{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T11:08:17Z","timestamp":1791112097302,"version":"4.1.0"},"reference-count":46,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2013,2,9]],"date-time":"2013-02-09T00:00:00Z","timestamp":1360368000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Environ and Mol Mutagen"],"published-print":{"date-parts":[[2013,4]]},"abstract":"<jats:p>Telomere integrity is important for chromosome stability. The main objective of our study was to investigate the relationship between telomere length modulation and mitotic chromosome segregation induced by ionizing radiation in human primary fibroblasts. We used X\u2010rays and low\u2010energy protons because of their ability to induce different telomeric responses. Samples irradiated with 4 Gy were fixed at different times up to 6 days from exposure and telomere length, anaphase abnormalities, and chromosome aberrations were analyzed. We observed that X\u2010rays induced telomere shortening in cells harvested at 96 hrs, whereas protons induced a significant increase in telomere length at short as well as at long harvesting times (24 and 96 hrs). Consistent with this, the analysis of anaphase bridges at 96 hrs showed a fourfold increase in X\u2010ray\u2010 compared with proton\u2010irradiated samples, suggesting a correlation between telomere length\/dysfunction and chromosome missegregation. In line with these findings, the frequency of dicentrics and rings decreased with time for protons whereas it remained stable after X\u2010rays irradiation. Telomeric FISH staining on anaphases revealed a higher percentage of bridges with telomere signals in X\u2010ray\u2010treated samples than that observed after proton irradiation, thus suggesting that the aberrations observed after X\u2010ray irradiation originated from telomere attrition and consequent chromosome end\u2010to\u2010end fusion. This study shows that, beside an expected \u201cearly\u201d chromosome instability induced shortly after irradiation, a delayed one occurs as a result of alterations in telomere metabolism and that this mechanism may play an important role in genomic stability. Environ. Mol. 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