Alterations in histone acetylation following exposure to 60Co γ-rays and their relationship with chromosome damage in human lymphoblastoid cells

• Published in: Radiation and environmental biophysics Vol. 57; no. 3; pp. 215 - 222
• Main Authors: Tian, Xue-Lei, Lu, Xue, Feng, Jiang-Bin, Cai, Tian-Jing, Li, Shuang, Tian, Mei, Liu, Qing-Jie
• Format: Journal Article
• Language: English
• Published: Berlin/Heidelberg Springer Berlin Heidelberg 01.08.2018; Springer Nature B.V
• Subjects: Acetylation; Biological and Medical Physics; Biophysics; Carcinogenesis; Carcinogens; Chromatin; Chromosomes; Deoxyribonucleic acid; DNA; DNA damage; DNA repair; DNA structure; Ecosystems; Effects of Radiation/Radiation Protection; Environmental Physics; Enzymatic activity; Enzyme activity; Exposure; Histone deacetylase; Hydroxamic acid; Ionizing radiation; Lymphocytes; Monitoring/Environmental Analysis; Original Article; Physics; Physics and Astronomy; Radiation damage; Radiation effects; Repair; Structural damage; γ Radiation; Histone deacetylase inhibitor; Ionizing radiation; Histone acetylation; Chromosome damage; Suberoylanilide hydroxamic acid
• ISSN: 0301-634X; 1432-2099
• DOI: 10.1007/s00411-018-0742-9

Chromosome damage is related to DNA damage and erroneous repair. It can cause cell dysfunction and ultimately induce carcinogenesis. Histone acetylation is crucial for regulating chromatin structure and DNA damage repair. Ionizing radiation (IR) can alter histone acetylation. However, variations in histone acetylation in response to IR exposure and the relationship between histone acetylation and IR-induced chromosome damage remains unclear. Hence, this study investigated the variation in the total acetylation levels of H3 and H4 in human lymphocytes exposed to 0–2 Gy 60 Co γ-rays. Suberoylanilide hydroxamic acid (SAHA), a histone deacetylase (HDAC) inhibitor, was added to modify the histone acetylation state of irradiated cells. Then, the total acetylation level, enzyme activity, dicentric plus centric rings (dic + r) frequencies, and micronucleus (MN) frequencies of the treated cells were analyzed. Results indicated that the acetylation levels of H3 and H4 significantly decreased at 1 and 24 h, respectively, after radiation exposure. The acetylation levels of H3 and H4 in irradiated groups treated with SAHA were significantly higher than those in irradiated groups that were not treated with SAHA. SAHA treatment inhibited HDAC activity in cells exposed to 0–1 Gy 60 Co γ-rays. SAHA treatment significantly decreased dic + r/cell and MN/cell in cells exposed to 0.5 or 1.0 Gy 60 Co γ-rays relative to that in cells that did not receive SAHA treatment. In conclusion, histone acetylation is significantly affected by IR and is involved in chromosome damage induced by 60 Co γ-radiation.