Effect of diesel exhaust inhalation on antioxidant and oxidative stress responses in adults with metabolic syndrome.

Effect of diesel exhaust inhalation on antioxidant and oxidative stress responses in adults with metabolic syndrome.
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DOI:
10.3109/08958370902721424
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发表时间:
2009-11
影响因子:
2.1
通讯作者:
Kaufman JD
Kaufman JD
中科院分区:
医学4区
文献类型:
--
作者:
Allen J;Trenga CA;Peretz A;Sullivan JH;Carlsten CC;Kaufman JD

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与交通相关的空气污染与心血管疾病的发病率和死亡率有关。虽然生物机制还不是很清楚,但氧化应激可能是主要途径。亚群,如代谢综合征(MES)患者,可能面临与空气污染相关的不良影响的风险增加。我们的目的是评估接触柴油废气(DE)与全身抗氧化剂和氧化反应指标之间的关系。我们假设,与过滤空气(FA)相比,DE暴露会导致更大的氧化应激和抗氧化反应。在双盲交叉实验中,10名患有MES的成年受试者在不同的日期分别暴露于FA或DE(200μg/m~3)中2小时。分别在暴露后3小时和22小时测定尿8-异前列腺素F2α(F2-异前列腺素)和8-羟基-2‘-脱氧鸟苷(8-OHdG)作为氧化应激标志物。为了评估短期抗氧化反应,我们在暴露开始后90分钟分析了血浆抗坏血酸(AA)。所有结果都与暴露前的水平进行了比较,并比较了FA和DE暴露之间的平均变化。尿F2-异前列腺素(ng/mg肌酐)(-0.0 5[95%CI=−0.2 9,0.15])和8-OHdG(μg/g肌酐)(-0.0 9[-0.13,0.31])的平均变化无统计学意义。血浆AA(mg/dl)的平均变化也不显著(-0.02[-0.78,0.04])。在这项精心控制的实验中,我们没有检测到暴露于200μg/m3DE的MES受试者的氧化应激或系统抗氧化反应的显著变化。
Traffic-related air pollution is associated with cardiovascular morbidity and mortality. Although the biological mechanisms are not well understood, oxidative stress may be a primary pathway. Subpopulations, such as individuals with metabolic syndrome (MeS), may be at increased risk of adverse effects associated with air pollution. Our aim was to assess the relationship between exposure to diesel exhaust (DE) and indicators of systemic antioxidant and oxidative responses in adults with MeS. We hypothesized that DE exposure would result in greater oxidative stress and antioxidant responses compared with filtered air (FA). Ten adult subjects with MeS were exposed on separate days for two hours to FA or DE (at 200μg/m3), in a double blind, crossover experiment. Urinary 8-isoPGF2α (F2-isoprostanes), and 8-hydroxy-2′-deoxyguanosine (8-OHdG) were assessed as markers of oxidative stress at 3 hrs and 22 hrs, respectively, after exposure initiation. To assess the short-term antioxidant response we analyzed plasma ascorbic acid (AA) 90 minutes after exposure initiation. All outcomes were compared to pre-exposure levels, and mean changes were compared between FA and DE exposures. Mean changes in urinary F2-isoprostanes (ng/mg creatinine), (-0.05 [95% CI = −0.29, 0.15]), and 8-OHdG (μg/g creatinine) (-0.09 [-0.13, 0.31]), were not statistically significant. Mean changes in plasma AA (mg/dl) were also not significant (-0.02 [-0.78, 0.04]). In this carefully controlled experiment, we did not detect significant changes in oxidative stress or systemic antioxidant responses in subjects with MeS exposed to 200μg/m3 DE.
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