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SCOPE: Acrolein (ACR), a lipid peroxidation product, pathologically participates in various chronic diseases. In vitro evidence suggested that dietary dihydrochalcones (DHCs) potentiate safe and alternative therapeutics to synthetic pharmaceuticals for ACR scavenging. Here, we aim to investigate whether ingested DHCs could trap ACR and thereof result in reductions in endogenous ACR in mice. METHODS AND RESULTS: Three doses of phloretin (25, 100, and 400 mg/kg), a major dietary DHC, were orally administrated to mice and 24 h urine and fecal samples were collected, respectively. High-resolution MS-based targeted metabolomics revealed for the first time that phloretin and its oxidized metabolite were able to trap endogenous ACR via formation of ACR conjugates. Quantification further demonstrated that a) more than 13% of ingested phloretin can dose-dependently trap 0.77−9.92 nmol of ACR within 24 h; b) phloretin ingestion leads to marked reductions in both free ACR and ACR metabolites in mouse urine compared to control; and c) trapping reactions by phloretin can account for up to 20.1% of the total decreases in endogenous ACR, depending on the administration doses. CONCLUSION: Findings from this study indicates that regular consumption of DHCs-rich diets holds great promise to alleviate the development of ACR-associated chronic diseases.