中国仓鼠肺成纤维细胞过氧化适应及其机理  

Adaptive Response of CHL to Hydrogen Peroxide Induced Oxidative Stress and the Mechanism

作　　者：薛丽君[1] 金中初[1] 

机构地区：[1]浙江医科大学病理生理学教研室

出　　处：《中华预防医学杂志》1998年第5期285-288,共4页Chinese Journal of Preventive Medicine

基　　金：国家自然科学基金

摘　　要：目的为研究真核细胞过氧化适应反应及其可能机理。方法在中国仓鼠肺成纤维细胞（ＣＨＬ）上，通过低剂量Ｈ２Ｏ２预处理，观察细胞和ＤＮＡ对高剂量Ｈ２Ｏ２再处理的适应反应，同时测定ＣＡＴ酶和ＰＡＲＰ的变化及其在适应ＤＮＡ断裂中的作用。结果在细胞活力和ＤＮＡ断裂水平上均观察到非致死性适应反应，然而这两种水平的适应模式（条件）有所不同，提示两者可能存在不同的诱导适应的途径。低剂量Ｈ２Ｏ２可诱导ＣＡＴ酶活性增高，并与抑制ＤＮＡ断裂的适应效应具有相关性（ｒ＝０．９５，Ｐ＜０．０５），同时ＰＡＲＰ阻断剂３氨基苯胺（３ＡＢ）可明显抑制ＤＮＡ断裂水平的适应反应。结论ＣＨＬ细胞系存在细胞活力变化和ＤＮＡ断裂的过氧化非致死性适应。Objective To study peroxidative adaptive response of eukaryocyte and its mechanisms. Methods Chinese hamster fibroblast cells (CHL) pretreated with low concentration of hydrogenperoxide(H 2O 2) were retreated by the following high concentration of H 2O 2. Cellular viability (MTT method) and DNA strand break (FADU method), as adaptive acting indicators were selected. Meanwhile, CAT activity and PARP were separately determined on the adaptive response to DNA strand break. Results There were peroxidative adaptive responses to non lethal damage of high concentration H 2O 2 in both cellular viability and DNA strand break levels; but adaptive models (conditions) between the two levels were different. The CAT activity induced by the low level of H 2O 2 was enhanced and related to peroxidative adaptation to DNA break. Furthermore, PARP blocker, 3 AB, markedly inhibited the adaptive response to DNA strand break. Conclusion Two models adaptation may be via different inducible adaptive pathways. CAT and PARP participated in the induction of peroxidative adaptation to DNA strand break.

关 键 词：过氧化氢 氧化性应激 肺 成纤维细胞 

分 类 号：R363[医药卫生—病理学]