Abstract

The oxidative stress theory predicts that the accumulation of oxidative damage causes aging. More generally, oxidative damage could be a cost of reproduction that reduces survival. Both of these hypotheses have mixed empirical support. To better understand the life-history consequences of oxidative damage, we fed male and female Australian field crickets (Teleogryllus commodus) four diets differing in their protein and carbohydrate content, which have sex-specific effects on reproductive effort and lifespan. We supplemented half of these crickets with the vitamin E isoform dl-alpha-tocopherol and measured the effects of nutrient intake on lifespan, reproduction, oxidative damage and antioxidant protection. We found a clear trade-off between reproductive effort and lifespan in females but not in males. In direct contrast to the oxidative stress theory, crickets fed diets that improved their lifespan had high levels of oxidative damage to proteins. Supplementation with dl-alpha-tocopherol did not significantly improve lifespan or reproductive effort. However, males fed diets that increased their reproductive investment experienced high oxidative damage to proteins. While this suggests that male reproductive effort could elevate oxidative damage, this was not associated with reduced male survival. Overall, these results provide little evidence that oxidative damage plays a central role in mediating life-history trade-offs in T. commodus.

Highlights

  • Aging is the decline in physiological performance over the life-course of an individual, which reduces fertility and increases the risk of mortality

  • There was a significant negative correlational coefficient showing that lifespan was maximized in females that consumed a high carbohydrate, low protein diet (Figure 1C, Table 1 (A))

  • Daily reproductive effort was influenced by intake of protein and carbohydrate (Table 1 (A))

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Summary

Introduction

Aging is the decline in physiological performance over the life-course of an individual, which reduces fertility and increases the risk of mortality. Because ROS are highly reactive, cells use them as signalling molecules to regulate cellular processes including repair and apoptosis [4]. This reactivity means that ROS can react with biological molecules, such as lipids, proteins and DNA, causing oxidative damage. When ROS production exceeds antioxidant defences, cells enter a pro-oxidant state called oxidative stress and damage occurs. If this damage is not repaired it accumulates in cells [6]. This accumulation of oxidative damage could cause aging [2]

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