| IAbstractl Objective Arsenic is a potent human carcinogen to which there is wor1dv~ide exposure through natural contamination of food and drinking water sources. But the molecular mechanism of caicinogenesis is not clear With human dem~l cell culttu~ and molecular biologic methods, we explored the change of dermal cell h~juiy induced by sodium arsenite. Methods Count cell number, M?17 reduction assay, transmission elecironmicmscope were performed. Results The growth of human keratinocytes(KC) and human dem-ial fibroblast(HDF1b) all showed three phases, sta~ant phase is vely short(<24h).Wtth different concentration of sodium ar~nite, the two cells were markedly st黱ulated(p <0.01) .The ha]f lethal doses were respectively 8 L?M and 20 1-i M. The low level dose group (0.8 ii M.. 1.614 M) improved the ii~lifemtkx1 of keratinocytes through MTh reduction assay, but the high level dose group (above 3.214 M )can inhibit the cell growth. When the human deimal fibmblast was exposed 1014 M sodium arsenite,there were remarkable pathological changes of LdtmsWmcture, such as Mitochondzia swelling~ polyiibosonie dropping from rough endoplasmic reticulum endc鏻asmic reticulum expending in human dermal fibroblast cells et al. As culture time prolonging, the cells coming to die. Conclusion The proliferation of dennal cell may pby a critical role in the development of arseniasis caused by arsenic; 1014 M sodium arsenite can induce injuiy of human demial fibmblast in culture. |
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