Biomarkers of oxidative damage in cigarette smokers: Which biomarkers might reflect acute versus chronic oxidative stress?

doi:10.1016/j.freeradbiomed.2011.03.019

Free Radical Biology and Medicine

Volume 50, Issue 12, 15 June 2011, Pages 1787-1793

https://doi.org/10.1016/j.freeradbiomed.2011.03.019 Get rights and content

Abstract

Cigarette smoking predisposes to the development of multiple diseases involving oxidative damage. We measured a range of oxidative damage biomarkers to understand which differ between smokers and nonsmokers and if the levels of these biomarkers change further during the act of smoking itself. Despite overnight abstinence from smoking, smokers had higher levels of plasma total and esterified F₂-isoprostanes, hydroxyeicosatetraenoic acid products (HETEs), F₄-neuroprostanes, 7-ketocholesterol, and 24- and 27-hydroxycholesterol. Levels of urinary F₂-isoprostanes, HETEs, and 8-hydroxy-2′-deoxyguanosine were also increased compared with age-matched nonsmokers. Several biomarkers (plasma free F₂-isoprostanes, allantoin, and 7β-hydroxycholesterol and urinary F₂-isoprostane metabolites) were not elevated. The smokers were then asked to smoke a cigarette; this acute smoking elevated plasma and urinary F₂-isoprostanes, plasma allantoin, and certain cholesterol oxidation products compared to presmoking levels, but not plasma HETEs or urinary 8-hydroxy-2′-deoxyguanosine. Smokers showed differences in plasma fatty acid composition. Our findings confirm that certain oxidative damage biomarkers are elevated in smokers even after a period of abstinence from smoking, whereas these plus some others are elevated after acute smoking. Thus, different biomarkers do not measure identical aspects of oxidative stress.

Section snippets

Subject recruitment

Community-based subjects were recruited through advertisements and referrals. Smokers were defined as otherwise healthy individuals age 21 years and above who had smoked for at least 5 years before their study participation, and controls were age-matched individuals who had never smoked, nor were they exposed to cigarette smoke at work or at home. The mean ± SD age of smokers (n = 119) was 32 ± 11 years and of controls (n = 59) 31 ± 10 years. Information on demographic characteristics, body mass index, blood

Comparison of biomarkers between chronic smokers and controls

Plasma lipid and liver function parameters were comparable between smokers and controls except for plasma HDL, which was slightly lower in smokers (Table 1). Plasma and urinary nicotine and cotinine levels were significantly higher in smokers compared to controls, as expected (Table 1). We measured plasma levels of arachidonate, docosahexaenoate, and urate, which are precursors of oxidative damage (isoprostanes and allantoin) and other (e.g., HETEs) biomarkers. Plasma arachidonate levels were

Discussion

Cigarette tar contains stable semiquinone radicals that can reduce oxygen to superoxide and subsequently to hydrogen peroxide in biological fluids [2], [4], [6]. Moreover, cigarette tar also contains metal ions that can form hydroxyl radicals from hydrogen peroxide, and the gas phase of cigarette smoke contains numerous free radicals that can remain in the smoke for relatively long times [6].

In this study, we investigated the effects of cigarette smoke on a range of oxidative damage biomarkers.

Acknowledgments

We thank Dr. Ginger Milne and the Eicosanoid Core Laboratory, Vanderbilt University (Nashville, TN, USA), for providing the standards for F₄-neuroprostane measurements. We are grateful to the National Medical Research Council (Grant NMRC/1157/2008) for their generous support of this study.

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Citation Excerpt :
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To study differences in oxidative stress markers and antioxidants among patients with bipolar depression (BPD) and unipolar depression (UPD).
Data sources. Electronic MEDLINE/PubMed/Cochrane Library/Scopus/TripDatabase database search until 30/06/2021.
Study selection. Included were articles comparing antioxidant or oxidative stress markers between adults with BPD or UPD and healthy controls (HCs).
Data extraction. Two authors extracted data independently. Random effects meta-analysis, calculating standardized mean differences for results from ≥3 studies.
Oxidative stress markers reported in 40 studies −1 published repeatedly– (UPD, studies = 30 n = 3072; their HCs, n = 2856; BPD, studies = 11 n = 393; their HCs, n = 540; with 1 study reporting on both UPD and BPD) included thiobarbituric acid reactive substances (TBARS), antioxidant uric acid and antioxidant-enhancing enzymes superoxide dismutase (SOD), catalase (CAT) and glutathione-peroxidase (GPX).
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Both BPD and UPD may be associated with an impaired oxidative stress balance, with significantly higher uric acid levels vs. HCs in UPD than in BPD.
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Original ContributionBiomarkers of oxidative damage in cigarette smokers: Which biomarkers might reflect acute versus chronic oxidative stress?

Abstract

Section snippets

Subject recruitment

Comparison of biomarkers between chronic smokers and controls

Discussion

Acknowledgments

Prev. Med.

Atherosclerosis

Free Radic. Biol. Med.

FEBS Lett.

Biochem. Pharmacol.

J. Biol. Chem.

Free Radic. Biol. Med.

Free Radic. Biol. Med.

Free Radic. Biol. Med.

J. Chromatogr. B

Toxicology

Free Radic. Biol. Med.

Fatty Acids

J. Biol. Chem.

J. Chromatogr. B

Free Radic. Biol. Med.

Biochem. Biophys. Res. Commun.

J. Chromatogr. B

J. Chromatogr. B

Fatty Acids

J. Lipid Res.

J. Lipid Res.

Fatty Acids

Methods Enzymol.

Prog. Lipid Res.

Cigarette Smoke and Oxidative Stress

Evaluation of biomarkers of exposure and potential harm in smokers, former smokers and never smokers

Clin. Chem. Lab. Med.

The effects of tobacco smoke and nicotine on cognition and the brain

Neuropsychol. Rev.

Acute effects of cigarette smoke on inflammation and oxidative stress: a review

Thorax

Original Contribution
Biomarkers of oxidative damage in cigarette smokers: Which biomarkers might reflect acute versus chronic oxidative stress?