Abstract: The selenium-induced cataract animal model is extensively utilized in investigating age-related cataracts due to its convenience and high reproducibility. In vivo models can be established by subcutaneous or intraperitoneal injection of sodium selenite solution into rats, while in vitro models can be created by incubating isolated rat lenses in a medium containing a high concentration of sodium selenite. Sodium selenite arrests lens epithelial cells in the cell cycle, accelerating apoptosis. Furthermore, it induces oxidative stress within the lens, reducing catalase and superoxide dismutase activities, increasing malondialdehyde levels, and decreasing nicotinamide adenine dinucleotide phosphate concentrations. These changes alter the metabolic state of lens cells, disrupt calcium ion homeostasis, and activate calpains, leading to proteolysis, phase transition of the lens, and loss of cytoskeletal proteins, ultimately resulting in lens opacification. Previous studies have confirmed that vitamin C and the calpain inhibitor E64 could delay the progression of selenium-induced cataracts; however, the effects of sodium selenite on oxidative stress in liver and kidney tissues should also be considered. (Int Rev Ophthalmol, 2025, 49:  19-24)

Key words: selenium, cataract, animal model