It has been suggested that
sugar cataracts associated with
diabetes mellitus result from the accumulation of excess
sorbitol within lens fibrils. Swelling of lens fibrils occurs when water moves in to maintain osmotic balance; the excess water causes disruption of fibrils and
cataract formation. Other studies have indicated that more than
sorbitol-induced osmotic stress is involved. Our study used
lenses collected from rats after 21 or 44 d of
streptozotocin diabetes.
Cataracts formed in untreated 44-d
streptozotocin diabetic rats, but were not apparent in the 21-d untreated diabetic animals. Lens
sorbitol increased in the diabetic animals both before and after
cataract formation. Lens
taurine varied inversely with the
sorbitol content in a fashion that resulted in no net change in total lens osmoles. Lens water did not increase in the diabetic animals with or without
cataracts. The
aldose reductase inhibitor
Sorbinil prevented the increase in lens
sorbitol in both the 21- and 44-d
streptozotocin diabetic rats;
cataract formation was prevented in the 44-d diabetic animals. The lens water in untreated diabetic animals with
cataracts did not differ from lens water in the
Sorbinil-treated diabetic animals that did not develop
cataracts.
Sorbinil treatment of diabetic animals was associated with normalization of both lens
sorbitol and
taurine levels.
Taurine has been shown to serve both as an osmoregulator and as an
antioxidant. The apparent increase in lens osmolality attributed to
sorbitol was counterbalanced by an equimolar reduction in
taurine concentration. The reciprocal relationship between
taurine and
sorbitol reduces the likelihood of an osmotic mechanism for
sugar cataractogenesis; the reduced lens
taurine, however, may increase the risk of lens
protein oxidation and subsequent
cataract formation. Thus in vivo
sugar cataract formation may be an oxidative process rather than an osmotic phenomenon.