The Effects Of Environmental Smoke Exposure On The Specific Injury In An Animal Model

Cigarette smoke is important sources of complicated air pollution.Many people use the bacterial mutagenicity,cytotoxicity,micronucleus to analyze the toxicity of cigarette smoke.There is less study on animal model.In this paper,we detected the mutation of three cigarette smoke extract.Then the SD rat COPD model was established to evaluate the specific injury of cigarette smoke exposure,as recommended by Cooperation Center for Scientific Research Relative to Tobacco(CORESTA).To determine the activity of CSC in vitro genetic toxicology test systems in mutagenicity using the Ames’ test.Using the plate incorporation assay,CSC were assayed for mutagenicity employing several histidine dependent salmonella strains(TA97,TA98,TA100 and TA102)both with and without metabolic activation using the liver fraction.To establish SD rat COPD model,the experimental rats were exposed to cigarette smoke for 8 weeks,10 cigarettes for 1 h/twice daily,6 days/wk,but the control animals inhaled ambient air.After the 14d,28d and 56d exposure,the rats were anesthetized by injecting pentobarbital sodium.We obtained blocks of lungs and tracheas for pathlogical analysis and collected lung tissue,serum and bronchoalveolar lavage fluid(BALF)for biochemical analysis.The changes of pulmonary mean lining intercept(MLI),mean alveolar numbers(MAN),smooth muscle layer thickness(Wam)and airway wall thickness(Wat)were observed with the semi-quantitative analysis on pathological sections.Subsequently,the SOD,GSH-Px,MDA,ROS,PCO,DPC,MMP-9,TIMP-1 and TGF-β1 were determined,by routine methods.The results showed that:(1)The Ames test results showed that S9 can increase the mutation rates of CSE.CS-1,CS-2 and CS-3 had different genotoxic effects,the three different CSE mutagenic ability followed by CS-1>CS-2>CS-3.(2)Pathological features such as inflammatory cells infiltration and airway remodeling were observed in lung of experimental rats.It was also found that MLI was significantly increased,but MAN was decreased in experimental rats(P<0.05).The Wat and Wam in the experimental groups have significant increase compared with the controls(P<0.05).(3)In lung tissue,the levels of SOD,GSH-Px,ROS,MDA and PCO in test groups had significant increase compared with the control group(P<0.05),the level of DPC in experimental rats was higher than controls,but there was no statistically significant(P>0.05).The activity of GSH-Px and the level of MDA were significant increase compared with normol controls(P<0.05),but SOD activity no significant change after smoke exposure.(4)After the 56 d exposure,in the BALF and serum,the contents of MMP-9,TIMP-1 and TGF-β1 of cigarette smoke exposure rats were markedly higher than controls(P<0.05),but MMP-9/TIMP-1 decreased obviously.Different cigarette smoke exposure induced different degree of injury which may relate to the different tobacco types.Conclusion:After the Ames test,we establish the animal model test in vivo.When SD rats were exposed to different cigarette smoke,the typical COPD pathological characteristics obviously occurred.Cigarette smoke exposure could induce oxidative stress and protease-antiprotease imbalance.The SD rat COPD model may be a used to reveal the biological effect of cigarette smoke exposure.