Sperm of patients with severe asthenozoospermia show biochemical, molecular and genomic alterations

Abstract

The multifactorial pathological condition, that is, severe low sperm motility is a frequent cause of infertility. However, mechanisms underlying the development of this condition are not completely understood. Single abnormalities have been reported in sperm of patients with asthenozoospermia. In this study, we characterized, in 22 normozoospermic men and in 37 patients with asthenozoospermia, biochemical, molecular and genomic abnormalities that frequently occur in sperm of patients with asthenozoospermia. We evaluated a panel of sperm biomarkers that may affect the motility and fertilizing ability of sperm of patients with severe asthenozoospermia. Since reactive oxygen species (ROS) production is involved in the pathogenesis of such sperm abnormalities, we determined the association between ROS production and sperm abnormalities. High percentage of patients with severe asthenozoospermia showed increased basal and stimulated ROS production. Moreover, these patients showed increased mitochondrial DNA (mtDNA) copy number but decreased mtDNA integrity and they were associated with elevated ROS levels. Furthermore, mitochondrial membrane potential was also significantly decreased and again associated with high ROS production in these patients. However, the rate of nuclear DNA fragmentation was increased only in less than one-fifth of these patients. An important cohort of these patients showed multiple identical biochemical, molecular and genomic abnormalities, which are typical manifestations of oxidative stress. The most frequent association was found in patients with high ROS levels, increased mtDNA copy number and decreased integrity, and low MMP. A smaller cohort of the aforementioned patients also showed nDNA fragmentation. Therefore, patients with asthezoospermia likely present reduced fertilizing potential because of such composed abnormalities.

Effect of in vitro selenium supplementation on sperm quality in asthenoteratozoospermic men

“…To overcome of these imbalances, researches tried to improve in vitro supplementation with antioxidant activity or some necessary element that participated in procedure that lead to maintain spermatozoa in functional and healthy condition (Banihani, Sharma, Bayachou, Sabanegh, & Agarwal, ; Im Yun, Gong, Song, & Lee, ). Previous studies revealed that spermatozoa from asthenoteratozoospermic men have increased the rate of membrane lipid peroxidation and DNA fragmentation and decreased MMP than normal fertile men (Abad et al., ; Bonanno et al., ; Colagar et al., ). Our descriptive data were in agreement with these studies (Table ).…”

Reactive oxygen species impact on sperm DNA and its role in male infertility

“…Subsequent increased mitochondrial copy number may lead to hypospermatogenesis due to meiotic arrest during sperm development and/or a disorganised axonemal complex as evidenced by asthenozoospermia (Feng, Song, Zou, & Mao, ). Additionally, in patients with asthenozoospermia, spermatozoa show significant increase in mtDNA copy number when compared to that of controls (Bonanno et al., ). Normally, there is minimal contribution of paternal mtDNA to the genome of an embryo as it is quickly eliminated in early embryonic development (May‐Panloup et al., ; reviewed in Benkhalifa et al., ).…”

Effect of metabolic and antioxidant supplementation on sperm parameters in oligo-astheno-teratozoospermia, with and without varicocele: A double-blind placebo-controlled study

“…In particular, elevated ROS exposure leads to membrane damage, membrane instability and functional alterations causing cell death (Agarwal et al., ). Latest evidence demonstrates an association between high ROS levels and increased mitochondrial DNA (mtDNA) copy number with decreased mtDNA integrity (Bonanno et al., ). Oxidative stress (OS) occurs when there is an imbalance between oxidants and antioxidants (Agarwal, Hamada, & Esteves, ).…”