Estrogenic and androgenic endpoints responses to bisphenols and atrazine in fish primary hepatocytes
- 1Department of Anatomy, Animal Physiology and Biophysics, Faculty of Biology, University of Bucharest
- 2Zoology Section, Department of Biochemistry and Molecular Biology, Faculty of Biology, University of Bucharest
Abstract
Primary hepatocytes isolated from Oreochromis niloticus were cultured under different serum media supplementation to establish the least stressful culturing conditions. Host-derived serum provided the highest metabolic support and the lowest cytotoxicity, outperforming the commonly used fetal bovine serum. Some non-host sera were toxic at 10% concentration but tolerable or even beneficial at 5% concentration. Separately, the primary hepatocytes were exposed to endocrine-disrupting chemicals (EDCs) and in vitro vitellogenin levels were measured after exposure to effective concentrations identified through estrogen receptor molecular docking analysis. The analysis predicted the strongest affinity for estradiol, bisphenol A and bisphenol S, whereas atrazine and its metabolites showed much weaker binding. After 48 h of exposure, except for estradiol, all of the compounds tested did not significantly induce vitellogenin secretion. However, transcriptional activation of the estrogen receptor was observed for both bisphenols and estradiol, but not for atrazine and its metabolites. Further assays of testosterone conversion to 11-ketotestosterone under exposure to the tested EDCs revealed a major impairment in conversion in the presence of atrazine. As such, it is concluded that some EDCs may fail to activate the estrogen receptor and induce VTG in vitro while still exerting endocrine-disrupting effects through the impairment of testosterone conversion to its more potent metabolite.
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BibTeX
@article{pop2026estrogenic,
title = {{Estrogenic and androgenic endpoints responses to bisphenols and atrazine in fish primary hepatocytes}},
author = {Cristian-Emilian Pop and Nicolai Crăciun and Andrea-Cristina Staicu and Maria Mernea and Dan-Florin Mihăilescu},
journal = {Scientific Reports},
year = {2026},
month = jul,
doi = {10.1038/s41598-026-63527-7},
url = {https://doi.org/10.1038/s41598-026-63527-7},
note = {CC BY},
}
RIS
TY - JOUR
TI - Estrogenic and androgenic endpoints responses to bisphenols and atrazine in fish primary hepatocytes
AU - Cristian-Emilian Pop
AU - Nicolai Crăciun
AU - Andrea-Cristina Staicu
AU - Maria Mernea
AU - Dan-Florin Mihăilescu
PY - 2026
DA - 2026/07/01
JO - Scientific Reports
DO - 10.1038/s41598-026-63527-7
UR - https://doi.org/10.1038/s41598-026-63527-7
AB - Primary hepatocytes isolated from Oreochromis niloticus were cultured under different serum media supplementation to establish the least stressful culturing conditions. Host-derived serum provided the highest metabolic support and the lowest cytotoxicity, outperforming the commonly used fetal bovine serum. Some non-host sera were toxic at 10% concentration but tolerable or even beneficial at 5% concentration. Separately, the primary hepatocytes were exposed to endocrine-disrupting chemicals (EDCs) and in vitro vitellogenin levels were measured after exposure to effective concentrations identified through estrogen receptor molecular docking analysis. The analysis predicted the strongest affinity for estradiol, bisphenol A and bisphenol S, whereas atrazine and its metabolites showed much weaker binding. After 48 h of exposure, except for estradiol, all of the compounds tested did not significantly induce vitellogenin secretion. However, transcriptional activation of the estrogen receptor was observed for both bisphenols and estradiol, but not for atrazine and its metabolites. Further assays of testosterone conversion to 11-ketotestosterone under exposure to the tested EDCs revealed a major impairment in conversion in the presence of atrazine. As such, it is concluded that some EDCs may fail to activate the estrogen receptor and induce VTG in vitro while still exerting endocrine-disrupting effects through the impairment of testosterone conversion to its more potent metabolite.
SN - 2045-2322
ER -