Protection by DMSO against Cell Death Caused by Intracellularly Localized Iodine-125, Iodine-131 and Polonium-210
Protection by DMSO against Cell Death Caused by Intracellularly Localized Iodine-125, Iodine-131 and Polonium-210
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DMSO 防止细胞内局部碘 125、碘 131 和钋 210 引起的细胞死亡
作者：
A. Bishayee;D. Rao;L. Bouchet;W. Bolch;R. W. Howell
摘要Bishayee，A.，拉奥，D.五、布谢湖G.，Bolch，W. E.和豪厄尔，R. W. DMSO对细胞内局部碘-125、碘-131和钋-210引起的细胞死亡的保护作用。通过检测二甲基亚砜（DMSO）对未结合氚（3 H2O）、DNA掺入的125 I-和131 I-碘脱氧尿苷（125 IdU，131 IdU）和胞质定位的210 Po柠檬酸盐引起的中国仓鼠V79细胞致死性损伤的保护能力，研究了DNA掺入的放射性核素对哺乳动物细胞造成致死性损伤的机制。放射性核素3 H和131 I分别发射低能量和中等能量的β粒子，125 I是一种多产的俄歇电子发射体，210 Po发射5.3 MeV的α粒子。将细胞放射性标记并在不同浓度的DMSO（5- 12.5%v/v）存在下在10.5°C下维持72小时，并测定与未标记对照相比的存活分数。DMSO对210 Po发射的高LET α粒子的致死效应没有保护作用。对未结合的~ 3 H、~（131）IdU和~（125）IdU引起的致死性损伤的保护作用依赖于培养基中DMSO的浓度。在所有情况下，10%的DMSO提供了最大的保护。在10% DMSO条件下，3 H2O、131 IdU、125 IdU和210 Po柠檬酸盐的剂量修正系数分别为2.9 ± 0.01、2.3 ± 0.5、2.6 ± 0.2和0.95 ± 0.07。这些结果表明，掺入哺乳动物细胞DNA中的俄歇电子和β粒子发射体的毒性主要是自由基介导的，因此本质上是间接的。这也是3 H2O发射的低能β粒子的情况。相比之下，α粒子主要通过直接作用造成致命的破坏。最后，细胞吸收剂量的计算表明，β-粒子发射体在掺入哺乳动物细胞DNA时比在细胞外定位时毒性更大。
Abstract Bishayee, A., Rao, D. V., Bouchet, L. G., Bolch, W. E. and Howell, R. W. Protection by DMSO against Cell Death Caused by Intracellularly Localized Iodine-125, Iodine-131 and Polonium-210. The mechanisms by which DNA-incorporated radionuclides impart lethal damage to mammalian cells were investigated by examining the capacity of dimethyl sulfoxide (DMSO) to protect against lethal damage to Chinese hamster V79 cells caused by unbound tritium (3H2O), DNA-incorporated 125I- and 131I-iododeoxyuridine (125IdU, 131IdU), and cytoplasmically localized 210Po citrate. The radionuclides 3H and 131I emit low- and medium-energy β particles, respectively, 125I is a prolific Auger electron emitter, and 210Po emits 5.3 MeV α particles. Cells were radiolabeled and maintained at 10.5°C for 72 h in the presence of different concentrations of DMSO (5–12.5% v/v), and the surviving fraction compared to that of unlabeled controls was determined. DMSO afforded no protection against the lethal effects of the high-LET α particles emitted by 210Po. Protection against lethal damage caused by unbound 3H, 131IdU and 125IdU depended on the concentration of DMSO in the culture medium. Ten percent DMSO provided maximum protection in all cases. The dose modification factors obtained at 10% DMSO for 3H2O, 131IdU, 125IdU and 210Po citrate were 2.9 ± 0.01, 2.3 ± 0.5, 2.6 ± 0.2 and 0.95 ± 0.07, respectively. These results indicate that the toxicity of Auger electron and β-particle emitters incorporated into the DNA of mammalian cells is largely radical-mediated and is therefore indirect in nature. This is also the case for the low-energy β particles emitted by 3H2O. In contrast, α particles impart lethal damage largely by direct effects. Finally, calculations of cellular absorbed doses indicate that β-particle emitters are substantially more toxic when incorporated into the DNA of mammalian cells than when they are localized extracellularly.
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DOI：
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影响因子：
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DOI：
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发表时间：
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期刊：
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影响因子：
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