ArticleCurrent protocols in toxicology2016
In Vivo Determination of Mitochondrial Function Using Luciferase-Expressing Caenorhabditis elegans: Contribution of Oxidative Phosphorylation, Glycolysis, and Fatty Acid Oxidation to Toxicant-Induced Dysfunction.
Article in Current protocols in toxicology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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.
The trial behind it
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Who cites it
22 citing papers in PubMed, 48 citations in OpenAlex.
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- Biochemical implications of robotic surgery: a new frontier in the operating room.Journal of robotic surgery · 2024Review
- Chronic high-sugar diet in adulthood protects Caenorhabditis elegans from 6-OHDA-induced dopaminergic neurodegeneration.BMC biology · 2023Article
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- ATP synthase FCellular and molecular life sciences : CMLS · 2022Review
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- Caenorhabditis elegans as a model for studies on quinolinic acid-induced NMDAR-dependent glutamatergic disorders.Brain research bulletin · 2021Article
- Mitochondria-affecting small molecules ameliorate proteostasis defects associated with neurodegenerative diseases.Scientific reports · 2021Article
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- Multiple metabolic changes mediate the response of Caenorhabditis elegans to the complex I inhibitor rotenone.Toxicology · 2021Article
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- Interplay between mitochondria and diet mediates pathogen and stress resistance in Caenorhabditis elegans.PLoS genetics · 2019Article
- Pyoverdine, a siderophore from Pseudomonas aeruginosa, translocates into C. elegans, removes iron, and activates a distinct host response.Virulence · 2018Article
- Nonselective autophagy reduces mitochondrial content during starvation in Caenorhabditis elegans.American journal of physiology. Cell physiology · 2018Article
- Mitochondrial Toxicity.Toxicological sciences : an official journal of the Society of Toxicology · 2018Review
- Cell Biology of the Mitochondrion.Genetics · 2017Review
- Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Mitochondria are a target of many drugs and environmental toxicants; however, how toxicant-induced mitochondrial dysfunction contributes to the progression of human disease remains poorly understood. To address this issue, in vivo assays capable of rapidly assessing mitochondrial function need to be developed. Here, using the model organism Caenorhabditis elegans, we describe how to rapidly assess the in vivo role of the electron transport chain, glycolysis, or fatty acid oxidation in energy metabolism following toxicant exposure, using a luciferase-expressing ATP reporter strain. Alterations in mitochondrial function subsequent to toxicant exposure are detected by depleting steady-state ATP levels with inhibitors of the mitochondrial electron transport chain, glycolysis, or fatty acid oxidation. Differential changes in ATP following short-term inhibitor exposure indicate toxicant-induced alterations at the site of inhibition. Because a microplate reader is the only major piece of equipment required, this is a highly accessible method for studying toxicant-induced mitochondrial dysfunction in vivo. © 2016 by John Wiley & Sons, Inc.
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Registered trials
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