The present study was undertaken to determine whether sulforaphane-derived 
reactive oxygen species (ROS) might cause growth arrest and apoptosis in human 
bladder cancer 5637 cells. Our results show that the reduced viability of 5637 
cells by sulforaphane is due to mitotic arrest, but not the G2 phase. The 
sulforaphane-induced mitotic arrest correlated with an induction of cyclin B1 
and phosphorylation of Cdk1, as well as a concomitant increased complex between 
cyclin B1 and Cdk1. Sulforaphane-induced apoptosis was associated with the 
activation of caspase-8 and -9, the initiators caspases of the extrinsic and 
intrinsic apoptotic pathways, respectively, and activation of effector caspase-3 
and cleavage of poly (ADP-ribose) polymerase. However, blockage of caspase 
activation inhibited apoptosis and abrogated growth inhibition in 
sulforaphane-treated 5637 cells. This study further investigated the roles of 
ROS with respect to mitotic arrest and the apoptotic effect of sulforaphane, and 
the maximum level of ROS accumulation was observed 3h after sulforaphane 
treatment. However, a ROS scavenger, N-acetyl-L-cysteine, notably attenuated 
sulforaphane-mediated apoptosis as well as mitotic arrest. Overall, these 
results suggest that sulforaphane induces mitotic arrest and apoptosis of 5637 
cells via a ROS-dependent pathway.