N-乙酰半胱氨酸对碳离子照射小鼠急性损伤的保护效应  

The protective effects of N-acetylcysteine on acute injury induced by ^(12)C^(6+) ions in mice

作　　者：刘阳[1,2] 张红[1,3] 张录卫[1,3] 赵卫平[1,2] 武振华[1,3] 

机构地区：[1]中国科学院近代物理研究所,兰州730000 [2]中国科学院研究生院,北京100049 [3]甘肃省重离子束辐射医学应用基础重点实验室,兰州730000

出　　处：《辐射研究与辐射工艺学报》2008年第6期367-370,共4页Journal of Radiation Research and Radiation Processing

基　　金：国家自然科学基金资助项目(1075151);甘肃省重大科技专项项目(O702NKDA045);兰州市科技攻关项目(07-2-07);中国科学院西部之光项目(O760160XB0)资助

摘　　要：探讨了N-乙酰半胱氨酸(N-acetylcysteine,NAC)对12C6+离子照射小鼠损伤的保护效应及可能的作用机制。预先给予昆明小鼠NAC(200mg/kg),后进行12C6+离子束4Gy的单次全身照射。照射后2h处死小鼠,取肝、肺组织,用化学法检测组织中超氧化物岐化酶(Superoxide dismutase,SOD)的活性,谷胱甘肽(Glutathione,GSH)含量及脂质过氧化产物丙二醛(Malondialdehyde,MDA)水平;用碱性单细胞凝胶电泳法检测DNA单链断裂;用流式细胞术检测组织细胞凋亡率。与照射对照组相比,提前给予NAC可极显著地减轻12C6+离子导致的肝、肺组织中DNA断裂(p<0.001)和细胞凋亡(p<0.001),并显著地提高组织中GSH的含量;NAC还明显地抑制了肺组织中碳离子辐照所致的MDA水平增高(p<0.01)并显著地诱导了组织中SOD活性的升高(p<0.01)。提示NAC可通过抵御组织内的氧化作用,合成、补充GSH的含量,阻止DNA链的断裂和细胞的凋亡,实现对碳离子辐照损伤的保护效应。The present study was designed to evaluate the effect and mechanism of N-acetylcysteine （NAC） against from acute injury of mice exposed to ^12C^6＋ ion beams. Pretreated with NAC （200mg/kg） Kun-Ming mice were exposed to whole-body irradiation of 4Gy and were killed at 2h after irradiation, and then their liver and lung tissues were quickly treated for further experiment. The Superoxide dismutase （SOD） activity, glutathione （GSH） content and malondialdehyde （MDA） level were measured by chemical method and DNA-single strand breaks were determined by single cell gel electrophoresis meanwhile the percentage of cell apoptosis were assayed by flow cytometry method. In comparison with the respective control, NAC pretreatment can significantly alleviate DNA-single strand breaks （p〈0.001）, cell apoptosis （p〈0.001） and obviously enhance GSH content in the liver and lung tissues. Moreover, NAC can prominently inhibit the increment of MDA level （p〈0.01） induced by ^12C^6＋ ion beams and can augment SOD activity （p〈0.01） in the lung.

关 键 词：N-乙酰半胱氨酸 ^12C^6+离子 小鼠 抗辐射损伤 

分 类 号：Q691[生物学—生物物理学] R818[医药卫生—放射医学]