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Carcinogenesis 5: Environmental and Endogenous Carcinogens

Abstract #1909

Diallyl sulfide inhibits 2,2’4,4’-tetra brominated biphenyl ether (BDE-47) induced DNA strand breaks and cell proliferation in MCF10A breast epithelial cells

Florida A&M University, Tallahassee, FL

Polybrominated diphenyl ethers (PBDEs) are a group of 209 congeners that are used in a variety of products as flame retardants, and have been found in the breast tissue and breast milk of women sampled in North America, Europe and Asia. 2,2’,4,4’-tetra brominated diphenyl ether (BDE-47) is the most abundant PBDE congener found in human, animal, and environmental samples, however the role of BDE-47 in breast cancer development is not known. Diallyl sulfide (DAS), an organosulfur compound found in garlic is a recognized chemo-preventive agent and has been shown to decrease DNA strand breaks induced by carcinogens. We hypothesize that BDE-47 will cause cell proliferation and induce DNA strand breaks in MCF10A cells, which will be inhibited by diallyl sulfide. To test this hypothesis MCF10A cells were pre-treated for 6 hours with various concentrations of DAS (1, 10, 100 µM) and treated for 24 hours with BDE-47 (1, 10, 100µM). DNA strand breaks were determined by Comet Assay analysis. To determine cell proliferation MCF10A cells were treated with BDE-47 (0.1 µM) for 24, 48, and 72 hours following a six hour pretreatment with 1.0 µM DAS. The MTS assay was used to determine cell viability. Cells treated with BDE-47 (1,10, & 100 µM) increased DNA strand breaks as indicated by an increase in the mean olive tail moment (8.885, 21.025, & 22.670) with increasing concentration. DAS at a concentration of 1 µM completely inhibited BDE-47 induced DNA strand breaks when compared to the control. BDE-47 (0.1 µM) decreased cell viability to 77% at 24 hours, and cell viability increased at 48 and 72 hours to 105% and 127% of the control. The addition of DAS (1 µM) increased the BDE-47 induced reduction in cell viability from 77% to 104% at 24 hours. However, DAS reduced BDE-47 induction in cell proliferation at 48 and 72 hours. We have demonstrated that BDE-47 causes DNA strand breaks and DAS inhibits these strand breaks. We have also demonstrated that BDE-47 decreases cell viability at 24 hours and stimulated cell proliferation at 48 and 72 hours. We conclude that BDE-47 causes initial genotoxicity that leads to cell proliferation. DAS inhibits this damage and also stimulates cell death in cells that are possibly damaged by BDE-47 in such a way as to prevent cancer formation. Further studies are under way to elucidate the mechanism by which BDE-47 may be involved in breast cancer formation. This research is sponsored by a generous grant from NIH/RCMI Number G12 RR03020