Human exposure to PM2.5 and PM10 has been linked to respiratory and cardiovascular diseases through inflammation activation. The kynurenine pathway is associated with inflammation, and it is necessary to investigate the effects of long-term PM2.5 and PM10 exposure on this pathway. This study aimed to conduct a cross-sectional analysis of long-term PM2.5 and PM10 exposure’s impact on the kynurenine pathway using proton NMR spectroscopy (¹H-NMR). The participants were divided into a low-PM-exposure group (LG; n = 98), and a high-PM-exposure group (HG; n = 92). The metabolites of tryptophan were determined in blood by ¹H-NMR. Serotonin, cinnabarinic acid, xanthurenic acid, 5-hydroxytryptophan, indoleacetic acid, tryptamine, melatonin, L-tryptophan, 5-hydroxy-L-tryptophol, indoxyl, 2-aminobenzoic acid, 5-HTOL, hydroxykynurenine, L-3-hydroxykynurenine, N-formyl kynurenine, 3-hydroxy anthranilic acid, kynurenic acid, and picolinic acid significantly increased (p < 0.05) in the HG group. Conversely, NAD and quinolinic acid significantly decreased in the HG group compared to the LG group. The enzyme activities of indoleamine 2,3-dioxygenase and formamidase significantly decreased, while kynureninase and kynurenine monooxygenase significantly increased. The kynurenine pathway is linked to inflammation and non-communicable diseases. Disruption of the kynurenine pathway from particulate matter might promote diseases. Reducing exposure to the particulate matter is crucial for preventing adverse health effects.

A new approach for assisting in the diagnosis of coronary artery disease (CAD) as a cause of death is essential in cases where complete autopsy examinations are not feasible. The purine pathway has been associated with CAD patients, but the understanding of this pathway in postmortem changes needs to be explored. This study investigated the levels of blood purine metabolites in CAD after death. Heart blood samples (n = 60) were collected and divided into CAD (n = 23) and control groups (n = 37). Purine metabolites were measured via proton nuclear magnetic resonance. Guanosine triphosphate (GTP), nicotinamide adenine dinucleotide (NAD), and xanthine levels significantly decreased (p < 0.05); conversely, adenine and deoxyribose 5-phosphate levels significantly increased (p < 0.05) in the CAD group compared to the control group. Decreasing xanthine levels may serve as a marker for predicting the cause of death in CAD (AUC = 0.7). Our findings suggest that the purine pathway was interrupted by physiological processes after death, causing the metabolism of the deceased to differ from that of the living. Additionally, xanthine levels should be studied further to better understand their relationship with CAD and used as a biomarker for CAD diagnosis under decomposition and skeletonization settings.

Background and purpose: Glyphosate-based herbicides, extensively utilized worldwide, raise concerns regarding potential human risks due to the detection of glyphosate (GLY) in human body fluids. This study aims to address critical knowledge gaps regarding whether GLY undergoes metabolism in humans, particularly considering the limited information available on human metabolism. Experimental approach: The study investigated GLY and its metabolites in eight amenity horticultural workers using proton nuclear magnetic resonance (1H-NMR) data analysis. Multiple spot urine samples were collected before and after herbicide applications. Key results: Findings reveal the presence of GLY and its metabolites (AMPA, formaldehyde, sarcosine, glyoxylic acid, and methylamine). Results demonstrate a moderate correlation between median GLY concentration and its metabolites within the studied population. Conclusion: Persuasive evidence suggests the potential metabolism of GLY in humans. 1H-NMR data analysis might be a promising technique for determining the metabolism of GLY in humans, offering valuable insights into urinary excretion patterns.

Background: Reliable identification remains a cornerstone of forensic investigations, particularly when encountering degraded remains or suboptimal biological evidence. This study evaluates the potential of dentine metabolomics, utilizing proton nuclear magnetic resonance (¹H-NMR) spectroscopy, to detect cancer-associated metabolic signatures in dental tissues for forensic applications. Methods: Forty-four non-carious second molars were analyzed, comprising 22 samples from deceased individuals with a documented history of cancer and 22 age- and sex-matched controls. Metabolomic profiling was conducted using ¹H-NMR spectroscopy to identify and quantify dentine metabolites. Statistical evaluation included unsupervised principal component analysis (PCA), partial least squares discriminant analysis (PLS-DA), receiver operating characteristic (ROC) curve analysis, and exploratory binary logistic regression. Results: Among the 209 identified metabolites, inosinic acid and 2-ketobutyric acid were identified as the most robust discriminative biomarkers across both multivariate and univariate frameworks. The exploration within-sample predictive model achieved a Nagelkerke R² of 0.822 and an overall classification accuracy of 90.9%, with a specificity of 95.5% and a sensitivity of 86.4%. These key metabolites are fundamentally associated with purine metabolism and oxidative stress pathways frequently dysregulated in oncogenesis. Conclusions: This pilot study suggests that dentine may retain metabolomic information associated with cancer comorbidity under heterogeneous postmortem conditions. However, the findings remain exploratory and require validation in larger cohorts with standardized postmortem variables before practical forensic implementation.