Department of Biology, University of Nevada, Reno, Reno, NV, USA; Program of Ecology, Evolution, and Conservation Biology, University of Nevada, Reno, Reno, NV, USA.
Department of Biology, University of Nevada, Reno, Reno, NV, USA.
Environ Pollut. 2021 Aug 1;282:117036. doi: 10.1016/j.envpol.2021.117036. Epub 2021 Mar 31.
Artificial light is transforming the nighttime environment and quickly becoming one of the most pervasive pollutants on earth. Across taxa, light entrains endogenous circadian clocks that function to synchronize behavioral and physiological rhythms with natural photoperiod. Artificial light at night (ALAN) disrupts these photoperiodic cues and has consequences for humans and wildlife including sleep disruption, physiological stress and increased risk of cardiovascular disease. However, the mechanisms underlying organismal responses to dim ALAN, resembling light pollution, remain elusive. Light pollution exists in the environment at lower levels (<5 lux) than tested in many laboratory studies that link ALAN to circadian rhythm disruption. Few studies have linked dim ALAN to both the upstream regulators of circadian rhythms and downstream behavioral and physiological consequences. We exposed zebra finches (Taeniopygia gutatta) to dim ALAN (1.5 lux) and measured circadian expression of five pacemaker genes in central and peripheral tissues, plasma melatonin, locomotor activity, and biomarkers of cardiovascular health. ALAN caused an increase in nighttime activity and, for males, cardiac hypertrophy. Moreover, downstream effects were detectable after just short duration exposure (10 days) and at dim levels that mimic the intensity of environmental light pollution. However, ALAN did not affect circulating melatonin nor oscillations of circadian gene expression in the central clock (brain) or liver. These findings suggest that dim ALAN can alter behavior and physiology without strong shifts in the rhythmic expression of molecular circadian pacemakers. Approaches that focus on ecologically-relevant ALAN and link complex biological pathways are necessary to understand the mechanisms underlying vertebrate responses to light pollution.
人造光正在改变夜间环境，迅速成为地球上最普遍的污染物之一。在各个分类群中，光会使内源性生物钟同步，使行为和生理节律与自然光周期同步。夜间人工光（ALAN）扰乱了这些光周期线索，对人类和野生动物都有影响，包括睡眠中断、生理压力和心血管疾病风险增加。然而，生物体对类似于光污染的暗淡 ALAN 的反应机制仍然难以捉摸。光污染存在于环境中的水平低于许多实验室研究中测试的水平，这些研究将 ALAN 与昼夜节律紊乱联系起来。很少有研究将暗淡的 ALAN 与昼夜节律的上游调节剂和下游行为和生理后果联系起来。我们将斑马雀（Taeniopygia gutatta）暴露于暗淡的 ALAN（1.5 勒克斯）下，测量了中央和外周组织中五个起搏器基因的昼夜节律表达、血浆褪黑素、运动活动以及心血管健康的生物标志物。ALAN 导致夜间活动增加，并且对雄性还导致心脏肥大。此外，仅在短暂暴露（10 天）和模拟环境光污染强度的暗淡水平下，就可以检测到下游效应。然而，ALAN 既不影响循环褪黑素，也不影响中央时钟（大脑）或肝脏中昼夜节律基因表达的振荡。这些发现表明，暗淡的 ALAN 可以改变行为和生理，而不会强烈改变分子昼夜节律起搏器的节律表达。需要采用关注生态相关的 ALAN 并将复杂的生物学途径联系起来的方法来理解脊椎动物对光污染的反应机制。
