Women have a higher incidence of cataracts, and epidemiologic data suggest
that the increased risk may be caused by a lack of estrogen in postmenopaus
al years. We have examined the effects of estrogen on methylnitrosourea (MN
U)-induced cataractogenesis in Sprague-Dawley rats, Animals were ovariectom
ized, injected with MNU, and treated with estradiol or estrone by a continu
ous-release, subcutaneous Silastic implant, or they received an empty Silas
tic implant (no hormone), In the no-hormone group, rats developed opaque le
nses approximately 6 months after MNU treatment, By 8 months, 74% (14/19) o
f the no-hormone rats had evident opacity in one or both eyes by simple gro
ss inspection; 58% (22/38) of the eyes in this group were opaque. Estradiol
or estrone treatment reduced the incidence of cataractous eyes to 12% or 2
5%, respectively. Lenses were examined under a dissecting microscope for li
ght transmission. The lenses of the group treated with no hormone had light
transmission of 26% +/- 9.2%, whereas lenses from the estradiol-treated an
imals had light transmission of 72% +/- 5.8%. Histological examination reve
aled that the anterior cortices of the opaque lenses were disrupted and she
lved the hallmark signs of age-related cataracts; in addition, some eyes th
at appeared clear by macroscopic examination showed the early histologic si
gns of cataractogenesis. It was demonstrated with reverse transcription-PCR
that lens cells express both alpha and beta types of estrogen receptor, su
ggesting that the protective effects of the hormones may be a direct, recep
tor-mediated phenomenon, Thus, the MNU-treated, ovariectomized rat serves a
s a model for age-related cataractogenesis, and observation of a clear prot
ective effect of estrogens in this system supports the implications of epid
emiologic data.