Tung Y H, Ko J L, Liang Y F, Yin L, Pu Y, Lin P
Institute of Toxicology, Chung-Shan Medical and Dental College, Taichung 40203, Taiwan, Republic of China.
Environ Res. 2001 Sep;87(1):47-54. doi: 10.1006/enrs.2001.4272.
Epidemiological studies have shown an association between exposure to indoor air pollution from Chinese-style cooking and risk of lung cancer among Chinese females. Several toxic substances have been identified in cooking oil fumes (COF) collected from heated rapeseed oil. In this study, we examined the biological effects of COF on CL3 human lung epithelial cells. Exposure to 200 microg/ml COF significantly reduced cell growth within 4 days. In addition, we examined the effect of COF on TGFbeta1, TGFbeta2, IL-6, IL-8, and IFN-gamma gene expressions with the RT-PCR method. We found that TGFbeta1 mRNA levels increased after exposure to 200 microg/ml COF for 24 h. Similarly, exposure to 10 microM benzo[a]pyrene or 100 nM 12-O-tetradecanoylphorbol-13-acetate increased TGFbeta1 mRNA levels at 24 h. The mRNA levels of TGFbeta2, IL-6, IL-8, and IFN-gamma did not increase after treatment with COF, benzo[a]pyrene, or 12-O-tetradecanoylphorbol-13-acetate. COF-induced TGFbeta1 production was confirmed by quantification of TGFbeta1 in conditioned medium with enzyme-linked immunosorbent assay. Exposure to 200 microg/ml COF significantly increased TGFbeta1 secretion in a time-dependent and dose-dependent manner. It has been demonstrated that reactive oxygen intermediates induce TGFbeta1 gene expression. When CL3 cells were exposed to 200 microg/ml COF for 15 min, there was an increase in intracellular peroxide formation with the dichlorofluorescein method. Furthermore, treatment with 200 microg/ml COF for 12 h also significantly induced lipid peroxidation in CL3 cells. Our results show that exposure to COF inhibits cell growth, increases TGFbeta1 secretion, and induces oxidative stress in CL3 lung epithelial cells. This suggests that TGFbeta1 and oxidative stress play a role in the biological effects of COF on lung epithelial cells.
流行病学研究表明，中式烹饪产生的室内空气污染与中国女性患肺癌的风险之间存在关联。在从加热的菜籽油中收集的烹饪油烟（COF）中已鉴定出几种有毒物质。在本研究中，我们检测了COF对CL3人肺上皮细胞的生物学效应。暴露于200微克/毫升的COF在4天内显著降低了细胞生长。此外，我们用RT-PCR方法检测了COF对TGFβ1、TGFβ2、IL-6、IL-8和IFN-γ基因表达的影响。我们发现，暴露于200微克/毫升的COF 24小时后，TGFβ1 mRNA水平升高。同样，暴露于10微摩尔苯并[a]芘或100纳摩尔12-O-十四烷酰佛波醇-13-乙酸酯24小时后，TGFβ1 mRNA水平升高。用COF、苯并[a]芘或12-O-十四烷酰佛波醇-13-乙酸酯处理后，TGFβ2、IL-6、IL-8和IFN-γ的mRNA水平没有升高。通过酶联免疫吸附测定法对条件培养基中的TGFβ1进行定量，证实了COF诱导的TGFβ1产生。暴露于200微克/毫升的COF以时间和剂量依赖性方式显著增加了TGFβ1的分泌。已经证明，活性氧中间体可诱导TGFβ1基因表达。当CL3细胞暴露于200微克/毫升的COF 15分钟时，用二氯荧光素法检测细胞内过氧化物形成增加。此外用200微克/毫升的COF处理12小时也显著诱导了CL3细胞中的脂质过氧化。我们的结果表明，暴露于COF会抑制细胞生长，增加TGFβ1分泌，并在CL3肺上皮细胞中诱导氧化应激。这表明TGFβ1和氧化应激在COF对肺上皮细胞的生物学效应中起作用。
