Abstract
Iron released from ferritin may trigger oxidative stress leading to progressive degeneration of brains from patients with neurodegenerative diseases. Previous studies have shown that oxidative damage of proteins and DNA was induced by catechol neurotoxin such as salsolinol (1-methyl-6,7-dihydroxy-1,2,3,4-tetrahydro-isoquinoline). In the present study, we have investigated oxidative damage of DNA induced by the reaction of salsolinol with ferritin. When DNA was incubated with ferritin and salsolinol, DNA strand breakage increased in a time-dependent manner. Hydroxyl radical scavengers, such as azide, mannitol and dimethyl sulfoxide, effectively inhibited the salsolinol/ferritin system-mediated DNA cleavage, whereas Cu,Zn-superoxide dismutase did not suppress DNA cleavage. Catalase significantly inhibited the salsolinol/ferritin system-mediated DNA cleavage. Iron specific chelator, deferoxamine, also inhibited DNA cleavage. Spectrophotometric study using a color reagent showed that the release of iron from salsolinol-treated ferritin was increased in a time dependent manner. These results suggest that DNA strand breakage is mediated in the reaction of salsolinol with ferritin via the generation of hydroxyl radicals by the Fenton-like reaction of free iron ions released from oxidatively damaged ferritin.
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