Current information about spontaneous cataract model animals of rats and mice is introduced in this review. Oxidative damages are considered to be related to cataract development in the heterozygote type in UPL rats, Ihara Cataract Rats (ICR), RCS rats, Emory mice and SAM mice. Abnormalities in ion-pomp were reported in the ICR and Nakano mice. Protein denaturation induced by activation in protease is occurred in the UPL rats and Shumiya Cataract rats. These hereditary cataract models may contribute a research in human cataract formation and a development of new therapeutic methods.

On the other hand, the cataract models in which morphological abnormalities are initiated during gestation period, for example, homozygote type in UPL rats, Bmn rats, Cts mice, Cataract-Fraser mice and Elo mice, also show microphthalmos. These models might be used for research in congenital human cataract with microphthalmos.

Retinal degeneration characterized by photoreceptor apoptosis was induced by a single systemic administration of N-methyl-N-nitrosourea (MNU) in a variety of adult animals: rodents (mouse, rat and hamster), insectivora (shrew; Suncus murinus), and non-human primates (monkey; Macaca Fuscata). Therefore, phylogenetically, MNU-induced photoreceptor apoptosis is a universal phenomenon. However, the lesions (similar to human retinitis pigmentosa) initiated from the equatorial zone in monkeys, whereas in the other species the lesions originated from the posterior pole. After the photoreceptor cell loss, an intraretinal migration of pigment epithelial cells was seen in rats and hamsters, but as in humans, the migrated pigment epithelial cells in contact with a blood vessel was seen only in the hamsters; no pigment epithelial cell migration was seen in the mice, shrews or monkeys. Retinal dysplasia characterized by dysplastic rosettes was induced in mice treated with MNU at day 0 or 3 (the stage of retinal cell proliferation), whereas no retinal response was seen when MNU was administered at day 5 or 8 (the stage of retinal cell differentiation), and retinal degeneration occurred when MNU was administered at or over day 11 (after cellular differentiation). Thus, from the ontogenetic point of view, the MNU response was related to retinal development in that there was a critical period for the time of MNU administration for the induction of retinal lesions.

We examined the diurnal changes in the electroretinogram (ERG) in rats to clarify whether a circadian rhythm exists in the retinal function.

ERGs were continuously recorded every 4 hours for 2 days from freely moving male Jcl: Wistar rats (4-7 months old) via electrodes implanted into the sclera of the left eye, and the amplitude and latency of the a-wave and b-wave and wavelet index (calculated from O1, O2, and O3 amplitudes) were determined. Under a 12-hour light/dark cycle (lights on from 7:00 to 19:00), the amplitude of the a-wave and b-wave and wavelet indices increased during the dark phase with maximum values at 23:00 or 3:00 and decreased during the light phase with minimum values at 11:00 or 15:00. In contrast, the latency of the a-wave and b-wave decreased during the dark phase with minimum values at 23:00 or 3:00 and increased during the light phase with maximum values at 11:00 or 15:00. A similar pattern of diurnal ERG changes was also observed under conditions of both continuous dark and continuous light. Therefore, the diurnal changes in the ERG were considered to be related to circadian rhythm of the retinal function. Additionally, the pattern of diurnal ERG changes was reversed one month after the 12-hour light/dark cycle was reversed (lights on from 19:00 to 7:00), suggesting light is one of the environmental synchronizers of circadian rhythm.

These results indicate that circadian rhythm of the retinal function similar to that of locomotor activity, which increases during the dark phase and decreases during the light phase, exists in the rat.

The optic fundi of 365 apparently healthy African green monkeys ranging in age from 0 day to 15 years were examined by an ophthalmoscope. Subtle differences in their findings by different ages were recorded. Colour of the ocular fundus showed significant changes with increasing ages. Retinal hemorrhage was found in neonates of natural delivery but not in those of caesarean section.

In this study, we measured the spherical equivalent transportation and the corneal radius of curvature of 140 normal dog eyes, using handy autorefract-keratometer. And we also discussed the correlation between corneal radius of curvature and spherical equivalent transportation as well as the correlation between the corneal radius of curvature, and age and body weight. The mean of their spherical equivalent transportation of dogs is +1.9±3.0 diopter (D) and has no correlation with their age and body weight. The mean of their corneal radius of curvature is +8.4±0.9 mm. It has no correlation with their age and spherical equivalent transportation, either. The heavier their body weight, the larger their corneal radius of curvature (r=0.58).

As a result, we understand about 80% of dogs are hyperopic and we believe these figures of measurement are very useful for development of IOL for dog.

To investigate mechanisms of cataract development in the late onset hereditary cataract of the UPL rat, lens reduced glutathione (GSH), sodium, potassium and calcium levels were determined at each stage of cataract development. Lenses of the UPL rat were delivered at various age. GSH and cation levels were measured by HPLC and atomic absorption methods, respectively. The GSH level was decreased from early stage of cataract development, and oxidative damage to the lens was suggested. In addition, the sodium/potassium ratio and calcium levels were increased at final stage of cataract development. In conclusion, it was suggested that disturbance in cation pumps and/or membrane function were caused by oxidative damage leading to swelling of lens and aggregation of lens proteins, and finally mature cataract was developed.