Cataracts in experimentally diabetic mouse: morphological and apoptotic changes.

AIM: The objective of these investigations was to extend our earlier study on the induction of cataracts in diabetic mice, a low aldose reductase (AR) animal model at morphological level. Previous studies were done primarily at biochemical level.
METHODS: Diabetes was induced by intraperitoneal administration of streptozotocin. The lenses isolated after the establishment of diabetes were then subjected to histologic and electron microscopic studies.
RESULTS: Morphological alterations were characterized by shrinkage, elongation and lobulization of the nuclei of the epithelial cells. This was associated with chromatin condensation and its margination. Similar structural aberrations were also observed in a significant number of the subepithelial fibre cells representing defect in fibre maturation. More interestingly, unlike that in other common animal models of diabetic cataract, such abnormally nucleated cells were also found to be prevalent in the posterior subcapsular region, a finding common in human diabetics also.
CONCLUSION: The present studies further affirm the suitability of the mouse model for a study of cataractogenesis induced by diabetes. Because of the findings reported herein, as well as the known biochemical similarity between the lenses of the mice and humans in respect of AR deficiency, contrary to the rat model where it is very high, use of this species is considered more useful towards understanding the basic aetiology as well as for evaluating the efficacy of various referred nutritional and metabolic antioxidants against such cataracts.