alexa Extracts from cigarette smoke induce DNA damage and cell adhesion molecule expression through different pathways.
Microbiology

Microbiology

Journal of Microbial & Biochemical Technology

Author(s): Chen HW, Chien ML, Chaung YH, Lii CK, Wang TS

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Abstract Cigarette smoke is a major risk factor for human diseases, such as lung cancer and atherosclerosis. The present study was undertaken to investigate the effect of non-fractionated water-soluble cigarette smoke extract (NFWS CSE) on DNA damage and cellular adhesion molecule expression in human umbilical vein endothelial cells (HUVECs). DNA damage and the surface expression of intercellular adhesion molecule-1 (ICAM-1) and E-selectin were determined by the use of the comet assay and flow cytometry, respectively. NFWS CSE-induced DNA damage in a dose-dependent manner during a 2 h exposure. Pretreatment with ascorbic acid or alpha-tocopherol completely inhibited the NFWS CSE-induced DNA damage. NFWS CSE exposure also up-regulated the surface expression of ICAM-1 and E-selectin in HUVECs. Pretreatment with ascorbic acid or alpha-tocopherol had no effect on NFWS CSE-induced E-selectin and ICAM-1 expression. In contrast, the non-antioxidant metal chelator 1,10-phenanthroline partially suppressed the surface expression of ICAM-1 and E-selectin. These results suggest that NFWS CSE exposure induces both DNA damage and the surface expression of adhesion molecules in HUVECs. However, the molecular mechanism of these effects may be through different pathways: reactive oxygen species are involved in NFWS CSE-induced DNA damage but have little relation to NFWS CSE-induced E-selectin and ICAM-1 expression. This article was published in Chem Biol Interact and referenced in Journal of Microbial & Biochemical Technology

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