Objectives: Human nucleus pulposus cells (HNPCs), the primary cellular constituents of the intervertebral disc, are central to the pathogenesis of intervertebral disc degeneration (IVDD). Oxidative stress–induced mitochondrial dysfunction leads to intracellular metabolic imbalance and has been implicated in IVDD. This study investigated the role and molecular mechanism of glutamate dehydrogenase 1 (GLUD1) in hydrogen peroxide (H₂O₂)–challenged HNPCs relevant to IVDD. Methods: HNPCs were exposed to H₂O₂ to establish an oxidative stress model. Cell viability was assessed using the CCK-8 assay. Mitochondrial function was evaluated by measuring the oxygen consumption rate (OCR) and mitochondrial membrane potential. GLUD1 expression was quantified by qRT-PCR and Western blotting. The regulatory relationship between METTL3 and GLUD1 was examined by MeRIP-qPCR and a luciferase reporter assay. Results: H₂O₂ treatment decreased OCR and mitochondrial membrane potential in HNPCs and reduced alpha-ketoglutarate (α-KG) levels and GLUD1 expression. GLUD1 knockdown exacerbated H₂O₂-induced mitochondrial dysfunction, whereas GLUD1 overexpression alleviated it. METTL3 regulated GLUD1 mRNA stability by inducing GLUD1 m6A modification via YTHDF2, thereby modulating H₂O₂-induced mitochondrial dysfunction. Conclusion: GLUD1 protects HNPCs from H₂O₂-induced mitochondrial dysfunction through the glutamate/α-KG metabolic axis.