Abstract
1- Introduction
2- Materials and methods
3- Results
4- Discussion
References
Abstract
Physiological stress markers may provide valuable insight for our understanding of costs of given life-history strategies or of wildlife health condition, most importantly in case of threatened species. In the last decade, there has been growing interest in the ecological relevance of cellular oxidative stress, which would provide complimentary information to that obtained by the classic analyses of glucocorticoid hormones. In this study, we analysed the sex and species variation of five blood-based markers of oxidative status, both molecular oxidative damage and antioxidant protection, in sympatric cheetahs (Acinonyx jubatus) and leopards (Panthera pardus) living on Namibian farmlands. Both these terrestrial carnivores are classified as vulnerable by the International Union for Conservation of Nature. We found that female cheetahs had significantly higher serum reactive oxygen metabolites of non-protein origin and lower glutathione peroxidase activity in whole blood than both male and female leopards and male cheetahs. We also found that cheetahs and leopards differed in the association between the two antioxidant enzymes glutathione peroxidase and superoxide dismutase. Correlations among oxidative status markers were stronger in female cheetahs than leopards or male cheetahs. Our results suggest that female cheetahs are more sensitive to local sources of stress. Our work did not corroborate the assumption that two species with different life histories consistently differ in key physiological traits.
Introduction
Measures of physiological stress are commonly used to assess the costs of given life-history events and the health status of free-living animals. Glucocorticoids are valuable biomarkers to assess the stress response of individuals (Romero, 2004; Angelier and Wingfield, 2013; Dantzer et al., 2014) and the population health in ecological and conservation studies (Busch and Hayward, 2009; Dantzer et al., 2014). However, glucocorticoids do not provide a direct quantification of actual physiological costs (e.g., cellular damage) an organism accrues when being exposed to a stressor or demanding activity. Thus, in the last decade, there has been a burgeoning of studies that tested the connections between oxidative stress and environmental stressors or key life-history functions in free-ranging animals (reviewed in Costantini, 2014). Body functions like aerobic metabolism and activity of immune cells are responsible for the production of several reactive oxygen chemicals (e.g. free radical or non-free radical chemicals such as superoxide anion, hydrogen peroxide, hypochlorous acid or peroxynitrite). While these reactive oxygen chemicals are counteracted by the antioxidant system (enzymatic and non-enzymatic), they cause oxidation of proteins, lipids and nucleic acids (Halliwell and Gutteridge, 2015). The resulting chemical modifications of biomolecules caused by the reactive chemicals are referred as molecular oxidative damage, which is classically being used as an endpoint to estimate the oxidative stress level (Halliwell and Gutteridge, 2015). Eco- and conservation physiologists have become interested in oxidative stress, recognizing that the mechanisms needed to keep oxidative damage under control may underlie adaptability of species to environmental stressors and many life-history trade-offs (Costantini, 2008, 2014; Isaksson et al., 2011; Stier et al., 2012; Beaulieu and Costantini, 2014; Speakman et al., 2015; Alonso-Alvarez et al., 2017).