Bleomycins are antitumor antibiotics that can chelate a metal center and cause 
site-specific DNA cleavage at 5'-Gpyrimidine-3' regions of DNA. These 
antibiotics are successful in the treatment of various cancers, but are known to 
cause pulmonary fibrosis to patients under bleomycin regimes. Substantial 
research has resulted in the development of over 300 bleomycin analogs, aiming 
to improve the therapeutic index of the drug. Previous studies have proposed 
that the lung toxicity caused by bleomycin is related to the C-terminal regions 
of these drugs, which have been shown to closely interact with DNA in 
metal-bleomycin-DNA complexes. Some of the research studying 
metallo-bleomycin-DNA interactions have suggested three different binding modes 
of the metal form of the drug to DNA, including total and/or partial 
intercalation, and minor groove binding. However, there is still lack of 
consensus regarding this matter, and solid conclusions on the subject have not 
yet been established. Previously we investigated the diverse levels of 
disruption caused to DNA hairpins containing 5'-GC-3' and 5'-GT-3' binding 
sites, which are consequence of the binding of bleomycins with different 
C-termini. The results of these investigation indicate that both the DNA-binding 
site and the bleomycin C-termini have an impact on the final conformations of 
drug and target. The present study focuses on the structural alterations 
exhibited by Zn(II)bleomycin-A2, -B2, -A5 and Zn(II)peplomycin upon binding to 
DNA hairpins containing 5'-GC-3' and 5'-GT-3' binding sites. Evidence that each 
Zn(II)bleomycin is structurally affected depending on both its C-terminus and 
the DNA-binding site present in the hairpin is provided.