Abstract

The life-prolonging effects of antioxidants have long entered popular culture, but the scientific community still debates whether free radicals and the resulting oxidative stress negatively affect longevity. Social insects are intriguing models for analysing the relationship between oxidative stress and senescence because life histories differ vastly between long-lived reproductives and the genetically similar but short-lived workers. Here, we present the results of an experiment on the accumulation of oxidative damage to proteins, and a comparative analysis of the expression of 20 selected genes commonly involved in managing oxidative damage, across four species of social insects: a termite, two bees and an ant. Although the source of analysed tissue varied across the four species, our results suggest that oxidative stress is a significant factor in senescence and that its manifestation and antioxidant defenses differ among species, making it difficult to find general patterns. More detailed and controlled investigations on why responses to oxidative stress may differ across social species may lead to a better understanding of the relations between oxidative stress, antioxidants, social life history and senescence.This article is part of the theme issue ‘Ageing and sociality: why, when and how does sociality change ageing patterns?'

Highlights

  • Social insects are excellent model organisms to investigate the evolution of senescence

  • The source of analysed tissue varied across the four species, our results suggest that oxidative stress is a significant factor in senescence and that its manifestation and antioxidant defenses differ among species, making it difficult to find general patterns

  • The genes differed in expression across species, with the exception of the gene Sod1, which was consistently overexpressed in workers relative to queens, and the gene Prx3, which was consistently overexpressed in old individuals

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Summary

Introduction

Social insects are excellent model organisms to investigate the evolution of senescence. Reproductive individuals, even though they carry the physiological costs of reproduction, can have extraordinary lifespans of up to 30 years, while non-reproductive workers die much younger [1,2,3] These findings challenge life-history theory, which assumes that limited resources lead to trade-offs between somatic and reproductive functions. Oxidative stress reflects an imbalance between the systemic manifestation of reactive oxygen species (ROS) and the organism’s ability to neutralize either the reactive molecules or the damage that they cause; the latter represents a proximate cause for senescence. Demanding activities such as reproduction should lead to increased production of ROS. As a side-product of mitochondrial metabolism, ROS are released that can cause oxidative stress by damaging important biomolecules such as proteins, lipids or nucleic acids [4], but can have an important function in homeostasis and cellular signalling [5]

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