Lead (Pb) exposure remains a major environmental risk factor for cognitive dysfunction, yet the cellular mechanisms underlying Pb-induced memory impairment are poorly understood. Here, we show that both developmental and adult-onset Pb exposure selectively disrupts protein-synthesis-dependent long-term memory (LTM) in Drosophila melanogaster while sparing other memory forms. Using a mitochondria-targeted redox biosensor (mito-roGFP2-Orp1), we found that Pb elevates mitochondrial oxidative stress and disrupts redox homeostasis in cholinergic neurons and in dorsal-anterior-lateral (DAL) neurons, a critical locus for LTM consolidation. Pb-induced redox imbalance suppresses training-induced de novo protein synthesis in DAL neurons, thereby impairing memory consolidation. Antioxidant treatment with epigallocatechin gallate restores mitochondrial redox balance and rescues LTM by reinstating activity-dependent protein synthesis in DAL neurons. These findings identify mitochondrial redox dysregulation as a key mechanism linking environmental Pb exposure to impaired memory consolidation. Our results further establish a genetically tractable platform for dissecting neurotoxic mechanisms and for evaluating antioxidant-based strategies to mitigate Pb-induced cognitive dysfunction.