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.
