"Low Doses of Bisphenol S Affect Post-translational Modifications of Sp" by Hedvika Řimnáčová, Miriam Štiavnická et al.
 

Document Type

Article

Publication Date

2020

Keywords

Male reproduction, endocrine disruptor, low dose effect, bisphenol S, post-translational modification

Digital Object Identifier (DOI)

https://doi.org/10.21203/rs.2.22155/v1

Abstract

Background: Bisphenol S (BPS) is increasingly used as a replacement for bisphenol A in the manufacture of products containing polycarbonates and epoxy resins. However, further studies of BPS exposure are needed for the assessment of health risks to humans. In this study we assessed the potential harmfulness of low-dose BPS on reproduction in male mice.

Methods: To simulate human exposure under experimental conditions, 8-week-old outbred ICR male mice received 8 weeks of drinking water containing a broad range of BPS doses [0.001, 1.0, or 100 µg/kg body weight (bw)/day, BPS1-3] or vehicle control. Mice were sacrificed and testicular tissue taken for histological analysis and protein identification by nano-liquid chromatography/mass spectrometry (MS) and sperm collected for immunodetection of acetylated lysine and phosphorylated tyrosine followed by protein characterisation using matrix-assisted laser desorption ionisation time-of-flight MS (MALDI-TOF MS).

Results: The results indicate that compared to vehicle, 100 µg/kg/day exposure (BPS3) leads to 1) significant histopathology in testicular tissue; and, 2) higher levels of the histone protein γH2AX, a reliable marker of DNA damage. There were fewer mature spermatozoa in the germ layer in the experimental group treated with 1 µg/kg bw (BPS2). Finally, Western blot and MALDI-TOF MS studies showed significant alterations in the sperm acetylome and phosphorylome in mice treated with the lowest (BPS1) exposure (0.001 µg/kg/day).

Conclusions: In summary, this range of qualitative and quantitative findings in young male mice raise the possibility that relatively low doses of BPS may impair mammalian reproduction through epigenetic modifications of sperm proteins.

Rights Information

Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 License.

Citation / Publisher Attribution

Research Square, v. 4, art. rs.2.22155

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