Method: The human acute monocytic leukemia cell line, THP-1, was used as a model system. Cell cycle analyses were performed using flow-cytometry and Multicycle analysis software (Phoenics Flow Systems, San Diego, CA, USA). The MTT ((3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) assay performed on cells attached to cell culture dishes was used as to measure the differentiation of THP-1 cells.
Result: Using THP-1 cells, we showed that exposure to 3mM HEMA reduced cell growth and shifted the cell culture towards more cells being in the S-phase of the cell cycle. Exposure to nicotine alone had no effect on cell-density and cell cycle distribution. In co-exposure experiments nicotine counteracted the effect of HEMA. Further, HEMA influenced phorbol-12-myristate-13-acetate (PMA) induced differentiation of THP-1 cells whereas nicotine alone had no effect. This effect of HEMA also seemed to be counteracted by nicotine. The underlying mechanism is currently being investigated and will be further discussed. Preliminary results exclude direct binding between HEMA and nicotine as a major mechanism.
Conclusion: Our results showed that nicotine interfered with HEMA induced cell responses.