N-Acetyltransferases (NATs) plays an important role in the first step of arylamine compounds metabolism. Polymorphic NAT is coded
for rapid or slow acetylatoion phenotypes, which are recognized to affect cancer risk related to environmental exposure. Aloe-emodin
has been shown to exit anticancer activity. The purpose of this study is to examine whether or not aloe-emodin could affect arylamine
N-acetyltransferase (NAT) activity and gene expression (NAT mRNA) and DNA–2-aminofluorene (DNA–AF) adduct formation in mouse
leukemia cells (L 1210). By using high performance liquid chromatography, N-acetylation and non-N-acetylation of AF were determined
and quantitated. By using reverse transcriptase-polymerase chain reaction (RT-PCR) and PCR,NATmRNAwas determined and quantitated.
Aloe-emodin displayed a dose-dependent inhibition to cytosolic NAT activity and intact mice leukemia cells. Time-course experiments
indicated that N-acetylation of AF measured from intact mice leukemia cells were inhibited by aloe-emodin for up to 24 h. Using standard
steady-state kinetic analysis, it was demonstrated that aloe-emodin was a possible uncompetitive inhibitor to NAT activity in cytosols. The
DNA–AF adduct formation in mouse leukemia cells were inhibited by aloe-emodin. The NAT1 mRNA in mouse leukemia cells were also
inhibited by aloe-emodin. This report is the first demonstration which showed aloe-emodin affect mice leukemia cells NAT activity, gene
expression (NAT1 mRNA) and DNA–AF on adduct formation.
