title: Anticataract action of vitamin E: its estimation using an in vitro steroid cataract model.
abstract: The aim of this study was to estimate the anticataract action of vitamin E using an in vitro methylprednisolone (MP)-induced cataract model. The same severity of early cortical cataract was induced in lenses isolated from male Wistar rats aged 6 weeks by incubation with MP (1.5 mg/ml) in TC-199 medium. The cataractous lenses showed slight increases in lipid peroxide (LPO) content and Na+/K+ ratio and slight decreases in reduced glutathione (GSH) content and glyceraldehyde-3-phosphate dehydrogenase (GAP-DH), a sensitive index of oxidative stress, and Na+,K(+)-ATPase activities. When the cataractous lenses were further incubated in TC-199 medium with and without vitamin E (250 micrograms/ml) for 48 h, the progression of cataract was prevented in the vitamin E-treated lenses, but not in the vitamin E-untreated lenses. The vitamin E-untreated lenses showed a decrease in vitamin E content and an increase in water content in addition to further increases in LPO content and Na+/K+ ratio and further decreases in GSH content and GAP-DH and Na+,K(+)-ATPase activities. In contrast, the changes of these components and enzymes except for GSH were attenuated in the vitamin E-treated lenses. From these results, it can be estimated that vitamin E prevents in vitro cataractogenesis in rat lenses treated with MP by protecting the lenses against oxidative damage and loss of membrane function.
authors.affiliation: Department of Biochemistry, School of Medicine, Fujita Health University, Aichi, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Ohta
authors.forename: H
authors.initials: H
authors.lastname: Okada
authors.forename: Y
authors.initials: Y
authors.lastname: Majima
authors.forename: I
authors.initials: I
authors.lastname: Ishiguro
mesh_terms: D000818:Animals; D001834:Body Water / Q000378:metabolism; D002386:Cataract / Q000139:chemically induced / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D004195:Disease Models, Animal; D005938:Glucocorticoids / Q000633:toxicity*; D005978:Glutathione / Q000378:metabolism; D005987:Glyceraldehyde-3-Phosphate Dehydrogenases / Q000378:metabolism; D007908:Lens, Crystalline / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D008054:Lipid Peroxides / Q000378:metabolism; D008297:Male; D008775:Methylprednisolone / Q000633:toxicity*; D009924:Organ Culture Techniques; D011188:Potassium / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012964:Sodium / Q000378:metabolism; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D014810:Vitamin E / Q000494:pharmacology*
chemical_list: D005938:Glucocorticoids; D008054:Lipid Peroxides; D014810:Vitamin E; D012964:Sodium; D005987:Glyceraldehyde-3-Phosphate Dehydrogenases; D000254:Sodium-Potassium-Exchanging ATPase; D005978:Glutathione; D011188:Potassium; D008775:Methylprednisolone