Young beagle dogs were fed a 30%
galactose diet, with or without the
aldose reductase inhibitors
sorbinil or
M79175.
Cataract formation was monitored by indirect ophthalmoscope and hand-held
slit-lamp microscopy and documented by retroillumination photography. In these dogs, the first sign of
cataract development was an accentuation of the anterior and posterior lens
sutures (1 month after feeding), then the appearance of cortical vacuoles (3 months after feeding), and finally, the formation of predominantly equatorial cortical opacities toward the posterior cortices (4-6 months after feeding). After long-term
galactose feeding, a progressive, irregular, clear zone formed at the cortical equatorial regions. Light microscopic examination of these
lenses shows that the
cataracts are osmotic, many of the lens fibers appear to be swollen or ruptured, and vacuoles are seen near the bow region. Moreover, these histologic changes were reduced in a dose-dependent manner in
galactose-fed dogs concomitantly treated with the
aldose reductase inhibitors
sorbinil or
M79175. The osmotic nature of these
cataracts and the observation that their formation can be reduced in a dose-dependent manner by
aldose reductase inhibitors are consistent with the concept that the
aldose-reductase catalyzed formation of polar
sugar alcohols (polyols) initiates
sugar cataract formation in the dog.