| Summary: | 碩士 === 國立中興大學 === 環境工程學系 === 90 === Oxidative DNA damage induced by quinoid metabolites of naphthalene, e.g., 1,2-naphthoquinone (1,2-NQ), 1,2-dihydroxynaphthalene (1,2-NCAT), was investigated in calf thymus DNA (ctDNA). Results indicated that in the presence of Cu(II) and NADPH, parallel increases in DNA strand breaks and abasic (AP) sites was detected in calf thymus DNA exposed to 1,2-NQ and 1,2-NCAT over the corresponding control. Further investigation indicated that the DNA damage induced by 1,2-NQ plus Cu(II) and NADPH was inhibited by the additions of catalase, copper(I)-specific chelator, hydroxyl radical scavenger and glutathione whereas superoxide dismutase did not prevent the induction of AP sites. These results suggest the involvement of Cu(I)、hydrogen peroxide and hydroxyl radical in the induction of oxidative DNA damage by 1,2-NQ. At high concentration ( 5 mM ), naphthalene quinoid alone may induce AP sites via epurination/ depyrimidination naphthalene quinone-DNA adducts. In contrast, of induced AP sites in.Further characterization of the AP sites confirmed that 1,2-NQ induced predominantly（70％）putrescine-excisable AP sites in ctDNA. In summary, quinononid derivatives of naphthalene may induce significant oxidative modifications in ctDNA via hydrogen abstract atome from deoxyribose, resulting in the parallel formation of AP sites and strand breaks.
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