摘要
Objective To dissect the molecular mechanism of toxic neuropathy induced by allyl chloride (AC). Methods 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 Ca^2+ , the contents of intracellular Ca^2+ percentage, Ca^2+ free calmodulin(CaM), the activity of Ca^2+ /CaM dependent protein kinase Ⅱ (Ca^2+ /CaM PK Ⅱ), and cytoskeletal protein synthesis in chicken embryo brain cells induced by AC. Results The contents of Ca^2+ percentage, the concentrations of cytosolic free Ca^2+ , and the activities of Ca^2+ /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 ). Conclusion The results suggest that one of the mechanism of AC induced cytoskeletal injury in vitro might be related to the elevation of intracellular Ca^2+ , activated CaM and Ca^2+ /CaM PK Ⅱ.
Objective To dissect the molecular mechanism of toxic neuropathy induced by allyl chloride (AC). Methods 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 Ca^2+ , the contents of intracellular Ca^2+ percentage, Ca^2+ free calmodulin(CaM), the activity of Ca^2+ /CaM dependent protein kinase Ⅱ (Ca^2+ /CaM PK Ⅱ), and cytoskeletal protein synthesis in chicken embryo brain cells induced by AC. Results The contents of Ca^2+ percentage, the concentrations of cytosolic free Ca^2+ , and the activities of Ca^2+ /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 ). Conclusion The results suggest that one of the mechanism of AC induced cytoskeletal injury in vitro might be related to the elevation of intracellular Ca^2+ , activated CaM and Ca^2+ /CaM PK Ⅱ.
