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

IF 2.5 3区医学 Q1 MEDICINE, LEGAL

Forensic science international Pub Date : 2025-09-04 DOI:10.1016/j.forsciint.2025.112643

Wilmar Alexander Ariza-Garcia , Daniel Pardo-Rodriguez , Gonzalo Taborda-Ocampo , Milton Rosero-Moreano , Mónica P. Cala

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引用次数: 0

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.

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致命一氧化碳中毒的代谢组学模式：法医毒理学视角

一氧化碳中毒由于其高致死率和诊断方面的挑战，仍然是一个主要的法医和公共卫生问题。其无色、无味的特性和有限的可靠的碳氧血红蛋白（COHb）水平——加上死后的变化——使毒理学解释复杂化。本研究采用非靶向代谢组学和脂质组学来表征致死性一氧化碳中毒病例的全身生化改变。综合代谢组学和脂质组学分析揭示了脂质相关途径的显著失调，包括类固醇生物合成、线粒体β氧化、脂肪酸和鞘脂代谢以及溶血磷脂介导的膜不稳定。高不饱和脂肪酸（HUFA）的生物合成也被破坏，可能损害膜结构和信号传导。这些发现强调了广泛的代谢破坏影响能量稳态和脂质信号。在改变的代谢物中，肉碱18:2 （CAR 18:2）在co中毒与对照之间表现出较强的鉴别力（AUC = 0.846），提示其作为法医生物标志物的价值。溶血磷脂酰胆碱18:2 (LPC 18:2)，鞘磷脂44:1；O₂（sm44:1;O₂）成为候选。这些结果强调了一氧化碳毒性对全身代谢的影响，并支持继续探索和实施靶向脂质组学作为致命中毒的替代法医生物标志物。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Forensic science international 医学-医学：法

CiteScore

5.00

自引率

9.10%

发文量

285

审稿时长

49 days

期刊介绍： Forensic Science International is the flagship journal in the prestigious Forensic Science International family, publishing the most innovative, cutting-edge, and influential contributions across the forensic sciences. Fields include: forensic pathology and histochemistry, chemistry, biochemistry and toxicology, biology, serology, odontology, psychiatry, anthropology, digital forensics, the physical sciences, firearms, and document examination, as well as investigations of value to public health in its broadest sense, and the important marginal area where science and medicine interact with the law. The journal publishes: Case Reports Commentaries Letters to the Editor Original Research Papers (Regular Papers) Rapid Communications Review Articles Technical Notes.