Sadani G R, Nadkarni G D
Radiation Medicine Centre, Bhabha Atomic Research Centre, Tata Memorial Centre Annexe, Parel, Bombay, India.
Thyroid. 1997 Dec;7(6):937-41. doi: 10.1089/thy.1997.7.937.
Exposure to ionizing radiation causes radiolysis of water in tissues leading to generation of reactive oxygen species (ROS), which are known to affect the antioxidant defense systems and induce lipid peroxidation (LP). Use of radioactive iodine (131I) for diagnosis and therapy of thyroid disorders may also generate ROS in the thyroid. Early (24 and 48 hours) and late (18 days) effects of subablation doses of 131I (370/555/1110 kBq) on the antioxidant defense and LP in the thyroid tissues have been studied. LP was elevated in all 131I treated groups by 10% to 41%. Although there was no change in catalase (CAT), the superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities showed evidence of change from 48 hours onwards--SOD decreased by 32% to 56% and GPx increased by 15% to 43%. Nonprotein thiols (reduced glutathione, GSH) showed an elevation of 16% at 24 hours, but later declined by 15% by day 18 after 370 KBq of 131I. Thus, the increase in LP observed may be due to beta irradiation induced ROS by 131I. The parallel decrease in SOD could be due to inactivation by ROS. The increase in GPx may be a consequence of induction due to elevated LP and/or ROS, which may be inadequate to lower the LP. In spite of elevated LP, the thyroid function appears to be normal.
暴露于电离辐射会导致组织中的水发生辐射分解，从而产生活性氧（ROS），已知这些活性氧会影响抗氧化防御系统并诱导脂质过氧化（LP）。使用放射性碘（131I）诊断和治疗甲状腺疾病也可能在甲状腺中产生活性氧。研究了亚消融剂量的131I（370/555/1110 kBq）对甲状腺组织抗氧化防御和脂质过氧化的早期（24小时和48小时）及晚期（18天）影响。所有接受131I治疗的组中脂质过氧化均升高了10%至41%。尽管过氧化氢酶（CAT）没有变化，但超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GPx）的活性从48小时起显示出变化迹象——SOD下降了32%至56%，GPx升高了15%至43%。非蛋白硫醇（还原型谷胱甘肽，GSH）在24小时时升高了16%，但在370 KBq的131I照射后第18天下降了15%。因此，观察到的脂质过氧化增加可能是由于131I的β辐射诱导产生活性氧所致。SOD的平行下降可能是由于活性氧使其失活。GPx的增加可能是脂质过氧化和/或活性氧升高诱导的结果，这可能不足以降低脂质过氧化。尽管脂质过氧化升高，但甲状腺功能似乎正常。
