Abstract

To clarify the histopathological changes of experimentally induced steroid cataract in Brown-Norway rat eyes, a scanning electron microscopic study was performed. The biomicroscopic appearance of the cataracts, which was quite similar to that of human eyes, was induced by daily application, either topically or systemically, of prednisolone acetate for 12 months. A single dose of 2 Gy X ray was given to the right eyes of all the animals 2 weeks before drug administration. Twenty-seven rats were divided into three groups: a control group (CTL), a group receiving topically administered prednisolone (TOP), and a group receiving systemically administered prednisolone (SYS). In vivo observation was performed through a slit-lamp microscope, and the lens findings were documented and objectively analyzed by an anterior eye segment analysis system over a period of 12 months. At the end of the 12-month period, X-ray-irradiated right eyes in the CTL group showed some minor lens changes on biomicroscopy, and non-X-ray-irradiated left eyes were almost normal. In the TOP and SYS groups, either with or without X-ray irradiation, lenses showed anterior and posterior subcapsular opacification; however, the grade and increase of lens opacification were higher and faster in the eyes with X-ray irradiation. Scanning electron microscopic findings of the three groups at the 12th month were as follows. In the CTL group, the X-ray-irradiated right eyes showed minor changes. In the TOP group, the X-ray-irradiated right eyes showed marked damage in the lens fibers of the anterior and posterior cortices, while the nonirradiated left eyes showed minor changes. In the SYS group, the X-ray-irradiated right eyes showed prominent cataractous disorganization of lens fibers in the shallow anterior and posterior cortices, and the non-X-ray-irradiated lenses were almost the same as those in the TOP group. These findings might suggest that even a minimum invasion of a low dose of X-ray irradiation plays a cocataractogenic or syncataractogenic role during the formation of steroid cataracts.

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