NNK诱发人支气管上皮细胞恶性转化及氧化损伤机理研究  

NNK INDUCED HUMAN BRONCHIAL EPITHELIAL CELL LINE NEOPLASTIC TRANSFORMATION AND ITS MECHANISM OF OXIDATIVE DAMAGE

作　　者：杨陟华[1,2] 朱茂祥[1,2] 龚诒芬 徐勇[1,2] 孙红琰 

机构地区：[1]军事医学科学院放射医学研究所 [2]美国印第安那大学医学院药理毒理研究室

出　　处：《癌变．畸变．突变》1999年第4期184-188,共5页Carcinogenesis,Teratogenesis & Mutagenesis

摘　　要：本文研究ＮＮＫ诱发人支气管上皮细胞（ＢＥＰ２Ｄ）恶性转化及其氧化损伤机理。结果表明，５００μｇ／ｍｌ的ＮＮＫ作用后的第５代细胞具有抗血清生长能力，第１５代细胞具有锚着独立生长特性，第２５代细胞具有裸鼠体内成瘤性，提示ＮＮＫ诱发ＢＥＰ２Ｄ细胞发生了恶性转化。ＮＮＫ作用后，ＢＥＰ２Ｄ细胞产生的过氧化氢（Ｈ２Ｏ２）、超氧阴离子（Ｏ÷２）和羟自由基（·ＯＨ），以及８－羟基脱氧鸟嘌呤（ＯＨ８ｄＧ）含量均显著增高，提示ＮＮＫ致ＢＥＰ２Ｄ细胞恶性转化过程中涉及到氧化损伤的机理。The HPV 16 immortalized human bronchial epithelial cell line (BEP2D) was used to study NNK induced cell transformation and its mechanism of oxidative damage. The 5th passage BEP2D cells treated with 500μg/ml NNK(NNK 500 cells) could grow in meduum containing fetal calf serum. The 15th passage NNK 500 cells increased significantly colony formation in soft agar. The 25th passage NK 500 cells had the ability to grow tumor in nude mice. The level of active oxygen species productions including hydrogen peroxides(H 2O 2), superoxide anions(O ÷ 2) and hydroxyl radicals(·OH), and the contents of 8 hydroxydeoxyguanosine(OH8dG) in NNK treated BEP2D cells, which maybe involved mechanism ofoxidative damage.

关 键 词：NNK BEP2D细胞 恶性转化 DNA加合物 肺癌 

分 类 号：R734.202[医药卫生—肿瘤]