Cellular senescence was involved in aging by irreversible loss of proliferative potential and growth arrest. It can be induced by several factors, such as telomere shortening below a crucial length, constitutive activation of oncogenes, tumor suppressor inactivation, mitochondrial oxidative stress and exposure to exogenous DNA damaging treatments including toxic agents and ionizing radiation.
In this report, we demonstrated that both X-rays and carbon ions could induce cellular senescence in a human uveal melanoma cell line, 92-1 cells. The results of senescence associated-β-galactosidase (SA-β-gal) positive cells showed that over 60% senescent cells were induced by 10 Gy of X-rays while the similar amount of senescent cells was induced by 3 Gy of carbon ions, implying the high relative biological effectiveness of heavy ions. Furthermore, we revealed that both telomere-DNA-damage and chromatin-DNA-damage are important for maintaining the senescence-associated growth arrest following exposure to ionizing radiation by immunofluorescence staining against the DNA damage response factor 53BP1, in conjunction with fluorescence in situ hybridization using a telomeric Cy3-conjugated peptide nucleic acid probe (immunoFISH). Although telomeres represent a very small fraction of the genome (around 0.02%), they play an important role in radiation-induced senescence. These findings not only enrich the knowledge of traditional radiobiology, but also provide useful reference data for the heavy ion therapy and the risk estimation of heavy ion radiation in space.