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Reduction in oxidatively generated DNA damage following smoking cessation.

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TLDR
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.
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.

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Journal ArticleDOI

Smoking and increased Alzheimer's disease risk: A review of potential mechanisms

TL;DR: Cigarette smoking has been linked with both increased and decreased risk for Alzheimer's disease (AD), which is relevant for the US military because the prevalence of smoking in the military is approximately 11% higher than in civilians.
Journal ArticleDOI

Occurrence, Biological Consequences, and Human Health Relevance of Oxidative Stress-Induced DNA Damage

TL;DR: The continuing development and improvement of LC-MS/MS coupled with the stable isotope-dilution method for DNA adduct quantification will further promote research about the clinical implications and diagnostic applications of oxidatively induced DNAAdducts.
Journal ArticleDOI

Mononuclear leukocyte DNA damage and oxidative stress: the association with smoking of hand-rolled and filter-cigarettes.

TL;DR: It is indicated that smoking of hand-rolled cigarettes has stronger genotoxic and oxidative effects on the metabolism than smoking of manufactured filter-cigarettes, and it is proposed that these harmful effects could be attributed to the higher level of oxidants.
Journal ArticleDOI

The influence of active and passive smoking during pregnancy on umbilical cord blood levels of vitamins A and E and neonatal anthropometric indices

TL;DR: An inverse association between smoking behaviour during pregnancy and birth length was observed, with shortest length in active smokers followed by passive smoking mothers, and the observed increase in umbilical cord serum levels of vitamins A and E may subserve antioxidative processes in response to tobacco smoke-induced oxidative stress.
References
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Journal ArticleDOI

The Role of Oxidative Stress in Carcinogenesis

TL;DR: This review examines the evidence of cellular oxidants' involvement in the carcinogenesis process, and focuses on the mechanisms for production, cellular damage produced, and the role of signaling cascades by reactive oxygen species.
Journal ArticleDOI

Increase in circulating products of lipid peroxidation (F2-isoprostanes) in smokers. Smoking as a cause of oxidative damage.

TL;DR: The increased levels of F2-isoprostanes in the circulation of persons who smoke support the hypothesis that smoking can cause the oxidative modification of important biologic molecules in vivo.
Journal ArticleDOI

Cancer risk and oxidative DNA damage in man

TL;DR: Human studies support the experimentally based notion of oxidative DNA damage as an important mutagenic and apparently carcinogenic factor in carcinogenesis, but the proof of a causal relationship in humans is still lacking.
Journal ArticleDOI

Oxidative Stress and Oxidative Damage in Carcinogenesis

TL;DR: Evidence demonstrates an association between a number of single nucleotide polymorphisms in oxidative DNA repair genes and antioxidant genes with human cancer susceptibility and the resultant altered gene expression patterns evoked by ROS contribute to the carcinogenesis process.
Book

The Chemical Components of Tobacco and Tobacco Smoke

TL;DR: In this article, the authors proposed a mechanism for the generation of free radicals in tobacco smoke using Free Radicals in Mainstream Smoke (FRS) and Free Radules in Tobacco Smoke (FR).
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