Rapid larval development under time stress reduces adult life span through increasing oxidative damage.

Abstract: While a trade‐off between larval development and adult life span is key to understand why not all animals develop at their maximum rate and why life histories align along a fast‐slow continuum, it has been rarely studied. More general, the physiological mechanisms underlying life‐history trade‐offs are poorly understood and there is ongoing debate about the mediatory role of oxidative stress. We explicitly investigated the role of oxidative stress in mediating the trade‐off between larval development and adult life span in the damselfly <italic>Lestes viridis</italic>. We exposed larvae to time stress (by manipulating photoperiods) and manipulated oxidative stress levels using the mitochondrial uncoupler 2,4‐dinitrophenol (DNP) that causes a reduced production of reactive oxygen species. In addition, we considered other costs of an accelerated development in terms of reductions in immune function (the activity of phenoloxidase [PO]) and energy storage (fat content). Larvae accelerated their development but not growth under time stress, allowing to identify costs of rapid development without confounding effects of rapid growth. Rapid development came at the cost of a much shorter life span, which was associated with an increase in oxidative damage to lipids, proteins and DNA. Other costs in the adult stage of a rapid larval development included a lower body mass and reduced immune function, while the fat and protein contents were not reduced. Time‐stressed animals exposed to DNP developed even faster and did not show the increase in oxidative damage. Notably, they did not suffer the costs of rapid development: they had no shorter life span, lower body mass or reduced PO activity. Our results provide strong experimental support for a trade‐off between rapid development and life span and for the mediatory role of oxidative stress in shaping this life‐history trade‐off. Our study highlights that manipulation of mitochondrial uncoupling may be a powerful method to study the mechanistic underpinnings of life‐history trade‐offs. A plain language summary is available for this article. [ABSTRACT FROM AUTHOR]