사람 유래의 MCF10A, Chang liver및 HaCaT 세포의 소핵형성 및 세포형질전환에 미치는 2,3,7,8-Tetrachlorodibenzo-p-dioxin의 영향

  • 엄미옥 (식품의약품안전청 국립독성연구원) ;
  • 박미영 (식품의약품안전청 국립독성연구원) ;
  • 김종원 (식품의약품안전청 생물의약품평가부) ;
  • 박미선 (식품의약품안전청 국립독성연구원) ;
  • 한의식 (식품의약품안전청 의약품평가부) ;
  • 오혜영 (식품의약품안전청 국립독성연구원) ;
  • 정해관 (식품의약품안전청 국립독성연구원)
  • Published : 2004.06.01

Abstract

Although 2,3,7,8-tetrachlorodibenzo-p-dioxin(TCDD) is a powerful carcinogen in several species, limited model system exist to study carcinogenicity of this compound at cellular level. To enhance our under-standing of carcinogenicity of TCDD at cellular level, we investigated micronucleus (MN) frequency as a index of genetic toxicity and whether TCDD can transform the human cells in culture. Normal human cell lines, skin keratinocyte HaCaT, Chang liver and breast MCF10A cells were used. TCDD did not affect the cell viability of the Chang liver, HaCaT and MCF10A cells. The frequency of micronucleus was increased after treatment of TCDD for 24hr in Chang liver and HaCaT cells, but not changed in MCF10A cells. And we observed putative transformed cells in Chang liver cells exposed to 1 $\mu$M TCDD for 2 weeks. The putative transformed cells were also observed in HaCaT cells with subsequent exposure to TCDD (0.1, 1, 10, 100 nM) for 2 weeks after initial exposure to MNNG, but not observed in MCF10A cells. Collectively, these results indicate that the ability of TCDD to induce micronuclei may be involved in cellular transformation of Chang liver and HaCaT cells. Our putative TCDD-transformed cells of Chang liver and HaCaT are expected to provide a clue to the elucidation of TCDD-induced transformation pathway.

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