Dynlacht Joseph R, Tyree Craig, Valluri Shailaja, DesRosiers Colleen, Caperell-Grant Andrea, Mendonca Marc S, Timmerman Robert, Bigsby Robert M
Department of Radiation Oncology, Indiana University School of Medicine, Indianapolis, Indiana 46202, USA.
Radiat Res. 2006 Jan;165(1):9-15. doi: 10.1667/rr3481.1.
Cataractogenesis is a widely reported late effect that is observed in patients receiving total-body irradiation (TBI) prior to bone marrow transplantation or radiotherapy for ocular or head and neck cancers. Recent studies indicate that estrogens may protect against age-related and drug-induced cataracts. Moreover, other reports suggest that estrogen possesses antioxidant properties. Since the effect of estrogen on radiation cataractogenesis is unknown, we wished to determine whether estrogen modulates radiation-induced opacification of the lens. Intact or ovariectomized Sprague-Dawley rats were treated with either 17-beta-estradiol or an empty silastic capsule. The right orbit was then irradiated with either 10 or 15 Gy of (60)Co gamma rays using a Leksell Gamma Knife, and lenses were examined at various times postirradiation with a slit lamp or evaluated for light transmission. We found that for ovariectomized rats irradiated with 15 Gy, the lens opacity and the incidence of cataract formation in the estradiol-treated group were significantly increased compared to the control group at the end of the 25-week period of observation. Cataract incidence was also high in irradiated eyes of ovary-intact animals at 25 weeks postirradiation but was greatly reduced in the ovariectomized control group, with less than half of irradiated eyes showing evidence of cataractogenesis. Thus, after irradiation with 15 Gy of gamma rays, estrogen increased the incidence of cataract formation. We also observed that although the incidence of cataract formation in rats irradiated with 10 Gy and receiving continuous estrogen treatment was not altered compared to rats in the control group that did not receive estrogen, the latent period for posterior subcapsular cataract formation decreased and the severity of the anterior cataract increased. Taken together, our data suggest that estrogen accelerates progression of radiation-induced opacification.
白内障形成是一种广泛报道的晚期效应,在接受骨髓移植前全身照射(TBI)或眼部、头颈癌放疗的患者中可见。近期研究表明,雌激素可能预防与年龄相关及药物诱导的白内障。此外,其他报告提示雌激素具有抗氧化特性。由于雌激素对放射性白内障形成的影响尚不清楚,我们希望确定雌激素是否能调节辐射诱导的晶状体混浊。将完整或去卵巢的Sprague-Dawley大鼠用17-β-雌二醇或空的硅橡胶胶囊处理。然后使用Leksell伽马刀对右侧眼眶进行10或15 Gy的钴-60γ射线照射,在照射后的不同时间用裂隙灯检查晶状体或评估透光率。我们发现,对于接受15 Gy照射的去卵巢大鼠,在25周观察期结束时,雌二醇处理组的晶状体混浊度和白内障形成发生率与对照组相比显著增加。在照射后25周,完整卵巢动物的照射眼白内障发生率也很高,但在去卵巢对照组中大大降低,不到一半的照射眼有白内障形成的迹象。因此,在接受15 Gyγ射线照射后,雌激素增加了白内障形成的发生率。我们还观察到,尽管接受10 Gy照射并持续接受雌激素治疗的大鼠白内障形成发生率与未接受雌激素的对照组大鼠相比没有改变,但后囊下白内障形成的潜伏期缩短,前白内障的严重程度增加。综合来看,我们的数据表明雌激素加速了辐射诱导的混浊进展。