NNK诱发BEP2D细胞产生活性氧及其对DNA的损伤

通过测定细胞内和细胞上清中活性氧（ｒｅａｃｔｉｖｅ ｏｘｙｇｅｎ ｓｐｅｃｉｅｓ，ＲＯＳ）水平，以及ＤＮＡ 加合物——８－羟基脱氧鸟嘌呤核苷（８－ｈｙｄｒｏｘｙｄｅｏｘｙｇｕａｎｏｓｉｎｅ，ＯＨ８ｄＧ）含量，对烟草特异亚硝胺类化合物４－甲基亚硝胺－１（３－吡啶基）－１－丁酮（４－（ｍ ｅｔｈｙｌｎｉｔｒｏｓａｍ ｉｎｏ）－１－（３－ｐｙｒｉｄｙｌ）－１－ｂｕｔａｎｏｎｅ，ＮＮＫ）诱发人乳头状病毒永生化的人支气管上皮细胞（ｈｕｍ ａｎ ｐａｐｉｌｌｏｍ ａｖｉｒｕｓ－ｉｍ ｍ ｏｒｔａｌｉｚｅｄ ｈｕｍ ａｎｂｒｏｎｃｈｉａｌｅｐｉｔｈｅｌｉａｌｃｅｌｌｌｉｎｅ，ＢＥＰ２Ｄ）产生的ＲＯＳ及其对ＤＮＡ 的氧化损伤进行研究，并观察纳米硒的保护作用．结果表明，ＢＥＰ２Ｄ 细胞经不同浓度的ＮＮＫ 作用后，细胞内和细胞上清中ＲＯＳ以及ＯＨ８ｄＧ含量均显著增加，并有较好的剂量效应关系．１ μｍ ｏｌ·Ｌ－ １纳米硒（ｎａｎｏｓｅｌｅｎｕｉｍ ，ＮＳ）能明显抑制ＮＮＫ 诱发ＢＥＰ２Ｄ细胞产生的ＲＯＳ及ＯＨ８ｄＧ 水平．揭示ＮＮＫ 能造成细胞的氧化损伤，而ＮＳ对ＮＮＫ 所致细胞的氧化损伤有保护作用．

Reactive Oxygen Species Productions and Oxidative DNA Damage in BEP2D Cells Treated with NNK

The reactive oxygen species(ROS) productions and oxidative DNA damage in human papillomavirus immortalized human bronchial epithelial cell(BEP2D)induced by 4 (methylnitrosamino) 1 (3 pyridyl) 1 butanone(NNK)were studied through measuring extracellular and intracellular ROS levels including superoxide anions(O -· 2),hydrogen peroxides (H 2O 2)and /or hydroxyl radicals(·OH),and 8 hydroxydeoxyguanosine(OH8dG) contents.The results showed that the ROS productions and DNA adduct OH8dG contents in NNK treated BEP2D cells increased remarkably,and these increments could be inhibited effectively by 1 μmol·L -1 nanoselenium.It is suggested that NNK caused oxidative damage to BEP2D cells,which could be protected efficaciously by nanoselenium.