Abstract

Exposure to unpredictable environmental stressors could influence animal health and fitness by inducing oxidative stress, potentially through downstream effects of glucocorticoid stress hormones (e.g. corticosterone) on mitochondrial function. Yet, it remains unclear whether species that have evolved in stochastic and challenging environments may present adaptations to alleviate the effects of stress exposure on oxidative stress. We tested this hypothesis in wild king penguins by investigating mitochondrial and oxidative stress responses to acute restraint-stress, and their relationships with baseline (potentially mirroring exposure to chronic stress) and stress-induced increase in corticosterone levels. Acute restraint-stress did not significantly influence mitochondrial function. However, acute restraint-stress led to a significant increase in endogenous antioxidant defences, while oxidative damage levels were mostly not affected or even decreased. High baseline corticosterone levels were associated with an up-regulation of the glutathione antioxidant system and a decrease in mitochondrial efficiency. Both processes might contribute to prevent oxidative damage, potentially explaining the negative relationship observed between baseline corticosterone and plasma oxidative damage to proteins. While stress exposure can represent an oxidative challenge for animals, protective mechanisms like up-regulating antioxidant defences and decreasing mitochondrial efficiency seem to occur in king penguins, allowing them to cope with their stochastic and challenging environment.

Highlights

  • Vertebrates respond to stressful and unpredictable environmental stimuli by activating a set of physiological and behavioural responses defined as a whole as the ‘stress response’[1]

  • We investigated the effects of the acute restraint stress on corticosterone, mitochondrial parameters and oxidative stress markers using repeated-measures Generalized Estimating Equations (GEE) with a Gaussian distribution, with bird ID as the individual factor, sampling time as the within-individual repeated effect, and sex as a fixed factor

  • We found a reduction in a proxy of mitochondrial efficiency to produce ATP both in relationship to the magnitude of the acute CORT response and with increasing levels of baseline CORT

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Summary

Introduction

Vertebrates respond to stressful and unpredictable environmental stimuli (e.g. food shortage, predation, adverse weather conditions, etc.) by activating a set of physiological and behavioural responses defined as a whole as the ‘stress response’[1]. It is possible that the relationships between GCs, mitochondrial function, and oxidative stress (see above) could differ between species, life history stages, and environmental conditions We tested this hypothesis in freely-breeding king penguins (Aptenodytes patagonicus) by investigating mitochondrial and oxidative stress responses to acute restraint-stress, and their relationships with baseline (potentially mirroring exposure to chronic stress) and stress-induced increase in corticosterone levels. King penguins are an interesting model to investigate the oxidative and mitochondrial responses to stress exposure These sub-Antarctic seabirds breed on-land while being exposed to numerous environmental stressors (predation, parasites, detrimental weather, aggressive social environment[33,34,35]). Our studies show that baseline corticosterone (CORT) levels in this species are positively associated with chronic stressors such as high intra-specific density in an aggressive social environment[39] and ectoparasites prevalence (Bize et al, unpublished)

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