A new steroid-induced cataract model in the rat: long-term prednisolone applications with a minimum of X-irradiation.
In order to induce experimental steroid cataracts in rat eyes similar morphologically to those seen in human eyes, prednisolone acetate was administered either topically or systemically for 12 months with a low dose of X-irradiation as a cocataractogenic factor. Twenty-seven Brown-Norway rats were randomly divided into a control group (group I) with no steroid administration; an eyedrop group (group II) with a daily 1% prednisolone acetate instillation of a total volume of 1.0 mg/kg in both eyes, and a systemic group (group III) with a daily intramuscular injection of 0.8-1.0 mg/kg prednisolone acetate. The right eyes of animals in each group were X-irradiated with a single dose of 2 Gy. Topical and systemic steroid administrations started 2 weeks after X-irradiation. Anterior segment changes were documented with a slitlamp microscope and an anterior eye segment analysis system once a month. Body weight and blood glucose levels were examined every week and every 2 weeks, respectively. The mortality rates in groups I, II and III were 0, 11 (1/9) and 25% (3/12), respectively. The both lenses in group I showed a gradual increase in light-scattering intensity in the nuclear and supranuclear regions over time. Initial lens changes in both steroid-treated groups were Y-suture dissociation and a slight increase in light-scattering intensity in the posterior supranuclear region 3 months after prednisolone administration. Opacification of the anterior shallow cortex and the posterior subcapsular layer was observed after 10 months. X-irradiated eyes showed more prominent lens opacification as compared with nonirradiated eyes after 10 months in both group II and group III. Either topical or systemic administrations of prednisolone acetate over a long term successfully induced morphological lenticular changes in the rat similar to those found in human steroid-induced cataracts. A low dose of X-irradiation effectively accelerated opacification as a cocataractogenic risk. This new model will allow future investigation of steroid cataracts.
Shui
Y B
YB
Department of Ophthalmology, Kanazawa Medical University, Uchinada, Japan.
Kojima
M
M
Sasaki
K
K
D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D001835:Body Weight; D002386:Cataract / Q000209:etiology* / Q000473:pathology; D004195:Disease Models, Animal; D005938:Glucocorticoids / Q000008:administration & dosage / Q000633:toxicity*; D007091:Image Processing, Computer-Assisted; D007273:Injections, Intramuscular; D007908:Lens, Crystalline / Q000187:drug effects* / Q000473:pathology / Q000528:radiation effects; D008297:Male; D009883:Ophthalmic Solutions; D010781:Photography; D011239:Prednisolone / Q000008:administration & dosage / Q000031:analogs & derivatives* / Q000633:toxicity; D011833:Radiation Injuries, Experimental / Q000209:etiology* / Q000473:pathology; D011897:Random Allocation; D051381:Rats; D011914:Rats, Inbred BN; D014965:X-Rays / Q000009:adverse effects
D001786:Blood Glucose; D005938:Glucocorticoids; D009883:Ophthalmic Solutions; C009935:prednisolone acetate; D011239:Prednisolone