Diquat (DQ) has emerged as an important cause of herbicide poisoning following restrictions on paraquat (PQ) and is associated with multi-organ injury involving the liver, kidneys, and brain. Acute DQ poisoning is characterized by marked lipid metabolic dysregulation, including elevated free fatty acids (FFA) and reduced triglycerides (TG). Nevertheless, the mechanisms responsible for these lipid abnormalities remain unclear. To further characterize the lipidomic landscape of acute DQ poisoning, we performed untargeted serum lipidomics using ultra-high-performance liquid chromatography in combination with high-resolution mass spectrometry in 52 confirmed bipyridyl poisoning cases (32 DQ and 20 PQ). KEGG pathway enrichment analysis revealed significant perturbations in glycerophospholipid, glycerolipid, linoleic acid, α-linolenic acid, and arachidonic acid metabolism following DQ exposure. Within 6 h after ingestion, several O-acylhydroxy fatty acids and fatty acids (20:4) tended to increase, and these lipid alterations appeared earlier than laboratory parameters. Triglyceride (26:0/18:2/18:2) and sphingomyelin (d42:8) were independently associated with 28-day mortality. Compared with DQ poisoning, PQ poisoning exhibited a more pronounced depletion of plasmalogen-phosphatidylethanolamines despite broadly similar overall lipidomic profiles. The observed lipidomic alterations suggest that acute DQ poisoning may promote excessive lipolysis, disrupt glycerophospholipid homeostasis, and impair mitochondria-associated membrane function, thereby potentially contributing to oxidative stress and organ dysfunction. These findings demonstrate substantial lipid metabolic disturbances following acute DQ poisoning and identify candidate lipid markers that warrant further evaluation for diagnosis and prognosis.
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