Reduction in oxidatively generated DNA damage following smoking cessation
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 redu...
| Main Authors: | , , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
European Publishing
2011-05-01
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| Series: | Tobacco Induced Diseases |
| Subjects: | |
| Online Access: | http://www.journalssystem.com/tid/Reduction-in-oxidatively-generated-DNA-damage-following-smoking-cessation,65985,0,2.html |
| _version_ | 1818756256819576832 |
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| author | Harold C. Box Richard J. O'Connor Helen B. Patrzyc Herbert Iijima Jean B. Dawidzik Harold G. Freund Edwin E. Budzinski K Michael Cummings Martin C. Mahoney |
| author_facet | Harold C. Box Richard J. O'Connor Helen B. Patrzyc Herbert Iijima Jean B. Dawidzik Harold G. Freund Edwin E. Budzinski K Michael Cummings Martin C. Mahoney |
| author_sort | Harold C. Box |
| collection | DOAJ |
| description | 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(Tg
pA)]; formamide breakdown of pyrimidine bases [d(Tg
pA)]; 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(Tg
pA) (c2
(3) = 8.068, p < 0.045), d(Pf
pA) (c2
(3) = 8.477, p < 0.037), and d(Gh
)
(c2
(3) = 37.599, p < 0.001) lesions were seen, indicating levels of each decreased significantly after CO-confirmed
smoking cessation. The d(Tg
pA) and d(Pf
pA) lesions show relatively greater rebound at Week 16 compared to the d
(Gh
) lesion (88% of baseline for d(Tg
pA), 64% of baseline for d(Pf
pA), 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. |
| first_indexed | 2024-12-18T05:52:09Z |
| format | Article |
| id | doaj.art-bfad29e7df0d470f90b5e49e5929ae43 |
| institution | Directory Open Access Journal |
| issn | 1617-9625 |
| language | English |
| last_indexed | 2024-12-18T05:52:09Z |
| publishDate | 2011-05-01 |
| publisher | European Publishing |
| record_format | Article |
| series | Tobacco Induced Diseases |
| spelling | doaj.art-bfad29e7df0d470f90b5e49e5929ae432022-12-21T21:18:53ZengEuropean PublishingTobacco Induced Diseases1617-96252011-05-019May10.1186/1617-9625-9-565985Reduction in oxidatively generated DNA damage following smoking cessationHarold C. Box0Richard J. O'Connor1Helen B. Patrzyc2Herbert Iijima3Jean B. Dawidzik4Harold G. Freund5Edwin E. Budzinski6K Michael Cummings7Martin C. Mahoney8Roswell Park Cancer Institute, Elm and Carlton Streets, Buffalo, NY 14263, USARoswell Park Cancer Institute, Elm and Carlton Streets, Buffalo, NY 14263, USARoswell Park Cancer Institute, Elm and Carlton Streets, Buffalo, NY 14263, USARoswell Park Cancer Institute, Elm and Carlton Streets, Buffalo, NY 14263, USARoswell Park Cancer Institute, Elm and Carlton Streets, Buffalo, NY 14263, USARoswell Park Cancer Institute, Elm and Carlton Streets, Buffalo, NY 14263, USARoswell Park Cancer Institute, Elm and Carlton Streets, Buffalo, NY 14263, USARoswell Park Cancer Institute, Elm and Carlton Streets, Buffalo, NY 14263, USARoswell Park Cancer Institute, Elm and Carlton Streets, Buffalo, NY 14263, USABackground 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(Tg pA)]; formamide breakdown of pyrimidine bases [d(Tg pA)]; 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(Tg pA) (c2 (3) = 8.068, p < 0.045), d(Pf pA) (c2 (3) = 8.477, p < 0.037), and d(Gh ) (c2 (3) = 37.599, p < 0.001) lesions were seen, indicating levels of each decreased significantly after CO-confirmed smoking cessation. The d(Tg pA) and d(Pf pA) lesions show relatively greater rebound at Week 16 compared to the d (Gh ) lesion (88% of baseline for d(Tg pA), 64% of baseline for d(Pf pA), 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.http://www.journalssystem.com/tid/Reduction-in-oxidatively-generated-DNA-damage-following-smoking-cessation,65985,0,2.htmlsmoking cessationgeneralize estimate equationvareniclineliquid chromatography tandem mass spectrometrysecondhand smoke |
| spellingShingle | Harold C. Box Richard J. O'Connor Helen B. Patrzyc Herbert Iijima Jean B. Dawidzik Harold G. Freund Edwin E. Budzinski K Michael Cummings Martin C. Mahoney Reduction in oxidatively generated DNA damage following smoking cessation Tobacco Induced Diseases smoking cessation generalize estimate equation varenicline liquid chromatography tandem mass spectrometry secondhand smoke |
| title | Reduction in oxidatively generated DNA damage following smoking cessation |
| title_full | Reduction in oxidatively generated DNA damage following smoking cessation |
| title_fullStr | Reduction in oxidatively generated DNA damage following smoking cessation |
| title_full_unstemmed | Reduction in oxidatively generated DNA damage following smoking cessation |
| title_short | Reduction in oxidatively generated DNA damage following smoking cessation |
| title_sort | reduction in oxidatively generated dna damage following smoking cessation |
| topic | smoking cessation generalize estimate equation varenicline liquid chromatography tandem mass spectrometry secondhand smoke |
| url | http://www.journalssystem.com/tid/Reduction-in-oxidatively-generated-DNA-damage-following-smoking-cessation,65985,0,2.html |
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