CAJ | 학술논문

目的探索镉的免疫毒性机制，系统性地研究镉体外诱导小鼠胸腺细胞凋亡的发生，解释其细胞毒性机制。方法通过以下方法检测凋亡：末端脱氧核苷酸转移酶介导的dUTP缺口末端标记(TUNEL)，DNA含量／细胞周期分析，DNA琼脂糖凝胶电泳。结果镉能引起原代培养的胸腺细胞发生凋亡，并呈时间-反应和剂量-效应关系。结论本研究为阐述镉免疫毒性机制提供了依据，尤其对解释镉引起的胸腺萎缩和导致的T细胞介导的免疫力损伤有重要意义。
목적탐색력적면역독성궤제，계통성지연구력체외유도소서흉선세포조망적발생，해석기세포독성궤제。방법통과이하방법검측조망：말단탈양핵감산전이매개도적dUTP결구말단표기(TUNEL)，DNA함량／세포주기분석，DNA경지당응효전영。결과력능인기원대배양적흉선세포발생조망，병정시간-반응화제량-효응관계。결론본연구위천술력면역독성궤제제공료의거，우기대해석력인기적흉선위축화도치적T세포개도적면역력손상유중요의의。
Objective To elucidate the immunotoxical mechanism of cadmium (Cd) which is a common occupational and environmental contaminant, apoptical effect of Cd on mouse thymoytes was studied. Methods The Cd-induced thymocyte apoptosis was systematically determined by ①TdT-mediated dUTP nick end labeling (TUNEL) assay; ②DNA content/cell cycle analysis; ③DNA agarose gel electrophoresis. Results The results showed that Cd might cause time-and dose-dependent apoptosis in primary cultured thymocytes. Conclusion These findings would be of significance in the understanding of immunotoxic mechanism of Cd, especially the induction of thymus atrophy and T cell mediated immunity.