Cooking oil fume-induced cytokine expression and oxidative stress in humanlung epithelial cells

Epidemiological studies have shown an association between exposure to indoo r air pollution from Chinese-style cooking and risk of lung cancer among Ch inese 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 mug/ml COF significantly reduced cell growth within 4 days. In addi tion, we examined the effect of COF on TGF beta1, TGF beta2, IL-6, IL-8, an d IFN-gamma gene expressions with the RT-PCR method. We found that TGF beta l mRNA levels increased after exposure to 200 mug/ml COF for 24 h. Similarl y, exposure to 10 muM benzo [a]pyrene or 100 nM 12-O-tetradecanoylphorbol-1 3-acetate increased TGF beta1 mRNA levels at 24 h. The mRNA levels of TGF b eta2, 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 TGF be ta1 production was confirmed by quantification of TGF beta1 in conditioned medium with enzyme-linked immunosorbent assay. Exposure to 200 mug/ml COF s ignificantly increased TGF beta1 secretion in a time-dependent and dose-dep endent manner. It has been demonstrated that reactive oxygen intermediates induce TGF beta1 gene expression. When CL3 cells were exposed to 200 mug/ml COF for 15 min, there was an increase in intracellular peroxide formation with the dichlorofluorescein method. Furthermore, treatment with 200 mug/ml COF for 12 h also significantly induced lipid peroxidation in CL3 cells. O ur results show that exposure to COF inhibits cell growth, increases TGF be ta1 secretion, and induces oxidative stress in CL3 lung epithelial cells. T his suggests that TGF beta1 and oxidative stress play a role in the biologi cal effects of COF on lung epithelial cells. (C) 2001 Academic Press.