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Antioxidants
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Disentangling the Association between Chronic Diseases and Oxidative Stress through...
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Disentangling the Association between Chronic Diseases and Oxidative Stress through Metabolomics

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (31 December 2023) | Viewed by 6617

Special Issue Editor

Dr. Daniel Monleon

E-Mail Website
Guest Editor
Department of Pathology, Medicine and Odontology Faculty, University of Valencia, 46010 Valencia, Spain
Interests: tumor metabolism for precision medicine in cancer; healthy aging; frailty and metabolic age; host- microbiota co-metabolism influence on health; cardiometabolic and cardiovascular disease; biophysical characterization of lipoproteins particles in plasma using NMR spectroscopy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Oxidative stress is the result of metabolic disbalance and can impact all components of the cell, including DNA, proteins, and metabolites. Many studies suggest an essential role of oxidative stress in the pathogenesis of chronic diseases, including cardiovascular diseases, diabetes, and neurodegenerative diseases. Studies analyzing the metabolic impact of oxidative stress on experimental models or human cohorts are scarce. Metabolomics provides information on a wide range of molecular processes through the measurement of individual metabolites. Metabolomics stands at the end of the -omic cascade (from genomics, transcriptomics, and proteomics to metabolomics), and changes in the metabolome represent the last response to genetic, chemical, and environmental alterations. As a consequence, the metabolome is closely linked to the phenotype and constitutes an important tool for detecting and understanding physiological and pathophysiological states. The goal of this Special Issue is to collect evidence and provide mechanistic insight to better understand the association between oxidative stress and chronic diseases through the analysis of metabolites.

Dr. Daniel Monleon
Guest Editor

Manuscript Submission Information

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Keywords

  • oxidative stress
  • metabolomics
  • chronic diseases
  • cardiovascular disease
  • diabetes
  • neurodegenerative diseases

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Published Papers (4 papers)

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Research

16 pages, 1177 KiB  
Article
Effects of Contagious Respiratory Pathogens on Breath Biomarkers
by Nele Kemnitz, Patricia Fuchs, Rasmus Remy, Leo Ruehrmund, Julia Bartels, Ann-Christin Klemenz, Phillip Trefz, Wolfram Miekisch, Jochen K. Schubert and Pritam Sukul
Antioxidants 2024, 13(2), 172; https://doi.org/10.3390/antiox13020172 - 29 Jan 2024
Viewed by 1518
Abstract
Due to their immediate exhalation after generation at the cellular/microbiome levels, exhaled volatile organic compounds (VOCs) may provide real-time information on pathophysiological mechanisms and the host response to infection. In recent years, the metabolic profiling of the most frequent respiratory infections has gained [...] Read more.
Due to their immediate exhalation after generation at the cellular/microbiome levels, exhaled volatile organic compounds (VOCs) may provide real-time information on pathophysiological mechanisms and the host response to infection. In recent years, the metabolic profiling of the most frequent respiratory infections has gained interest as it holds potential for the early, non-invasive detection of pathogens and the monitoring of disease progression and the response to therapy. Using previously unpublished data, randomly selected individuals from a COVID-19 test center were included in the study. Based on multiplex PCR results (non-SARS-CoV-2 respiratory pathogens), the breath profiles of 479 subjects with the presence or absence of flu-like symptoms were obtained using proton-transfer-reaction time-of-flight mass spectrometry. Among 223 individuals, one respiratory pathogen was detected in 171 cases, and more than one pathogen in 52 cases. A total of 256 subjects had negative PCR test results and had no symptoms. The exhaled VOC profiles were affected by the presence of Haemophilus influenzae, Streptococcus pneumoniae, and Rhinovirus. The endogenous ketone, short-chain fatty acid, organosulfur, aldehyde, and terpene concentrations changed, but only a few compounds exhibited concentration changes above inter-individual physiological variations. Based on the VOC origins, the observed concentration changes may be attributed to oxidative stress and antioxidative defense, energy metabolism, systemic microbial immune homeostasis, and inflammation. In contrast to previous studies with pre-selected patient groups, the results of this study demonstrate the broad inter-individual variations in VOC profiles in real-life screening conditions. As no unique infection markers exist, only concentration changes clearly above the mentioned variations can be regarded as indicative of infection or colonization. Full article
(This article belongs to the Special Issue Disentangling the Association between Chronic Diseases and Oxidative Stress through Metabolomics)
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26 pages, 11707 KiB  
Article
Methylglyoxal-Derived Nucleoside Adducts Drive Vascular Dysfunction in a RAGE-Dependent Manner
by Seigmund Wai Tsuen Lai, Supriyo Bhattacharya, Edwin De Jesus Lopez Gonzalez and Sarah C. Shuck
Antioxidants 2024, 13(1), 85; https://doi.org/10.3390/antiox13010085 - 10 Jan 2024
Viewed by 1620
Abstract
Diabetic kidney disease (DKD) is a leading cause of death in patients with diabetes. An early precursor to DKD is endothelial cell dysfunction (ECD), which often precedes and exacerbates vascular disease progression. We previously discovered that covalent adducts formed on DNA, RNA, and [...] Read more.
Diabetic kidney disease (DKD) is a leading cause of death in patients with diabetes. An early precursor to DKD is endothelial cell dysfunction (ECD), which often precedes and exacerbates vascular disease progression. We previously discovered that covalent adducts formed on DNA, RNA, and proteins by the reactive metabolic by-product methylglyoxal (MG) predict DKD risk in patients with type 1 diabetes up to 16 years pre-diagnosis. However, the mechanisms by which MG adducts contribute to vascular disease onset and progression remain unclear. Here, we report that the most predominant MG-induced nucleoside adducts, N2-(1-carboxyethyl)-deoxyguanosine (CEdG) and N2-(1-carboxyethyl)-guanosine (CEG), drive endothelial dysfunction. Following CEdG or CEG exposure, primary human umbilical vein endothelial cells (HUVECs) undergo endothelial dysfunction, resulting in enhanced monocyte adhesion, increased reactive oxygen species production, endothelial permeability, impaired endothelial homeostasis, and exhibit a dysfunctional transcriptomic signature. These effects were discovered to be mediated through the receptor for advanced glycation end products (RAGE), as an inhibitor for intracellular RAGE signaling diminished these dysfunctional phenotypes. Therefore, we found that not only are MG adducts biomarkers for DKD, but that they may also have a role as potential drivers of vascular disease onset and progression and a new therapeutic modality. Full article
(This article belongs to the Special Issue Disentangling the Association between Chronic Diseases and Oxidative Stress through Metabolomics)
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33 pages, 4686 KiB  
Article
Definition of the Neurotoxicity-Associated Metabolic Signature Triggered by Berberine and Other Respiratory Chain Inhibitors
by Ilinca Suciu, Johannes Delp, Simon Gutbier, Julian Suess, Lars Henschke, Ivana Celardo, Thomas U. Mayer, Ivano Amelio and Marcel Leist
Antioxidants 2024, 13(1), 49; https://doi.org/10.3390/antiox13010049 - 28 Dec 2023
Cited by 1 | Viewed by 1554
Abstract
To characterize the hits from a phenotypic neurotoxicity screen, we obtained transcriptomics data for valinomycin, diethylstilbestrol, colchicine, rotenone, 1-methyl-4-phenylpyridinium (MPP), carbaryl and berberine (Ber). For all compounds, the concentration triggering neurite degeneration correlated with the onset of gene expression changes. The mechanistically diverse [...] Read more.
To characterize the hits from a phenotypic neurotoxicity screen, we obtained transcriptomics data for valinomycin, diethylstilbestrol, colchicine, rotenone, 1-methyl-4-phenylpyridinium (MPP), carbaryl and berberine (Ber). For all compounds, the concentration triggering neurite degeneration correlated with the onset of gene expression changes. The mechanistically diverse toxicants caused similar patterns of gene regulation: the responses were dominated by cell de-differentiation and a triggering of canonical stress response pathways driven by ATF4 and NRF2. To obtain more detailed and specific information on the modes-of-action, the effects on energy metabolism (respiration and glycolysis) were measured. Ber, rotenone and MPP inhibited the mitochondrial respiratory chain and they shared complex I as the target. This group of toxicants was further evaluated by metabolomics under experimental conditions that did not deplete ATP. Ber (204 changed metabolites) showed similar effects as MPP and rotenone. The overall metabolic situation was characterized by oxidative stress, an over-abundance of NADH (>1000% increase) and a re-routing of metabolism in order to dispose of the nitrogen resulting from increased amino acid turnover. This unique overall pattern led to the accumulation of metabolites known as biomarkers of neurodegeneration (saccharopine, aminoadipate and branched-chain ketoacids). These findings suggest that neurotoxicity of mitochondrial inhibitors may result from an ensemble of metabolic changes rather than from a simple ATP depletion. The combi-omics approach used here provided richer and more specific MoA data than the more common transcriptomics analysis alone. As Ber, a human drug and food supplement, mimicked closely the mode-of-action of known neurotoxicants, its potential hazard requires further investigation. Full article
(This article belongs to the Special Issue Disentangling the Association between Chronic Diseases and Oxidative Stress through Metabolomics)
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18 pages, 7246 KiB  
Article
Altered Lipid Moieties and Carbonyls in a Wistar Rat Dietary Model of Subclinical Fatty Liver: Potential Sex-Specific Biomarkers of Early Fatty Liver Disease?
by María Martín-Grau, Mercedes Pardo-Tendero, Pilar Casanova, Mar Dromant, Vannina G. Marrachelli, Jose Manuel Morales, Consuelo Borrás, Serena Pisoni, Sabrina Maestrini, Anna M. Di Blasio and Daniel Monleon
Antioxidants 2023, 12(10), 1808; https://doi.org/10.3390/antiox12101808 - 28 Sep 2023
Cited by 3 | Viewed by 1157
Abstract
Non-alcoholic fatty liver disease (NAFLD) is a condition in which excess fat builds up in the liver. To date, there is a lack of knowledge about the subtype of lipid structures affected in the early stages of NAFLD. The aim of this study [...] Read more.
Non-alcoholic fatty liver disease (NAFLD) is a condition in which excess fat builds up in the liver. To date, there is a lack of knowledge about the subtype of lipid structures affected in the early stages of NAFLD. The aim of this study was to analyze serum and liver lipid moieties, specifically unsaturations and carbonyls, by nuclear magnetic resonance (NMR) in a subclinical Wistar rat model of NAFLD for detecting early alterations and potential sex dimorphisms. Twelve weeks of a high-fat diet (HFD) induced fat accumulation in the liver to a similar extent in male and female Wistar rats. In addition to total liver fat accumulation, Wistar rats showed a shift in lipid subtype composition. HFD rats displayed increased lipid carbonyls in both liver and serum, and decreased in unsaturated fatty acids (UFAs) and polyunsaturated fatty acids (PUFAs), with a much stronger effect in male than female animals. Our results revealed that the change in fat was not only quantitative but also qualitative, with dramatic shifts in relevant lipid structures. Finally, we compared the results found in Wistar rats with an analysis in a human patient cohort of extreme obesity. For the first time to our knowledge, lipid carbonyl levels and lipoproteins profiles were analyzed in the context of subclinical NAFLD. The association found between lipid carbonyls and alanine aminotransferase (ALT) in a human cohort of extremely obese individuals further supports the potential role of lipid moieties as biomarkers of early NAFLD. Full article
(This article belongs to the Special Issue Disentangling the Association between Chronic Diseases and Oxidative Stress through Metabolomics)
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