癌变·畸变·突变 ›› 2009, Vol. 21 ›› Issue (1): 50-053.doi: 10.3969/j.issn.1004-616x.2009.01.012

• 论著 • 上一篇    下一篇

吸烟引起人体氧化损伤的可能机制

宋 雁,张晓鹏,贾旭东,张文众,王 伟,崔文明,张 馨,李 宁   

  1. 中国疾病预防控制中心营养与食品安全所,北京 100021
  • 收稿日期:2008-05-29 修回日期:2008-09-09 出版日期:2009-01-30 发布日期:2009-01-30

Potential Mechanisms of Oxidative Damage Mechanisms by Smoking

SONG Yan, ZHANG Xiao-peng, JIA Xu-dong, ZHANG Wen-zhong, WANG Wei, CUI Wen-ming, ZHANG Xin, LI Ning   

  1. National Institute for Nutrition and Food Safety, Chinese Center for Disease Control and Prevention, Beijing 100021
  • Received:2008-05-29 Revised:2008-09-09 Online:2009-01-30 Published:2009-01-30

摘要: 背景与目的: 通过多项生物标志物研究吸烟对DNA氧化损伤、脂质过氧化和氧化防御机制的影响。 材料与方法: 选取年龄在18~25岁的男性吸烟志愿者60名和非吸烟者30名,分为吸烟组和非吸烟组。分别通过高效液相色谱-电化学检测法(HPLC-ECD)测定24 h尿样中8-羟基脱氧鸟苷(8-OHdG)水平;应用彗星实验测定外周血淋巴细胞DNA链的断裂情况;采用高效液相色谱-紫外线检测法(HPLC-UV)测定24 h尿样中丙二醛(MDA)、丙酮(ACON)和戊醛(PP)水平;采静脉血测定血浆超氧化物歧化酶(SOD)、谷胱苷肽过氧化氢酶(GPX)和过氧化氢酶含量。 结果: 吸烟组尿8-OHdG和外周血淋巴细胞DNA的断裂分别比非吸烟组高185%和97 %(P均<0.01),尿MDA、ACON和PP较非吸烟组显著增高(P均<0.01),SOD、GPX和过氧化氢酶分别较非吸烟组低15%,10%和9%(P≤0.01)。 结论: 吸烟可以引起机体的氧负荷,造成DNA氧化损伤、脂质过氧化和抗氧化酶的改变。

关键词: 吸烟, DNA损伤, 脂质过氧化, 抗氧化酶, 活性氧

Abstract: BACKGROUND AND AIM: To investigate the effects of oxidative stress induced by smoking by quantifying various biomarkers of oxidative DNA damage, lipid peroxidation and antioxidative defense mechanisms. MATERIALS AND METHODS: Sixty male smokers and thirty male nonsmokers aged 18-25 were recruited and divided into two groups.8-OHdG in 24 h urine was analysed by HPLC-ECD; peripheral lymphocyte DNA strand breaks by comet assay; MDA, ACON and PP in 24 h urine were analysed by HPLC-UV and plasma antioxidant enzymes were assessed. RESULTS: 8-OHdG and DNA strand breaks were significantly greater by 185% and 97%,respectively, in 60 smokers than in 30 nonsmokers. MDA, ACON and PP in urine were significantly higher than nonsmokers(P<0.01). Superoxide dismutase(SOD), glutathione peroxidase (GPX), and catalase were significantly lower by 15%,10%,and 9%, respectively, in smokers than nonsmokers(P≤0.01). CONCLUSION: Oxidative stress imposed by cigarette smoking had an impact upon certain pathways involved in DNA damage, lipid peroxidation and antioxidative defense system.

Key words: smoking, DNA damage, lipid peroxidation, antioxidative enzymes, reactive oxygen species