Aging of the human eye lens—A morphological point of view

Age-related cortical lens changes are mainly due to oxidative stress induced membrane disorganization increasing with time to (1) membrane ruptures, (2) local fibre opacification, (3) local opacities and eventually to (4) more advanced segmental and annular opacities and mature cataract. Early occurrence of these cortical opacities is delayed by the presence of several defence systems: (1) radical scavengers, (2) a membrane repair-lysosomal system, (3) a segregation system and (4) the inertness of the deep cortical and nuclear membranes. Posterior subcapsular age-related changes As shown by Spector (1991), oxidative stress also affects the DNA of lenticular epithelial cells leading to single strand breaks. Although these DNA breaks are efficiently repaired by excision repair, longlasting low dose insults, as in the human lens or massive insults as in experimental studies, can lead to incomplete repair and therefore to germinative epithelial cells with aberrant DNA. These will give rise to cohorts of deviating cells with an abnormal developmental programme. That abnormal DNA, e.g. regarding the genes for cytoskeletal proteins, leads to abnormal development of fibres has been shown in studies in transgenic mice (Dunia et al., 1991). Irradiation in animals leading to abnormal development of fibres and finally to posterior subcapsular cataract has been extensively documented (Worgul, 1989). In our studies of donor eye lenses, we have incidentally found lenses with one or two regions with abnormal and abnormally interdigitating lens fibres which would beyond doubt have led to posterior subcapsular cataract. Compared with the other two types of age-related changes, posterior subcapsular changes are rather infrequent (Sasaki et al., 1987, 1989).(ABSTRACT TRUNCATED AT 250 WORDS)