ArticleToxicological sciences : an official journal of the Society of Toxicology2014
Epigenetic events determine tissue-specific toxicity of inhalational exposure to the genotoxic chemical 1,3-butadiene in male C57BL/6J mice.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- Epigenetic alterations induced by genotoxic occupational and environmental human chemical carcinogens: A systematic literature review.Mutation research. Reviews in mutation researchPooled it
- Characterization of population variability of 1,3-butadiene derived protein adducts in humans and mice.Regulatory toxicology and pharmacology : RTP · 2022Article
- Commentary: Novel strategies and new tools to curtail the health effects of pesticides.Environmental health : a global access science source · 2021Article
- An Assessment on Ethanol-Blended Gasoline/Diesel Fuels on Cancer Risk and Mortality.International journal of environmental research and public health · 2021Review
- Population-Based Analysis of DNA Damage and Epigenetic Effects of 1,3-Butadiene in the Mouse.Chemical research in toxicology · 2019Article
- Sex-specific differences in genotoxic and epigenetic effects of 1,3-butadiene among mouse tissues.Archives of toxicology · 2019Article
- Effects of continuous bisphenol A exposure from early gestation on 90 day old rat testes function and sperm molecular profiles: A CLARITY-BPA consortium study.Toxicology and applied pharmacology · 2018Article
- Tissue- and strain-specific effects of a genotoxic carcinogen 1,3-butadiene on chromatin and transcription.Mammalian genome : official journal of the International Mammalian Genome Society · 2018Article
- Application of epigenetic data in human health risk assessment.Current opinion in toxicology · 2017Article
- Variation in DNA-Damage Responses to an Inhalational Carcinogen (1,3-Butadiene) in Relation to Strain-Specific Differences in Chromatin Accessibility and Gene Transcription Profiles in C57BL/6J and CAST/EiJ Mice.Environmental health perspectives · 2017Article
- From the Cover: Sperm Molecular Biomarkers Are Sensitive Indicators of Testicular Injury following Subchronic Model Toxicant Exposure.Toxicological sciences : an official journal of the Society of Toxicology · 2016Article
- Enhanced Antifungal Activity by Ab-Modified Amphotericin B-Loaded Nanoparticles Using a pH-Responsive Block Copolymer.Nanoscale research letters · 2015Article
- Environmental pollution and DNA methylation: carcinogenesis, clinical significance, and practical applications.Frontiers of medicine · 2015Review
- Response of transposable elements to environmental stressors.Mutation research. Reviews in mutation researchReview
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
1,3-Butadiene (BD), a widely used industrial chemical and a ubiquitous environmental pollutant, is a known human carcinogen. Although genotoxicity is an established mechanism of the tumorigenicity of BD, epigenetic effects have also been observed in livers of mice exposed to the chemical. To better characterize the diverse molecular mechanisms of BD tumorigenicity, we evaluated genotoxic and epigenotoxic effects of BD exposure in mouse tissues that are target (lung and liver) and non-target (kidney) for BD-induced tumors. We hypothesized that epigenetic alterations may explain, at least in part, the tissue-specific differences in BD tumorigenicity in mice. We evaluated the level of N-7-(2,3,4-trihydroxybut-1-yl)guanine adducts and 1,4-bis-(guan-7-yl)-2,3-butanediol crosslinks, DNA methylation, and histone modifications in male C57BL/6 mice exposed to filtered air or 425 ppm of BD by inhalation (6 h/day, 5 days/week) for 2 weeks. Although DNA damage was observed in all three tissues of BD-exposed mice, variation in epigenetic effects clearly existed between the kidneys, liver, and lungs. Epigenetic alterations indicative of genomic instability, including demethylation of repetitive DNA sequences and alterations in histone-lysine acetylation, were evident in the liver and lung tissues of BD-exposed mice. Changes in DNA methylation were insignificant in the kidneys of treated mice, whereas marks of condensed heterochromatin and transcriptional silencing (histone-lysine trimethylation) were increased. These modifications may represent a potential mechanistic explanation for the lack of tumorigenesis in the kidney. Our results indicate that differential tissue susceptibility to chemical-induced tumorigenesis may be attributed to tissue-specific epigenetic alterations.
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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.