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A Metabolomics Approach to Tackling Toxicological and Pharmacological Issues: 2nd Edition

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Toxicology".

Deadline for manuscript submissions: 20 January 2025 | Viewed by 2418

Special Issue Editors

Dr. Nuno G. Oliveira

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Guest Editor
Research Institute for Medicines (iMed.ULisboa), Faculty of Pharmacy, Universidade de Lisboa, 1649-003 Lisbon, Portugal
Interests: mechanisms of toxicity; genotoxicity; DNA damage; oxidative stress inducers; antioxidants; SOD mimics; chemotherapeutic drugs; DNA repair inhibitors; cytotoxicity
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Paula Guedes de Pinho

E-Mail Website
Guest Editor
UCIBIO-REQUIMTE, Laboratory of Toxicology, Department of Biological Sciences, Faculty of Pharmacy, University of Porto, 4050-313 Porto, Portugal
Interests: metabolomics; urological cancers; toxicology; toxicometabolomics; drugs of abuse
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The identification and quantification of metabolites responding to a specific stimulus is of the utmost importance in tackling toxicological and pharmacological issues. In the field of metabolomics, information concerning the pattern of the low-molecular-weight compounds generated in a biological system upon exposure to xenobiotics provides new insights into the cellular and organ-specific pathways involved.

Metabolomics thus represents a powerful tool with which to evaluate the mode of action of drugs and chemical contaminants. Moreover, toxicometabolomics and pharmacometabolomics data may clarify the differences observed in drug responses (i.e., responders vs. non-responders) and help identify biomarkers related to drug efficacy or toxicity. These approaches are also critical to providing pharmacokinetics (PK) and pharmacodynamics (PD) data for use in precision medicine.

In view of this, we are inviting submissions of experimental work and review articles on pertinent subjects within the scope of this Special Issue. This is an excellent opportunity for researchers from different fields of expertise to disseminate their recent findings and stay up to date on this emerging topic.

Dr. Nuno G. Oliveira
Dr. Paula Guedes De Pinho
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • metabolomics
  • metabolites
  • drugs
  • contaminants
  • xenobiotics
  • toxicity
  • pharmacology
  • toxicology

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Published Papers (2 papers)

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Research

18 pages, 8545 KiB  
Article
Probiotics as Potential Tool to Mitigate Nucleotide Metabolism Alterations Induced by DiNP Dietary Exposure in Danio rerio
by Christian Giommi, Francesca Maradonna, Claudia Ladisa, Hamid R. Habibi and Oliana Carnevali
Int. J. Mol. Sci. 2024, 25(20), 11151; https://doi.org/10.3390/ijms252011151 - 17 Oct 2024
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Abstract
Diisononyl phthalate, classified as endocrine disruptor, has been investigate to trigger lipid biosynthesis in both mammalian and teleostean animal models. Despite this, little is known about the effects of DiNP exposure at tolerable daily intake level and the possible mechanisms of its toxicity. [...] Read more.
Diisononyl phthalate, classified as endocrine disruptor, has been investigate to trigger lipid biosynthesis in both mammalian and teleostean animal models. Despite this, little is known about the effects of DiNP exposure at tolerable daily intake level and the possible mechanisms of its toxicity. Probiotics, on the other hand, were demonstrated to have beneficial effects on the organism’s metabolism and recently emerged as a possible tool to mitigate the EDC toxicity. In the present study, using a metabolomic approach, the potential hepatic sex-related toxicity of DiNP was investigated in adult zebrafish together with the mitigating action of the probiotic formulation SLAB51, which has already demonstrated its ability to ameliorate gastrointestinal pathologies in animals including humans. Zebrafish were exposed for 28 days to 50 µg/kg body weight (bw)/day of DiNP (DiNP) through their diet and treated with 109 CFU/g bw of SLAB51 (P) and the combination of DiNP and SLAB51 (DiNP + P), and the results were compared to those of an untreated control group (C). DiNP reduced AMP, IMP, and GMP in the purine metabolism, while such alterations were not observed in the DiNP + P group, for which the phenotype overlapped that of C fish. In addition, in male, DiNP reduced UMP and CMP levels in the pyrimidine metabolism, while the co-administration of probiotic shifted the DiNP + P metabolic phenotype toward that of P male and closed to C male, suggesting the beneficial effects of probiotics also in male fish. Overall, these results provide the first evidence of the disruptive actions of DiNP on hepatic nucleotide metabolism and mitigating action of the probiotic to reduce a DiNP-induced response in a sex-related manner. Full article
(This article belongs to the Special Issue A Metabolomics Approach to Tackling Toxicological and Pharmacological Issues: 2nd Edition)
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22 pages, 3085 KiB  
Article
Metabolomics Reveals Tyrosine Kinase Inhibitor Resistance-Associated Metabolic Events in Human Metastatic Renal Cancer Cells
by Filipa Amaro, Márcia Carvalho, Maria de Lourdes Bastos, Paula Guedes de Pinho and Joana Pinto
Int. J. Mol. Sci. 2024, 25(12), 6328; https://doi.org/10.3390/ijms25126328 - 7 Jun 2024
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Abstract
The development of resistance to tyrosine kinase inhibitors (TKIs) is a major cause of treatment failure in metastatic renal cell carcinoma (mRCC). A deeper understanding of the metabolic mechanisms associated with TKI resistance is critical for refining therapeutic strategies. In this study, we [...] Read more.
The development of resistance to tyrosine kinase inhibitors (TKIs) is a major cause of treatment failure in metastatic renal cell carcinoma (mRCC). A deeper understanding of the metabolic mechanisms associated with TKI resistance is critical for refining therapeutic strategies. In this study, we established resistance to sunitinib and pazopanib by exposing a parental Caki-1 cell line to increasing concentrations of sunitinib and pazopanib. The intracellular and extracellular metabolome of sunitinib- and pazopanib-resistant mRCC cells were investigated using a nuclear magnetic resonance (NMR)-based metabolomics approach. Data analysis included multivariate and univariate methods, as well as pathway and network analyses. Distinct metabolic signatures in sunitinib- and pazopanib-resistant RCC cells were found for the first time in this study. A common metabolic reprogramming pattern was observed in amino acid, glycerophospholipid, and nicotinate and nicotinamide metabolism. Sunitinib-resistant cells exhibited marked alterations in metabolites involved in antioxidant defence mechanisms, while pazopanib-resistant cells showed alterations in metabolites associated with energy pathways. Sunitinib-resistant RCC cells demonstrated an increased ability to proliferate, whereas pazopanib-resistant cells appeared to restructure their energy metabolism and undergo alterations in pathways associated with cell death. These findings provide potential targets for novel therapeutic strategies to overcome TKI resistance in mRCC through metabolic regulation. Full article
(This article belongs to the Special Issue A Metabolomics Approach to Tackling Toxicological and Pharmacological Issues: 2nd Edition)
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