EYE LENS OPACITY IN CORTICAL CATARACTS ASSOCIATED WITH ACTIN-RELATED GLOBULAR DEGENERATION

Incubation of rat lenses with intact capsules in vitro in Medium 199 as described by Patterson and Fournier 1976 resulted in no change in clarity or morphological appearance of the lens cells during one week when examined by scanning electron microscopy. Incubation of such lenses in medium containing the specific inhibitor of microfilament function, cytochalasin D, for one week, gave rise to a cortical cataract. These lenses exhibited loss of acuity, opacity and associated globular degeneration of the lens cortex similar to that previously observed by scanning electron microscopy in human and animal cataracts. Although several mechanisms have been suggested for cytochalasin D, the most likely one, from our reading of the literature, is that it appears to act on actin microfilaments; this suggests that microfilaments may be important components of the lens cell architecture since disorganization of only one cellular element-actin microfilaments, may be sufficient to cause the opacity and globular degeneration. Study of the time course of appearance of the globular degeneration indicates that the loss of acuity and opacity occur concurrently with it, and are related to the extent of the globular degeneration. Up to 24 hr, the globular degeneration was almost completely reversible, along with the opacity. Since the effect of cytochalasin D on microfilaments is reversible, this is consistent with the opacity and globular degeneration being caused by disorganization of microfilaments by cytochalasin D. Such actin-related globular degeneration may be a contributing factor in cortical cataractogenesis. © 1979.