N-pentyl-nitrofurantoin induces apoptosis in HL-60 leukemia cell line by upregulating BAX and downregulating BCL-xL gene expression

Background nitrofurantoin is a nitroderivative antibiotic that has bactericidal activity against pathogens causing urinary tract infection. a few studies have reported that nitrofurantoin has cytotoxic activity against cancer cells; however,nitrofurans remain a poorly explored class of compounds with respect to their anticancer potential. the aim of this study was to investigate the anticancer effects of a nitrofurantoin derivative,n-pentyl-nitrofurantoin (nfp),on hl-60 leukemia cells. methods cytotoxicity was assayed by the mtt assay. cell morphology and phosphatidylserine externalization were visualized after giemsa-may-grunwald and annexin v staining,respectively. dna content and mitochondrial depolarization were measured by flow cytometry. bax and bcl-xl expression was examined by rt-pcr. results nfp was 3.8-fold more cytotoxic against hl‐60 leukemia cells than against normal cells. nfp reduced the number of viable cells 24 h after the treatment with a concomitant increase in the number of apoptotic cells indicated by the externalization of phosphatidylserine,dna fragmentation,and mitochondrial depolarization. the mrna levels of bax increased,whereas the mrna levels of bcl-xl decreased. conclusion the results indicate that nfp induces apoptosis in hl-60 cells by upregulating bax and downregulating bcl-xl. © 2016 institute of pharmacology,polish academy of sciences