摘要
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.
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.
出处
《中国生物化学与分子生物学报》
CAS
CSCD
1999年第6期992-996,共5页
Chinese Journal of Biochemistry and Molecular Biology
基金
国家自然科学青年基金
关键词
NNK
BEP2D细胞
活性氧
DNA损伤
纳米硒
氧化损伤
Methylnitrosamino)-1-(3-pyridyl)-1-butanone(NNK),Human papillomavirus immortalized human bronchial epithelial cell line(BEP2D),Reactive oxygen species(ROS),8-Hydroxydeoxyguanosine(OH8dG),Nanoselenium(NS)