Ellagic Acid Inhibits Growth and Arylamine N-Acetyltransferase Activity and Gene Expression in Staphylococcus aureus

It is well documented that N-acetyltransferase (NAT) plays a key role in the N-acetylation of arylamine compounds. Ellagic acid was demonstrated to elicit dose- dependent bacteriostatic activity and inhibition of N-acetylation of 2-aminofluorene (AF). N-acetylation of AF in S. aureus was determined by high preformance liquid chromatography. The apparent values of Km and Vmax of NAT were decreased after co-treatment with 0.5 mM ellagic acid in the cytosol of S. aureus. PCR also indicated that ellagic acid inhibited NAT gene expression (NAT mRNA) in S. aureus. Several arylamines require N-acetylation to form metabolites before leading to carcinogenesis. N-acetylation is catalyzed by cytosolic arylamine N-acetyltransferase (NAT) using acetyl coenzyme A as a cofactor (1). Individuals can be classified into slow and rapid acetylator phenotypes based on liver cytosolic NAT activity (2, 3). After individuals have been exposed to these arylamines, the slow or rapid acetylator phenotype can influence both therapeutic response and toxicity (1). Some common fruits and nuts had been demonstrated to contain ellagic acid, which is a phenolic compound. Many studies in animal models have demonstrated that ellagic acid can inhibit tumor growth caused by chemical carcinogens (4- 8) and inhibit TPA-induced ornithine decarboxylase activity,