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Low Vitamin E Level as a Subliminal Risk Factor in a Rat Model of Prednisolone-Induced Cataract

¹ From the Department of Ophthalmology and the ³ Division of Basic Science, Medical Research Institute, Kanazawa Medical University, Uchinada, Japan.

PURPOSE. To investigate the relationship between vitamin E deficiency and prednisolone-induced cataract formation, long-term examination of lens changes was performed in rats under the condition of vitamin E deficiency or supplementation and administration of prednisolone.

METHODS. Rats were divided into six groups: normal chow (N), vitamin E–deficient chow (ED), normal chow with prednisolone instillation (NP), vitamin E–deficient chow with prednisolone instillation (EDP), NP treatment with vitamin E supplementation (NP+VE), and EDP treatment with vitamin E supplementation (EDP+VE). Prednisolone (1 mg/kg · d) and vitamin E (5%; 10 µL per administration per eye, 1 mg/kg · d) were applied in the cul-de-sac. Lens changes were documented and analyzed. Vitamin E status was confirmed by measuring peroxide-induced hemolysis.

RESULTS. After 15 months, 91.7% of the eyes in the EDP group showed development of anterior and posterior cortical cataracts. Supplementation with vitamin E significantly reduced cataract formation (to 38.9% of eyes). Neither a vitamin E–deficient diet nor prednisolone treatment alone significantly increased cataract formation. Hemolysis-susceptibility tests confirmed the expected vitamin E status of rats fed vitamin E–deficient chow and rats supplemented with eye drops containing vitamin E.

CONCLUSIONS. Vitamin E deficiency and long-term prednisolone treatment together cause cataracts. Singly, however, both conditions are subliminal cataractogenic risk factors.

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