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This study investigated the protective effect of carbon monoxide releasing molecule-3 (CORM-3), the classical donor of carbon monoxide, on selenite-induced cataract in rats and explore its possible mechanism. Sprague-Dawley rat pups treated with sodium selenite (Na 2 SeO 3 ) were chosen as the cataract model. Fifty rat pups were randomly divided into 5 groups: Control group, Na 2 SeO 3  (3.46 mg/kg) group, low-dose CORM-3 (8 mg/kg/d) + Na 2 SeO 3  group, high-dose CORM-3 (16 mg/kg/d) + Na 2 SeO 3  group, and inactivated CORM-3 (iCORM-3) (8 mg/kg/d) + Na 2 SeO 3  group. The protective effect of CORM-3 was tested by lens opacity scores, hematoxylin and eosin staining, TdT-mediated dUTP nick-end labeling assay, and enzyme-linked immunosorbent assay. Besides, quantitative real-time PCR and western blotting were used for mechanism validation. Na 2 SeO 3  induced nuclear cataract rapidly and stably, and the achievement ratio of Na 2 SeO 3  group was 100%. CORM-3 alleviated lens opacity of selenite-induced cataract and attenuated the morphological changes of the rat lens. The levels of antioxidant enzymes GSH and SOD in rat lens were also increased by CORM-3 treatment. CORM-3 significantly reduced the ratio of apoptotic lens epithelial cells, besides, CORM-3 decreased the expression of Cleaved Caspase-3 and Bax induced by selenite and increased the expression of Bcl-2 in rat lens inhibited by selenite. Moreover, Nrf-2 and HO-1 were upregulated and Keap1 was downregulated after CORM-3 treatment. While iCORM-3 did not exert the same effect as CORM-3. Exogenous CO released from CORM-3 alleviates oxidative stress and apoptosis in selenite-induced rat cataract  via  activating Nrf2/HO-1 pathway. CORM-3 may serve as a promising preventive and therapeutic strategy for cataract.

Carbon Monoxide Releasing Molecule-3 Alleviates Oxidative Stress and Apoptosis in Selenite-Induced Cataract in Rats via Activating Nrf2/HO-1 Pathway