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      Interacting effects of early dietary conditions and reproductive effort on the oxidative costs of reproduction

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      PeerJ
      PeerJ Inc.
      Antioxidants, Oxidative stress, Predictive adaptive responses, Trade-offs

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          Abstract

          The hypothesis that oxidative damage accumulation can mediate the trade-off between reproduction and lifespan has recently been questioned. However, in captive conditions, studies reporting no evidence in support of this hypothesis have usually provided easy access to food which may have mitigated the cost of reproduction. Here, I test the hypothesis that greater investment in reproduction should lead to oxidative damage accumulation and telomere loss in domestic zebra finches Taeniopygia guttata. Moreover, since the change or fluctuation in diet composition between early and late postnatal period can impair the ability to produce antioxidant defences in zebra finches, I also tested if early nutritional conditions (constant vs fluctuating early diet) influenced the magnitude of any subsequent costs of reproduction (e.g., oxidative damage and/or telomere shortening). In comparison to pairs with reduced broods, the birds that had to feed enlarged broods showed a higher level of oxidative DNA damage (8-OHdG), but brood size had no effect on telomeres. Fluctuating early diet composition reduced the capacity to maintain the activity of endogenous antioxidants (GPx), particularly when reproductive costs were increased (enlarged brood). The decline in GPx in birds feeding enlarged broods was accompanied by a change in bill colouration. This suggests that birds with lower endogenous antioxidant defences might have strategically increased the mobilization of antioxidants previously stored in other tissues (i.e., bill and liver) and thus, preventing an excessive accumulation of damage during reproduction.

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          Oxidative stress shortens telomeres.

          Telomeres in most human cells shorten with each round of DNA replication, because they lack the enzyme telomerase. This is not, however, the only determinant of the rate of loss of telomeric DNA. Oxidative damage is repaired less well in telomeric DNA than elsewhere in the chromosome, and oxidative stress accelerates telomere loss, whereas antioxidants decelerate it. I suggest here that oxidative stress is an important modulator of telomere loss and that telomere-driven replicative senescence is primarily a stress response. This might have evolved to block the growth of cells that have been exposed to a high risk of mutation.
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            Glutathione peroxidases.

            With increasing evidence that hydroperoxides are not only toxic but rather exert essential physiological functions, also hydroperoxide removing enzymes have to be re-viewed. In mammals, the peroxidases inter alia comprise the 8 glutathione peroxidases (GPx1-GPx8) so far identified. Since GPxs have recently been reviewed under various aspects, we here focus on novel findings considering their diverse physiological roles exceeding an antioxidant activity. GPxs are involved in balancing the H2O2 homeostasis in signalling cascades, e.g. in the insulin signalling pathway by GPx1; GPx2 plays a dual role in carcinogenesis depending on the mode of initiation and cancer stage; GPx3 is membrane associated possibly explaining a peroxidatic function despite low plasma concentrations of GSH; GPx4 has novel roles in the regulation of apoptosis and, together with GPx5, in male fertility. Functions of GPx6 are still unknown, and the proposed involvement of GPx7 and GPx8 in protein folding awaits elucidation. Collectively, selenium-containing GPxs (GPx1-4 and 6) as well as their non-selenium congeners (GPx5, 7 and 8) became key players in important biological contexts far beyond the detoxification of hydroperoxides. This article is part of a Special Issue entitled Cellular functions of glutathione. Copyright © 2012 Elsevier B.V. All rights reserved.
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              Free Radicals in Biology and Medicine

              Free Radicals in Biology and Medicine has become a classic text in the field of free radical and antioxidant research. Now in its fifth edition, the book has been comprehensively rewritten and updated whilst maintaining the clarity of its predecessors. Two new chapters discuss 'in vivo' and 'dietary' antioxidants, the first emphasising the role of peroxiredoxins and integrated defence mechanisms which allow useful roles for ROS, and the second containing new information on the role of fruits, vegetables, and vitamins in health and disease. This new edition also contains expanded coverage of the mechanisms of oxidative damage to lipids, DNA, and proteins (and the repair of such damage), and the roles played by reactive species in signal transduction, cell survival, death, human reproduction, defence mechanisms of animals and plants against pathogens, and other important biological events. The methodologies available to measure reactive species and oxidative damage (and their potential pitfalls) have been fully updated, as have the topics of phagocyte ROS production, NADPH oxidase enzymes, and toxicology. There is a detailed and critical evaluation of the role of free radicals and other reactive species in human diseases, especially cancer, cardiovascular, chronic inflammatory and neurodegenerative diseases. New aspects of ageing are discussed in the context of the free radical theory of ageing. This book is recommended as a comprehensive introduction to the field for students, educators, clinicians, and researchers. It will also be an invaluable companion to all those interested in the role of free radicals in the life and biomedical sciences.
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                Author and article information

                Contributors
                Journal
                PeerJ
                PeerJ
                peerj
                peerj
                PeerJ
                PeerJ Inc. (San Francisco, USA )
                2167-8359
                14 March 2017
                2017
                : 5
                : e3094
                Affiliations
                [-1]Departamento de Ecología y Biología Animal, Universidad de Vigo , Vigo, Galicia, Spain
                Article
                3094
                10.7717/peerj.3094
                5354074
                9696c463-b619-4d5a-b48e-15ffdd67fc47
                ©2017 Noguera

                This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, reproduction and adaptation in any medium and for any purpose provided that it is properly attributed. For attribution, the original author(s), title, publication source (PeerJ) and either DOI or URL of the article must be cited.

                History
                : 21 November 2016
                : 15 February 2017
                Funding
                Funded by: AXA Research Fund
                Award ID: PDOC2013W1
                Funded by: Juan de la Cierva Fellowship
                Award ID: IJCI-2014-20246
                The study and the author were supported by the AXA Research Fund (PDOC2013W1) and a Juan de la Cierva Fellowship (IJCI-2014-20246). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
                Categories
                Ecology
                Evolutionary Studies

                antioxidants,oxidative stress,predictive adaptive responses,trade-offs

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