ArticleDifferentiation; research in biological diversity
The cellular and molecular progression of mitochondrial dysfunction induced by 2,4-dinitrophenol in developing zebrafish embryos.
Article in Differentiation; research in biological diversity. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 54 citations in OpenAlex.
- Non-Mammalian Models for Mitochondria Research in CNS Disorders.Biomolecules · 2026Review
- Mitochondrial regulation of brain development: evidence from zebrafish models.Fish physiology and biochemistry · 2026Review
- Precision Medicine: Therapeutically Targeting Mitochondrial Alterations in Heart Failure.JACC. Basic to translational science · 2025Review
- Mitochondria-Targeted COUPY Photocages: Synthesis and Visible-Light Photoactivation in Living Cells.The Journal of organic chemistry · 2023Article
- In vitro biochemical assessment of mixture effects of two endocrine disruptors on INS-1 cells.Scientific reports · 2022Article
- Altered epidermal proliferation, differentiation, and lipid composition: Novel key elements in the vitiligo puzzle.Science advances · 2022Article
- XJB-5-131 Is a Mild Uncoupler of Oxidative Phosphorylation.Journal of Huntington's disease · 2022Article
- AOP Report: Uncoupling of Oxidative Phosphorylation Leading to Growth Inhibition via Decreased Cell Proliferation.Environmental toxicology and chemistry · 2021Article
- Article
- Fishing in the Cell Powerhouse: Zebrafish as A Tool for Exploration of Mitochondrial Defects Affecting the Nervous System.International journal of molecular sciences · 2019Review
- Organelle-Targeted BODIPY Photocages: Visible-Light-Mediated Subcellular Photorelease.Angewandte Chemie (International ed. in English) · 2019Article
- Developmental toxicity of the triazole fungicide cyproconazole in embryo-larval stages of zebrafish (Danio rerio).Environmental science and pollution research international · 2019Article
- Niclosamide Induces Epiboly Delay During Early Zebrafish Embryogenesis.Toxicological sciences : an official journal of the Society of Toxicology · 2018Article
- Mitochondrial Toxicity.Toxicological sciences : an official journal of the Society of Toxicology · 2018Review
- Mitochondrial fusion, fission, and mitochondrial toxicity.Toxicology · 2017Review
- Clinical effects of chemical exposures on mitochondrial function.Toxicology · 2017Review
- Article
- Article
- Triclosan is a mitochondrial uncoupler in live zebrafish.Journal of applied toxicology : JAT · 2016Article
- Zebrafish lacking functional DNA polymerase gamma survive to juvenile stage, despite rapid and sustained mitochondrial DNA depletion, altered energetics and growth.Nucleic acids research · 2015Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The etiology of mitochondrial disease is poorly understood. Furthermore, treatment options are limited, and diagnostic methods often lack the sensitivity to detect disease in its early stages. Disrupted oxidative phosphorylation (OXPHOS) that inhibits ATP production is a common phenotype of mitochondrial disorders that can be induced in zebrafish by exposure to 2,4-dinitrophenol (DNP), a FDA-banned weight-loss agent and EPA-regulated environmental toxicant, traditionally used in research labs as an uncoupler of OXPHOS. Despite the DNP-induced OXPHOS inhibition we observed using in vivo respirometry, the development of the DNP-treated and control zebrafish were largely similar during the first half of embryogenesis. During this period, DNP-treated embryos induced gene expression of mitochondrial and nuclear genes that stimulated the production of new mitochondria and increased glycolysis to yield normal levels of ATP. DNP-treated embryos were incapable of sustaining this mitochondrial biogenic response past mid-embryogenesis, as shown by significantly lowered ATP production and ATP levels, decreased gene expression, and the onset of developmental defects. Examining neural tissues commonly affected by mitochondrial disease, we found that DNP exposure also inhibited motor neuron axon arbor outgrowth and the proper formation of the retina. We observed and quantified the molecular and physiological progression of mitochondrial dysfunction during development with this new model of OXPHOS dysfunction, which has great potential for use in diagnostics and therapies for mitochondrial disease.
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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.