ArticlePloS one2014
Smoking cessation reverses DNA double-strand breaks in human mononuclear cells.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 48 citations in OpenAlex.
- Smoking Status and Survival in Patients With Early-Stage Primary Cutaneous Melanoma.JAMA network open · 2024Trial
- Polysialic acid is associated with immune activation in human peripheral blood nuclear cells.Glycobiology · 2026Article
- A Review of the Repair of DNA Double Strand Breaks in the Development of Oral Cancer.International journal of molecular sciences · 2024Review
- Mitochondrial DNA is a key driver in cigarette smoke extract-induced IL-6 expression.Hypertension research : official journal of the Japanese Society of Hypertension · 2024Article
- Adipose-derived mesenchymal stem cells cultured in serum-free medium attenuate acute contrast-induced nephropathy by exerting anti-apoptotic effects.Stem cell research & therapy · 2023Article
- A possible role for proinflammatory activation via cGAS-STING pathway in atherosclerosis induced by accumulation of DNA double-strand breaks.Scientific reports · 2023Article
- Effects of heated tobacco products and conventional cigarettes on dental implant wound healing: experimental research.Annals of medicine and surgery (2012) · 2023Article
- Cigarette smoke induces mitochondrial DNA damage and activates cGAS-STING pathway: application to a biomarker for atherosclerosis.Clinical science (London, England : 1979) · 2023Article
- Review
- Insight into the pulmonary molecular toxicity of heated tobacco products using human bronchial and alveolar mucosa models at air-liquid interface.Scientific reports · 2022Article
- Reactive Oxygen Species in the Adverse Outcome Pathway Framework: Toward Creation of Harmonized Consensus Key Events.Frontiers in toxicology · 2022Review
- Spoken and Unspoken Matters Regarding the Use of Opioids in Cancer.Journal of pain research · 2022Review
- Cytotoxic, genotoxic, and toxicogenomic effects of heated tobacco products and cigarette smoke in human primary keratinocytes.Tobacco induced diseases · 2022Article
- Vitamin-Containing Antioxidant Formulation Reduces Carcinogen-Induced DNA Damage through ATR/Chk1 Signaling in Bronchial Epithelial Cells In Vitro.Biomedicines · 2021Article
- CUL4 E3 ligase regulates the proliferation and apoptosis of lung squamous cell carcinoma and small cell lung carcinoma.Cancer biology & medicine · 2020Article
- Cigarette smoke exposure redirects Staphylococcus aureus to a virulence profile associated with persistent infection.Scientific reports · 2019Article
- Cigarette smoke activates the parthanatos pathway of cell death in human bronchial epithelial cells.Cell death discovery · 2019Article
- Genetic modifiers of radon-induced lung cancer risk: a genome-wide interaction study in former uranium miners.International archives of occupational and environmental health · 2018Article
- DNA damage in lymphocytes induced by cardiac CT and comparison with physical exposure parameters.European radiology · 2017Article
- Dysregulation of CUL4A and CUL4B Ubiquitin Ligases in Lung Cancer.The Journal of biological chemistry · 2017Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveCigarette smoking is a major risk factor for atherosclerotic cardiovascular disease, which is responsible for a significant proportion of smoking-related deaths. However, the precise mechanism whereby smoking induces this pathology has not been fully delineated. Based on observation of DNA double-strand breaks (DSBs), the most harmful type of DNA damage, in atherosclerotic lesions, we hypothesized that there is a direct association between smoking and DSBs. The goal of this study was to investigate whether smoking induces DSBs and smoking cessation reverses DSBs in vivo through examination of peripheral mononuclear cells (MNCs). APPROACH AND
resultsImmunoreactivity of oxidative modification of DNA and DSBs were increased in human atherosclerotic lesions but not in the adjacent normal area. DSBs in human MNCs isolated from the blood of volunteers can be detected as cytologically visible "foci" using an antibody against the phosphorylated form of the histone H2AX (γ-H2AX). Young healthy active smokers (n = 15) showed increased γ-H2AX foci number when compared with non-smokers (n = 12) (foci number/cell: median, 0.37/cell; interquartile range [IQR], 0.31-0.58 vs. 4.36/cell; IQR, 3.09-7.39, p<0.0001). Smoking cessation for 1 month reduced the γ-H2AX foci number (median, 4.44/cell; IQR, 4.36-5.24 to 0.28/cell; IQR, 0.12-0.53, p<0.05). A positive correlation was noted between γ-H2AX foci number and exhaled carbon monoxide levels (r = 0.75, p<0.01).
conclusionsSmoking induces DSBs in human MNCs in vivo, and importantly, smoking cessation for 1 month resulted in a decrease in DSBs to a level comparable to that seen in non-smokers. These data reinforce the notion that the cigarette smoking induces DSBs and highlight the importance of smoking cessation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.