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Background Smoke induced-lung tumor has become one of the malignancies with highest incidence and mortality worldwide.Therefore,increasing attention has been paid to searching for effective approaches to the prevention and treatment of smoke-induced lung tumor,including the use of antioxidants.Epidemiological and in vitro studies suggest that antioxidauts such as quercetin and vitamin E (VE) can prevent lung tumor caused by smoking;however,there is limited evidence from animal studies.Sethods In the present study,Swiss mouse was used to examine the potential of quercetin and VE for prevention lung tumor induced by smoking.Four hundred and fifty mice were randomly divided into 7 groups : control (C) group and tobacco smoke exposure (TS) group (n =100,both sexes in each group);quercetin control (C + Q) group,VE (alpha-tocopherol) control (C + VE) group,tobacco smoke plus quercetin (TS+ Q) group,tobacco smoke plus VE (TS + VE) group,tobacco smoke plus quercetin and VE (TS + Q + VE) group (n=50,ioth sexes in each group).The mice were exposed to 6h of smoke each day,5 d a week for 5 months,followed by a 4month recovery period.The VE and quercetin dose was 100 ur 80 mg/kg mouse/d.,respectively.The activities of superoxide dismutase (SOD),glutathione peroxidase (GSH-Px),the levels of malondialdehyde (MDA) and reactive oxygen species (ROS) in each group were measured to examine the oxidation and antioxidation index in mouse serum.Single cell gel electrophoresis (SCGE) assay was used to evaluate the DNA damage of lung cells.Apeptosis was determined by analysis of the percentages of cells with subdiploid DNA content by propidium iodide staining followed by flow cytometry.Results In the TS exposure group,the incidence of lung tumor anj tumor multiplicity were 43.5% and 1.00 ± 0.29,which were significantly higher than those in the normal control group and the C + VE group (v < 0.05).The incidknce of lung tumor and tumor multiplicity in VE-treated mice were 17.0%and 0.32 ± 0.16,which were significant lower than those in the TS group (p < 0.05).Serum ROS activity in the TY group was significantly higher than the three control groups (C,C +Q,and C + VE) and the VE-treated (TS + VE) group (p < 0.05),these results suggest that the TS exposure induces the production of ROS,which can be scavenged by VE;The serum SOD levels in the TS exposure group were the lowest among all the groups.The serum SOD activity in TS + Q group increased slightly,but did not reach a statistically significant level (p > 0.05).The serum SOD levels in each of the VE-treated groups (C+ VE,TS + VE,and TS + VE + Q) were significantly higher than in the TS (untreated) group (p <0.05).There were little or no differences in the serum MDA levels between the different groups (p > 0.05).The GSH-Px activities in the three control groups were much higher than in the treated groups (p < 0.05).The length of the DNA comet tail in mouse lung cells exposed to TS was not only longer than in the three control groups (p < 0.05),but was also higher than that in VE-treated and combination treatment groups (p < 0.05).However,no significant differences were observed between the TS and quercetin-treated groups (p > 0.05).Apoptosis was more prevalent in the group exposed to TS compared to all of the control groups (p < 0.05).WE treatment significantly decreased the TS-induced apoptosis (p < 0.05).This effect was also observed in mice receiving the combined treatment (p < 0.05).However,the quereetin treatment did not result in significant changes in apoptosis compared to the TS group (p > 0.05).The findings suggest that TS promotes apoptosis in mouse lung cells,which can be reversed by WE treatment,but not quercetin.Conclusions We found that TS could induce lung tumor in mice,and that quercetin did not exhibit significant preventive effects under the current experimental conditions.Moreover,no antioxidant effects or reduction in DNA damage induced by TS,or inhibition of TS-induced apoptosis in vivo were observed in quercetin-treated mice.In contrast,VE significantly decreased the carcinogenic potential of TS,and significantly reduced TSinduced DNA damage and cell apoptosis.The combination of VE and quercetin did not show any obvious synergistic or additive effects compared with VE alone.We conclude that VE might prevent lung tumor induced by smoking in Swiss mice.