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.
Highlights
In animals, early development is a critical life stage that strongly affects life-history trajectories and fitness[1]
We examined the effect of mitoQ supplementation on chick growth, oxidative stress, Mitochondrial DNA (mtDNA) damage, mitochondrial density, and the expression of redox-regulated genes involved in mitochondrial biogenesis and cell turnover during early development
In relation to mitochondrial proliferation, we examined the expression of the nuclear respiratory factor 1 (NRF1), a transcriptional factor that activates nuclear genes required for mtDNA replication[20], and the expression of sirtuin 1 (SIRT1), a histone deacetylase that stimulates transcriptional pathways promoting mitochondrial biogenesis[37]
Summary
Early development is a critical life stage that strongly affects life-history trajectories and fitness[1]. Previous studies of vertebrates indicate that antioxidant supplementation increases growth rates, suggesting that oxidative stress constrains growth (reviewed in[25]). It is unclear whether antioxidants alleviate the damaging effects of mtROS or ROS of non-mitochondrial origin (e.g. NADPH oxidases) in developing animals, or alter the redox-regulation in the mitochondrial and cellular processes. We explored physiological and molecular mechanisms, which potentially mediate the link between mitochondrial activity and chick growth In this species, antioxidant supplementation (vitamin E) increases growth in some circumstances[27,28], but it is unclear whether these results can be attributed to a mitigation of growth-related oxidative damage[28]
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