| Summary: | 碩士 === 國立臺灣大學 === 職業醫學與工業衛生研究所 === 90 === Particulate matter (PM) and Ozone (O3) are major air pollutants in Taiwan. Previous epidemiological studies have reported that these pollutants are associated with respiratory cancer, but their carcinogenic mechanism is not clear. This study investigated DNA damage induced by ozone and particulate matters alone and in combination on human lung epithelial cell. A549 cell line was exposed to ozone (0、60、80、120 ppb) for 1 hour and PM2.5 (0、50、100 µg/ml) for 4 hours alone and in combination. We used 8-oxoguanine and DNA breakage to evaluate the effects of ozone and particles. 8-oxoguanine was measured by flow cytometry and comet assay was used to assess DNA breakage. Moreover, formamidipyrimidine glycosylase (Fpg) repair enzyme was added to increase the power of detecting oxidative damage. Our study revealed that after ozone exposure, percentage of tail intensity was not significantly associated with exposure concentration. After-adding Fpg repair enzyme, percentage of tail intensity in higher exposure group (80、120 ppb) was significantly higher than control group (0 ppb) (p=0.03 and 0.03, respectively). Furthermore, 8-oxoguanine levels in exposure group (80、120 ppb) were also significantly higher, as compared control group. After particulate matter exposure, percentage of tail intensity was also not significantly associated with exposure concentration. 8-oxoguanine levels in 100 µg/ml were significantly higher than that in control group (p<0.05). As to co-exposure, the combination effects in DNA damage did not show an additive effect. Futher, the antioxidants, vitamin C and vitamin E could significantly inhibit 8-oxoguanine induced by ozone exposure of 120ppb.
This study reveals adding Fpg enzyme could increase the sensitivity of comet assay for detecting oxidative stress. Importantly, ozone 80 ppb exposure for 1 hour could induce significant DNA damage. Thus, our finding may be useful in standard setti
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