ArticleToxicological sciences : an official journal of the Society of Toxicology2011
Aflatoxin B1-DNA adduct formation and mutagenicity in livers of neonatal male and female B6C3F1 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. An erratum has been issued. Cited by 44 papers.
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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.
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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
44 citing papers in PubMed, 84 citations in OpenAlex.
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- Sex-Specific Renal Proteomic Responses to Mycotoxins and Their Mitigation by Bioactive Food Ingredients.Molecular nutrition & food research · 2026Article
- The Comet Assay in Human Biomonitoring.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Cancer and Environmental Xenobiotics: Mechanisms, Controversies, and Innovations.Journal of xenobiotics · 2025Review
- Mycotoxins in food and agriculture: from occurrence to economic consequences.Archives of microbiology · 2025Review
- Food contaminants: mechanisms of toxicity, computational assessment, and mitigation.Frontiers in toxicology · 2025Review
- Mass Spectrometry-Based Method to Measure Aflatoxin BChemical research in toxicology · 2024Article
- Frequencies and spectra of aflatoxin BNAR molecular medicine · 2024Article
- Tissue Organoid Cultures Metabolize Dietary Carcinogens Proficiently and Are Effective Models for DNA Adduct Formation.Chemical research in toxicology · 2024Article
- Intervention mechanism of marine-based chito-oligosaccharide on acute liver injury induced by AFBBioresources and bioprocessing · 2024Article
- Comparative metabolism of aflatoxin BArchives of toxicology · 2023Article
- AflatoxinBVeterinary medicine and science · 2023Review
- Article
- Recent Advances in Anticancer Activity of Novel Plant Extracts and Compounds from Curcuma longa in Hepatocellular Carcinoma.Journal of gastrointestinal cancer · 2023Review
- Effects of Prenatal Exposure to Aflatoxin B1: A Review.Molecules (Basel, Switzerland) · 2021Review
- Quantification of aflatoxin and ochratoxin contamination in animal milk using UHPLC-MS/SRM method: a small-scale study.Journal of food science and technology · 2021Article
- Review
- Risk Factors, Pathogenesis, and Strategies for Hepatocellular Carcinoma Prevention: Emphasis on Secondary Prevention and Its Translational Challenges.Journal of clinical medicine · 2020Review
- Risk assessment of aflatoxins in food.EFSA journal. European Food Safety Authority · 2020Article
- Modulation ofChemical research in toxicology · 2020Article
Corrections and comments
- Erratum issuedBouhenguel, Jason T [added]
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Exposure to genotoxic chemicals at a young age increases cancer incidence later in life. Aflatoxin B(1) (AFB(1)) is a potent genotoxin that induces hepatocellular carcinoma (HCC) in many animal species and in humans. Whereas adult mice are insensitive to aflatoxin-induced carcinogenesis, mice treated with AFB(1) shortly after birth develop a high incidence of HCC in adulthood. Furthermore, the incidence of HCC in adult male mice treated as infants is much greater than in females, reasons for which are unclear. In this study, treatment with AFB(1) produced similar levels of DNA damage and mutations in the liver of newborn male and female gpt delta B6C3F1 mice. Twenty-four hours after dosing with AFB(1) (6 mg/kg), the highly mutagenic AFB(1)-FAPY adduct was present at twice the level of AFB(1)-N(7)-guanine in liver DNA of males and females. A multiple dose regimen (3 × 2 mg/kg), while delivering the same total dose, resulted in lower AFB(1) adduct levels. Mutation frequencies in the gpt transgene in liver were increased by 20- to 30-fold. The most prominent mutations in AFB(1)-treated mice were G:C to T:A transversions and G:C to A:T transitions. At this 21-day time point, no significant differences were found in mutation frequency or types of mutations between males and females. These results show that infant male and female B6C3F1 mice experience similar amounts of DNA damage and mutation from AFB(1) that may initiate the neoplastic process. The gender difference in the subsequent development of HCC highlights the importance of elucidating additional factors that modulate HCC development.
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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.