Effect of smoking cessation on oxidative DNA modification estimated by 8-oxo-7,8-dihydro-2'-deoxyguanosine excretion

Priemé, Helene; Loft, Steffen; Klarlund, Mette; Grønbæk, K.; Tønnesen, Philip; Poulsen, Henrik E.

doi:10.1093/carcin/19.2.347

Cited by 100 publications

(47 citation statements)

References 37 publications

(37 reference statements)

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“…Interestingly, treatment with oxidants has been shown to cause similar mutations in codons 248 -250 of p53 (Hussain et al, 1994). Prieme et al (1998) found a statistically significant effect of smoking cessation for 4 and 26 weeks on the urinary excretion rate of the DNA repair products between the control group and the smoking cessation group. The study gives direct evidence that smoking induces oxidative DNA modification.…”

Section: Cigarette Smokementioning

confidence: 79%

Biologic damage resulting from exposure to tobacco smoke and from radon: implication for preventive interventions

Alavanja

2002

Oncogene

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Section: Cigarette Smokementioning

confidence: 79%

Biologic damage resulting from exposure to tobacco smoke and from radon: implication for preventive interventions

Alavanja

2002

Oncogene

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“…Leanness may represent decreased biological functions against oxidative DNA stress induced by smoking and thus could be used as a marker of host susceptibility to smoking-related cancer. Because smoking cessation leads to a substantial decline of 8-OHdG levels (20), it is expected that lean smokers may have large health benefit from smoking cessation. It remains uncertain, however, whether leanness itself or factor related to leanness modulates the carcinogenic effect of smoking, and this point deserves further investigations, including a search for genetic profiles regarding metabolism of tobacco smoke or repair of DNA damage.…”

Section: Discussionmentioning

confidence: 99%

Leanness, Smoking, and Enhanced Oxidative DNA Damage

Mizoue

Kasai

Kubo

et al. 2006

Cancer Epidemiology, Biomarkers &Amp; Prevention

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An increased risk of some forms of cancer, including lung cancer, among lean individuals has been consistent; however, there is a paucity of biological evidence supporting this relation. Subjects analyzed were 177 healthy Japanese workers who participated in a lifestyle intervention study. The levels of urinary 8-hydroxydeoxyguanosine (8-OHdG), a marker of oxidative DNA damage, were measured using an automated high-pressure liquid chromatography and urinary creatinine levels were adjusted for before statistical analysis. A clear inverse association was found between body mass index (BMI) and 8-OHdG levels among smokers [Pearson correlation coefficient (r) = À0.48], and the association did not materially change after adjustment for potential confounding factors. In contrast, no apparent relation was observed between BMI and 8-OHdG levels among nonsmokers (r = À0.12), although lean nonsmokers had a slightly higher mean of 8-OHdG levels compared with nonlean nonsmokers. The interaction of smoking and BMI reached statistical significance (P = 0.04). Leanness may enhance oxidative DNA damage induced by smoking and thus serve as a marker of host susceptibility to smoking-related cancers. (Cancer Epidemiol Biomarkers Prev 2006;15(3):582 -5)

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“…The major consequence for cell biology of the increase in ROS content is to enhance oxidative damage of some biological molecules of crucial relevance for cellular functions, such as deoxyribonucleic acid (DNA), proteins and lipids, which leads to a deterioration or loss of their physicochemical properties and functions [3]. Increasing attention has been paid in the recognition of relevance that such an oxidative damage could play in tobacco-mediated diseases, since greater lipid peroxidation [4], DNA oxidation and DNA repair activity [5][6][7] have been demonstrated in smokers compared with nonsmokers [8].…”

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confidence: 99%

Reversible inhibition of mitochondrial complex IV activity in PBMC following acute smoking

Alonso¹,

Cardellach²,

Casademont³

et al. 2004

Eur Respir J

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Smoking causes a decrease of mitochondrial complex IV activity in chronic smokers. However, it is not known if this toxic effect is due to the acute effect of cigarette smoke itself or is a secondary phenomenon related to other smoking factors.The study assessed mitochondrial respiratory chain function in peripheral blood mononuclear cells of 15 healthy nonsmoker individuals before smoking (t0), immediately after smoking five cigarettes in 45 min (t1) and 24 h later (t2). Blood carboxyhaemoglobin (COHb) and carbon monoxide concentrations in exhaled air (COEA) were determined to ascertain smoke inhalation status.After acute smoking, COHb increased from 0.5¡0.3% to 3.3¡1.5%, and COEA from 2.9¡2.5 to 26.1¡9.9 ppm. Complex II and III enzyme activities did not change along the study. Complex IV activity showed a 23% inhibition at t1 but returned to initial (t0) levels at t2. A decay in oxygen consumption was observed after the correction for mitochondrial content. Lipid peroxidation of cell membranes remained unchanged.Short-time smoking causes an acute and reversible mitochondrial complex IV inhibition in human mononuclear cells. These results suggest that smoke itself is one of the causes for the decrease of complex IV activity observed in chronic smokers.

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Effect of smoking cessation on oxidative DNA modification estimated by 8-oxo-7,8-dihydro-2'-deoxyguanosine excretion

Abstract: Smoking cessation significantly reduces the urinary excretion rate of 8-oxodG, giving direct and controlled evidence that cigarette smoking causes an increased rate of oxidative DNA modification. This could represent a mechanism by which tobacco smoke is carcinogenic.

Cited by 100 publications

References 37 publications

Biologic damage resulting from exposure to tobacco smoke and from radon: implication for preventive interventions

Biologic damage resulting from exposure to tobacco smoke and from radon: implication for preventive interventions

Leanness, Smoking, and Enhanced Oxidative DNA Damage

Reversible inhibition of mitochondrial complex IV activity in PBMC following acute smoking

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