Dracorhodin perchlorate inhibited proliferation of several tumor cell lines. The 
drug induced oligonucleosomal fragmentation of DNA in HeLa cells and increased 
caspase-3, -8, -9 activities followed by the degradation of caspase-3 
substrates, inhibitor of caspase-dependent DNase, and poly-(ADP-ribose) 
polymerase. It also increased caspase-1 activity and a caspase-1 inhibitor, 
Ac-YVAD-cmk, and a caspase-10 inhibitor z-AEVD-fmk, also reduced 
dracorhodin-perchlorate-induced HeLa cell death. Dracorhodin perchlorate 
decreased the expression of anti-apoptotic mitochondrial protein, Bcl-X(L), but 
not Bcl-2; and it increased the expression of pro-apoptotic protein, Bax. 
Dracorhodin perchlorate induced a sustained generation of reactive oxygen 
species (ROS) in HeLa cells; caspase-1 inhibitor, Ac-YVAD-cmk, and caspase-3 
inhibitor, z-DEVD-fmk, attenuated the generation of ROS. Taken together, our 
results indicate that dracorhodin perchlorate alters the intracellular redox 
status, changed the balance of Bcl-X(L) and Bax protein expression, and induces 
apoptosis through caspase pathways in HeLa cells.