19The length of telomeres, the protective caps of chromosomes, is increasingly used as a biomarker 20 of individual health state since it has been shown to predict chances of survival in a range of 21 endothermic species including humans. Oxidative stress is presumed to be a major cause of 22 telomere shortening, but most evidence to date comes from in vitro cultured cells. The 23 importance of oxidative stress as a determinant of telomere shortening in vivo remains less clear 24 and has recently been questioned. 25We therefore reviewed correlative and experimental studies investigating the links between 26 oxidative stress and telomere shortening in vivo. While correlative studies provide equivocal 27 support for a connection between oxidative stress and telomere attrition (10/18 studies), most 28 experimental studies published so far (7/8 studies) partially or fully support this hypothesis. Yet, 29 this link seems to be tissue-dependent in some cases, or restricted to particular categories of 30 individual (e.g. sex-dependent) in other cases. 31More experimental studies, especially those decreasing antioxidant protection or increasing pro-32 oxidant generation, are required to further our understanding of the importance of oxidative 33 stress in determining telomere length in vivo. Studies comparing growing vs. adult individuals, or 34 proliferative vs. non-proliferative tissues would provide particularly important insights. 35 36

One of the reasons for animals not to grow as fast as they potentially could is that fast growth has been shown to be associated with reduced lifespan. However, we are still lacking a clear description of the reality of growth-dependent modulation of ageing mechanisms in wild animals. Using the particular growth trajectory of small king penguin chicks naturally exhibiting higher-than-normal growth rate to compensate for the winter break, we tested whether oxidative stress and telomere shortening are related to growth trajectories. Plasma antioxidant defences, oxidative damage levels and telomere length were measured at the beginning and at the end of the post-winter growth period in three groups of chicks (small chicks, which either passed away or survived the growth period, and large chicks). Small chicks that died early during the growth period had the highest level of oxidative damage and the shortest telomere lengths prior to death. Here, we show that small chicks that grew faster did it at the detriment of body maintenance mechanisms as shown by (i) higher oxidative damage and (ii) accelerated telomere loss. Our study provides the first evidence for a mechanistic link between growth and ageing rates under natural conditions.

BackgroundOne central concept in evolutionary ecology is that current and residual reproductive values are negatively linked by the so-called cost of reproduction. Previous studies examining the nature of this cost suggested a possible involvement of oxidative stress resulting from the imbalance between pro- and anti-oxidant processes. Still, data remain conflictory probably because, although oxidative damage increases during reproduction, high systemic levels of oxidative stress might also constrain parental investment in reproduction. Here, we investigated variation in oxidative balance (i.e. oxidative damage and antioxidant defences) over the course of reproduction by comparing female laboratory mice rearing or not pups.ResultsA significant increase in oxidative damage over time was only observed in females caring for offspring, whereas antioxidant defences increased over time regardless of reproductive status. Interestingly, oxidative damage measured prior to reproduction was negatively associated with litter size at birth (constraint), whereas damage measured after reproduction was positively related to litter size at weaning (cost).ConclusionsGlobally, our correlative results and the review of literature describing the links between reproduction and oxidative stress underline the importance of timing/dynamics when studying and interpreting oxidative balance in relation to reproduction. Our study highlights the duality (constraint and cost) of oxidative stress in life-history trade-offs, thus supporting the theory that oxidative stress plays a key role in life-history evolution.