PURPOSE:The present study was aimed at investigating the possible antioxidant potential of curcumin at a dose of 75 mg/kg body weight on selenite-induced cataract in experimental rat pups.

METHODS:Group I: Control rat pups receiving physiological saline; Group II: Selenite-induced group (15 microM/kg body wt); Group III: Selenite-induced group co-treated with curcumin (single dose of curcumin orally 75 mg/kg body wt); Group IV: Selenite-induced animals post-treated (after 24 hrs) with curcumin at a dose mentioned for group III; Group V: Rat pups were pretreated with curcumin (dose as mentioned in Group III), 24 hrs before the administration of selenite. Encapsulated lenses liver, kidney, and serum were analyzed for antioxidant enzymes and malondialdehyde, a marker of lipid peroxidation.

RESULTS:Intraperitoneal injection of sodium selenite (15 microM/kg body wt) to 8-10-day-old rat pups led to severe oxidative stress in eye lens as evidenced by enhanced LPO levels that led to cataract formation. Sodium selenite also led to decrease in activities of SOD, GST, GPx, CAT with simultaneous decrease in the levels of GSH, vitamin C, and vitamin E. Treatment with curcumin (75 mg/kg body wt) led to a significant decrease in the levels of LPO, enzymic antioxidants, and nonenzymic antioxidants, which were similar to that of control.

CONCLUSIONS:Curcumin suppressed selenite-induced oxidative stress and cataract formation in rat pups. The presence of oxidative stress in selenite cataract development and its prevention by curcumin support the possibility that the natural consumption of curcumin in food can help prevent the onset of senile cataract.

Several studies have suggested that antioxidants retard the process of cataractogenesis by scavenging free oxygen radicals. The present study sought to assess the efficacy of the antioxidant acetyl-L-carnitine (ALCAR) in preventing selenite-induced 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 degrees C in Dulbecco's Modified Eagle Medium (DMEM) alone (control, Group I), or in DMEM containing 100 microM of selenite (Group II) or in DMEM containing 100 microM of selenite and 200 microM/ml ALCAR added at the same time as selenite (Group IIIa) or 30 min, 1 h or 2 h later (Groups IIIb, IIIc and IIId, respectively). Gross morphological examination of these lenses revealed dense opacification (cataract formation) in Group II, minimal opacification in some Group IIIa lenses and no opacification in Group I. The mean activities of the antioxidant enzymes catalase and glutathione peroxidase were significantly lower in Group II than in Group I or Group IIIa lenses, while malondialdehyde concentration (an indicator of lipid peroxidation) was significantly higher in Group II lenses than that in Group I or Group IIIa lenses. The second, in vivo phase of the study revealed dense opacification (cataract formation) in 100% of Wistar rat pups receiving subcutaneous sodium selenite alone (19 microM/kg body weight) but in only 37.5% of those receiving subcutaneous selenite and intraperitoneal ALCAR. These data suggest that ALCAR is able to significantly retard experimental selenite-induced cataractogenesis.