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The present study sought to assess the efficacy of the allylmercaptocaptopril in preventing seleniteinduced cataractogenesis in an experimental setting. The first, in vitro phase of the study was performed on lenses from Wistar rats incubated for 24 h at 37°C in Dulbeccous Modified Eagle Medium (DMEM) alone (control, Group I), or in DMEM containing 100 µM of selenite (Group II) or in DMEM containing 100 µM of selenite and 5 mM allylmercaptocaptopril was added (Group III). The second, in vivo phase of the study, 9 days old Wistar rat pups divided into normal, control and test groups were injected subcutaneously with 19 µM/kg sodium selenite except normal group. One day before the selenite challenge, the pups in the test group were injected intraperitoneally a single dose of 50 mg/kg of allylmercaptocaptopril and was repeated once daily for five consecutive days thereafter. When the pups first opened their eyes (when the pups were 15 days old), their eyes were examined by slit-lamp biomicroscopy. In the first phase, the mean activities of reduced glutathione, total protein, water soluble protein, Ca 2+ -ATPase activity and the antioxidant enzymes activity were significantly lower in Group II than in Group I or Group III lenses, while malondialdehyde concentration (an indicator of lipid peroxidation) and lens calcium ion concentration was significantly higher in Group II lenses than that in Group I or Group III lenses. The second, in vivo phase of the study revealed dense opacification (cataract formation) in 100% of Wistar rat pups receiving sodium selenite alone (19 µM/kg s.c) but in only 12.5% of those receiving subcutaneous selenite and allylmercaptocaptopril (50 mg/kg i.p). The study on the evaluation of the anticataract potential of allylmercaptocaptopril in experimental animals indicated that it modulates antioxidant parameters in the enucleated eye lenses. It also attenuates selenite-induced cataract both in vitro and in vivo, so it may be useful for cataract therapy.
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A 2011 study studied this question.
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