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Influence of smoking on levels of urinary 8-iso Prostaglandin F2α

机译:吸烟对尿8-ISO前列腺素水平的影响

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摘要

Background: To evaluate the reduced-risk potential of alternative tobacco products, biomarkers that are involved in the biological pathways affected by cigarette smoking and smoking cessation are needed. Isoprostanes, a measure of oxidative stress, appear to be influenced by smoking and reversible upon smoking cessation and therefore could be a good biomarker. This review aims at quantifying the effect of smoking and smoking cessation on levels of urinary 8-iso prostaglandin F2α (8-epi-PGF2α), an isoprostane. Methods: PubMed and Scopus databases were searched for publications that reported 8-epi-PGF2α levels in smokers and nonsmokers as well as articles reporting the effect of smoking cessation on 8-epi-PGF2α levels. Results: Eighteen studies assessing 8-epi-PGF2α levels by smoking status were identified. Five of the papers reported the results as quantity excreted in 24-hour urine (μg/24 h), and 15 reported creatinine adjusted values. The meta-analyses show increased levels of 8-epi-PGF2α in current smokers compared with nonsmokers (mean difference = 0.16, 95% confidence interval [95%CI]: 0.14–0.19 μg/24 h with inconsistency statistic [I2] = 98%; mean difference = 172.38, 95%CI: 152.75–192.01 pg/mg creatinine with I2 = 89%, respectively). There were too few publications to perform a meta-analysis assessing the effects of smoking cessation on 8-epi-PGF2α levels. Conclusions: Due to the high heterogeneity among the studies included in these meta-analyses, it is difficult to generalize the results; however, our study indicates increased levels of 8-epi-PGF2α and therefore increased oxidative stress in smokers compared with nonsmokers. More studies are still needed to assess if 8-epi-PGF2α levels are reversible after cessation. Keywords: Oxidative stress, Prostaglandin, Smoking
机译:背景技术:为了评估替代烟草产品的减少风险潜力,需要参与受吸烟和吸烟的生物途径的生物标志物。异丙醇是一种氧化应激的量度,似乎受到吸烟和可逆时受到吸烟的影响,因此可能是一个很好的生物标志物。本综述旨在量化吸烟和吸烟停止对尿8-ISO前列腺素F2α(8-EPI-PGF2α),一种异前列烷的影响。方法:搜查了PubMed和Scopus数据库的出版物,报告了吸烟者和非吸烟者中的8-EPI-PGF2α水平以及报告吸烟对8-EPI-PGF2α水平影响的文章。结果:确定了通过吸烟状态评估8-EPI-PGF2α水平的十八研究。其中五篇论文报告了结果作为在24小时尿液中排出的量(μg/ 24h)和15个报告的肌酐调节值。 Meta-Analyzes显示出与非吸烟者中的8-EPI-PGF2α的水平增加(平均差异= 0.16,95%置信区间[95%CI]:0.14-0.19μg/ 24小时,不一致统计[I2] = 98 %;平均差异= 172.38,95%CI:152.75-192.01 pg / mg肌酐,分别为I2 = 89%)。出版物太少用于进行荟萃分析,评估吸烟对8-EPI-PGF2α水平的影响。结论:由于这些荟萃分析中的研究中的研究中的高异质性,难以概括结果;然而,我们的研究表明,8-EPI-PGF2α的水平增加,因此与非闻名者相比,吸烟者的氧化应激增加。仍需要更多的研究来评估在停止后8-EPI-PGF2α水平是否可逆。关键词:氧化应激,前列腺素,吸烟

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