International Journal of Medical Laboratory
Shahid Sadoughi University of Medical Sciences
Mon, Dec 29, 2025
[Archive]
Reproductive Immunology Research Center, Shahid Sadoughi University of Medical Sciences, Yazd, Iran
Abstract: (42 Views)
Emerging evidence implicates DNA repair dysfunction as a central contributor to male infertility, driving spermatogenic failure, genomic instability, and compromised sperm function. During spermatogenesis, germ cells rely on coordinated activity of homologous recombination, non-homologous end joining, base excision repair, and mismatch repair pathways to maintain genomic integrity under oxidative and replicative stress. Disruption of these systems leads to defective meiotic recombination, aberrant chromatin remodeling, and increased sperm DNA fragmentation, manifesting as oligozoospermia, azoospermia, or reduced fertilization potential. Recent advances in molecular diagnostics, such as phosphorylated H2A histone family member X immunostaining, DNA fragmentation assays, comet and terminal deoxynucleotidyl transferase dUTP nick end labeling tests, and next-generation sequencing of DNA repair genes, offer mechanistically anchored biomarkers for patient stratification. Integration of DNA repair profiling with oxidative stress and chromatin packaging assessments enhances diagnostic resolution and supports personalized therapeutic strategies. Translating these molecular insights into clinical practice provides a novel framework for precision reproductive medicine, informing assisted reproductive technology selection, therapeutic targeting, and genetic counseling to improve outcomes in male infertility.
Keywords: Assisted reproductive technology, DNA repair pathways, Male infertility, Molecular diagnostics, Spermatogenesis
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