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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2005.12
- 수록면
- 97 - 103 (7page)
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The genotoxic effect of antimalarial drugs amodiaquine (AQ), mefloquine (MQ) and
halofantrine (HF) was investigated in rat liver cells using the alkaline comet assay. AQ, MQ and HF at concentrations between 0-1000 μmol/L significantly increased DNA strand breaks of rat liver cells dosedependently. The order of induction of strand breaks was AQ > MQ > HF. The rat liver cells exposed to AQ and HF (200 and 400 μmol/L) and treated with (Fpg) the bacterial DNA repair enzyme that recognizes oxidized purine showed greater DNA damage than those not treated with the enzyme, providing evidence that AQ and HF induced oxidation of purines. Such an effect was not observed when MQ was treated with the enzyme. Treatment of cells with catalase, an enzyme inactivating hydrogen peroxide, decreased significantly the extent of DNA damage induced by AQ, and HF but not the one induced by MQ. Similarly quercetin, an antioxidant flavonoid at 50 μmol/L attenuated the extent of the formation of DNA strand breaks by both AQ and HF. Quercetin, however, did not modify the effects of MQ. These results indicate the genotoxicity of AQ, MQ and HF in rat liver cells. In addition, the results suggest that reactive oxygen species may be involved in the formation of DNA lesions induced by AQ and HF and that, free radical scavengers may elicit protective effects against genotoxicity of these antimalarial drugs.
halofantrine (HF) was investigated in rat liver cells using the alkaline comet assay. AQ, MQ and HF at concentrations between 0-1000 μmol/L significantly increased DNA strand breaks of rat liver cells dosedependently. The order of induction of strand breaks was AQ > MQ > HF. The rat liver cells exposed to AQ and HF (200 and 400 μmol/L) and treated with (Fpg) the bacterial DNA repair enzyme that recognizes oxidized purine showed greater DNA damage than those not treated with the enzyme, providing evidence that AQ and HF induced oxidation of purines. Such an effect was not observed when MQ was treated with the enzyme. Treatment of cells with catalase, an enzyme inactivating hydrogen peroxide, decreased significantly the extent of DNA damage induced by AQ, and HF but not the one induced by MQ. Similarly quercetin, an antioxidant flavonoid at 50 μmol/L attenuated the extent of the formation of DNA strand breaks by both AQ and HF. Quercetin, however, did not modify the effects of MQ. These results indicate the genotoxicity of AQ, MQ and HF in rat liver cells. In addition, the results suggest that reactive oxygen species may be involved in the formation of DNA lesions induced by AQ and HF and that, free radical scavengers may elicit protective effects against genotoxicity of these antimalarial drugs.
목차
ABSTRACT
Abbreviations
Introduction
Materials and Methods
Results
Discussion
Acknowledgments
References
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UCI(KEPA) : I410-ECN-0101-2009-476-015284807