Ursodeoxycholic acid prevents selenite-induced oxidative stress and alleviates cataract formation: In vitro and in vivo studies.Mol Vis. 2012; 18:151-60.MV
To evaluate the antioxidative and anticataractogenic potential effect of ursodeoxycholic acid (UDCA) on selenite-induced cataract in vitro and in vivo.
Enucleated rat lenses were incubated in M199 medium alone (Group I), with 200 μM selenite (Group II), or with 200 μM selenite and 500 μM UDCA (Group III). Selenite was administered on the third day and UDCA treatment was from the second to the fifth day. The development of cataracts was observed under an inverted microscope. Total antioxidative capabilities (T-AOC), mean activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (Gpx), glutathione reductase (GR) and glutathione S-transferase (GST), levels of reduced glutathione (GSH), malondialdehyde (MDA), and total sulfhydryl content were analyzed in lenticular samples. In vivo, cataracts were induced in 12-day-old pups by single subcutaneous injections of sodium selenite. The test groups received 180 mg/kg bodyweight/day of UDCA intraperitoneally on postpartum days 11-16 or 0.5% UDCA drops four times daily on postpartum days 11-25.
In vitro, morphological examination of the lenses revealed dense vacuolization and opacification in Group II, minimal vacuolization in 12.5% of Group III, and no opacification in 87.5% of Group III. In Group I, all lenses were clear. UDCA significantly (p<0.05) restored GSH and total sulfhydryl, and decreased MDA levels. T-AOC and the mean activities of the antioxidant enzymes were elevated following treatment with UDCA. In vivo, 0.5% UDCA drops resulted in only 20% nuclear cataract development and 180 mg/kg of UDCA intraperitoneally led to 50% development, compared to 100% in the control group (p<0.05).
UDCA prevents selenite toxicity and cataractogenesis by maintaining antioxidant status and GSH, protecting the sulfhydryl group, and inhibiting lipid peroxidation in lenses.