Cataract from ultraviolet radiation

Abstract: Cataract is the major cause of low vision and blindness in the world. Epidemiological and experimental studies link cataract to (solar) ultraviolet radiation (UVR) exposure. Current safety limits of UVR exposure are based on animal experiments, but many factors are less well known in UVR cataractogenesis. This thesis aims at strengthening the foundation for experimental UVR cataract research and to aid in future revisions of UVR safety limits. Using lactate as a marker of glycolytic activity, it was shown that in vivo UVR exposure, but not blue light, inhibits lens glycolysis. With optimised histochemistry of the glycolytic enzyme lactate dehydrogenase (LDH), it was determined that lens epithelium and nucleus have high LDH activity and cortex lower activity. LDH in the anterior parts of the lens was inhibited by in vivo UVR exposure, probably by direct photochemical action. A short penetration of UVR-B in the lens was shown using LDH activity as end-point. After in vivo exposure, young rats develop more severe cataract than old rats, with no difference between sexes, and the time for maximal cataract to develop is dependent on age. The degree of cataract was quantified by measurement of in vitro lens forward fight scattering. Iris pigmentation is highly UVR protective, with little importance of pupil size in pigmented eyes, while the opposite holds for albino eyes where a large pupil is more protective than a small pupil. In vitro UVR exposed lenses from albino rats are more sensitive than lenses from pigmented rats. The cataract type is similar in the two strains after in vitro UVR exposure, opposite of the in vivo exposure situation, where cataract type differs.