Mechanism of allyl chloride-induced cytoskeletal injury to nerve cells
	    		
		   		
	    	
    	
    	
   		
        
        	
        	
        	
        		- Author:
	        		
		        		
		        		
			        		Keqin XIE
			        		
			        		
			        		
			        			1
			        			
			        		
			        		
			        		
			        		
			        		;
		        		
		        		
		        		
			        		Keren SUN
			        		
			        		;
		        		
		        		
		        		
			        		Shujun GAO
			        		
			        		;
		        		
		        		
		        		
			        		Lei ZHANG
			        		
			        		;
		        		
		        		
		        		
			        		Min ZHANG
			        		
			        		
		        		
		        		
		        		
		        		
		        			
			        		
			        		Author Information
			        		
		        		
		        		
			        		
			        		
			        			1. 山东医科大学
			        		
		        		
	        		
        		 
        	
        	
        	
        	
            
            
            	- From:
	            		
	            			Chinese Medical Journal
	            		
	            		 1998;(6):556-559
	            	
            	
 
            
            
            	- CountryChina
 
            
            
            	- Language:Chinese
 
            
            
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		        	Abstract:
			       	
			       		
				        
				        	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 Ca2+, the contents of intracellular Ca2+ percentage, Ca2+-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. Results 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 Ca2+-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 Ca2+, activated CaM and Ca2+/CaM-PK Ⅱ.