Repair of Chromate induced DNA-Protein Crosslinks in Rat Lymphocyte

크롬에 의해 유발된 백서 임파구 DNA-Protein Crosslinks의 복구

  • Lee, Hun-Jae (Inha University Medical College, Department of Preventive Medicine) ;
  • Lee, Kwan-Hee (Inha University Medical College, Department of Preventive Medicine) ;
  • Hong, Yun-Chul (Inha University Medical College, Department of Preventive Medicine)
  • 이훈재 (인하대학교 의과대학 예방의학교실) ;
  • 이관희 (인하대학교 의과대학 예방의학교실) ;
  • 홍윤철 (인하대학교 의과대학 예방의학교실)
  • Published : 1996.09.01

Abstract

Genotoxic agents can induce various DNA lesions. DNA-Protein Crosslinks(DPCs) were known as the important DNA lesions which could impair gene expression because DPCs had a high probability of resisting repair and persisting through cell cycle. This repair resistance of DPCs could have biological significance but had not been evaluated clearly yet. Most of the studies that have evaluated the repair of DPCs only compared the extent of DPCs repair with other DNA lesions. We injected $K_2CrO_4$, a genotoxic agent, into Sprague-Dawley rats intraperitoneally(5mg/kg) and isolated blood lymphocytes 12 hours later. These lymphocytes were cultured in the mitogen added growth media and mitogen free media separately. The degree of the repair of DPCs was monitored for 4 days by the K-SDS assay. 4 days later, the amount of DPCs decreased by 4.6% in the mitogen added media high increased by 10.9% in the mitogen free media. These results showed that DPCs induced by $K_2CrO_4$ were not repaired easily and the DPCs were biologically significant DNA lesions. We thought the decrease of DPCs in the mitogen added media was not due to the repair of DPCs, but from the increase of normal cell proliferation. Therefore, it is very important to consider the proliferation of normal cells when estimating the repair of DPCs.

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