ArticleJournal of translational medicine2025
Paternal ribosome biogenesis dysfunction caused by cyclophosphamide-busulfan chemotherapy contributes to early embryonic developmental impairment in mice.
Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundCombined cyclophosphamide (CTX) and busulfan (BUS) chemotherapy, while effective against malignancies, poses significant risks to male reproductive health. This study systematically investigates the proteomic basis underlying CTX + BUS-induced paternal reproductive toxicity and its impact on early embryonic development in mice.
methodsWe utilized a mouse model of acute CTX + BUS exposure. Systemic germ cell apoptosis, sperm parameters (concentration, motility, morphology), and fertilization rates were assessed. Testicular and sperm proteomic profiling was performed. Embryonic developmental outcomes were evaluated following fertilization with sperm from treated males.
resultsAcute CTX + BUS exposure induced systemic germ cell apoptosis and profound sperm head teratozoospermia, despite preserved sperm concentration and motility. Proteomic profiling revealed testicular dysregulation of ribosome biogenesis, DNA replication, and cell cycle control, alongside sperm-specific depletion of ribosomal proteins. Sperm from CTX + BUS-treated mice exhibited a reduced fertilization rate and induced severe embryonic developmental defects. Molecularly, ribosomal insufficiency in sperm is linked to lower ribosomal protein levels in early embryos, potentially compromising the paternal role in translational activation.
conclusionsOur findings establish ribosome biogenesis defects as a novel pathway mediating paternal-derived embryotoxicity following CTX + BUS chemotherapy. They challenge the reliance on conventional semen parameters (motility, count) for fertility assessment, highlighting that significant molecular lesions in sperm can persist despite normal traditional metrics. These results advocate for incorporating protein biomarker analysis into clinical fertility risk stratification for cancer survivors. This work provides critical insights into the early embryonic consequences of chemotherapy and underscores the imperative to safeguard paternal genomic and epigenetic integrity in oncological care.
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