Summary: | 碩士 === 國立清華大學 === 分子醫學研究所 === 93 === Colcemid, a well-known inhibitor of mitotic spindle, enhances UVC-induced cell death in Chinese hamster ovary cells (CHO-K1) according to previous studies. In this study, the enhancement of UV-induced cell death by colcemid was related to its effect on DNA repair. The evidence for this correlation was obtained from the experimental results described below. First, an accumulation of DNA breaks was detected when colcemid was added to cells following UV-irradiation. The increase of DNA breaks was not formed in cells treated with colcemid alone, neither was the phenomenon a result of DNA fragmentation, a hallmark associated with the programmed cell death. Furthermore, the increase of DNA breaks is not cell-cycle dependent but depends on nucleotide excision repair. Second, colcemid inhibited the rejoining of DNA breaks accumulated by hydroxyurea and cytosine-β-D-arabinofuranoside following UV irradiation in a dose dependent manner. On the other hand, colcemid did not affect the excision of UV-induced DNA lesions. Thus, colcemid may inhibit the steps of gap-filling of nucleotide excision repair by a yet-unknown mechanism.
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