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Oxidative and genotoxic damage after radio-iodine therapy of Graves' hyperthyroidism.

机译:放射性碘治疗格雷夫斯甲状腺功能亢进症后的氧化和遗传毒性损害。

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摘要

PURPOSE: To evaluate genetic damage and oxidative stress following a single therapeutic dose of 131I in Graves' disease patients monitored up to 180 days after treatment. MATERIALS AND METHODS: Genetic damage induction was estimated as the increase in micronuclei in peripheral lymphocytes of patients. As indicators of radiogenic oxidative stress, vitamin E and lipoperoxide levels were assessed in the plasma of patients, as well as the release of plasmic clastogenic factors measured by the induction of micronuclei in vitro in peripheral lymphocytes of a healthy donor. RESULTS: Vitamin E depletion lasted at least 3 days and the basal level was restored within 7 days. No statistically significant variations were observed in lipoperoxide plasma levels. A sharp increase of micronuclei in the peripheral lymphocytes of patients was correlated (p < 0.001) with the release of clastogenic factor in the plasma. The highest micronucleus value was negatively correlated (p < 0.03) with the lowest vitamin E level observed in each patient. CONCLUSIONS: Micronuclei induction was the direct consequence not only of the energy deposition of 131I on the genetic material, but also of oxidative stress, likely via the release of clastogenic factor.
机译:目的:评估在接受治疗后180天以监测的Graves病患者中单次131I治疗后的遗传损伤和氧化应激。材料与方法:遗传损伤诱导被估计为患者外周淋巴细胞中微核的增加。作为放射源氧化应激的指标,评估了患者血浆中的维生素E和脂过氧化物水平,以及通过体外诱导健康捐献者外周淋巴细胞中的微核测量了血浆裂解性因子的释放。结果:维生素E耗竭至少持续3天,基础水平在7天内恢复。脂过氧化物血浆水平未观察到统计学上的显着变化。患者外周淋巴细胞中微核的急剧增加与血浆中致死因子的释放相关(p <0.001)。在每位患者中观察到的最高微核值与最低的维生素E水平呈负相关(p <0.03)。结论:微核诱导不仅是131I在遗传物质上的能量沉积的直接结果,而且是氧化应激的直接结果,可能是通过释放致胶化因子引起的。

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