Lisinopril Attenuates Selenite Induced Experimental Cataract Development: an in Vitro Study

Several studies have suggested that angiotensin converting enzyme inhibitors retard the process of cataractogenesis by scavenging free oxygen radicals. The present study sought to assess the efficacy of the ACE inhibitor Lisinopril in preventing selenite-induced cataractogenesis in an experimental setting. The in vitro phase of the study was performed on lenses from wistar rats incubated for 24 h at 37C in Dulbecco’s 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 10 μM lisinopril (Group III). Gross morphological examination of these lenses revealed dense opacification (cataract formation) in Group II, minimal opacification in Group III lenses and no opacification in Group I. The mean activities of the reduced glutathione, total protein and water soluble protein were significantly lower in Group II than in Group I or Group III lenses, while malondialdehyde concentration (an indicator of lipid peroxidation), insoluble protein and lens Ca concentration was significantly higher in Group II lenses than that in Group I or Group III lenses. Reversal of these changes was found to be significant in lisinopril treated group of lenses. These data suggest that lisinopril is able to significantly retard experimental selenite-induced cataractogenesis.