IOVS
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Originally published In Press as doi:10.1167/iovs.08-3262 on February 28, 2009
 (Investigative Ophthalmology and Visual Science. 2009;50:3304-3310.)
© 2009 by The Association for Research in Vision and Ophthalmology, Inc.
doi:10.1167/iovs.08-3262
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
iovs.08-3262v1
50/7/3304    most recent
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Bigsby, R. M.
Right arrow Articles by Dynlacht, J. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bigsby, R. M.
Right arrow Articles by Dynlacht, J. R.

Ovarian Hormone Modulation of Radiation-Induced Cataractogenesis: Dose-Response Studies

Robert M. Bigsby,1 Shailaja Valluri,2 Jennifer Lopez,3 Marc S. Mendonca,3 Andrea Caperell-Grant,1 Colleen DesRosiers,3 and Joseph R. Dynlacht3

1From the Departments of Obstetrics and Gynecology, 2Ophthalmology, and 3Radiation Oncology, Indiana University School of Medicine, Indianapolis, Indiana.

PURPOSE. Epidemiologic data on the effects of female sex hormones in cataract formation are conflicting. With the use of a rat model of radiation-induced cataractogenesis, it was found that estrogen can either enhance or inhibit the progression of radiation cataracts, depending on when the hormone is administered. The present study was performed to further define radiation-hormone interactions during cataractogenesis.

METHODS. In one experiment, rats were left ovary-intact or ovariectomized and were then irradiated with 2.5, 5, 10, or 15 Gy to one eye. In another experiment, ovariectomized rats were treated continuously with three different doses of estradiol through a slow-release capsule implanted subcutaneously, after which one eye was irradiated with 15 Gy. In all animals, cataract formation was followed by slit lamp examination at regular intervals.

RESULTS. Latency to identification of cataracts decreased exponentially with increasing radiation dose. The presence of ovaries enhanced cataractogenesis when the eye was irradiated with 15 Gy, but there was no difference between ovary-intact and ovariectomized rats that were irradiated at lower doses. In ovariectomized rats irradiated with 15 Gy, estradiol increased the rate of progression of cataracts in a dose-dependent manner. The rate of cataract progression increased linearly with increasing estradiol dose; there was no sign of saturation at high estradiol doses, as would be expected from a receptor-mediated effect.

CONCLUSIONS. Ovarian hormones enhance radiation-induced cataract formation; hormone supplementation experiments indicate that estrogen is responsible for this effect. The data suggest that the enhancing effect of estradiol is not mediated by its receptor, but this requires further study.






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2009 by the Association for Research in Vision and Ophthalmology