RT info:eu-repo/semantics/article
T1 Male exposure to bisphenol a impairs spermatogenesis and triggers histone hyperacetylation in zebrafish testes
A1 González Rojo, Silvia
A1 Lombó Alonso, Marta
A1 Fernández Díez, Cristina
A1 Herráez Ortega, María Paz
A2 Biologia Celular
K1 Biología
K1 Bisphenol A
K1 Histone acetylation
K1 DNA methylation
K1 Zebrafish testes
K1 Sperm transcripts
K1 GPER
K1 2407 Biología Celular
K1 3214 Toxicología
K1 2401.07 Embriología Animal
K1 2409.99 Otros (Epigenética)
AB [EN] Bisphenol A (BPA) is an endocrine disruptor whose ubiquitous presence in the environment has been related with impairment of male reproduction. BPA can cause both transcriptomic and epigenetic changes during spermatogenesis. To evaluate the potential effects of male exposure to BPA, adult zebrafish males were exposed during spermatogenesis to doses of 100 and 2000 μg/L, which were reported in contaminated water bodies and higher than those allowed for human consumption. Fertilization capacity and survival at hatching were analysed after mating with untreated females. Spermatogenic progress was analysed through a morphometrical study of testes and apoptosis was evaluated by TUNEL assay. Testicular gene expression was evaluated by RT-qPCR and epigenetics by using ELISA and immunocytochemistry. In vitro studies were performed to investigate the role of Gper. Chromatin fragmentation and the presence of transcripts were also evaluated in ejaculated sperm. Results on testes from males treated with the highest dose showed a significant decrease in spermatocytes, an increase in apoptosis, a downregulation of ccnb1 and sycp3, all of which point to an alteration of spermatogenesis and to meiotic arrest and an upregulation of gper1 and esrrga receptors. Additionally, BPA at 2000 μg/L caused missregulation of epigenetic remodelling enzymes transcripts in testes and promoted DNA hypermethylation and H3K27me3 demethylation. BPA also triggered an increase in histone acetyltransferase activity, which led to hyperacetylation of histones (H3K9ac, H3K14ac, H4K12ac). In vitro reversion of histone acetylation changes using a specific GPER antagonist, G-36, suggested this receptor as mediator of histone hyperacetylation. Males treated with the lower dose only showed an increase in some histone acetylation marks (H3K14ac, H4K12ac) but their progeny displayed very limited survival at hatching, revealing the deleterious effects of unbalanced paternal epigenetic information. Furthermore, the highest dose of BPA led to chromatin fragmentation, promoting direct reproductive effects, which are incompatible with embryo development
PB Elsevier
SN 0269-7491
LK https://hdl.handle.net/10612/18122
UL https://hdl.handle.net/10612/18122
NO González-Rojo, S., Lombó, M.,  Fernández-Díez, C., & Herráez, M. P. (2019). Male exposure to bisphenol a impairs spermatogenesis and triggers histone hyperacetylation in zebrafish testes. Environmental Pollution, 248, 368-379. https://doi.org/10.1016/J.ENVPOL.2019.01.127
DS BULERIA. Repositorio Institucional de la Universidad de León
RD 19-may-2024