Jha J C, Maharjan B R, Adhikari D, Vishwanath P, Nagamma T, Azhari S, Singh P P
Department of Biochemistry, Manipal College of Medical Sciences, Pokhara, Nepal.
Kathmandu Univ Med J (KUMJ). 2007 Oct-Dec;5(4):511-7.
To assess the effect of cigarette smoking on lipid peroxidation induced oxidative stress, antioxidants, uric acid and blood sugar in normal subjects.
The study included 61 normal subjects with regular smoking habit and 57 never-smokers normal subjects matched in respect to socio-economic status, age and BMI. Information regarding smoking habit and other personal details were collected by oral questionnaire. Total antioxidant activity (TAA), reduced glutathione (GSH), alpha-tocopherol (alpha-T), ascorbic acid (AA), uric acid (UA), plasma and urinary thiobarbituric acid reactive substances (TBARS), fasting blood sugar (FBS) and urinary creatinine (Cr) were estimated by standard procedures in both the groups. Ferric Reducing Antioxidant Power (FRAP) procedure is used to estimate TAA which measures total dietary antioxidants. Statistical analysis was done with SPSS version 10.
The mean pack years smoked by smokers was 14.4 +/- 15.8. The plasma TBARS level in smokers and never-smokers was 2.6 +/- 0.8 and 2.5 +/- 0.6 micromol/L respectively. The respective figure for urinary TBARS level was 4.6 +/- 2.7 and 3.7 +/- 1.4 micromol/gmCr. Smokers did not show any significant difference from never-smokers with respect to GSH, alpha-T, AA, plasma TBARS and FBS. However, the smokers had significantly lower levels of TAA (p<0.05) and raised level of urinary TBARS (p<0.05) and uric acid (p<0.01) as compared to never-smokers.
Our study suggests that smoking induces mild lipid peroxidation but the body is able to compensate for it by removing its adducts. Importantly it also indicates enhanced oxidation of purines which are essential components of both DNA and RNA. Dietary antioxidants are consumed to scavenge free radicals (FR) and other reactive species (RS) in smoke. Female smokers are more prone to oxidative insult than male smokers. In summary RS present in smoke induce mild lipid peroxidation but are not the major contributors of redox imbalance in smoke induced toxicity in the selected subjects.
评估吸烟对正常受试者脂质过氧化诱导的氧化应激、抗氧化剂、尿酸和血糖的影响。
该研究纳入了61名有规律吸烟习惯的正常受试者和57名在社会经济地位、年龄和体重指数方面相匹配的从不吸烟者。通过口头问卷收集吸烟习惯和其他个人信息。两组均采用标准程序测定总抗氧化活性（TAA）、还原型谷胱甘肽（GSH）、α-生育酚（α-T）、抗坏血酸（AA）、尿酸（UA）、血浆和尿中硫代巴比妥酸反应性物质（TBARS）、空腹血糖（FBS）和尿肌酐（Cr）。采用铁还原抗氧化能力（FRAP）法测定TAA，该方法可测量总膳食抗氧化剂。使用SPSS 10版进行统计分析。
吸烟者的平均吸烟包年数为14.4±15.8。吸烟者和从不吸烟者的血浆TBARS水平分别为2.6±0.8和2.5±0.6微摩尔/升。尿TBARS水平的相应数值分别为4.6±2.7和3.7±1.4微摩尔/克肌酐。吸烟者在GSH、α-T、AA、血浆TBARS和FBS方面与从不吸烟者无显著差异。然而，与从不吸烟者相比，吸烟者的TAA水平显著降低（p<0.05），尿TBARS水平升高（p<0.05），尿酸水平升高（p<0.01）。
我们的研究表明，吸烟会诱导轻度脂质过氧化，但身体能够通过清除其加合物来进行补偿。重要的是，它还表明嘌呤的氧化增强，嘌呤是DNA和RNA的重要组成部分。膳食抗氧化剂被消耗以清除烟雾中的自由基（FR）和其他活性物质（RS）。女性吸烟者比男性吸烟者更容易受到氧化损伤。总之，烟雾中的RS会诱导轻度脂质过氧化，但不是所选受试者烟雾诱导毒性中氧化还原失衡的主要原因。
