| In recent years,people have a stronger interest in indoor air quality.Cigarette smoke is a major air pollutant in indoor and severely harm to body health.This paper simulated the exposure of environmental smoke through the custom-made exposure apparatus.The SD rats were exposed to various materials of tobacco(NDY-1,NDY-2 and NDY-3)or ambient air.Then the SD rat COPD model was established.We analyzed the effects of smoke exposure on inflammatory reaction in bronchial alveolar lavage fluid,pathologic feature of lung,the micronucleus rates of polychromatic erythrocyte,the biomarkers of oxidative stress(SOD and GSH-Px activities,ROS,MDA,PCO and DPC levels)and the pathologic features of liver and spleen.It was designed to provide a theoretical basis for the research of the mechanism of toxicity of complex environmental air pollutant exposure.The results showed that:(1)After the exposure of cigarette smoke,the ratio of the neutrophils showed a clear upward trend but the ratio of the macrophages showed obvious decline in the tested rats when compared with the controls;there wasn’t a significant difference between the experimental groups.The typical COPD pathological characteristics obviously occurred:different degrees of inflammatory cells infiltration,partial alveolar septum fracture and alveolar irregular expansion,bronchial wall thickening and luminal area narrowing.These results collectively indicated that exposure of smoke caused inflammation and damage in lung tissue;there were differences of airway inflammatory degree between three experimental groups.(2)Biochemical analyses resulted that the levels of ROS,MDA and PCO and the coefficient of DPC were significantly increased while the enzymatic activities of SOD and GSH-Px were reducing in liver and spleen of the experimental groups when compared with the control group(P<0.05).There were significant differences of ROS,MDA,PCO,DPC contents and SOD,GSH-Px activities between NDY-2 and NDY-1 groups(P<0.05);but there weren’t obvious differences between NDY-3 and NDY-1 groups.These results indicated that exposure of smoke caused oxidative stress and injury in liver and spleen tissue;there were significant differences of injury degree between three experimental groups.After exposure of cigarette smoke,pathological section of liver demonstrated inflammatory cells infiltration and central venous dilation,congestion and hemorrhage,nuclear disintegration.The pathological section of spleen displayed chaotic distribution of white pulp and red pulp,loosened arrangement of lymphocytes,markedly narrowed lumen of central artery.These results indicated that exposure of smoke caused pathologic changes in liver and spleen tissue;there were differences of pathologic changes degree between NDY-2 or NDY-3 group and NDY-1 group.(3)After the exposure of cigarette smoke,the micronucleus rates of the experiment groups was clearly higher than those of control group.There were significant differences of the micronucleus rates between three experimental groups.This result indicate that different materials of cigarette smoke exposure induced the different injury degree of chromosome.In summary,the exposure of cigarette smoke could cause airway inflammation,oxidative stress and chromosomal damage.There were significant differences of injury severity between the different materials of cigarette smoke exposure.This may be related to the genotype and ingredient of cigarette.The mechanism of environmental smoke induced COPD rats tissue damage may be related with oxidative stress.These may affect some biological functions,such as the gas exchange,metabolism,immunity,and induce various diseases. |