Food‐Borne Advanced Lipoxidation End Products: From Processing‐Induced Formation to Systemic Health Effects

Advanced lipoxidation end products (ALEs), formed via lipid-derived reactive carbonyl species (RCS), are critical dietary hazards originating from food processing and endogenous metabolism. To systematically elucidate their health impacts, this review introduces a "processing-bioavailability-toxicity" framework. We emphasize that thermal stress in foods rich in polyunsaturated fatty acids drives ALE accumulation and nutritional deterioration. Crucially, the systemic absorption and metabolic fate of these adducts are fundamentally governed by their physical states-specifically, their distribution between free electrophiles and protein-bound adducts. Upon ingestion, these distinct forms exert toxicity by irreversibly damaging biomolecules and triggering oxidative stress via receptor-mediated pathways, including the receptor for advanced glycation end products (RAGE) and CD36 signaling axes, thereby exacerbating cardiometabolic risks. Accurate evaluation of these hazards requires robust analytical platforms, while LC-MS carbonylomics offers superior specificity for precise site mapping, and advanced spectroscopic techniques (e.g., SERS) provide indispensable complementary insights into macroscopic structural degradation. However, quantifying ultralow-abundance isomers remains a significant bottleneck. Despite these challenges, immediate risk mitigation is achievable through antioxidant application and optimized processing parameters. Ultimately, future research must prioritize establishing integrated exposure databases and applying systems carbonylomics, translating mechanistic insights into evidence-based precision food safety regulations.