ArticleToxicological sciences : an official journal of the Society of Toxicology2014
Mitochondrial DNA damage as a peripheral biomarker for mitochondrial toxin exposure in rats.
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 18 papers.
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Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
- Alterations in mitochondrial DNA copy number and oxidative stress markers in blood and muscle tissues of mice following snake envenomation.Environmental analysis, health and toxicology · 2026Article
- Parkinson's disease linked LRRK2 G2019S drives oxidative nuclear DNA damage and PARP1 hyperactive signaling.bioRxiv : the preprint server for biology · 2026Article
- L-Carnitine and Mildronate Demonstrate Divergent Protective Effects on Mitochondrial DNA Quality Control and Inflammation Following Traumatic Brain Injury.International journal of molecular sciences · 2025Article
- Article
- G2019S selective LRRK2 kinase inhibitor abrogates mitochondrial DNA damage.NPJ Parkinson's disease · 2024Article
- A blood-based marker of mitochondrial DNA damage in Parkinson's disease.Science translational medicine · 2023Article
- High Doses of Pesticides Induce mtDNA Damage in Intact Mitochondria of Potato In Vitro and Do Not Impact on mtDNA Integrity of Mitochondria of Shoots and Tubers under In Vivo Exposure.International journal of molecular sciences · 2022Article
- Mitochondrial DNA Mutagenesis: Feature of and Biomarker for Environmental Exposures and Aging.Current environmental health reports · 2021Review
- Multiple metabolic changes mediate the response of Caenorhabditis elegans to the complex I inhibitor rotenone.Toxicology · 2021Article
- Mitochondrial DNA damage as a potential biomarker of LRRK2 kinase activity in LRRK2 Parkinson's disease.Scientific reports · 2020Article
- Predictors of mitochondrial DNA copy number and damage in a mercury-exposed rural Peruvian population near artisanal and small-scale gold mining: An exploratory study.Environmental and molecular mutagenesis · 2019Article
- Age-related declines in α-Klotho drive progenitor cell mitochondrial dysfunction and impaired muscle regeneration.Nature communications · 2018Article
- Newly Revised Quantitative PCR-Based Assay for Mitochondrial and Nuclear DNA Damage.Current protocols in toxicology · 2018Article
- Autophagy Disruptions Associated With Altered Optineurin Expression in Extranigral Regions in a Rotenone Model of Parkinson's Disease.Frontiers in neuroscience · 2018Article
- LRRK2 G2019S-induced mitochondrial DNA damage is LRRK2 kinase dependent and inhibition restores mtDNA integrity in Parkinson's disease.Human molecular genetics · 2017Article
- Editor's Highlight: Base Excision Repair Variants and Pesticide Exposure Increase Parkinson's Disease Risk.Toxicological sciences : an official journal of the Society of Toxicology · 2017Article
- From the Cover: Alterations in Optineurin Expression and Localization in Pre-clinical Parkinson's Disease Models.Toxicological sciences : an official journal of the Society of Toxicology · 2016Article
- LC/MS analysis of cardiolipins in substantia nigra and plasma of rotenone-treated rats: Implication for mitochondrial dysfunction in Parkinson's disease.Free radical research · 2015Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Demonstrating or verifying a current or past exposure to an environmental mitochondrial toxin or toxicant is extraordinarily difficult. Thus, there is a pressing need to develop a biomarker for exposure to environmental mitochondrial inhibitors. Rotenone, an environmental toxicant, is a potent inhibitor of the mitochondrial electron transfer chain. Rotenone specifically inhibits complex I throughout the body and brain, thereby producing systemic mitochondrial impairment. As such, rotenone is a prototypical clinically relevant, environmental mitochondrial toxicant that may be used as an ideal initial platform to develop accessible biomarkers of exposure. The over-arching goal of this work is to explore and validate peripheral (blood and skeletal muscle) DNA damage as a biomarker of mitochondrial toxicant exposure using the rat rotenone model. In this effort, we utilized an extremely sensitive quantitative polymerase chain reaction (QPCR)-based assay that simultaneously allows the assessment of multiple forms of mitochondrial DNA (mtDNA) and nuclear DNA (nDNA) damage. We found mtDNA damage in blood is detected after subclinical rotenone exposure and the damage persists even after complex I activity has returned to normal. With a more sustained rotenone exposure, mtDNA damage is also detected in skeletal muscle, suggesting that mtDNA damage in this tissue simply lags behind blood. Using the QPCR-based assay, we have no evidence for nDNA damage in peripheral tissues after rotenone exposure either acutely or chronically. Overall, these data support the idea that mtDNA damage in peripheral tissues in the rotenone model may provide a biomarker of past or ongoing mitochondrial toxin exposure.
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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.