首页> 外文期刊>Mutation Research - Genetic Toxicology and Environmental Mutagenesis >Role of DNA methylation in the adaptive responses induced in a human B lymphoblast cell line by long-term low-dose exposures to gamma-rays and cadmium
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Role of DNA methylation in the adaptive responses induced in a human B lymphoblast cell line by long-term low-dose exposures to gamma-rays and cadmium

机译:DNA甲基化在长期低剂量暴露于伽玛射线和镉的人B淋巴母细胞系诱导的适应性反应中的作用

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摘要

The possible involvement of epigenetic factors in health risks due to exposures to environmental toxicants and ionizing radiation is poorly understood. We have tested the hypothesis that DNA methylation contributes to the adaptive response (AR) to ionizing radiation or Cd. Human B lymphoblast cells HMy2.CIR were irradiated (0.032 Gy gamma-rays) three times per week for 4 weeks or exposed to CdCb (0.005, 0.01, or 0.1 |jlM) for 3 months, and then challenged with a high dose ofCd (50 or 100 muM) or-gamma-rays (2Gy). Long-term low-dose radiation (LDR) or long-term low-dose Cd exposure induced AR against challenging doses of Cd and irradiation, respectively. When the primed cells were treated with 5-aza-2'-deoxycytidine (5-aza-dC), a DNA methyltransferase inhibitor, the ARs were eliminated. These results indicate that DNA methylation is involved in the induction of AR in HMy2.CIR cells.
机译:表观遗传因素可能由于暴露于环境毒物和电离辐射而导致健康风险,对此知之甚少。我们已经验证了DNA甲基化有助于电离辐射或Cd的适应性反应(AR)的假设。每周对人类B淋巴母细胞HMy2.CIR进行3次照射(0.032 Gyγ射线),持续4周,或将其暴露于CdCb(0.005、0.01或0.1 | jlM)3个月,然后用高剂量的Cd( 50或100μM)或伽马射线(2Gy)。长期低剂量辐射(LDR)或长期低剂量Cd暴露分别诱导挑战性的Cd和辐射剂量引起的AR。当用DNA甲基转移酶抑制剂5-氮杂-2'-脱氧胞苷(5-氮杂-dC)处理致敏细胞后,消除了AR。这些结果表明DNA甲基化参与了HMy2.CIR细胞中AR的诱导。

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