ArticleToxicological sciences : an official journal of the Society of Toxicology2020
Genome-Scale Model-Based Identification of Metabolite Indicators for Early Detection of Kidney Toxicity.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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9 citing papers in PubMed, 10 citations in OpenAlex.
- Personalized metabolite biomarker predictions reveal heterogeneous characteristics of Parkinson's disease.NPJ Parkinson's disease · 2026Article
- A Metabolism-Informed Neural Network Identifies Pathways Influencing the Potency and Toxicity of Antimicrobial Combinations.npj drug discovery · 2026Article
- A systems-level integration of liver-kidney transcriptomics and genome-scale metabolic models reveals organ-specific injury mechanisms.Frontiers in toxicology · 2026Article
- Article
- Quantifying liver-toxic responses from dose-dependent chemical exposures using a rat genome-scale metabolic model.Toxicological sciences : an official journal of the Society of Toxicology · 2025Article
- Comparative Proteomics Highlights that GenX Exposure Leads to Metabolic Defects and Inflammation in Astrocytes.Environmental science & technology · 2024Article
- Identifying metabolic adaptations characteristic of cardiotoxicity using paired transcriptomics and metabolomics data integrated with a computational model of heart metabolism.PLoS computational biology · 2024Article
- Transcriptome-based biomarker prediction for Parkinson's disease using genome-scale metabolic modeling.Scientific reports · 2024Article
- Toxicant-Induced Metabolic Alterations in Lipid and Amino Acid Pathways Are Predictive of Acute Liver Toxicity in Rats.International journal of molecular sciences · 2020Article
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Authors and funding
12 authors at 4 institutions in 1 country.
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Abstract
Identifying early indicators of toxicant-induced organ damage is critical to provide effective treatment. To discover such indicators and the underlying mechanisms of toxicity, we used gentamicin as an exemplar kidney toxicant and performed systematic perturbation studies in Sprague Dawley rats. We obtained high-throughput data 7 and 13 h after administration of a single dose of gentamicin (0.5 g/kg) and identified global changes in genes in the liver and kidneys, metabolites in the plasma and urine, and absolute fluxes in central carbon metabolism. We used these measured changes in genes in the liver and kidney as constraints to a rat multitissue genome-scale metabolic network model to investigate the mechanism of gentamicin-induced kidney toxicity and identify metabolites associated with changes in tissue gene expression. Our experimental analysis revealed that gentamicin-induced metabolic perturbations could be detected as early as 7 h postexposure. Our integrated systems-level analyses suggest that changes in kidney gene expression drive most of the significant metabolite alterations in the urine. The analyses thus allowed us to identify several significantly enriched injury-specific pathways in the kidney underlying gentamicin-induced toxicity, as well as metabolites in these pathways that could serve as potential early indicators of kidney damage.
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