Skip Navigation
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Your Environment. Your Health.

Publication Detail

Title: Intergenerational response to the endocrine disruptor vinclozolin is influenced by maternal genotype and crossing scheme.

Authors: Pietryk, Edward W; Clement, Kiristin; Elnagheeb, Marwa; Kuster, Ryan; Kilpatrick, Kayla; Love, Michael I; Ideraabdullah, Folami Y

Published In Reprod Toxicol, (2018 06)

Abstract: In utero exposure to vinclozolin (VIN), an antiandrogenic fungicide, is linked to multigenerational phenotypic and epigenetic effects. Mechanisms remain unclear. We assessed the role of antiandrogenic activity and DNA sequence context by comparing effects of VIN vs. M2 (metabolite with greater antiandrogenic activity) and wild-type C57BL/6 (B6) mice vs. mice carrying mutations at the previously reported VIN-responsive H19/Igf2 locus. First generation offspring from VIN-treated 8nrCG mutant dams exhibited increased body weight and decreased sperm ICR methylation. Second generation pups sired by affected males exhibited decreased neonatal body weight but only when dam was unexposed. Offspring from M2 treatments, B6 dams, 8nrCG sires or additional mutant lines were not similarly affected. Therefore, pup response to VIN over two generations detected here was an 8nrCG-specific maternal effect, independent of antiandrogenic activity. These findings demonstrate that maternal effects and crossing scheme play a major role in multigenerational response to in utero exposures.

PubMed ID: 29535025 Exiting the NIEHS site

MeSH Terms: Animals; Body Weight/drug effects; Breeding; DNA Methylation; Endocrine Disruptors/toxicity*; Epigenesis, Genetic; Female; Fungicides, Industrial/toxicity*; Genotype; Male; Maternal-Fetal Exchange; Mice, Inbred C57BL; Mice, Mutant Strains; Oxazoles/toxicity*; Phenotype; Pregnancy; Prenatal Exposure Delayed Effects*; Sperm Count; Spermatozoa/drug effects

Back
to Top