Ultraviolet Radiation–Induced Cataract in Mice: The Effect of Age and the Potential Biochemical Mechanism

Authors

Jie Zhang, University of Nebraska- Lincoln & the Fourth Military Medical University
Hong Yan, the Fourth Military Medical University
Stefan Lofgren, Karolinska Institutet
Xiaoli Tian, University of Nebraska- Lincoln
Marjorie F. Lou, University of Nebraska-LincolnFollow

Date of this Version

9-18-2012

Citation

2012 The Association for Research in Vision and Ophthalmology, Inc.

Comments

(Invest Ophthalmol Vis Sci. 2012;53:7276–7285) DOI: 10.1167/iovs.12-10482

Abstract

PURPOSE. To study the effect of age on the morphologic and biochemical alterations induced by in vivo exposure of ultraviolet radiation (UV).

METHODS. Young and old C57BL/6 mice were exposed to broadband UVBþUVA and euthanized after 2 days. Another batch of UV-exposed young mice was monitored for changes after 1, 2, 4, and 8 days. Age-matched nonexposed mice served as controls. Lens changes were documented in vivo by slit-lamp biomicroscopy and dark field microscopy photographs ex vivo. Lens homogenates were analyzed for glutathione (GSH) level, and the activities of thioredoxin (Trx), thioltransferase (TTase), and glyceraldehyde-3-phosphate dehydrogenase (G3PD). Glutathionylated lens proteins (PSSGs) were detected by immunoblotting using GSH antibody. Western blot analysis was also done for the expression levels of TTase and Trx.

RESULTS. Both age groups developed epithelial and superficial anterior subcapsular cataract at 2 days postexposure. The lens GSH level and G3PD activity were decreased, and PSSGs were elevated in both age groups, but more prominent in the older mice. TTase and Trx activity and protein expression were elevated only in the young mice. Interestingly, lens TTase and Trx in the young mice showed a transient increase, peaking at 2 days after UV exposure and returning to baseline at day 8, corroborated by lens transparency.

CONCLUSIONS. The lenses of old mice were more susceptible to UV radiation–induced cataract. The upregulated TTase and Trx likely provided oxidation damage repair in the young mice.