Published Paper Details:

Abstract The ecosystems of cities place wildlife at risk of a combination of anthropogenic stressors, where artificial night-time light (ALAN) and man-made noise are two examples of chemically mediated pollutants that have quantifiable biochemical effects on fauna. In this paper, we will discuss, in a chemistry way the science behind how light and noise pollution dysregulate endocrine signalling, favor oxidative stress and inhibit immune competence in urban wildlife. Light pollution interferes with the synthesis of melatonin by the pineal gland involving the action of N-acetyltransferase, phase-shifts the expression of circadian clock genes (BMAL1, CLOCK, Per2, Cry1) and increases reactive oxygen species (ROS) by mitochondrial uncoupling. The chronic effect of noise pollution is the activation of the hypothalamic-pituitary-adrenal (HPA) axis, which increases the levels of glucocorticoids and inhibits the pulsatility of the gonadotropin-releasing hormone (GnRH) and stimulates lipid peroxidation. Symbiotic environmental pollutants, such as polycyclic aromatic hydrocarbons (PAHs), volatile organic compounds (VOCs) and nitrogen oxides (NOx) amplify these biochemical insults by stimulating the cytochrome P450 enzymes and producing the actions of secondary oxidative intermediates. An overview of published biochemical and Eco physiological evidence in avian, amphibian, and mammalian taxa has shown convergent evidence of hormonal perturbation and genotoxic stress. The results of this study demonstrate that incorporating environmental chemistry within urban wildlife management is critical, and such biomarkers as urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG) in a 2-hydroxydeoxyuridine (H2O) form, plasma malondialdehyde (MDA), and faecal corticosterone metabolites are logical as routine surveillance tools of urban wildlife health.