ArticleJournal of neurochemistry2012
Alterations in bioenergetic function induced by Parkinson's disease mimetic compounds: lack of correlation with superoxide generation.
Article in Journal of neurochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
41 citing papers in PubMed, 56 citations in OpenAlex.
- The role of energy deficit in autophagy failure in Parkinson's disease.Frontiers in aging neuroscience · 2026Review
- An iridium(iii)-based photosensitizer disrupting the mitochondrial respiratory chain induces ferritinophagy-mediated immunogenic cell death.Chemical science · 2024Article
- Metabolic dysfunctions in the intranigral rotenone model of Parkinson's disease.Experimental brain research · 2023Article
- Nanostars Carrying Multifunctional Neurotrophic Dendrimers Protect Neurons in Preclinical In Vitro Models of Neurodegenerative Disorders.ACS applied materials & interfaces · 2022Article
- Multiple metabolic changes mediate the response of Caenorhabditis elegans to the complex I inhibitor rotenone.Toxicology · 2021Article
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- Article
- Intrinsic Effects of Gold Nanoparticles on Oxygen-Glucose Deprivation/Reperfusion Injury in Rat Cortical Neurons.Neurochemical research · 2019Article
- Tetramethylpyrazine Analogue T-006 Exerts Neuroprotective Effects against 6-Hydroxydopamine-Induced Parkinson's DiseaseOxidative medicine and cellular longevity · 2019Article
- Methods for assessing mitochondrial quality control mechanisms and cellular consequences in cell culture.Redox biology · 2018Article
- Rapamycin increases oxidative metabolism and enhances metabolic flexibility in human cardiac fibroblasts.GeroScience · 2018Article
- Teaching the basics of reactive oxygen species and their relevance to cancer biology: Mitochondrial reactive oxygen species detection, redox signaling, and targeted therapies.Redox biology · 2018Review
- Review
- Glycolysis-Derived Compounds From Astrocytes That Modulate Synaptic Communication.Frontiers in neuroscience · 2018Review
- Mitochondrial Complex I Reversible S-Nitrosation Improves Bioenergetics and Is Protective in Parkinson's Disease.Antioxidants & redox signaling · 2018Article
- Mito-Apocynin Prevents Mitochondrial Dysfunction, Microglial Activation, Oxidative Damage, and Progressive Neurodegeneration in MitoPark Transgenic Mice.Antioxidants & redox signaling · 2017Article
- Metabolic Dysfunction in Parkinson's Disease: Bioenergetics, Redox Homeostasis and Central Carbon Metabolism.Brain research bulletin · 2017Review
- Redox-based therapeutics in neurodegenerative disease.British journal of pharmacology · 2017Review
- Mitochondria-regulated formation of endothelium-derived extracellular vesicles shifts the mediator of flow-induced vasodilation.American journal of physiology. Heart and circulatory physiology · 2017Article
- Mitochondria-targeted metformins: anti-tumour and redox signalling mechanisms.Interface focus · 2017Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
In vitro and in vivo models of Parkinson's disease (PD) suggest that increased oxidant production leads to mitochondrial dysfunction in dopaminergic neurons and subsequent cell death. However, it remains unclear if cell death in these models is caused by inhibition of mitochondrial function or oxidant production. The objective of this study was to determine the relationship between mitochondrial dysfunction and oxidant production in response to multiple PD neurotoxicant mimetics. MPP(+) caused a dose-dependent decrease in the basal oxygen consumption rate in dopaminergic N27 cells, indicating a loss of mitochondrial function. In parallel, we found that MPP(+) only modestly increased oxidation of hydroethidine as a diagnostic marker of superoxide production in these cells. Similar results were found using rotenone as a mitochondrial inhibitor, or 6-hydroxydopamine (6-OHDA) as a mechanistically distinct PD neurotoxicant, but not with exposure to paraquat. In addition, the extracellular acidification rate, used as a marker of glycolysis, was stimulated to compensate for oxygen consumption rate inhibition after exposure to MPP(+), rotenone, or 6-OHDA, but not paraquat. Together these data indicate that MPP(+), rotenone, and 6-OHDA dramatically shift bioenergetic function away from the mitochondria and towards glycolysis in N27 cells.
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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.