Copper ion-dependent oxy-radical mediated DNA damage from dihydroxy derivative of etoposide.
The dihydroxy etoposide, a metabolite of the clinically active anticancer drug, VP-16, induced extensive DNA damage in the presence of copper ions. While superoxide dismutase was without any effect on the DNA damage, catalase and inhibitors of free hydroxyl radicals inhibited the DNA degradation, indicating that hydroxyl radicals were responsible for this drug-Cu-dependent DNA damage.
Sinha
B K
BK
Biochemical Pharmacology Section, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.
Antholine
W M
WM
Kalyanaraman
B
B
Eliot
H M
HM
D000818:Animals; D002374:Catalase / Q000378:metabolism; D003300:Copper / Q000378:metabolism*; D004249:DNA Damage; D005047:Etoposide / Q000031:analogs & derivatives* / Q000494:pharmacology; D005609:Free Radicals; D006868:Hydrolysis; D006878:Hydroxides / Q000378:metabolism*; D017665:Hydroxyl Radical; D013482:Superoxide Dismutase / Q000378:metabolism
D005609:Free Radicals; D006878:Hydroxides; C051505:3',4'-dihydroxyetoposide; D017665:Hydroxyl Radical; D005047:Etoposide; D003300:Copper; D002374:Catalase; D013482:Superoxide Dismutase