Establishment of the Mouse as a Model Animal for the Study of Diabetic Cataracts

Abstract

The purpose of the present study was to investigate the suitability of using the mouse, a species known to have a low lens aldose reductase activity, as a model animal for studying the pathogenesis of diabetic cataract. Earlier studies with diabetic rats whose cataract development is much faster can only partially explain the etiology of cataracts in humans where lens aldose reductase is substantially low. CD-1 mice were injected intraperitoneally with streptozotocin according to Rossini’s method. Blood glucose levels were estimated after 7 days, and animals having blood glucose between 300 and 400 mg/dl were selected for further experiments. Development of lenticular opacity was followed by examining the animals every 3–4 weeks by direct ophthalmoscopy, slitlamp examination and Scheimpflug photography. Additionally, the animals were sacrificed at appropriate intervals, eyes enucleated and subjected to morphological studies. The presence of refractive changes and early cataract in the diabetic mice was initially ascertained by the distorted appearance of the grid pattern when seen through the isolated lenses. Early cataracts were visible on slitlamp examination and by ophthalmoscopy as early as 3–4 weeks after the establishment of diabetes. Advanced opacity was clearly documentable by photography after 5–6 months. Similar to that in other species, a single layer of anterior epithelial cells abutting the anterior capsule was seen in the histological sections of normal mouse lenses. On the contrary, the epithelium in the diabetic lens was multilayered, and numerous nucleated cells were visible in the superficial anterior cortex. These studies therefore suggest that further studies with mice may throw additional light on the contribution of diabetes in the pathogenesis of cataracts in low lens aldose reductase models.