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Low vitamin E level as a subliminal risk factor in a rat model of prednisolone-induced cataract
Masami Kojima1, Ying Bo Shui, Hidekazu Murano
1Department of Ophthalmology, Medical Research Institute, Kanazawa Medical University, Uchinada, Kahoku-gun, Ishikawa, Japan. m-kojima@kanazawa-med.ac.jp
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 small middle dot d) and vitamin E (5%; 10 microL per administration per eye, 1 mg/kg small middle dot 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.