ArticlePloS one2025
Busulfan damages spermatogenic function by inducing orchitis.
Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Article
- Inflammation-Driven Remodeling of the Blood-Testis Barrier: Roles of Junctional Complexes, Actin Dynamics, and Kinase Signaling.Biomedicines · 2026Review
- Immunological mechanisms and precision stratification in male infertility: from testicular immune privilege and danger signal amplification to seminal immune biomarkers and mechanism-tailored intervention.Frontiers in immunology · 2026Review
- Paternal ribosome biogenesis dysfunction caused by cyclophosphamide-busulfan chemotherapy contributes to early embryonic developmental impairment in mice.Journal of translational medicine · 2025Article
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In order to clarify injure mechanism of busulfan to spermatogenic function, we treated mice with busulfan, the testicular and epididymal weights and sperm concentration significantly decreased and the sperm malformation rate increased over time. Moreover, testicular interstitial cell infiltration, a smaller seminiferous tubule, and disorganized and shed spermatogenic cells were also observed by immunohistochemical, immunofluorescence detection after the busulfan treatment. Furthermore, the enzyme-linked absorbance assays showed serum interleukin (IL)-6, IL-1β, and tumor necrosis factor-apha levels (inflammatory factors) were significantly upregulated; blood-testis barrier (BTB)-related protein levels (e.g., N-Cadherin, occludin, and connexin 43) and vimentine gradually decreased. So we infer busulfan treatment induced orchitis, further disrupted the BTB and disrupted the spermatogenic microenvironment, then decreased vimentine and gradually damaged the cytoskeleton, which cause spermatogenic cells losing their supporting from sertoli cells, androgen regulation was also affected, which was detrimental to spermatogenesis. The study result will improve the efficiency and safety in spermatogonial stem cell transplant recipients.
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Registered trials
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