Mass spectrometric measurement of formaldehyde generated in breast cancer cells upon treatment with anthracycline antitumor drugs.

  title={Mass spectrometric measurement of formaldehyde generated in breast cancer cells upon treatment with anthracycline antitumor drugs.},
  author={Shuji Kato and Patrick J. Burke and David J. Fenick and Dylan J. Taatjes and Veronica M Bierbaum and Tad H. Koch},
  journal={Chemical research in toxicology},
  volume={13 6},
Selected ion flow tube-chemical ionization mass spectrometry was used to measure formaldehyde levels in human breast cancer cells in comparison with levels in cells treated with the antitumor drugs doxorubicin (DOX) and daunorubicin (DAU) and the daunorubicin-formaldehyde conjugate Daunoform (DAUF). The measurement was performed on cell lysates and showed only background levels of formaldehyde in untreated cells and drug-treated resistant cells (MCF-7/Adr cells) but levels above background in… 
Chemical ionization mass spectrometric determination of acrolein in human breast cancer cells.
A selected ion flow tube-chemical ionization mass spectrometric method is presented for the first determination of acrolein metabolically produced in biological tissues. Acrolein in aqueous samples
Quantification of acetaldehyde released by lung cancer cells in vitro using selected ion flow tube mass spectrometry.
The discovery that acetaldehyde is released by the lung cancer cell lines SK-MES and CALU-1 is reported, and the potential value of this new technique in cell biology and in industrial cell biotechnology is discussed.
Doxazolidine induction of apoptosis by a topoisomerase II independent mechanism.
The data indicate that doxorubicin and doxazolidine induce apoptosis via different mechanisms andDoxzolidine cytotoxicity is topoisomerase II independent.
Exposure of Tumor Cells to Chemotherapeutic Agents Progression and Enhancement of Metastatic Potential after Updated Version
In vitro exposure of tumor cells to chemotherapeutic agents either selects more aggressive cells or enhances the metastatic potential of the surviving cells, as shown in experiments on nonmetastatic MCF-7 breast carcinoma cells.
Doxorubicin-DNA adducts induce a non-topoisomerase II-mediated form of cell death.
It is shown that doxorubicin-DNA adducts induce a more cytotoxic response in HL-60 cells than doxorbicin as a single agent, and that theseAdducts are more cytOToxic than topoisomerase II-mediated lesions.
Progression and enhancement of metastatic potential after exposure of tumor cells to chemotherapeutic agents.
In vitro exposure of tumor cells to chemotherapeutic agents either selects more aggressive cells or enhances the metastatic potential of the surviving cells, as indicated by in vitro treatment of nonmetastatic MCF-7 breast carcinoma cells.
ABT-737 overcomes Bcl-2 mediated resistance to doxorubicin-DNA adducts.
On the Synergistic Effect of Doxorubicin and Mitomycin C Against Breast Cancer Cells
The results suggest that poisoning of topoisomerase IIalpha by doxorubicin may interact with drug-induced DNA cross-links to enhance the formation of DNA double-strand breaks.
Analysis of covalent ellipticine- and doxorubicin-derived adducts in DNA of neuroblastoma cells by the ³²P-postlabeling technique.
The results suggest that covalent binding of ellipticine to DNA of UKF-NB-3 and UKF -NB-4 neuroblastoma cell lines is the predominant mechanism responsible for the cytotoxicity of this drug.


Doxoform and Daunoform: anthracycline-formaldehyde conjugates toxic to resistant tumor cells.
Daunoform reacts with the self-complementary deoxyoligonucleotide (GC)4 faster than the combination of daunorubicin and formaldehyde at an equivalent concentration to given drug-DNA adducts, and in spite of hydrolytic instability, Doxoform is 150-fold more toxic to MCF-7 human breast cancer cells and 10000-foldMore toxic toMCF- 7/ADR resistant cells.
Redox pathway leading to the alkylation of DNA by the anthracycline, antitumor drugs adriamycin and daunomycin.
The results suggest a pathway to the inhibition of transcription by reductively activated adriamycin and daunomycin and the proposed molecular structure is duplex DNA containing two molecules of anthracycline bound to a separate strand of the DNA via a methylene group.
Comparison of different iron chelators as protective agents against acute doxorubicin-induced cardiotoxicity.
DFO was the most effective agent to afford protection against Dox-mediated atrial malfunction, however, at 500 microM, DFO was not effective whereas ICRF-187 afforded partial protection.
Volatile carbonyl levels in tissues of transgenic mice with nerve sheath tumors.
The secondary alcohol metabolite of doxorubicin irreversibly inactivates aconitase/iron regulatory protein‐1 in cytosolic fractions from human myocardium
  • G. Minotti, S. Recalcati, G. Cairo
  • Biology, Chemistry
    FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • 1998
It is demonstrated thatDOXol delocalizes low molecular weight Fe(II) from the [4Fe‐4S] cluster of cytoplasmic aconitase, suggesting that intramyocardial formation of DOXol may perturb the homeostatic processes associated with cluster assembly or disassembly and the reversible switch between acon itase and IRP‐1.
Quantitative analysis by gas chromatography of volatile carbonyl compounds in expired air from mice and human.
Stability of adriamycin-induced DNA adducts and interstrand crosslinks
Values serve to define a model of the interstrand crosslink with unstable sites of attachment at both ends of the crosslink, with half-lives at either end being approximately 5 and 40 h.
Base Specific and Regioselective Chemical Cross-Linking of Daunorubicin to DNA
The potent anticancer drug daunorubicin binds to DNA by the process of intercalation. Formaldehyde (HCOH) was found to rapidly and efficiently cross-link the drug to DNA in solution in a reaction t...
Formaldehyde adducts of glutathione. Structure elucidation by two-dimensional n.m.r. spectroscopy and fast-atom-bombardment tandem mass spectrometry.
The structures of two of the other major adducts were determined by concerted application of 13C-1H two-dimensional chemical-shift correlation, fast-atom-bombardment mass spectrometry and tandem mass Spectrometry to the adduct mixtures in aqueous solution.