ArticleChemical research in toxicology2013
Systematic study of mitochondrial toxicity of environmental chemicals using quantitative high throughput screening.
Article in Chemical research in toxicology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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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.
The trial behind it
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Who cites it
38 citing papers in PubMed.
- Review of in vitro approaches for assessing the toxicity of chemical stressors across diverse physiological systems.Toxicological sciences : an official journal of the Society of Toxicology · 2026Review
- Article
- High-concentration MEHP triggers mtDNA depletion in undifferentiated HepaRG and C2C12 cultures and disrupts mitochondrial homeostasis in both HepaRG culture states.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- Progeny effects of rotenone exposure depend on parental toxicity.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- Use of Tox21 screening data to profile PFAS bioactivities on nuclear receptors, cellular stress pathways, and cytochrome p450 enzymes.Journal of hazardous materials · 2024Article
- Lack of detectable sex differences in the mitochondrial function of Caenorhabditis elegans.BMC ecology and evolution · 2024Article
- Water Quality Monitoring with the Multiplexed Assay MitoOxTox for Mitochondrial Toxicity, Oxidative Stress Response, and Cytotoxicity in AREc32 Cells.Environmental science & technology · 2024Article
- High-Throughput Screening to Advance In Vitro Toxicology: Accomplishments, Challenges, and Future Directions.Annual review of pharmacology and toxicology · 2024Review
- Sex-specific DNA methylation and associations withEpigenetics · 2022Article
- Assessing Drug-Induced Mitochondrial Toxicity in Cardiomyocytes: Implications for Preclinical Cardiac Safety Evaluation.Pharmaceutics · 2022Review
- 3D Spheroids of Human Primary Urine-Derived Stem Cells in the Assessment of Drug-Induced Mitochondrial Toxicity.Pharmaceutics · 2022Article
- A Quantitative High-Throughput Screening Data Analysis Pipeline for Activity Profiling.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Mild pentachlorophenol-mediated uncoupling of mitochondria depletes ATP but does not cause an oxidized redox state or dopaminergic neurodegeneration inCurrent research in toxicology · 2022Article
- Mitochondrial Membrane Potential Assay.Methods in molecular biology (Clifton, N.J.) · 2022Article
- MitoTox: a comprehensive mitochondrial toxicity database.BMC bioinformatics · 2021Article
- Deep Graph Learning with Property Augmentation for Predicting Drug-Induced Liver Injury.Chemical research in toxicology · 2021Article
- Effective Antitumor of Orally Intestinal Targeting Penetrating Peptide-Loaded Tyroserleutide/PLGA Nanoparticles in Hepatocellular Carcinoma.International journal of nanomedicine · 2021Article
- Respirometric Screening and Characterization of Mitochondrial Toxicants Within the ToxCast Phase I and II Chemical Libraries.Toxicological sciences : an official journal of the Society of Toxicology · 2020Article
- Identifying and Characterizing Stress Pathways of Concern for Consumer Safety in Next-Generation Risk Assessment.Toxicological sciences : an official journal of the Society of Toxicology · 2020Article
- Quantitative Proteomic Profiling of Mitochondrial Toxicants in a Human Cardiomyocyte Cell Line.Frontiers in genetics · 2020Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
A goal of the Tox21 program is to transit toxicity testing from traditional in vivo models to in vitro assays that assess how chemicals affect cellular responses and toxicity pathways. A critical contribution of the NIH Chemical Genomics center (NCGC) to the Tox21 program is the implementation of a quantitative high throughput screening (qHTS) approach, using cell- and biochemical-based assays to generate toxicological profiles for thousands of environmental compounds. Here, we evaluated the effect of chemical compounds on mitochondrial membrane potential in HepG2 cells by screening a library of 1,408 compounds provided by the National Toxicology Program (NTP) in a qHTS platform. Compounds were screened over 14 concentrations, and results showed that 91 and 88 compounds disrupted mitochondrial membrane potential after treatment for 1 or 5 h, respectively. Seventy-six compounds active at both time points were clustered by structural similarity, producing 11 clusters and 23 singletons. Thirty-eight compounds covering most of the active chemical space were more extensively evaluated. Thirty-six of the 38 compounds were confirmed to disrupt mitochondrial membrane potential using a fluorescence plate reader, and 35 were confirmed using a high content imaging approach. Among the 38 compounds, 4 and 6 induced LDH release, a measure of cytotoxicity, at 1 or 5 h, respectively. Compounds were further assessed for mechanism of action (MOA) by measuring changes in oxygen consumption rate, which enabled the identification of 20 compounds as uncouplers. This comprehensive approach allows for the evaluation of thousands of environmental chemicals for mitochondrial toxicity and identification of possible MOAs.
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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.