ArticleToxicological sciences : an official journal of the Society of Toxicology2014
Integrated redox proteomics and metabolomics of mitochondria to identify mechanisms of cd toxicity.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
61 citing papers in PubMed, 96 citations in OpenAlex.
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- Cadmium exposure at low environmental levels induces cognitive decline in aged male mice.Neurotoxicology · 2026Article
- The effects of combined low-dose cadmium and deltamethrin on mitochondrial bioenergetics and metabolism in human lung fibroblasts.Toxicology reports · 2025Article
- Cadmium exposure following early-life respiratory syncytial virus infection promotes lung fibrosis through autophagy inhibition.Toxicological sciences : an official journal of the Society of Toxicology · 2025Article
- The Protective Effects ofToxics · 2024Article
- Redox organization of living systems.Free radical biology & medicine · 2024Review
- Cadmium Highlights Common and Specific Responses of Two Freshwater Sentinel Species,Proteomes · 2024Article
- ALTERATIONS IN HISTIDINE METABOLISM IS A FEATURE OF EARLY AUTOSOMAL DOMINANT POLYCYSTIC KIDNEY DISEASE (ADPKD).Transactions of the American Clinical and Climatological Association · 2024Article
- Harnessing redox proteomics to study metabolic regulation and stress response in lignin-fed Rhodococci.Biotechnology for biofuels and bioproducts · 2023Article
- Metabolite Stability in Archived Neonatal Dried Blood Spots Used for Epidemiologic Research.American journal of epidemiology · 2023Article
- Study on the relationship between selenium and cadmium in diseased human lungs.Advances in redox research · 2023Article
- Antagonistic Interactions in Mitochondria ROS Signaling Responses to Manganese.Antioxidants (Basel, Switzerland) · 2023Article
- Acylcarnitines in Ophthalmology: Promising Emerging Biomarkers.International journal of molecular sciences · 2022Review
- Low-Dose Cadmium Potentiates Metabolic Reprogramming Following Early-Life Respiratory Syncytial Virus Infection.Toxicological sciences : an official journal of the Society of Toxicology · 2022Article
- Sub-Cellular Metabolomics Contributes Mitochondria-Specific Metabolic Insights to a Mouse Model of Leigh Syndrome.Metabolites · 2021Article
- Stoichiometric Thiol Redox Proteomics for Quantifying Cellular Responses to Perturbations.Antioxidants (Basel, Switzerland) · 2021Review
- Human Serum Albumin Cys34 Adducts in Newborn Dried Blood Spots: Associations With Air Pollution Exposure During Pregnancy.Frontiers in public health · 2021Article
- Novel mitochondrial and cytosolic purification pipeline for compartment-specific metabolomics in mammalian disease model tissues.Metabolomics : Official journal of the Metabolomic Society · 2020Article
- S-Nitroso-Proteome Revealed in Stomatal Guard Cell Response to Flg22.International journal of molecular sciences · 2020Article
- Neutrophil-Derived Reactive Oxygen Orchestrates Epithelial Cell Signaling Events during Intestinal Repair.The American journal of pathology · 2019Article
1 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Cadmium (Cd) exposure contributes to human diseases affecting liver, kidney, lung, and other organ systems, but mechanisms underlying the pleotropic nature of these toxicities are poorly understood. Cd accumulates in humans from dietary, environmental (including cigarette smoke), and occupational sources, and has a twenty-year biologic half-life. Our previous mouse and cell studies showed that environmental low-dose Cd exposure altered protein redox states resulting in stimulation of inflammatory signaling and disruption of the actin cytoskeleton system, suggesting that Cd could impact multiple mechanisms of disease. In the current study, we investigated the effects of acute Cd exposure on the redox proteome and metabolome of mouse liver mitochondria to gain insight into associated toxicological mechanisms and functions. We analyzed redox states of liver mitochondrial proteins by redox proteomics using isotope coded affinity tag (ICAT) combined mass spectrometry. Redox ICAT identified 2687 cysteine-containing peptides (peptidyl Cys) of which 1667 peptidyl Cys (657 proteins) were detected in both control and Cd-exposed samples. Of these, 46% (1247 peptidyl Cys, 547 proteins) were oxidized by Cd more than 1.5-fold relative to controls. Bioinformatics analysis using MetaCore software showed that Cd affected 86 pathways, including 24 Cys in proteins functioning in branched chain amino acid (BCAA) and 14 Cys in proteins functioning in fatty acid (acylcarnitine/carnitine) metabolism. Consistently, high-resolution metabolomics data showed that Cd treatment altered levels of BCAA and carnitine metabolites. Together, these results show that mitochondrial protein redox and metabolites are targets in Cd-induced hepatotoxicity. The results further indicate that redox proteomics and metabolomics can be used in an integrated systems approach to investigate complex disease mechanisms.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.