Airway epithelial injury induced by peroxynitrite
	    		
		   		
	    	
    	
    	
   		
        
        	
        		- VernacularTitle:过氧亚硝基阴离子对气道上皮细胞的损伤作用
 
        	
        	
        	
        		- Author:
	        		
		        		
		        		
			        		Tienian ZHU
			        		
			        		;
		        		
		        		
		        		
			        		Ruijing ZHAO
			        		
			        		;
		        		
		        		
		        		
			        		Yiling LING
			        		
			        		;
		        		
		        		
		        		
			        		Zhenyong GU
			        		
			        		;
		        		
		        		
		        		
			        		Junlin ZHOU
			        		
			        		
		        		
		        		
		        		
		        		
		        		
			        		
			        		
		        		
	        		
        		 
        	
        	
        	
        		- Publication Type:Journal Article
 
        	
        	
            
            
            	- From:
	            		
	            			Chinese Journal of Pathophysiology
	            		
	            		 2001;17(6):527-530
	            	
            	
 
            
            
            	- CountryChina
 
            
            
            	- Language:Chinese
 
            
            
            	- 
		        	Abstract:
			       	
			       		
				        
				        	AIM:To study the effect of ONOO- on the airway epithelial injury. METHODS: The mitochondrial respiration, the amount of lactate dedydrogenase (LDH) release into the cell culture medium, the levels of 8-hydroxy-2′-deoxyguanosine (8-OHdG), and the cellular apoptosis were examined after exposure of cultured rat tracheal epithelial (RTE) cells to ONOO-. RESULTS: Exposure of RTE cells to 0.25, 0.5 and 1 mmol/L ONOO- caused a dose-dependent suppression of the mitochondrial respiration . ONOO- also caused a dose-dependent increase in the percentage of LDH release. Exposure of RTE cells to ONOO- resulted in an increased generation of 8-OHdG in a dose-dependent manner. ONOO- caused an increase in apoptotic percentage in RTE cells in a time-dependent manner at different concentrations. CONCLUSION: ONOO- could cause necrosis and apoptosis in cultured RTE cells. Low concentration of ONOO- caused apoptosis in a time-dependent manner. Whereas exposure to high concentration of ONOO- resulted in cell necrosis, ONOO- caused a dose-dependent increase in the percentage of LDH release. Suppression of mitochondrial respiration and oxidative DNA damage by ONOO- may be the major cause of cellular injury induced by ONOO-.