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Direct and delayed X-ray-induced DNA damage in male mouse germ cells.

TitoloDirect and delayed X-ray-induced DNA damage in male mouse germ cells.
Tipo di pubblicazioneArticolo su Rivista peer-reviewed
Anno di Pubblicazione2012
AutoriCordelli, Eugenia, Eleuteri Patrizia, Grollino Maria Giuseppa, Benassi Barbara, Blandino Giovanni, Bartoleschi Cecilia, Pardini Maria Chiara, Di Caprio Edoardo Vittorio, Spanò M., Pacchierotti Francesca, and Villani Paola
RivistaEnviron Mol Mutagen
Volume53
Issue6
Paginazione429-39
Data di pubblicazione2012 Jul
ISSN08936692
Parole chiaveAnimals, DNA damage, DNA repair, male, Mice, Mice, Inbred C57BL, Mutagenicity Tests, mutation, spermatogenesis, Spermatozoa, testis, X-Rays
Abstract

Sperm DNA integrity is essential for the accurate transmission of paternal genetic information. Various stages of spermatogenesis are characterized by large differences in radiosensitivity. Differentiating spermatogonia are susceptible to radiation-induced cell killing, but some of them can repair DNA damage and progress through differentiation. In this study, we applied the neutral comet assay, immunodetection of phosphorylated H2AX (γ-H2AX) and the Sperm Chromatin Structure Assay (SCSA) to detect DNA strand breaks in testicular cells and spermatozoa at different times following in vivo X-ray irradiation. Radiation produced DNA strand breaks in testicular cells that were repaired within the first few hours after exposure. Spermatozoa were resistant to the induction of DNA damage, but non-targeted DNA lesions were detected in spermatozoa derived from surviving irradiated spermatogonia. These lesions formed while round spermatids started to elongate within the testicular seminiferous tubules. The transcription of pro-apoptotic genes at this time was also enhanced, suggesting that an apoptotic-like process was involved in DNA break production. Our results suggest that proliferating spermatogonia retain a memory of the radiation insult that is recognized at a later developmental stage and activates a process leading to DNA fragmentation.

Note

cited By 10

URLhttps://www.scopus.com/inward/record.uri?eid=2-s2.0-84863780019&doi=10.1002%2fem.21703&partnerID=40&md5=8805a50fbb871ddc6b47e6b5ba6e0b82
DOI10.1002/em.21703
Alternate JournalEnviron. Mol. Mutagen.
Citation Key4908
PubMed ID22730201