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Metabolomic patterns in fatal carbon monoxide poisoning: A forensic toxicology perspective.

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Title: Metabolomic patterns in fatal carbon monoxide poisoning: A forensic toxicology perspective.
Authors: Ariza-Garcia, Wilmar Alexander1,2 (AUTHOR), Pardo-Rodriguez, Daniel3 (AUTHOR), Taborda-Ocampo, Gonzalo4 (AUTHOR), Rosero-Moreano, Milton4 (AUTHOR), Cala, Mónica P.1,3 (AUTHOR)
Source: Forensic Science International. Dec2025, Vol. 377, pN.PAG-N.PAG. 1p.
Subjects: Carbon monoxide poisoning, Forensic toxicology, Biomarkers, Lipidomics, Metabolomics, Lipid metabolism, Poisons
Abstract: Carbon monoxide (CO) poisoning remains a major forensic and public health concern due to its high lethality and diagnostic challenges. Its colorless, odorless nature and the limited reliability of carboxyhemoglobin (COHb) levels—compounded by postmortem changes—complicate toxicological interpretation. This study employed untargeted metabolomics and lipidomics to characterize systemic biochemical alterations in fatal CO poisoning cases. Integrated metabolomic and lipidomic analyses revealed significant dysregulation in lipid-related pathways, including steroid biosynthesis, mitochondrial β-oxidation, fatty acid and sphingolipid metabolism, and lysophospholipid-mediated membrane destabilization. Impaired biosynthesis of highly unsaturated fatty acids (HUFA) was also observed, potentially compromising membrane structure and signaling. These findings highlight widespread metabolic disruption affecting energy homeostasis and lipid signaling. Among the altered metabolites, carnitine 18:2 (CAR 18:2) demonstrated strong discriminative power (AUC = 0.846) between CO-poisoned and control cases, suggesting its value as a forensic biomarker. Additionally, lysophosphatidylcholine 18:2 (LPC 18:2) and sphingomyelin 44:1;O₂ (SM 44:1;O₂) emerged as promising candidates. These results underscore the systemic metabolic impact of CO toxicity and support the continued exploration and implementation of targeted lipidomics as alternative forensic biomarkers in fatal poisonings. • Untargeted metabolomics and lipidomics revealed systemic biochemical disruptions in fatal CO poisoning. • Lipid pathway dysregulation involved β-oxidation, steroid biosynthesis, and sphingolipid metabolism. • Oxidative stress and impaired lipid homeostasis emerged as central toxicodynamic mechanisms. • CAR 18:2, LPC 18:2, and SM 44:1;O₂ demonstrated strong potential as forensic biomarkers. [ABSTRACT FROM AUTHOR]
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Database: Engineering Source
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Abstract:Carbon monoxide (CO) poisoning remains a major forensic and public health concern due to its high lethality and diagnostic challenges. Its colorless, odorless nature and the limited reliability of carboxyhemoglobin (COHb) levels—compounded by postmortem changes—complicate toxicological interpretation. This study employed untargeted metabolomics and lipidomics to characterize systemic biochemical alterations in fatal CO poisoning cases. Integrated metabolomic and lipidomic analyses revealed significant dysregulation in lipid-related pathways, including steroid biosynthesis, mitochondrial β-oxidation, fatty acid and sphingolipid metabolism, and lysophospholipid-mediated membrane destabilization. Impaired biosynthesis of highly unsaturated fatty acids (HUFA) was also observed, potentially compromising membrane structure and signaling. These findings highlight widespread metabolic disruption affecting energy homeostasis and lipid signaling. Among the altered metabolites, carnitine 18:2 (CAR 18:2) demonstrated strong discriminative power (AUC = 0.846) between CO-poisoned and control cases, suggesting its value as a forensic biomarker. Additionally, lysophosphatidylcholine 18:2 (LPC 18:2) and sphingomyelin 44:1;O₂ (SM 44:1;O₂) emerged as promising candidates. These results underscore the systemic metabolic impact of CO toxicity and support the continued exploration and implementation of targeted lipidomics as alternative forensic biomarkers in fatal poisonings. • Untargeted metabolomics and lipidomics revealed systemic biochemical disruptions in fatal CO poisoning. • Lipid pathway dysregulation involved β-oxidation, steroid biosynthesis, and sphingolipid metabolism. • Oxidative stress and impaired lipid homeostasis emerged as central toxicodynamic mechanisms. • CAR 18:2, LPC 18:2, and SM 44:1;O₂ demonstrated strong potential as forensic biomarkers. [ABSTRACT FROM AUTHOR]
ISSN:03790738
DOI:10.1016/j.forsciint.2025.112643