ArticleInternational journal of molecular sciences2013
X-ray induced DNA damage and repair in germ cells of PARP1(-/-) male mice.
Article in International journal of molecular sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 14 citations in OpenAlex.
- Revealing DNA damage levels in rat testicular germ cells in vivo using an adapted version of the alkaline comet assay.Archives of toxicology · 2026Article
- Different responses of normal cells (red blood cells) and cancer cells (K562 and K562/Dox cells) to low-doseMolecular and clinical oncology · 2021Article
- Role of PARP1 regulation in radiation-induced rescue effect.Journal of radiation research · 2020Article
- Differential gene expression in mouse spermatogonial stem cells and embryonic stem cells.International journal of molecular medicine · 2016Article
- The Effects of Levofloxacin on Testis Tissue and Spermatogenesis in Rat.Cell journal · 2016Article
- DNA Double Strand Break Response and Limited Repair Capacity in Mouse Elongated Spermatids.International journal of molecular sciences · 2015Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Poly(ADP-ribose)polymerase-1 (PARP1) is a nuclear protein implicated in DNA repair, recombination, replication, and chromatin remodeling. The aim of this study was to evaluate possible differences between PARP1(-/-) and wild-type mice regarding induction and repair of DNA lesions in irradiated male germ cells. Comet assay was applied to detect DNA damage in testicular cells immediately, and two hours after 4 Gy X-ray irradiation. A similar level of spontaneous and radiation-induced DNA damage was observed in PARP1(-/-) and wild-type mice. Conversely, two hours after irradiation, a significant level of residual damage was observed in PARP1(-/-) cells only. This finding was particularly evident in round spermatids. To evaluate if PARP1 had also a role in the dynamics of H2AX phosphorylation in round spermatids, in which γ-H2AX foci had been shown to persist after completion of DNA repair, we carried out a parallel analysis of γ-H2AX foci at 0.5, 2, and 48 h after irradiation in wild-type and PARP1(-/-) mice. No evidence was obtained of an effect of PARP1 depletion on H2AX phosphorylation induction and removal. Our results suggest that, in round spermatids, under the tested experimental conditions, PARP1 has a role in radiation-induced DNA damage repair rather than in long-term chromatin modifications signaled by phosphorylated H2AX.
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