Ultrastructural studies of traumatic cataractogenesis: observations of a repair process in mouse lens.

Lenses of CFI mice were studied with the transmission electron microscope at frequent intervals through 13 months following a transcorneal needle injury to the lens. While this kind of injury causes a high incidence of traumatic cataract in the human and frog, it elicits a repair process in the mouse lens whereby the damaged capsule, epithelium and lens fibers are rapidly renewed and permanent lens opacity seldom occurs. Ultrastructural changes in lens epithelial cells adjacent to the wound, which precede and accompany localized cellular proliferation and production of new capsule, involve a rapid increase or enlargement of organelles associated with protein synthesis and assembly. The capsule and epithelium are repaired within a couple of months. Cortical lens fibers in the wound area undergo conformational changes into smaller, ordered arrays of "membranous sacs". These are replaced within a week by normal appearing lens fibers. There is minimal degeneration or hyperplasia noted, and except for a few fibroblastic cells on the lens surface, little evidence remains of the injury by two months. Ultrastructural differences between mouse and human lens, such as presence or absence of dense bundles of microfilaments and desmosomes are considered in relation to lens shape and tension, and susceptibility to injury-induced cataract.