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- Ouyang, Jenny Q., et al.
(författare)
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A New Framework for Urban Ecology : An Integration of Proximate and Ultimate Responses to Anthropogenic Change
- 2018
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Ingår i: Integrative and Comparative Biology. - : Oxford University Press (OUP). - 1557-7023 .- 1540-7063. ; 58:5, s. 915-928
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Tidskriftsartikel (refereegranskat)abstract
- As urban areas continue to grow, understanding how species respond and adapt to urban habitats is becoming increasingly important. Knowledge of the mechanisms behind observed phenotypic changes of urban-dwelling animals will enable us to better evaluate the impact of urbanization on current and future generations of wildlife and predict how animals respond to novel environments. Recently, urban ecology has emerged not only as a means of understanding organismal adaptation but also as a framework for exploring mechanisms mediating evolutionary phenomena. Here, we have identified four important research topics that will advance the field of urban ecology and shed light on the proximate and ultimate causes of the phenotypic differences commonly seen among species and populations that vary in their responses to urbanization. First, we address the ecological and socio-economic factors that characterize cities, how they might interact with each other, and how they affect urban species. Second, we ask which are the proximate mechanisms underlying the emergence over time of novel traits in urban organisms, focusing on developmental effects. Third, we emphasize the importance of understanding the ultimate causations that link phenotypic shifts to function. This question highlights the need to quantify the strength and direction of selection that urban individuals are exposed to, and whether the phenotypic shifts associated with life in the city are adaptive. Lastly, we stress the need to translate how individual-level responses scale up to population dynamics. Understanding the mechanistic underpinnings of variation among populations and species in their responses to urbanization will unravel species resilience to environmental perturbation, which will facilitate predictive models for sustainability and development of green cities that maintain or even increase urban biodiversity and wildlife health and wellbeing.
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| 2. |
- Salmon, Pablo, et al.
(författare)
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Effects of the Urban Environment on Oxidative Stress in Early Life : Insights from a Cross-fostering Experiment
- 2018
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Ingår i: Integrative and Comparative Biology. - : Oxford University Press (OUP). - 1557-7023 .- 1540-7063. ; , s. 986-994
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Tidskriftsartikel (refereegranskat)abstract
- As urban areas expand rapidly worldwide, wildlife is exposed to a wide range of novel environmental stressors, such as increased air pollution and artificial light at night. Birds in highly polluted and/or urbanized habitats have been found to have increased antioxidant protection, which is likely important to avoid accumulation of oxidative damage, which can have negative fitness consequences. Yet, the current knowledge about the ontogeny of antioxidant protection in urban areas is limited; i.e., is the capacity to up-regulate the antioxidant defences already established during pre-natal development, or does it manifest itself during post-natal development? We cross-fostered great tit (Parus major) nestlings within and between urban and rural habitats, to determine if oxidative stress (measured as non-enzymatic total antioxidant capacity, superoxide dismutase (SOD), and plasma lipid peroxidation) is affected by habitat of origin and/or by habitat of rearing. The results demonstrate that being reared in the urban environment triggers an increase in SOD (an intracellular, enzymatic antioxidant) independent of natal habitat. Oxidative damage increased with hatching date in urban-reared nestlings, but there was little seasonal change in rural-reared nestlings. Total antioxidant capacity was neither affected by habitat of rearing or habitat of origin, but we observed a decline with hatching date in both rearing habitats. Taken together, our results support the growing evidence that the urban environment induces a direct plastic adjustment in antioxidant protection, but that up-regulation is not sufficient to avoid increased oxidative damage in late-hatched broods. Future studies should explore the underlying causes for this effect in late-hatched broods and whether it has any negative long-term implications, both at the individual- and the population level.
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| 3. |
- Treberg, Jason R., et al.
(författare)
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Comparing Electron Leak in Vertebrate Muscle Mitochondria
- 2018
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Ingår i: Integrative and Comparative Biology. - : Oxford University Press (OUP). - 1540-7063 .- 1557-7023. ; 58:3, s. 495-505
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Tidskriftsartikel (refereegranskat)abstract
- Mitochondrial electron transfer for oxidative ATP regeneration is linked to reactive oxygen species (ROS) production in aerobic eukaryotic cells. Because they can contribute to signaling as well as oxidative damage in cells, these ROS have profound impact for the physiology and survival of the organism. Although mitochondria have been recognized as a potential source for ROS for about 50 years, the mechanistic understanding on molecular sites and processes has advanced recently. Most experimental approaches neglect thermal variability among species although temperature impacts mitochondrial processes significantly. Here we delineate the importance of temperature by comparing muscle mitochondrial ROS formation across species. Measuring the thermal sensitivity of respiration, electron leak rate (ROS formation), and the antioxidant capacity (measured as H2O2 consumption) in intact mitochondria of representative ectothermic and endothermic vertebrate species, our results suggest that using a common assay temperature is inappropriate for comparisons of organisms with differing body temperatures. Moreover, we propose that measuring electron leak relative to the mitochondrial antioxidant capacity (the oxidant ratio) may be superior to normalizing relative to respiration rates or mitochondrial protein for comparisons of mitochondrial metabolism of ROS across species of varying mitochondrial respiratory capacities.
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