PUBLICATION
Genetic and epigenetic alterations induced by bisphenol A exposure during different periods of spermatogenesis: from spermatozoa to the progeny
- Authors
- Lombó, M., Fernández-Díez, C., González-Rojo, S., Herráez, M.P.
- ID
- ZDB-PUB-191204-18
- Date
- 2019
- Source
- Scientific Reports 9: 18029 (Journal)
- Registered Authors
- Keywords
- none
- MeSH Terms
-
- Acetylation/drug effects
- Animals
- Benzhydryl Compounds/toxicity*
- Chromatin/drug effects
- DNA Repair/drug effects
- Embryo, Nonmammalian
- Embryonic Development/drug effects*
- Endocrine Disruptors/toxicity*
- Epigenesis, Genetic/drug effects*
- Histones/metabolism
- Male
- Models, Animal
- Phenols/toxicity*
- Spermatogenesis/drug effects*
- Spermatozoa/drug effects
- Spermatozoa/metabolism
- Spermatozoa/pathology
- Time Factors
- Zebrafish
- PubMed
- 31792261 Full text @ Sci. Rep.
Citation
Lombó, M., Fernández-Díez, C., González-Rojo, S., Herráez, M.P. (2019) Genetic and epigenetic alterations induced by bisphenol A exposure during different periods of spermatogenesis: from spermatozoa to the progeny. Scientific Reports. 9:18029.
Abstract
Exposure to bisphenol A (BPA) has been related to male reproductive disorders. Since this endocrine disruptor also displays genotoxic and epigenotoxic effects, it likely alters the spermatogenesis, a process in which both hormones and chromatin remodeling play crucial roles. The hypothesis of this work is that BPA impairs early embryo development by modifying the spermatic genetic and epigenetic information. Zebrafish males were exposed to 100 and 2000 μg/L BPA during early spermatogenesis and during the whole process. Genotoxic and epigenotoxic effects on spermatozoa (comet assay and immunocytochemistry) as well as progeny development (mortality, DNA repairing activity, apoptosis and epigenetic profile) were evaluated. Exposure to 100 µg/L BPA during mitosis slightly increased sperm chromatin fragmentation, enhancing DNA repairing activity in embryos. The rest of treatments promoted high levels of sperm DNA damage, triggering apoptosis in early embryo and severely impairing survival. Regarding epigenetics, histone acetylation (H3K9Ac and H3K27Ac) was similarly enhanced in spermatozoa and embryos from males exposed to all the treatments. Therefore, BPA male exposure jeopardizes embryonic survival and development due to the transmission of a paternal damaged genome and of a hyper-acetylated histone profile, both alterations depending on the dose of the toxicant and the temporal window of exposure.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping