Background. Fractalkine is produced in seminal plasma in small amounts and correlates with sperm motility. Purpose. To investigate\nthe possible effect of low-level leucospermia on spermatozoa oxidative stress and sDNA fragmentation in patients with subclinical\nvaricocele and apparently normal seminogram, and also to study the role of spermatozoal fractalkine and its receptor (CX3CR1) gene\nexpression as a marker of spermatozoa inflammatory response. Methods. This study included 80 patients with subclinical varicocele\n(45 fertile and 35 infertile) and 45 age-matched fertile volunteers. In semen samples, fractalkine and CX3CR1 gene expression were\ninvestigated by qRT-PCR. Moreover, seminal plasma malondialdehyde (MDA) and total antioxidant capacity (TAC) were measured.\nResults. There are significant decrease in semen quality and significant increase in seminal leucocytes count in subclinical varicocele.\nOur results show a significant increase in MDA and TAC levels, DNA fragmentation, and expression levels of fractalkine and its\nreceptor (CX3CR1) in subclinical varicocele groups. Conclusion. Subclinical varicocele induces seminal and spermatozoal subclinical\ninflammatory response in the form of low-level leucospermia and increased mRNA expression of the fractalkine signaling pathway,\nleading to increased spermatozoal ROS production, oxidative stress, and DNA fragmentation. These could cooperate in the\npathogenesis of delayed fertility in males with subclinical varicocele.
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