OBJECTIVES: To investigate the effects of particulate matter (PM), a marker of environmental pollution derived from combustion sources, on lung epithelial cells (A549) and macrophage (RAW 264.7). METHODS: The production of reactive radicals from lung cells, the lipid peroxidation of cell membrane, and the cytotoxicity of PM were measured using an in vitro model. The results were compared with a control group. RESULTS: The presence of PM significantly increased the production of reactive oxygen species and reactive nitrogen species with time and in a dose dependent pattern and also increased the malondialdehyde concentration in lung epithelial cells. The cytotoxicity of PM was increased with increasing concentration of PM. CONCLUSIONS: It has been suggested that urban particulate matter causes an inflammatory reaction in lung tissue through the production of hydroxyl radicals, nitric oxides and numerous cytokines. The causal chemical determinant responsible for these biologic effects are not well understood, but the bioavailable metal in PM seems to determine the toxicity of inhaled PM.
Cell Membrane ; Cytokines ; Environmental Pollution ; Epithelial Cells ; Lipid Peroxidation ; Lung ; Macrophages ; Malondialdehyde ; Oxides ; Particulate Matter ; Reactive Nitrogen Species ; Reactive Oxygen Species

BACKGROUND AND OBJECTIVES: Aberrant activation of hepatocyte growth factor (HGF) and its receptor, c-Met, has been known to be involved in many human cancer development and progression. During the search for an effective molecule inhibitor of HGF/ c-Met signaling, we have found that Epigallocatechin-3-gallate (EGCG) in green tea might inhibit HGF/c-Met signaling. Studies were performed to address whether EGCG inhibited HGF-dependent tumor proliferation and invasion in HNSCC. MATERIALS AND METHOD: For EGCG inhibition of HGF/c-Met signaling, Western blot was performed. The proliferation of FaDu cells was assayed by counting the number of the cells after treatment by HGF 0, 10 ng/ml, EGCG 1 micrometer, EGCG 10 micrometer, HGF 10+EGCG 1 micrometer, HGF 10+EGCG 10 micrometer. The dispersion of cells was observed by measuring the separation and morphologic changes of the cells after treatment with HGF 0, 10 ng/ml HGF 10+EGCG 1 micrometer, HGF 10+EGCG 10 micrometer for 24 hours. Tumor cell migration was assessed by wound healing assay and tumor cell invasiveness was assessed by the membrane invasion assay. RESULTS: HGF treatment induced rapid activation of c-Met and EGCG inhibited HGF-induced c-Met signaling in FaDu cells. HGF significantly enhanced the growth of HNSCC cells and this phenomenon was inhibited by EGCG in a dose-dependant manner (p<0.05). EGCG inhibited HGF-induced scattering, migration, and invasion of HNSCC cells in a dose-dependent manner (p<0.05). CONCLUSION: Inhibition of HGF/Met by EGCG leads to decreased proliferation, scattering, migration and invasion in vitro, suggesting the possible use of EGCG in HNSCC associated with down-regulation of HGF/Met signaling.
Blotting, Western ; Catechin ; Cell Movement ; Down-Regulation ; Hepatocyte Growth Factor ; Humans ; Hypopharyngeal Neoplasms ; Membranes ; Tea ; Wound Healing