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Reduction in oxidatively generated DNA damage following smoking cessation.

Box HC, O'Connor RJ, Patrzyc HB, Iijima H, Dawidzik JB, Freund HG, Budzinski EE, Cummings KM, Mahoney MC - Tob Induc Dis (2011)

Bottom Line: The current study sought to examine the extent to which three DNA lesions showed significant reductions after participants quit smoking.The d(TgpA) and d(PfpA) lesions show relatively greater rebound at Week 16 compared to the d(Gh) lesion (88% of baseline for d(TgpA), 64% of baseline for d(PfpA), vs 46% of baseline for d(Gh)).Future research may shed light on the broader array of oxidative damage influenced by smoking and over longer durations of abstinence, to provide further insights into mechanisms underlying carcinogenesis.

View Article: PubMed Central - HTML - PubMed

Affiliation: Roswell Park Cancer Institute, Elm and Carlton Streets, Buffalo, NY 14263, USA. richard.oconnor@roswellpark.org.

ABSTRACT

Background: Cigarette smoking is a known cause of cancer, and cancer may be in part due to effects of oxidative stress. However, whether smoking cessation reverses oxidatively induced DNA damage unclear. The current study sought to examine the extent to which three DNA lesions showed significant reductions after participants quit smoking.

Methods: Participants (n = 19) in this study were recruited from an ongoing 16-week smoking cessation clinical trial and provided blood samples from which leukocyte DNA was extracted and assessed for 3 DNA lesions (thymine glycol modification [d(TgpA)]; formamide breakdown of pyrimidine bases [d(TgpA)]; 8-oxo-7,8-dihydroguanine [d(Gh)]) via liquid chromatography tandem mass spectrometry (LC-MS/MS). Change in lesions over time was assessed using generalized estimating equations, controlling for gender, age, and treatment condition.

Results: Overall time effects for the d(TgpA) (χ2(3) = 8.068, p < 0.045), d(PfpA) (χ2(3) = 8.477, p < 0.037), and d(Gh) (χ2(3) = 37.599, p < 0.001) lesions were seen, indicating levels of each decreased significantly after CO-confirmed smoking cessation. The d(TgpA) and d(PfpA) lesions show relatively greater rebound at Week 16 compared to the d(Gh) lesion (88% of baseline for d(TgpA), 64% of baseline for d(PfpA), vs 46% of baseline for d(Gh)).

Conclusions: Overall, results from this analysis suggest that cigarette smoking contributes to oxidatively induced DNA damage, and that smoking cessation appears to reduce levels of specific damage markers between 30-50 percent in the short term. Future research may shed light on the broader array of oxidative damage influenced by smoking and over longer durations of abstinence, to provide further insights into mechanisms underlying carcinogenesis.

No MeSH data available.


Related in: MedlinePlus

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Figure 2: Study timeline.

Mentions: Participants (n = 19) in this study were recruited from an ongoing 16-week smoking cessation clinical trial using varenicline. Criteria for inclusion were smoking at least 15 cigarettes per day, general good health, and willingness to make a quit attempt. Persons were excluded if they currently used tobacco products other than cigarettes; were using smoking cessation drugs at time of enrollment (e.g., varenicline, bupropion, nicotine); had a serious medical or mental health condition in the past year; abused alcohol or other drugs; or were pregnant or planning to become pregnant. Eligible participants received either medication (varenicline) or a placebo as part of a double-blind cessation study. Both self-reported tobacco use and measured breath carbon monoxide (CO) levels were used to determine tobacco use status at each visit. Blood samples were obtained from volunteer donors at baseline (4 weeks prior to target quit ), on the target quit date (Study Week 0), 4 weeks following target quit date (Study Week 4), and 11 weeks after target quit date (Study Week 11). (see Figure 2) Participants received $25 remuneration for each blood sample provided. The study protocol was reviewed and approved by the Roswell Park Cancer Institute Institutional Review Board. All participants provided written informed consent, and provision of blood samples was an optional component of the clinical trial.


Reduction in oxidatively generated DNA damage following smoking cessation.

Box HC, O'Connor RJ, Patrzyc HB, Iijima H, Dawidzik JB, Freund HG, Budzinski EE, Cummings KM, Mahoney MC - Tob Induc Dis (2011)

Study timeline.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3104490&req=5

Figure 2: Study timeline.
Mentions: Participants (n = 19) in this study were recruited from an ongoing 16-week smoking cessation clinical trial using varenicline. Criteria for inclusion were smoking at least 15 cigarettes per day, general good health, and willingness to make a quit attempt. Persons were excluded if they currently used tobacco products other than cigarettes; were using smoking cessation drugs at time of enrollment (e.g., varenicline, bupropion, nicotine); had a serious medical or mental health condition in the past year; abused alcohol or other drugs; or were pregnant or planning to become pregnant. Eligible participants received either medication (varenicline) or a placebo as part of a double-blind cessation study. Both self-reported tobacco use and measured breath carbon monoxide (CO) levels were used to determine tobacco use status at each visit. Blood samples were obtained from volunteer donors at baseline (4 weeks prior to target quit ), on the target quit date (Study Week 0), 4 weeks following target quit date (Study Week 4), and 11 weeks after target quit date (Study Week 11). (see Figure 2) Participants received $25 remuneration for each blood sample provided. The study protocol was reviewed and approved by the Roswell Park Cancer Institute Institutional Review Board. All participants provided written informed consent, and provision of blood samples was an optional component of the clinical trial.

Bottom Line: The current study sought to examine the extent to which three DNA lesions showed significant reductions after participants quit smoking.The d(TgpA) and d(PfpA) lesions show relatively greater rebound at Week 16 compared to the d(Gh) lesion (88% of baseline for d(TgpA), 64% of baseline for d(PfpA), vs 46% of baseline for d(Gh)).Future research may shed light on the broader array of oxidative damage influenced by smoking and over longer durations of abstinence, to provide further insights into mechanisms underlying carcinogenesis.

View Article: PubMed Central - HTML - PubMed

Affiliation: Roswell Park Cancer Institute, Elm and Carlton Streets, Buffalo, NY 14263, USA. richard.oconnor@roswellpark.org.

ABSTRACT

Background: Cigarette smoking is a known cause of cancer, and cancer may be in part due to effects of oxidative stress. However, whether smoking cessation reverses oxidatively induced DNA damage unclear. The current study sought to examine the extent to which three DNA lesions showed significant reductions after participants quit smoking.

Methods: Participants (n = 19) in this study were recruited from an ongoing 16-week smoking cessation clinical trial and provided blood samples from which leukocyte DNA was extracted and assessed for 3 DNA lesions (thymine glycol modification [d(TgpA)]; formamide breakdown of pyrimidine bases [d(TgpA)]; 8-oxo-7,8-dihydroguanine [d(Gh)]) via liquid chromatography tandem mass spectrometry (LC-MS/MS). Change in lesions over time was assessed using generalized estimating equations, controlling for gender, age, and treatment condition.

Results: Overall time effects for the d(TgpA) (χ2(3) = 8.068, p < 0.045), d(PfpA) (χ2(3) = 8.477, p < 0.037), and d(Gh) (χ2(3) = 37.599, p < 0.001) lesions were seen, indicating levels of each decreased significantly after CO-confirmed smoking cessation. The d(TgpA) and d(PfpA) lesions show relatively greater rebound at Week 16 compared to the d(Gh) lesion (88% of baseline for d(TgpA), 64% of baseline for d(PfpA), vs 46% of baseline for d(Gh)).

Conclusions: Overall, results from this analysis suggest that cigarette smoking contributes to oxidatively induced DNA damage, and that smoking cessation appears to reduce levels of specific damage markers between 30-50 percent in the short term. Future research may shed light on the broader array of oxidative damage influenced by smoking and over longer durations of abstinence, to provide further insights into mechanisms underlying carcinogenesis.

No MeSH data available.


Related in: MedlinePlus