Goddu S M, Narra V R, Harapanhalli R S, Howell R W, Rao D V
Department of Radiology, New Jersey Medical School, University of Medicine and Dentistry of New Jersey, Newark 07103, USA.
Acta Oncol. 1996;35(7):901-7. doi: 10.3109/02841869609104044.
Dimethyl sulfoxide (DMSO) was studied for its capacity to protect against the biological effects of chronic irradiation by incorporated radionuclides. Spermatogenesis in mice was used as experimental model and spermatogonial cell survival was the biological endpoint. DMSO was injected intratesticularly 4 h prior to a similar injection of the radiochemical and the spermhead survival determined. Iodine-125 was localized in either the cytoplasm (H125IPDM) or in the DNA (125IUdR) of the testicular cells. Protection was observed against the high-LET type effects of DNA-bound 125I as well as the low-LET effects of cytoplasmically localized 125I with dose modification factors (DMF) of 3.1+/-1.0 and 4.4+/-1.0 respectively. No protection (DMF = 1.1+/-0.1) was observed against the effects of high-LET 5.3 MeV alpha particles of 210Po. The present findings provide supporting evidence that the mechanism responsible for the extreme biological damage caused by DNA-bound Auger emitters is largely radical mediated and therefore indirect in nature.
研究了二甲基亚砜(DMSO)对掺入放射性核素引起的慢性辐射生物学效应的防护能力。以小鼠精子发生作为实验模型,精原细胞存活作为生物学终点。在注射放射性化学物质前4小时,将DMSO经睾丸内注射,然后测定精子头部的存活率。碘-125定位于睾丸细胞的细胞质(H125IPDM)或DNA(125IUdR)中。观察到对与DNA结合的125I的高传能线密度(LET)类型效应以及细胞质中定位的125I的低LET效应均有防护作用,剂量修正因子(DMF)分别为3.1±1.0和4.4±1.0。未观察到对210Po的5.3 MeV高LETα粒子效应的防护作用(DMF = 1.1±0.1)。目前的研究结果提供了支持性证据,即由与DNA结合的俄歇电子发射体引起的极端生物损伤的机制在很大程度上是自由基介导的,因此本质上是间接的。