Bleomycin cancer cells selectively

The DNA-damaging agent bleomycin arrests the cell cycle of Jurkat cells defective in the G1 checkpoint in the G2 phase, and microtubule-affecting colchicine arrests it in the M phase [40]. Boromycin showed no effect on the cell cycle status of Jurkat cells at least up to 340 nM but potentiated anti-tumor activity of bleomycin in SCID mice inoculated with Jurkat cells. These data suggest that boromycin disrupts the cell cycle at the G2 checkpoint of cancer cells selectively, leading to sensitization of cancer cells to anti-cancer reagents. 

The dimerization has a second-order rate constant of 200 50 M s at 25 C, which is lowered by a factor of 2 X 10 in the presence of DNA [21]. An apparent equilibrium binding constant of 8.4 X 10 was found for the Co(III)—O2—Co(III)/DNA adduct, with binding of one //-peroxo complex approximately every three base pairs [21]. Of interest is the fact that the variously colored Co complexes have the ability to nick DNA in the presence of light [42, 43], reminiscent of the reaction of simple Co(III) complexes (Section 1.3.1). As the Co-substituted bleomycin has been extensively investigated for tumour imaging and found to accumulate selectively in certain cancer cells, the possibility of selective attack by a later light-induced reaction is attractive. 

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