Acetyl-L-Carnitine Prevents Selenite-Induced Cataractogenesis in an Experimental Animal Model

Abstract

Purpose: To investigate whether acetyl-L-carnitine (ALCAR) retards selenite-induced cataractogenesis in vivo. Methods: On postpartum day 10, group I pups received intraperitoneal saline and group II and group III pups received subcutaneous sodium selenite; Group III pups also received intraperitoneal ALCAR once daily on postpartum days 9–14. Both eyes of each pup were examined up to postpartum day 30. After sacrifice, extricated pup lenses were analyzed for antioxidant and redox system components. Results: There was dense lenticular opacification in all group II pups, minimal opacification in 33% of group III pups, and no opacification in 67% of group III and in all group I pups. Group II lenses exhibited significantly lower values of antioxidant and redox system components and higher malondialdehyde concentrations than group I or group III lenses. Conclusion: ALCAR prevents selenite-induced cataractogenesis in Wistar rat pups, possibly by inhibiting depletion of antioxidant enzyme and redox system components and inhibiting lipid peroxidation.

KEYWORDS:

• acetyl-L-carnitine
• antioxidant enzymes
• cataractogenesis
• oxidative stress
• selenite cataract