ArticleToxicological sciences : an official journal of the Society of Toxicology2011
Cigarette smoke induces DNA damage and alters base-excision repair and tau levels in the brain of neonatal mice.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- Pooled it
- The Influence of DNA Repair Genes and Prenatal Tobacco Exposure on Risk of Childhood Acute Lymphoblastic Leukemia: A Gene-Environment Interaction Study.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2025Article
- World no-tobacco: effects of second-hand smoke (SHS) and vapors on the developing and adult brain.Frontiers in pharmacology · 2025Review
- Correlation analysis between smoke exposure and serum neurofilament light chain in adults: a cross-sectional study.BMC public health · 2024Article
- Cigarette smoke sustains immunosuppressive microenvironment inducing M2 macrophage polarization and viability in lung cancer settings.PloS one · 2024Article
- miR-153-3p via PIK3R1 Is Involved in Cigarette Smoke-Induced Neurotoxicity in the Brain.Toxics · 2023Article
- Neuropathological Examination of Mice Chronically Exposed to Secondhand Smoke.Military medicine · 2023Article
- Circular RNA circNIPBL promotes NNK-induced DNA damage in bronchial epithelial cells via the base excision repair pathway.Archives of toxicology · 2022Article
- Early-Life Environment Influence on Late-Onset Alzheimer's Disease.Frontiers in cell and developmental biology · 2022Review
- Smoking and Neuropsychiatric Disease-Associations and Underlying Mechanisms.International journal of molecular sciences · 2021Review
- Effects of Chronic Secondhand Smoke (SHS) Exposure on Cognitive Performance and Metabolic Pathways in the Hippocampus of Wild-Type and Human Tau Mice.Environmental health perspectives · 2021Article
- Fruit and vegetable consumption, cigarette smoke, and leukocyte mitochondrial DNA copy number.The American journal of clinical nutrition · 2019Article
- Release of MicroRNAs into Body Fluids from Ten Organs of Mice Exposed to Cigarette Smoke.Theranostics · 2018Article
- Current status of research and treatment for non-small cell lung cancer in never-smoking females.Cancer biology & therapy · 2017Review
- Prenatal and Early Postnatal Exposure to Cigarette Smoke Decreases BDNF/TrkB Signaling and Increases Abnormal Behaviors Later in Life.The international journal of neuropsychopharmacology · 2016Article
- Xenobiotic pulmonary exposure and systemic cardiovascular response via neurological links.American journal of physiology. Heart and circulatory physiology · 2015Review
- Article
- Article
- [Correlation between drinking behavior and polymorphisms of extracellular superoxide dismutase, aldehyde dehydrogenase 2 genes, and oral squamous cell carcinoma].Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2014Article
- Human AP endonuclease 1: a potential marker for the prediction of environmental carcinogenesis risk.Oxidative medicine and cellular longevity · 2014Review
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
The prenatal and perinatal periods of brain development are especially vulnerable to insults by environmental agents. Early life exposure to cigarette smoke (CS), which contains both genotoxicants and oxidants, is considered an important risk factor for both neurodevelopmental and neurodegenerative disorders. Yet, little is known regarding the underlying pathogenetic mechanisms. In the present study, neonatal Swiss ICR (CD-1) albino mice were exposed to various concentrations of CS for 4 weeks and the brain examined for lipid peroxides, DNA damage, base-excision repair (BER) enzymes, apoptosis, and levels of the microtubule protein tau. CS induced a dose-dependent increase in both malondialdehyde and various types of DNA damage, including single-strand breaks, double-strand breaks, and DNA-protein cross-links. However, the CS-induced DNA damage in the brain returned to basal levels 1 week after smoking cessation. CS also modulated the activity and distribution of the BER enzymes 8-oxoguanine-DNA-glycosylase (OGG1) and apyrimidinic/apurinic endonuclease (APE1) in several brain regions. Normal tau (i.e., three-repeat tau, 3R tau) and various pathological forms of tau were also measured in the brain of CS-exposed neonatal mice, but only 3R tau and tau phosphorylated at serine 199 were significantly elevated. The oxidative stress, genomic dysregulation, and alterations in tau metabolism caused by CS during a critical period of brain development could explain why CS is an important risk factor for both neurodevelopmental and neurodegenerative disorders appearing in later life.
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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.