Selenite reaches the lens of ocular tissues through systemic circulation. On one hand, it oxidizes protein sulfhydryl groups, inhibiting Ca²⁺-ATPase, which leads to massive accumulation of Ca²⁺ in lens nucleus fibers. This activates calpains in the nucleus fibers, hydrolyzing β-crystallin and other lens proteins, turning partially hydrolyzed lens proteins insoluble. On the other hand, selenite can react with trace amounts of hydroxyl radicals in aqueous humor to generate various reactive oxygen species (ROS). These ROS attack lens proteins and various amino acids, damaging and cross-linking lens proteins to form insoluble high-molecular-weight aggregates that deposit in the lens, resulting in lens opacification and the formation of selenite-induced cataract.

SD suckling rats (male and female, 10 days old)
Modeling method: Sodium selenite at different concentrations was subcutaneously injected into the nape once every other day for a total of 3 injections to successfully establish a selenite-induced cataract model.
Evaluation indicators: ophthalmoscope observation, lens opacity score, HE staining

Ophthalmoscope observation

Lens opacity score

HE staining of eyeball tissue