@article {LI399, author = {YU-CHING LI and YU-SHENG TYAN and YIH-MIN LEE and TANG-YI TSAO and JING-YUAN CHUANG and HSIU-MAAN KUO and TE-CHUN HSIA and JEN-HUNG YANG and JING-GUNG CHUNG}, title = {N-Acetyltransferase is Involved in Baicalein-induced N-Acetylation of 2-Aminofluorene and DNA-2-Aminofluorene Adduct Formation in Human Leukemia HL-60 Cells}, volume = {19}, number = {2}, pages = {399--405}, year = {2005}, publisher = {International Institute of Anticancer Research}, abstract = {Many arylamine and hydrazine drugs are acetylated by cytosolic N-acetyltransferase (NAT). The human promyelocytic leukemia cell line (HL-60) has been shown to acetylate arylamine and contain NAT activity. The purpose of this study was to determine whether or not baicalein could affect N-acetylation of 2-aminofluorene (AF) in HL-60 cells. Acetylated and nonacetylated AF were determined by using high performance liquid chromatography. Baicalein displayed a dose-dependent inhibition of cytosolic and intact cells{\textquoteright} NAT activity and reduced the number of viable cells. Time-course experiments showed that N-acetylation of AF, measured from intact HL-60 cells, was inhibited by baicalein for up to 48 h. Baicalein also decreased AF-DNA adduct formation in the examined cells. The effects of baicalein on NAT were examined by flow cytometry and NAT gene expression was examined by polymerase chain reaction. The results demonstrated that baicalein inhibited NAT1 mRNA gene expression and reduced the level of NAT in HL-60 cells. These results show that baicalein can affect the NAT activity of human leukemia cells in vitro.}, issn = {0258-851X}, URL = {https://iv.iiarjournals.org/content/19/2/399}, eprint = {https://iv.iiarjournals.org/content/19/2/399.full.pdf}, journal = {In Vivo} }