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Abstract
Abnormalities in corneal epithelial healing in diabetic patients have been described recently. Defects in corneal re-epithelialization in diabetic rats have been reported, and it was found that treatment with aldose reductase (AR) inhibitors effectively prevented these defects. Experiments using galactosemic rats to study further the role of AR in these defects, since AR is known to be the common factor involved in sugar cataractogeneses, are reported herein. Similar defects in corneal re-epithelialization in galactosemic rats as in diabetic rats were found. The delay in re-epithelialization was documented by computer planimetry. Light microscopy showed marked corneal stroma edema and wider intercellular spaces in the epithelium after complete re-epithelialization, while scanning electron microscopy revealed fewer filopodia projecting from the leading margin during the active migration stage. These defects were prevented by treating galactosemic rats with the aldose reductase inhibitor, Pfizer's Sorbinil. These suggest that AR plays a role in the defects in corneal re-epithelialization observed in diabetes.