 0.01).The results suggest that one of the mechanism of AC-induced cytoskeletal injury in vitro might be related to the elevation of intracellular Ca2+, activated CaM and Ca2+/CaM-PK II.