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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2000.3
- 수록면
- 7 - 13 (7page)
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The mechanisms of benzene toxicity is not fully elucidated, although the metabolism of benzene is very well understood. In order to study the mechanism of benzene toxicity, we investigated DNA damage induced by benzene metabolite, 1,2,4-benzenetriol (BT) in HL-60 cells by alkaline comet assay. To investigate the
mechanism of cellular DNA damage induced by BT, the cells were treated with antioxidant such as vitamin C, SOD, catalase, and chelating agent such as deferoxamine (DFO), bathocuproinedisulfonic acid (BCDS). BT induced DNA damage in dose-dependent manner at concentration between 10 μM and 100 μM. The antioxidant vitamin C itself induced DNA damage at higher concentration. The DNA damage induced by BT in HL-60 cells was protected at low concentration of vitamin C whereas no protective effect was found at high concentration. Inhibitory effect of SOD on DNA damage by BT was observed and this suggested that BT produce superoxide anion (O₂
-) causing DNA damage. Catalase protected BT-induced DNA damage suggesting that BT produce H₂O₂ during autooxidation of BT. Both Fe(Ⅱ)-specific chelating agent, deferoxamine (DFO) and Cu(Ⅰ)-
specific chelating agent, bathocuproinedisulfonic acid (BCDS) inhibited BT-induced DNA damage. This suggested that DNA damage was caused by active species which was produced by the autooxidation of BT in the presence of Cu(Ⅱ) and Fe(Ⅲ). These findings suggest that reactive oxygen species play an important role in the
mechanism of toxicity induced by benzene metabolites.
mechanism of cellular DNA damage induced by BT, the cells were treated with antioxidant such as vitamin C, SOD, catalase, and chelating agent such as deferoxamine (DFO), bathocuproinedisulfonic acid (BCDS). BT induced DNA damage in dose-dependent manner at concentration between 10 μM and 100 μM. The antioxidant vitamin C itself induced DNA damage at higher concentration. The DNA damage induced by BT in HL-60 cells was protected at low concentration of vitamin C whereas no protective effect was found at high concentration. Inhibitory effect of SOD on DNA damage by BT was observed and this suggested that BT produce superoxide anion (O₂
-) causing DNA damage. Catalase protected BT-induced DNA damage suggesting that BT produce H₂O₂ during autooxidation of BT. Both Fe(Ⅱ)-specific chelating agent, deferoxamine (DFO) and Cu(Ⅰ)-
specific chelating agent, bathocuproinedisulfonic acid (BCDS) inhibited BT-induced DNA damage. This suggested that DNA damage was caused by active species which was produced by the autooxidation of BT in the presence of Cu(Ⅱ) and Fe(Ⅲ). These findings suggest that reactive oxygen species play an important role in the
mechanism of toxicity induced by benzene metabolites.
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