Urbanization, oxidative stress and inflammation: a question of evolving, acclimatizing or coping with urban environmental stress

To estimate the impact of urbanization on wild animals, it is important to know how different species, populations and/or individuals deal with and respond to environmental stress. Are more urbanized species adapted to their environment, or do individuals acclimatize over the course of their life? Alternatively, do they simply cope at the expense of other functions? These are three key processes that I will address using two important physiological responses as case traits, namely oxidative stress and inflammation, - which are known to be under genetic control as well as showing great plasticity. Oxidative stress is a state of more reactive oxidants than antioxidants, which may cause tissue damage linked to disease and senescence. Inflammation, on the other hand, is the response of vascular tissues to harmful stimuli. However, under progressive stimuli, inflammation may also cause tissue destruction and pathology. Although patterns and strengths of effects are not always clear cut, the often interconnected oxidative stress and inflammation have the potential to be severely affected by urban stressors, thereby mechanistically linking ecology to fitness. Here I discuss five major urban stressors: chemical, noise and artificial night light pollution, disease and diet, and how their individual and combinatory effects may affect these two physiological responses. To start to disentangle whether physiological responses are a question of evolving, acclimatizing or coping with the urban environment, population genetics along with regulatory mechanisms of gene expression will shed light on the costs' of urban life and help to understand why some species or genotypes thrive, while others are absent, in urban areas. Single nucleotide polymorphism (SNP) has been successful for explaining local adaptation and tolerance towards acute toxic substances. However, for multiple stressors acting in concert, at low chronic exposure, investigations of epigenetic mechanisms regulating gene expression may be more illuminating. Here I review the pathways by which genetic and epigenetic mechanisms can affect oxidative stress and inflammatory responses in urban environments, thereby affecting overall fitness. By doing so, I identify the major outstanding gaps of knowledge in the interfaces between ecology, toxicology, evolutionary and molecular biology to inform future studies of urban wildlife