Smoking-induced increasing of oxidative stress in Spanish adults: A urinary biomonitoring study.

IF 4.2 3区 环境科学与生态学 Q2 ENVIRONMENTAL SCIENCES
Borja Peris-Camarasa , Iván Claros Garrido , Olga Pardo , Francesc A. Esteve-Turrillas , Pablo Dualde , Clara Coscollà
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引用次数: 0

Abstract

Oxidative stress (OS) arises from an imbalance between excessive oxidant radicals and insufficient antioxidant defences, leading to damage to lipids, proteins or DNA. OS levels in humans are influenced by health, nutrition, and environmental exposures. A key biomarker of endogenous oxidative DNA damage is 8-hydroxy-2’-deoxyguanosine (8-OHdG). To assess baseline OS, we analysed 8-OHdG levels in first-morning urine samples from adults in the Valencia Community (Spain) using a UHPLC-MS/MS method based on a “dilute-and-shoot” sample preparation. Both 8-OHdG and the nucleoside 2’-dG were quantified in over 92 % of samples, with geometric means of 6.23 and 3.26 µg/L, respectively. Urinary 8-OHdG was directly associated with smoking status, and the levels of urinary metabolites of acrylamide. The oxidation ratio (8-OHdG/2’-dG) also showed correlations with sex and age. The results provide valuable reference data for future epidemiological and toxicological studies and highlight the oxidative stress effects of smoking.
西班牙成年人吸烟引起的氧化应激增加:一项尿液生物监测研究。
氧化应激(OS)源于过量的氧化自由基和不足的抗氧化防御之间的不平衡,导致脂质,蛋白质或DNA的损害。人体的OS水平受健康、营养和环境暴露的影响。内源性氧化DNA损伤的关键生物标志物是8-羟基-2 ' -脱氧鸟苷(8-OHdG)。为了评估基线OS,我们使用UHPLC-MS/MS方法分析了西班牙瓦伦西亚社区成年人早晨尿液样本中的8-OHdG水平,该方法基于“稀释-射击”样品制备。8-OHdG和核苷2′-dG在超过92% %的样品中均被定量,几何平均值分别为6.23和3.26 µg/L。尿中8-OHdG与吸烟状况和尿中丙烯酰胺代谢物的水平直接相关。氧化比(8-OHdG/2′-dG)也与性别和年龄相关。结果为今后的流行病学和毒理学研究提供了有价值的参考数据,并突出了吸烟的氧化应激效应。
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来源期刊
CiteScore
7.00
自引率
4.70%
发文量
185
审稿时长
34 days
期刊介绍: Environmental Toxicology and Pharmacology publishes the results of studies concerning toxic and pharmacological effects of (human and veterinary) drugs and of environmental contaminants in animals and man. Areas of special interest are: molecular mechanisms of toxicity, biotransformation and toxicokinetics (including toxicokinetic modelling), molecular, biochemical and physiological mechanisms explaining differences in sensitivity between species and individuals, the characterisation of pathophysiological models and mechanisms involved in the development of effects and the identification of biological markers that can be used to study exposure and effects in man and animals. In addition to full length papers, short communications, full-length reviews and mini-reviews, Environmental Toxicology and Pharmacology will publish in depth assessments of special problem areas. The latter publications may exceed the length of a full length paper three to fourfold. A basic requirement is that the assessments are made under the auspices of international groups of leading experts in the fields concerned. The information examined may either consist of data that were already published, or of new data that were obtained within the framework of collaborative research programmes. Provision is also made for the acceptance of minireviews on (classes of) compounds, toxicities or mechanisms, debating recent advances in rapidly developing fields that fall within the scope of the journal.
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