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在年轻吸烟者中,体力劳动引起的氧化应激会加剧。

Physical work-induced oxidative stress is exacerbated in young cigarette smokers.

作者信息

Bloomer Richard J, Creasy Andrea K, Smith Webb A

机构信息

Department of Health and Sport Sciences, The University of Memphis, TN 38152, USA.

出版信息

Nicotine Tob Res. 2007 Feb;9(2):205-11. doi: 10.1080/14622200601078541.

Abstract

Both cigarette smoking and strenuous physical work are associated with increased oxidative stress, which is implicated in the pathogenesis of cardiovascular disease. No study to date has measured oxidative stress in response to graded exercise in cigarette smokers. We compared oxidative stress biomarkers before and after strenuous exercise (Bruce treadmill protocol) in 14 cigarette smokers and 15 nonsmokers of similar age (24+/-6 years) and fitness status. Plasma protein carbonyls (PC), malondialdehyde (MDA), and 8-hydroxydeoxyguanosine (8-OHdG) were measured pre- and postexercise. Smoking status (p<.01) and time (p<.01) effects were noted for PC with values higher for smokers than nonsmokers and increasing from pre- to postexercise (52% vs. 25%, respectively). The smoking statusxtime interaction for PC approached statistical significance (p=.07). The change in PC from pre- to postexercise was positively correlated with the number of cigarettes smoked per day (r=.5782, p=.03). A smoking statusxtime interaction was noted for MDA (p<.01), with values increasing 37% from pre- (0.6140+/-0.0708 micromol/L) to postexercise (0.8440+/-0.0687 micromol/L) for smokers and remaining relatively unchanged for nonsmokers (from 0.7664+/-0.0901 to 0.7419+/-0.0776 micromol/L). 8-OHdG was unaffected by smoking status (p=.43) or exercise (p=.40). These findings indicate that young cigarette smokers experience an exaggerated oxidative stress response to strenuous physical work, compared with nonsmokers of similar age. These results highlight yet another detrimental impact of cigarette smoking on human health. Future investigations should focus on older, more established smokers.

摘要

吸烟和高强度体力劳动均与氧化应激增加有关,而氧化应激与心血管疾病的发病机制有关。迄今为止,尚无研究测量吸烟者在分级运动后的氧化应激情况。我们比较了14名吸烟者和15名年龄相仿(24±6岁)且健康状况相似的非吸烟者在剧烈运动(布鲁斯跑步机方案)前后的氧化应激生物标志物。在运动前后测量血浆蛋白羰基(PC)、丙二醛(MDA)和8-羟基脱氧鸟苷(8-OHdG)。发现PC存在吸烟状态(p<0.01)和时间(p<0.01)效应,吸烟者的值高于非吸烟者,且从运动前到运动后增加(分别为52%和25%)。PC的吸烟状态×时间交互作用接近统计学意义(p = 0.07)。运动前后PC的变化与每日吸烟量呈正相关(r = 0.5782,p = 0.03)。MDA存在吸烟状态×时间交互作用(p<0.01),吸烟者的值从运动前(0.6140±0.0708微摩尔/升)到运动后(0.8440±0.0687微摩尔/升)增加37%,而非吸烟者相对保持不变(从0.7664±0.0901到0.7419±0.0776微摩尔/升)。8-OHdG不受吸烟状态(p = 0.43)或运动(p = 0.40)的影响。这些发现表明,与年龄相仿的非吸烟者相比,年轻吸烟者在剧烈体力劳动时会经历过度的氧化应激反应。这些结果凸显了吸烟对人类健康的又一有害影响。未来的研究应关注年龄较大、吸烟时间较长的吸烟者。

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