Abstract

Oxidative stress experienced during early development can negatively affect diverse life-history traits, and organisms have evolved complex defence systems against its detrimental effects. Bird eggs contain maternally derived exogenous antioxidants that play a major role in embryo protection from oxidative damage, including the negative effects on telomere dynamics. In this study on the yellow-legged gull (Larus michahellis), we manipulated the concentration of vitamin E (VE) in the egg yolk and analysed the consequences on oxidative status markers and telomere length in the hatchlings. This study provides the first experimental evidence that, contrary to the expectation, a physiological increase in yolk VE concentration boosted total antioxidant capacity and reduced the concentration of pro-oxidant molecules in the plasma, but did not reduce telomere attrition or ameliorate oxidative damage to proteins and lipids in the early postnatal period.

Highlights

  • Early-life development is characterized by rapid growth requiring high metabolic activity and oxygen consumption, which imposes notable reactive oxygen species (ROS) production [1], even if there is still ambiguity regarding the relationship between oxygen consumption and ROS production [2]

  • An linear mixed models (LMMs) showed that vitamin E (VE) treatment caused a statistically significant increase in Total antioxidant capacity (TAC) in the hatchlings from VE-injected eggs compared to controls (EMM: controls: 1.27 (0.02); VE-treated: 1.36 (0.02); figure 1)

  • The experimental increase in yolk VE concentration within physiological limits ameliorated plasma TAC and TOS, but this was not mirrored in a reduction in oxidative damage to proteins and lipids

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Summary

Introduction

Early-life development is characterized by rapid growth requiring high metabolic activity and oxygen consumption, which imposes notable reactive oxygen species (ROS) production [1], even if there is still ambiguity regarding the relationship between oxygen consumption and ROS production [2]. To efficiently counteract the detrimental effects of oxidizing molecules, organisms have evolved a complex antioxidant machinery, which relies on enzymatic and non-enzymatic defence. Embryo protection against ROS largely depends on egg exogenous non-enzymatic antioxidants of maternal origin [3].

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