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Persistent Polar Depletion of Stratospheric Ozone and Emergent Mechanisms of Ultraviolet Radiation-Mediated Health Dysregulation

机译：平流层臭氧的持续极性消耗和紫外线辐射介导的健康失调的紧急机制

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Year 2011 noted the first definable ozone “hole” in the Arctic region, serving as an indicator to the continued threat of dangerous ultraviolet radiation (UVR) exposure caused by the deterioration of stratospheric ozone in the northern hemisphere. Despite mandates of the Montreal Protocol to phase out the production of ozone depleting chemicals (ODCs), the relative stability of ODCs validates popular notions of persistent stratospheric ozone for several decades. Moreover, increased UVR exposure through stratospheric ozone depletion is occurring within a larger context of physiological stress and climate change across the biosphere. In this review, we provide commentaries on stratospheric ozone depletion with relative comparisons between the well-known Antarctic ozone hole and the newly defined ozone hole in the Arctic. Compared to the Antarctic region, increased UVR exposure in the Northern Hemisphere poses a threat to denser human populations across North America, Europe and Asia. In this context, we discuss emerging targets of UVR exposure that can potentially offset normal biological rhythms in terms of taxonomically conserved photoperiod dependent seasonal signaling and entrainment of circadian clocks. Consequences of seasonal shifts during critical life history stages can alter the fitness and condition, while circadian disruption is increasingly becoming associated as a causal link to increased carcinogenesis. We further review the significance of genomic alterations via UVR induced modulations of phase I and phase II transcription factors, the aryl hydrocarbon receptor (AhR) and the Nuclear factor (erythroid-derived 2)-like 2 (Nrf2), with emphasis on mechanism that can lead to metabolic shifts and cancer. While concern for adverse health consequences due to increased UVR exposure are longstanding, recent advances in biochemical research suggest that AhR and Nrf2 transcriptional regulators are likely targets for UVR mediated dysregulations of rhymicity and homeostasis among animals, including humans.

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