Apoptosis of lens epithelial cells (LECs) is a key feature of age-related cataracts. With the aging process, the energy supply mechanism of LEC changes, resulting in impaired glucose metabolism, which in turn causes increased oxidative stress and apoptosis of cells. However, the exact intrinsic mechanism has not been fully clarified. This study shows that in the Sodium selenite-induced cataract rat model, the level of lactylation in LECs increases significantly as the disease progressed. Inhibiting lactylation can reduce cell apoptosis and delay the formation of cataracts. Specifically, the excessive lactylation of the H4K8 site directly regulates the expression of RNA-binding protein ZMAT3. After the ZMAT3 level is elevated, it can directly bind to the downstream target gene-the key glutamate metabolic enzyme GLS and regulate its mRNA stability. This leads to the downregulation of GLS expression, thus inhibiting glutamate metabolism. As a result, glutathione and other antioxidants are rapidly exhausted, reducing the antioxidant ability of LEC and eventually inducing cell apoptosis. These findings elucidate the disruption of the balance between oxidative phosphorylation and glycolysis in LECs, promoting cell apoptosis by regulating specific lactylation. This study further indicates that H4K8la and ZMAT3 are potential therapeutic targets for the prevention and treatment of age-related cataracts.