BACKGROUND: Cataract, the leading cause of blindness, is associated with oxidative damage and protein modification in the lens. The present study was carried out to assess the efficacy of rutin on rat-lens crystallins in selenite-induced in-vivo cataract models. METHODS: Eight-day-old Sprague-Dawley rat pups were grouped as control (G I), experimental (G II) and rutin-treated (G III). The rat pups in G II, and G III received a single subcutaneous injection of sodium selenite (4 μg/g body weight) and G I received a single subcutaneous injection of sterile water on the 10th day. The treatment groups (G III) were administered with rutin (1 μg/g body weight) respectively from the 8th to 15th day. Cataract was visualized from the 16th day. Lens crystallins (α, β, and γ) were isolated by size exclusion chromatography. Chaperone activity of isolated crystallins was measured by heat, DTT, and oxidation-induced aggregation and refolding assays. Concentration of total protein (soluble and insoluble) and SDS-PAGE analysis of soluble proteins were also done. RESULTS: Treatment with rutin prevented the loss of α crystallin chaperone property, and protein insolubilization prevailed during selenite-induced cataract. CONCLUSIONS: These results suggest the therapeutic potential of rutin, a bioflavonoid, against selenite-induced cataract, which has been reported in this paper for the first time. The work assumes significance, as this is a novel approach in modulating the chaperone activity of lens crystallins in selenite-induced cataract by a natural product.
BACKGROUND:Cataract, the leading cause of blindness, is associated with oxidative damage and protein modification in the lens. The present study was carried out to assess the efficacy of rutin on rat-lens crystallins in selenite-induced in-vivo cataract models. METHODS: Eight-day-old Sprague-Dawley rat pups were grouped as control (G I), experimental (G II) and rutin-treated (G III). The rat pups in G II, and G III received a single subcutaneous injection of sodium selenite (4 μg/g body weight) and G I received a single subcutaneous injection of sterile water on the 10th day. The treatment groups (G III) were administered with rutin (1 μg/g body weight) respectively from the 8th to 15th day. Cataract was visualized from the 16th day. Lens crystallins (α, β, and γ) were isolated by size exclusion chromatography. Chaperone activity of isolated crystallins was measured by heat, DTT, and oxidation-induced aggregation and refolding assays. Concentration of total protein (soluble and insoluble) and SDS-PAGE analysis of soluble proteins were also done. RESULTS: Treatment with rutin prevented the loss of α crystallin chaperone property, and protein insolubilization prevailed during selenite-induced cataract. CONCLUSIONS: These results suggest the therapeutic potential of rutin, a bioflavonoid, against selenite-induced cataract, which has been reported in this paper for the first time. The work assumes significance, as this is a novel approach in modulating the chaperone activity of lens crystallins in selenite-induced cataract by a natural product.