Preventive Effects of Tomatidine Against Sodium Selenite-induced Oxidative Damage and Cataractogenesis in Rats via Activating Nrf-2 Pathway

Background: Cataracts, characterized by the gradual opacification of the crystalline lens, represent a primary cause of vision impairment worldwide, placing a considerable burden on individuals and healthcare systems. Understanding the precise mechanisms behind cataract formation is essential to developing targeted preventive and treatment approaches. Objectives: The current study was performed to investigate the preventive mechanisms of tomatidine against seleniteinduced cataractogenesis in a rat pup model. Materials and Methods: Cataracts were experimentally induced in rat pups by administering sodium selenite, followed by administration of tomatidine at dosages of 10 and 20 mg/kg, respectively. The lens opacification level, oxidative stress biomarker levels, calcium, and ascorbic acid concentrations in the lens tissues of rat pups were assessed. The concentrations of antioxidants, inflammatory cytokines, nuclear factor erythroid 2-related factor 2 (Nrf-2), nuclear factor-κB (NF-κB), and cyclooxygenase-2 (COX-2) were evaluated in the lenses of rat pups using kits. Results: The results of this study indicate that tomatidine administration significantly diminished lens opacification level, calcium, oxidative stress biomarkers, and increased ascorbic acid and antioxidant levels in the lens tissues of cataract-induced rat pups. Moreover, the tomatidine treatment significantly reduced the inflammatory cytokine levels, elevated antioxidant concentrations, reduced COX-2 and NF-κB levels, and enhanced Nrf-2 levels in the lens tissues of cataract-induced rat pups. Conclusion: The findings of this study suggested that tomatidine may be effective in preventing the formation of seleniteinduced cataract in rat pups. These outcomes highlight that tomatidine shows promise as a potential therapeutic agent for cataracts.