ArticleInternational journal of cancer2015
Prenatal exposure of mice to the human liver carcinogen aflatoxin B1 reveals a critical window of susceptibility to genetic change.
Article in International journal of cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 33 citations in OpenAlex.
- Application of error-corrected sequencing technologies for in vivo regulatory mutagenicity assessment.Regulatory toxicology and pharmacology : RTP · 2026Review
- 5-Chloro-2'-deoxycytidine Induces a Distinctive High-Resolution Mutational Spectrum of Transition Mutations In Vivo.Chemical research in toxicology · 2024Article
- Aflatoxins Contamination in Feed Commodities: From Occurrence and Toxicity to Recent Advances in Analytical Methods and Detoxification.Microorganisms · 2023Review
- A Novel Multicellular Placental Barrier Model to Investigate the Effect of Maternal Aflatoxin BToxins · 2023Article
- Effects of Prenatal Exposure to Aflatoxin B1: A Review.Molecules (Basel, Switzerland) · 2021Review
- Aflatoxin exposure in pregnant women of mixed status of human immunodeficiency virus infection and rate of gestational weight gain: a Ugandan cohort study.Tropical medicine & international health : TM & IH · 2020Article
- Risk assessment of aflatoxins in food.EFSA journal. European Food Safety Authority · 2020Article
- Modulation ofChemical research in toxicology · 2020Article
- Article
- In utero Exposure to Genotoxicants Leading to Genetic Mosaicism: An Overlooked Window of Susceptibility in Genetic Toxicology Testing?Environmental and molecular mutagenesis · 2020Article
- Mechanisms underlying aflatoxin-associated mutagenesis - Implications in carcinogenesis.DNA repair · 2019Review
- Impact of DNA lesion repair, replication and formation on the mutational spectra of environmental carcinogens: Aflatoxin BDNA repair · 2018Review
- Aflatoxin-lysine adducts in blood serum of the Malawian rural population and aflatoxin contamination in foods (groundnuts, maize) in the corresponding areas.Mycotoxin research · 2018Article
- HAfTs are novel lncRNA transcripts from aflatoxin exposure.PloS one · 2018Article
- Editor's Highlight: Pregnancy Alters Aflatoxin B1 Metabolism and Increases DNA Damage in Mouse Liver.Toxicological sciences : an official journal of the Society of Toxicology · 2017Article
- Mutational spectra of aflatoxin BProceedings of the National Academy of Sciences of the United States of America · 2017Article
- Characterization of nitrogen mustard formamidopyrimidine adduct formation of bis(2-chloroethyl)ethylamine with calf thymus DNA and a human mammary cancer cell line.Chemical research in toxicology · 2015Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
It has become axiomatic that critical windows of susceptibility to genotoxins exist and that genetic damage in utero may be a trigger for later life cancers. Data supporting this critical window hypothesis are remarkably few. This study provides a quantitative bridge between DNA damage by the liver carcinogen aflatoxin B1 (AFB1 ) during prenatal development and the risk of later life genetic disease. AFB1 was given to pregnant C57BL/6J mice, carrying F1 gestation day 14 (GD14) embryos of the B6C3F1 genotype. Ultra-high performance liquid chromatography and mass spectrometry (UPLC-MS) using aflatoxin-(15) N5 -guanine adduct standards afforded measurement of the AFB1 -N(7) -Gua and AFB1 -FAPY adducts 6-hr post dosing in liver DNA of mothers and embryos. A parallel cohort gave birth and the livers of the F1 were analyzed for mutations in the gpt gene at 3 and 10 weeks of age. The data revealed mutational spectra dominated by G:C to T:A mutations in both the mother and offspring that are characteristic of AFB1 and distinct from background. It was shown that adducts in GD14 embryos were 20-fold more potent inducers of mutagenesis than adducts in parallel-dosed adults. This sensitivity enhancement correlated with Ki67 staining of the liver, reflecting the proliferative potential of the tissue. Taken together, these data provide insight into the relative genetic risks of prenatal and adult exposures to AFB1 . Early life exposure, especially during the embryonic period, is strikingly more mutagenic than treatment later in life. Moreover the data provide a baseline against which risk prevention strategies can be evaluated.
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