ArticleScientific reports2019
Redox-regulation and life-history trade-offs: scavenging mitochondrial ROS improves growth in a wild bird.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 27 citations in OpenAlex.
- Genomic Integrity in Gull Chicks Predicts Colony Departure and Postfledging Movements.Ecology and evolution · 2026Article
- Photoperiod, but not testosterone, increases basal metabolic rate in house sparrows.Integrative organismal biology (Oxford, England) · 2026Article
- Does colour-morph variation in metabolic physiology and oxidative stress match morph-specific life-history strategies?Oecologia · 2025Article
- Gull chicks grow faster but lose telomeres when prenatal cues mismatch the real presence of sibling competitors.Proceedings. Biological sciences · 2020Article
- Plastic but repeatable: rapid adjustments of mitochondrial function and density during reproduction in a wild bird species.Biology letters · 2019Article
- Oxidative status and metabolic profile in a long-lived bird preparing for extreme endurance migration.Scientific reports · 2019Article
- Carotenoid-based coloration predicts both longevity and lifetime fecundity in male birds, but testosterone disrupts signal reliability.PloS one · 2019Article
- Corticosterone-implanted chicks transmit stress to parents and neighbors in a colonial seabird.Behavioral ecology : official journal of the International Society for Behavioral EcologyArticle
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It has been proposed that animals usually restrain their growth because fast growth leads to an increased production of mitochondrial reactive oxygen species (mtROS), which can damage mitochondrial DNA and promote mitochondrial dysfunction. Here, we explicitly test whether this occurs in a wild bird by supplementing chicks with a mitochondria-targeted ROS scavenger, mitoubiquinone (mitoQ), and examining growth rates and mtDNA damage. In the yellow-legged gull Larus michahellis, mitoQ supplementation increased the early growth rate of chicks but did not reduce mtDNA damage. The level of mtDNA damage was negatively correlated with chick mass, but this relationship was not affected by the mitoQ treatment. We also found that chick growth was positively correlated with both mtDNA copy number and the mitochondrial enzymatic activity of citrate synthase, suggesting a link between mitochondrial content and growth. Additionally, we found that MitoQ supplementation increased mitochondrial content (in males), altered the relationship between mtDNA copy number and damage, and downregulated some transcriptional pathways related to cell rejuvenation, suggesting that scavenging mtROS during development enhanced growth rates but at the expense of cellular turnover. Our study confirms the central role of mitochondria modulating life-history trade-offs during development by other mechanisms than mtROS-inflicted damage.
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