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- W47466700 abstract "The anthracycline antitumor drug, doxorubicin (DOX), is proposed to catalyze the production of formaldehyde and bond to the formaldehyde at its amino sugar to produce an active metabolite that subsequently crosslinks DNA as part of the cytotoxic mechanism. Doxoform (DOXF), a synthetic formaldehyde conjugate of DOX, exhibits enhanced toxicity to numerous sensitive and resistant cancer cell lines. The aim of this study was to demonstrate that DOXF, at much lower drug levels, retains the apoptosis-inducing characteristics of DOX, consistent with DOXF being a prodrug to the DOX active metabolite.HeLa S3 and MCF-7 cells were treated with IC50-equivalent concentrations of DOX and DOXF and analyzed for DNA fragmentation and phosphatidylserine externalization, common morphological features of apoptosis. DNA fragmentation was detected by gel electrophoresis and TUNEL assay; phosphatidylserine externalization was detected by annexin V binding.DNA fragmentation and phosphatidylserine externalization were detected in HeLa S3 cells following a 3 h treatment with either 86 nM equiv. DOXF or 1 microM DOX. No apoptotic features were observed for MCF-7 cells following a 3 h treatment with either DOXF (100 nM equiv.) or DOX (1 microM).DOXF induced cell death in both cell lines at drug levels an order of magnitude lower than DOX. The similar behavior of DOXF and DOX supports the role of formaldehyde in the cytotoxic mechanism of the clinical anthracycline antitumor agents and provides further support for the proposition that DOXF is a prodrug to the DOX active metabolite." @default.
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- W47466700 date "2001-11-29" @default.
- W47466700 modified "2023-09-23" @default.
- W47466700 title "Doxorubicin-formaldehyde conjugate, doxoform: induction of apoptosis relative to doxorubicin." @default.
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