Abstract:Thyroid hormones (TH) are major contributor to oxidative stress in mammals because they (1) stimulate reactive oxygen species generation (ROS), (2) impair antioxidant defenses, and (3) increase the susceptibility to free radicals of most tissues. Unlike mammals, THs seem to diminish mitochondrial ROS while they have limited effect on the antioxidant machinery in birds. However, how THs modify the susceptibility to ROS has never been explored in an avian model, and very little is known about their effect on oxi… Show more
“…While there is some evidence from laboratory acute heat stress studies that thyroid hormones could be up-regulated when facing increased ambient temperatures [12,13], we show here that even a small increase in early-life temperature can increase thyroid hormones levels. Importantly, high thyroid hormone levels have been linked to increased mortality risks in adult humans [35] and increased susceptibility to free radicals in birds [36]. Yet, we found no significant effect of nest heating on two oxidative stress biomarkers (glutathione and oxidative damage to lipids), nor on NRF2 gene expression (an oxidative-stress-induced regulator of several antioxidants).…”
Climate change is increasing both the average ambient temperature and the frequency and severity of heat waves. While direct mortality induced by heat waves is increasingly reported, sub-lethal effects are also likely to impact wild populations. We hypothesized that accelerated ageing could be a cost of being exposed to higher ambient temperature, especially in early-life when thermoregulatory capacities are not fully developed. We tested this hypothesis in wild great tit (Parus major) by experimentally increasing nest box temperature by ca. 2 degrees during postnatal growth and measuring telomere length, a biomarker of cellular ageing predictive of survival prospects in many bird species. While increasing early-life temperature does not affect growth or survival to fledging, it accelerates telomere shortening and reduces medium-term survival from 34% to 19%. Heat-induced telomere shortening was not explained by oxidative stress, but more likely by an increase in energy demand (i.e. higher thyroid hormones levels, increased expression of glucocorticoid receptor, increased mitochondrial density) leading to a reduction in telomere maintenance mechanisms (i.e. decrease in the gene expression of telomerase and protective shelterin). Our results thus suggest that climate warming can affect ageing rate in wild birds, with potential impact on population dynamics and persistence.
“…While there is some evidence from laboratory acute heat stress studies that thyroid hormones could be up-regulated when facing increased ambient temperatures [12,13], we show here that even a small increase in early-life temperature can increase thyroid hormones levels. Importantly, high thyroid hormone levels have been linked to increased mortality risks in adult humans [35] and increased susceptibility to free radicals in birds [36]. Yet, we found no significant effect of nest heating on two oxidative stress biomarkers (glutathione and oxidative damage to lipids), nor on NRF2 gene expression (an oxidative-stress-induced regulator of several antioxidants).…”
Climate change is increasing both the average ambient temperature and the frequency and severity of heat waves. While direct mortality induced by heat waves is increasingly reported, sub-lethal effects are also likely to impact wild populations. We hypothesized that accelerated ageing could be a cost of being exposed to higher ambient temperature, especially in early-life when thermoregulatory capacities are not fully developed. We tested this hypothesis in wild great tit (Parus major) by experimentally increasing nest box temperature by ca. 2 degrees during postnatal growth and measuring telomere length, a biomarker of cellular ageing predictive of survival prospects in many bird species. While increasing early-life temperature does not affect growth or survival to fledging, it accelerates telomere shortening and reduces medium-term survival from 34% to 19%. Heat-induced telomere shortening was not explained by oxidative stress, but more likely by an increase in energy demand (i.e. higher thyroid hormones levels, increased expression of glucocorticoid receptor, increased mitochondrial density) leading to a reduction in telomere maintenance mechanisms (i.e. decrease in the gene expression of telomerase and protective shelterin). Our results thus suggest that climate warming can affect ageing rate in wild birds, with potential impact on population dynamics and persistence.
“…By contrast, the hormone treatment inhibited CYP2J19 expression in the same dosage range when administered alone. Thyroid hormones have been linked to high ROS generation and oxidative stress both in mammals and birds (reviewed in [33,[64][65][66]) due to increased oxidative metabolism (i.e. oxygen consumption rate) (e.g.…”
Ornaments can evolve to reveal individual quality when their production/maintenance costs make them reliable as ‘signals’ or if their expression level is intrinsically linked to condition by some unfalsifiable mechanism (indices). The latter has been mostly associated with traits constrained by body size. In red ketocarotenoid-based colorations, that link could, instead, be established with cell respiration at the inner mitochondrial membrane (IMM). The production mechanism could be independent of resource (yellow carotenoids) availability, thus discarding costs linked to allocation trade-offs. A gene coding for a ketolase enzyme (CYP2J19) responsible for converting dietary yellow carotenoids to red ketocarotenoids has recently been described. We treated male zebra finches with an antioxidant designed to penetrate the IMM (mitoTEMPO) and a thyroid hormone (triiodothyronine) with known hypermetabolic effects. Among hormone controls, MitoTEMPO downregulated
CYP2J19
in the bill (a red ketocarotenoid-based ornament), supporting the mitochondrial involvement in ketolase function. Both treatments interacted when increasing hormone dosage, indicating that mitochondria and thyroid metabolisms could simultaneously regulate coloration. Moreover,
CYP2J19
expression was positively correlated to redness but also to yellow carotenoid levels in the blood. However, treatment effects were not annulated when controlling for blood carotenoid variability, which suggests that costs linked to resource availability could be minor.
“…The complexity of the relationship between antioxidants and reproductive effort highlight the need for a finer‐scale picture of antioxidant strategies. For that purpose, combining multiple assays and taking advantage of high‐throughput sequencing fitted to nonmodel species (Dégletagne et al ) might help exploring complementary aspects of the oxidative balance, such as the efficiency of the DNA repair mechanism, or the intrinsic susceptibility of biomolecules to ROS (Rey et al ). In complement, studying mitochondrial plasticity regarding ROS generation versus their ability to supply ATP remains to be investigated in the context of life‐history evolution (Salin et al , b; Pichaud et al ).…”
The idea that oxidative stress could be a major force governing evolutionary trade-offs has recently been challenged by experimental approaches in laboratory conditions, triggering extensive debates centered on theoretical and methodological issues. Here, we revisited the link between oxidative stress and reproduction by measuring multiple antioxidant and oxidative damages in wild-caught females of two sibling weevil species (Curculio elephas, C. glandium). The strength of our study arised from (1) studied species that were sympatric and exploited similar resource, but displayed contrasting reproductive strategies and (2) individuals were sampled throughout adult life so as to relate oxidative status to breeding effort. We found that the short-lived C. elephas sacrifices red-ox homeostasis for immediate reproduction upon emergence as characterized by low antioxidant defenses and elevated oxidative damage. Comparatively, C. glandium massively invests in antioxidant and maintains low oxidative damage, which may contribute to their extended prereproductive period. Intriguingly, we also reveal, for the first time in a field study, an unexpected reactivation of antioxidant defenses with the onset of reproduction. Our results thus support the existence of a strong, but complex relationship between oxidative stress and life-history evolution and highlight the need for a finer-scale picture of antioxidant strategies.
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