Oxidative Stress Is Associated with Telomere Interaction Impairment and Chromatin Condensation Defects in Spermatozoa of Infertile Males.

Benoit Berby,Véronique Sétif,Chistine Rondanino,Cynthia Bichara,Pierre Di Pizio,Fanny Jumeau,Louis Sibert,Aurélie Rives-Feraille,Nathalie Rives,Ludovic Dumont

doi:10.3390/antiox10040593

Benoit Berby, Véronique Sétif + Show 8 more

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https://doi.org/10.3390/antiox10040593

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Journal: Antioxidants	Publication Date: Apr 12, 2021
Citations: 22	License type: CC BY 4.0

Affiliation: University of Rouen, Normandie Université

Abstract

Telomere length can be influenced by reactive oxygen species (ROS) generated by lifestyle factors or environmental exposure. We sought to determine whether oxidative stress has an impact on sperm nuclear alterations, especially on chromatin organization and telomere interactions in the spermatozoa of infertile males. We performed an observational and prospective study including fifty-two males, allocated in the “case group” (30 infertile males presenting conventional semen parameter alterations) and the “control group” (22 males with normal conventional semen parameters). ROS detection was determined on spermatozoa using CellROX© probes. Sperm nuclear damage was assessed using quantitative fluorescence in situ hybridization (Q-FISH) for relative telomere length and telomere number, aniline blue staining for chromatin condensation, terminal deoxynucleotidyl transferase dUTP nick-end labeling for DNA fragmentation, and FISH for aneuploidy and 8-hydroxy-2′-deoxyguanosine immunostaining for oxidative DNA damages. Infertile males had significantly increased levels of cytoplasmic ROS and chromatin condensation defects as well as a higher mean number of telomere signals per spermatozoon in comparison with controls. In addition, the mean number of sperm telomere signals were positively correlated with the percentage of spermatozoa with chromatin condensation defect. In infertile males with conventional semen parameter alterations, oxidative stress is associated with telomere interaction impairment and chromatin condensation defects.

Highlights

Oxidative stress, defined as a perturbation of local or systemic redox regulation, may be responsible for male infertility [1]
A total of 52 individuals were included in the study, allocated in two groups: a control group of 22 males aged between 21 and 53 years and a case group of 30 infertile males aged between 23 to 45 years (Table 1)
Normozoospermic males with unexplained infertility did not differ significantly in any features compared to normozoospermic males who had previously conceived spontaneously (Supplementary Table S1)

Summary

Introduction

Oxidative stress, defined as a perturbation of local or systemic redox regulation, may be responsible for male infertility [1]. In the male urogenital tract, ROS originate mainly from leukocytes and immature abnormal spermatozoa, their production is triggered by various clinical conditions such as infection or inflammation, varicocele, cryptorchidism, testicular torsion, and toxic exposure [3,4]. Due to their extremely reduced cytoplasm, spermatozoa have low amounts of antioxidant agents, notably enzymatic ones and they use the high antioxidant capacity of seminal plasma [3,5]. ROS participate in the phosphorylation of membranous tyrosine, which allows capacitation and flagellar hyperactivation [7]

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