Dani Vijayta, Dhawan Davinder
Department of Biophysics, Panjab University, Chandigarh-160014, India.
Hell J Nucl Med. 2006 Jan-Apr;9(1):22-6.
Iodine-131 ((131)I) irradiation is the first line treatment for Graves' disease and thyroid carcinoma. In such cases, (131)I gets accumulated in the thyroid, and is released in the form of radioiodinated triiodothyronine (T3) and tetraiodothronine (T4). Various reports describe changes in the blood picture after radioiodine treatment. Zinc, on the other hand, has been reported to maintain the integrity of red blood cells (RBC) under certain toxic conditions. The present study was conducted to evaluate the adverse effects of (131)I on the antioxidant defense system and morphology of RBC and also to assess the possible protection by zinc under irradiation by (131)I. Thirty two female Wistar rats were equally segregated into four main groups. Animals with Group I served as normal controls; Group II animals were administered a dose of 3.7 MBq of (131)I (carrier free) intraperitoneally, Group III rats were supplemented with zinc (227 mg/L drinking water) and Group IV rats were given a combined treatment of (131)I and zinc, in a similar way as in Group II and IV rats. After seven days of (131)I treatment, RBC lysate was prepared and its antioxidant status assessed. The activity of superoxide dismutase (SOD), reduced glutathione (GSH) and malondialdehyde (MDA) in the lysate of RBC was increased. On the contrary, the activity of catalase was found to be significantly decreased. The activity of glutathione reductase (GR) remained unchanged. Marked changes in the shape of RBC from normal discocytes to echinocytes, spherocytes, stomatocytes and acanthocytes were also observed in the blood of the rats treated with (131)I. Zinc supplementation to (131)I treated rats, significantly attenuated the adverse effects caused by (131)I on the levels of MDA, GSH, SOD and catalase. In conclusion, the study revealed significant oxidant/antioxidant changes in RBC following (131)I administration in rats, while zinc was shown to act as a radioprotector agent.
碘-131（¹³¹I）照射是格雷夫斯病和甲状腺癌的一线治疗方法。在这些情况下，¹³¹I会在甲状腺中蓄积，并以放射性碘化三碘甲状腺原氨酸（T3）和四碘甲状腺原氨酸（T4）的形式释放。各种报告描述了放射性碘治疗后血细胞图像的变化。另一方面，据报道锌在某些毒性条件下可维持红细胞（RBC）的完整性。本研究旨在评估¹³¹I对红细胞抗氧化防御系统和形态的不良影响，并评估锌在¹³¹I照射下可能提供的保护作用。32只雌性Wistar大鼠被平均分为四个主要组。第一组动物作为正常对照；第二组动物腹腔注射3.7 MBq的¹³¹I（无载体），第三组大鼠补充锌（227 mg/L饮用水），第四组大鼠以与第二组和第三组大鼠类似的方式接受¹³¹I和锌的联合治疗。¹³¹I治疗7天后，制备红细胞裂解物并评估其抗氧化状态。红细胞裂解物中超氧化物歧化酶（SOD）、还原型谷胱甘肽（GSH）和丙二醛（MDA）的活性增加。相反，过氧化氢酶的活性显著降低。谷胱甘肽还原酶（GR）的活性保持不变。在用¹³¹I治疗的大鼠血液中还观察到红细胞形状从正常的双凹圆盘状明显变为棘状红细胞、球形红细胞、口形红细胞和刺状红细胞。给¹³¹I治疗的大鼠补充锌可显著减轻¹³¹I对MDA、GSH、SOD和过氧化氢酶水平的不良影响。总之，该研究揭示了大鼠给予¹³¹I后红细胞中显著的氧化/抗氧化变化，而锌被证明可作为一种辐射防护剂。
