Loss of Nuclear/DNA Integrity in Mouse Epididymal Spermatozoa after Short-Term Exposure to Low Doses of Dibutyl Phthalate or Bisphenol AF and Its Mitigation by Oral Antioxidant Supplementation

Author:

Hug Elisa1,Villeneuve Pauline1,Bravard Stephanie1,Chorfa Areski1,Damon-Soubeyrand Christelle1,Somkuti Stephen G.2,Moazamian Aron13ORCID,Aitken R. John4ORCID,Gharagozloo Parviz3,Drevet Joël R.1ORCID,Saez Fabrice1ORCID

Affiliation:

1. GReD Institute, CNRS UMR6293-Université Clermont Auvergne, Faculté de Médecine, CRBC, 28 Place Henri Dunant, 63001 Clermont-Ferrand, France

2. Sincera Reproductive Medicine, Fort Washington, PA 19034, USA

3. CellOxess LLC, Ewing, NJ 08540, USA

4. School of Environmental and Life Sciences, Priority Research Centre for Reproductive Sciences, The University of Newcastle, Callaghan, Newcastle 2308, Australia

Abstract

Routine exposure to chemicals omnipresent in the environment, particularly the so-called endocrine-disrupting chemicals (EDCs), has been associated with decreased sperm quality and increased anomalies in testis. The decline in semen quality and testicular abnormalities have been attributed to the disruption of endocrine signaling as well as oxidative stress. The present study set out to examine the effect of short-term exposure of two common EDCs widely used in the plastic industry: Dibutyl Phthalate (DBP) and Bisphenol AF (BPAF). Our research objective was to focus on the post-testicular compartment of the epididymis, where spermatozoa acquire their functional capacity and are stored. The data obtained indicated no significant effect for either chemicals on sperm viability, motility or acrosome integrity. Neither of the EDCs had a noticeable effect on the structures of the testis and epididymis. However, substantial impact on the integrity of the sperm nucleus and DNA structure was evidenced by a significant increase in nuclear decondensation and DNA base oxidation. The damage observed was postulated to arise from the pro-oxidant properties of the EDCs generating excess of reactive oxygen species (ROS) and triggering a state of oxidative stress. This hypothesis was confirmed when the observed damage was largely blocked by co-administering EDCs with an evidenced-based antioxidant formulation.

Funder

Regional Council FEDER/AURA

Publisher

MDPI AG

Subject

Cell Biology,Clinical Biochemistry,Molecular Biology,Biochemistry,Physiology

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