吸烟引起人体氧化损伤的可能机制

Potential Mechanisms of Oxidative Damage Mechanisms by Smoking

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24h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24h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。

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 nonstnokers（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.