Cataracts in the Aging Rat Lens

Abstract

Two types of cortical cataract were observed in senile Wistar rats: posterior subcapsular (PSC) and supranuclear (SNC). The beginning of PSC was denoted clinically by vacuole accumulation in the posterior suture. The appearance of vacuoles, granules and cloudiness spread laterally in all directions, maintaining a primarily superficial cortical distribution. Microscopic comparison of rat and human forms showed the opacity to represent subcapsular accumulations of fluid and cytoplasmic residues, generated by the swelling and disintegration of basal extremities of fiber cells. The clinical onset of murine SNC was usually represented by small vacuole accumulation in the anterior cortical suture system. Later, lamellar separations formed in the outer cortex, followed by the development of water clefts in the deeper cortex. Microscopically, advanced forms showed extensive swelling and coalescence of cortical fibers, associated with Morgagnian globules and myelin figures.

Normal Mouse and Rat Strains as Models for Age-related Cataract and the Effect of Caloric Restriction on its Development

“…However, most of these differ from the human age-related cataract, in that the time of cataract appearance or the initiation of the precataractous changes take place early in post-natal life, or even in utero (Hosokawa et al, 1988;Kruk, 1990;Zigler, 1990;Tripathi et al, 1991;Phelps Brown and Bron, 1996a;Smith, Sundberg and Linder, 1997). Other possible models develop cataracts late in life but all of these in the reports we accessed were found to be pink-eyed albino animals that have been shown to be susceptible to both light-induced cataract and retinitis (Coleman et al, 1977;Gorthy, 1977;Anver and Cohen, 1979;Rao, 1991;Toyoda et al, 1992). It is important that an animal model parallel human cataracts in time of appearance, lens regions involved, and the occurrence and progression of the lesion during late life span, as well as its development in a pigmented eye.…”

“…We are not the ®rst to report the development of cataracts in mice and rats. However, in all previous studies that we have been able to access the animals were from strains predisposed to develop congenital or early cataracts (Hosakawa et al, 1988;Kruk, 1990;Zigler, 1990;Taylor et al, 1995;Phelps Brown and Bron, 1996a;Smith et al, 1997) or, if of otherwise normal genetic eye inheritance, were albinos, which have been shown to develop light-induced retinal damage and cataracts (LaVail, Sidman and Gerhardt, 1975;Gorthy, 1977;Rao, 1991;Toyoda et al, 1992). Light-induced cataracts in albino F344 rats were reported in studies by Rao (1991) and by Toyoda et al (1992), in which the percentage of animals developing cataracts over a 24 month period was related tō uorescent light intensity in the cages.…”

“…However, no relationships between the treatment groups and the incidence of cataracts were observed. Gorthy (1977) reported a 66 % incidence of advanced posterior subcapsular and/or supranuclear cataracts in albino Wistar rats with`a normal life expectancy of 32 months' by 29±30 months of age, with lighting conditions not reported. A study in otherwise untreated young albino A/J mice found lens opacities developing by 50±60 weeks, correlated with a decrease in the development of lens epithelial cells (LECs) into ®ber cells, when the mice were exposed to near UV light 12 hr per day (Zigman, Yulo and Schultz, 1974).…”