| Budget Amount *help |
¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Outline of Final Research Achievements |
Histone modifications like acetylation and phosphorylation were detected after exposure to several chemicals. The pattern was different according to classes of chemicals. 17-β-Estradiol (E2) induced remarkable acetylation of histone H3 (K9, K14 and global) and phosphorylation of histone H3 (S10). In the condition of the disruption of histone modifications, the sensitivity to ultraviolet (UV) increased. UVB-induced cell death was enhanced in E2-treated cells. This might be due to delay of DNA damage repair: the formation of cyclobutane pyrimidine dimers (CPD) did not change, whereas the repair of CPD was delayed in E2-treated cells. Furthermore, we could find some chemicals to induce similar histone acetylation and phosphorylation. These results suggested that the disruption of histone modifications by the chemicals might suppress the repair of DNA damage, indicating the contribution to cancer initiation and promotion in the case of coexposure to UV.
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