JEN-HUNG YANG2026-10-162026-10-162004-01-01Pure ID: 15254382Pure UUID: 3136761a-d33f-46e3-8fc2-6f93573f80e4https://www.scopus.com/pages/publications/34447272216https://scholars.csmu.edu.tw/handle/123456789/27913Evidence has shown that N-acetyltransferase (NAT) acetylated 2-aminofluorene (AF) to form N-acetyl-2-aminofluorene (AAF). Then it was metabolized by cytochrome P450 (CYP) enzyme to form ring or N-hydroxylated metabolites. Sulfotransferase and other enzymes participated to form the ultimate metabolites which bind to DNA to form DNA-AF adducts which may have led to cancer development. The aim of the present study is to demonstrate whether paclitaxel (taxol) can inhibit the NAT activity, NAT gene expression and DNA-AF adduct formation in human stomach tumor cell line (SC-M1). The activity of NAT was determined by high performance liquid chromatography (HPLC) assaying for the amounts of acetylated AF (AAF) or p-aminobenzoic acid (N-Ac-PABA) and nonacetylated AF or PABA. While SC-M1 cell cytosols were used for examining NAT activity, intacts cells were used for examining all three: NAT activity, gene expression and DNA-AF adduct formation. As compared with the control group, the paclitaxel- treated group showed decreased NAT activity and DNA-AF adduct formation in SC-M1 cells and the decrease was dose-dependent. The results also indicated that paclitaxel decreased the apparent values of Km and Vmax from SC-M1 cells in both cytosol and intact cells. Palitaxel did significantly affect NAT gene expression (NAT1 mRNA) in SC-M1 cells.18enjournal article