ArticleBMC pharmacology & toxicology2013
Effects of early life exposure to ultraviolet C radiation on mitochondrial DNA content, transcription, ATP production, and oxygen consumption in developing Caenorhabditis elegans.
Article in BMC pharmacology & toxicology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 65 citations in OpenAlex.
- Toxicity Evaluation of Nano-Sized Particles by Analysis of mtDNA Content and Expression Levels of Genes Required for mtDNA Maintenance: A Meta-Analysis of Pre-Clinical Studies.Antioxidants (Basel, Switzerland) · 2026Review
- Lysosomal control of proteostasis and reproductive capacity by conserved LMD-3 protein inScience advances · 2025Article
- Seminar: Functional Exposomics and Mechanisms of Toxicity-Insights from Model Systems and NAMs.Environmental health perspectives · 2024Review
- Comprehensive characterization of mitochondrial bioenergetics at different larval stages reveals novel insights about the developmental metabolism ofbioRxiv : the preprint server for biology · 2024Article
- L-Theanine Prolongs the Lifespan by Activating Multiple Molecular Pathways in Ultraviolet C-ExposedMolecules (Basel, Switzerland) · 2024Article
- Lack of detectable sex differences in the mitochondrial function of Caenorhabditis elegans.BMC ecology and evolution · 2024Article
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- Cytochromes P450 ofBiomolecules · 2022Review
- Mitochondrial DNA Mutagenesis: Feature of and Biomarker for Environmental Exposures and Aging.Current environmental health reports · 2021Review
- Mitochondrial DNA copy number in human disease: the more the better?FEBS letters · 2021Review
- Multiple metabolic changes mediate the response of Caenorhabditis elegans to the complex I inhibitor rotenone.Toxicology · 2021Article
- PCR-Based Determination of Mitochondrial DNA Copy Number in Multiple Species.Methods in molecular biology (Clifton, N.J.) · 2021Article
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- KLF-1 orchestrates a xenobiotic detoxification program essential for longevity of mitochondrial mutants.Nature communications · 2019Article
- Genetic Defects in Mitochondrial Dynamics inInternational journal of molecular sciences · 2019Article
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- Mitochondrial DNA Damage Does Not DetermineFrontiers in genetics · 2019Article
- Stress pre-conditioning with temperature, UV and gamma radiation induces tolerance against phosphine toxicity.PloS one · 2018Article
- Mitochondrial fusion, fission, and mitochondrial toxicity.Toxicology · 2017Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
backgroundMitochondrial DNA (mtDNA) is present in multiple copies per cell and undergoes dramatic amplification during development. The impacts of mtDNA damage incurred early in development are not well understood, especially in the case of types of mtDNA damage that are irreparable, such as ultraviolet C radiation (UVC)-induced photodimers.
methodsWe exposed first larval stage nematodes to UVC using a protocol that results in accumulated mtDNA damage but permits nuclear DNA (nDNA) repair. We then measured the transcriptional response, as well as oxygen consumption, ATP levels, and mtDNA copy number through adulthood.
resultsAlthough the mtDNA damage persisted to the fourth larval stage, we observed only a relatively minor ~40% decrease in mtDNA copy number. Transcriptomic analysis suggested an inhibition of aerobic metabolism and developmental processes; mRNA levels for mtDNA-encoded genes were reduced ~50% at 3 hours post-treatment, but recovered and, in some cases, were upregulated at 24 and 48 hours post-exposure. The mtDNA polymerase γ was also induced ~8-fold at 48 hours post-exposure. Moreover, ATP levels and oxygen consumption were reduced in response to UVC exposure, with marked reductions of ~50% at the later larval stages.
conclusionsThese results support the hypothesis that early life exposure to mitochondrial genotoxicants could result in mitochondrial dysfunction at later stages of life, thereby highlighting the potential health hazards of time-delayed effects of these genotoxicants in the environment.
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