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Author Grunst, M.L.; Raap, T.; Grunst, A.S.; Pinxten, R.; Eens, M.
Title Artificial light at night does not affect telomere shortening in a developing free-living songbird: A field experiment Type Journal Article
Year 2019 Publication Science of The Total Environment Abbreviated Journal Science of The Total Environment
Volume 662 Issue Pages 266-275
Keywords Animals; birds; Great tit; Parus major; telomere shortening; Stress
Abstract Artificial light at night (ALAN) is an increasingly pervasive anthropogenic disturbance factor. ALAN can seriously disrupt physiological systems that follow circadian rhythms, and may be particularly influential early in life, when developmental trajectories are sensitive to stressful conditions. Using great tits (Parus major) as a model species, we experimentally examined how ALAN affects physiological stress in developing nestlings. We used a repeated-measure design to assess effects of ALAN on telomere shortening, body mass, tarsus length and body condition. Telomeres are repetitive nucleotide sequences that protect chromosomes from damage and malfunction. Early-life telomere shortening can be accelerated by environmental stressors, and has been linked to later-life declines in survival and reproduction. We also assayed nitric oxide, as an additional metric of physiological stress, and determined fledging success. Change in body condition between day 8 and 15 differed according to treatment. Nestlings exposed to ALAN displayed a trend towards a decline in condition, whereas control nestlings displayed a trend towards increased condition. This pattern was driven by a greater increase in tarsus length relative to mass in nestlings exposed to ALAN. Nestlings in poorer condition and nestlings that were smaller than their nest mates had shorter telomeres. However, exposure to ALAN was unrelated to telomere shortening, and also had no effect on nitric oxide concentrations or fledging success. Thus, exposure to ALAN may not have led to sufficient stress to induce telomere shortening. Indeed, plasticity in other physiological systems could allow nestlings to maintain telomere length despite moderate stress. Alternatively, the cascade of physiological and behavioral responses associated with light exposure may have no net effect on telomere dynamics.
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Language Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0048-9697 ISBN Medium
Area Expedition Conference
Notes Approved no
Call Number (up) GFZ @ kyba @ Serial 2161
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Author Ayalon, I.; de Barros Marangoni, L.F.; Benichou, J.I.C.; Avisar, D.; Levy, O.
Title Red Sea corals under Artificial Light Pollution at Night (ALAN) undergo oxidative stress and photosynthetic impairment Type Journal Article
Year 2019 Publication Global Change Biology Abbreviated Journal Glob Chang Biol
Volume 25 Issue 12 Pages 4194-4207
Keywords Animals; *Anthozoa; Coral Reefs; Ecosystem; Indian Ocean; Oxidative Stress; Photosynthesis; Alan; Ros; corals; light pollution; photosynthesis; physiology
Abstract Coral reefs represent the most diverse marine ecosystem on the planet, yet they are undergoing an unprecedented decline due to a combination of increasing global and local stressors. Despite the wealth of research investigating these stressors, Artificial Light Pollution at Night (ALAN) or “ecological light pollution” represents an emerging threat that has received little attention in the context of coral reefs, despite the potential of disrupting the chronobiology, physiology, behavior, and other biological processes of coral reef organisms. Scleractinian corals, the framework builders of coral reefs, depend on lunar illumination cues to synchronize their biological rhythms such as behavior, reproduction and physiology. While, light pollution (POL) may mask and lead de-synchronization of these biological rhythms process. To reveal if ALAN impacts coral physiology, we have studied two coral species, Acropora eurystoma and Pocillopora damicornis, from the Gulf of Eilat/Aqaba, Red Sea, which is undergoing urban development that has led to severe POL at night. Our two experimental design data revealed that corals exposed to ALAN face an oxidative stress condition, show lower photosynthesis performances measured by electron transport rate (ETR), as well as changes in chlorophyll and algae density parameters. Testing different lights such as Blue LED and White LED spectrum showed more extreme impact in comparison to Yellow LEDs on coral physiology. The finding of this work sheds light on the emerging threat of POL and the impacts on the biology and ecology of Scleractinian corals, and will help to formulate specific management implementations to mitigate its potentially harmful impacts.
Address Mina and Everard Goodman Faculty of Life Sciences, Bar-Ilan University, Ramat Gan, Israel
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Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 1354-1013 ISBN Medium
Area Expedition Conference
Notes PMID:31512309; PMCID:PMC6900201 Approved no
Call Number (up) GFZ @ kyba @ Serial 2809
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Author Sharma, A.; Goyal, R.
Title Long-term exposure to constant light induces dementia, oxidative stress and promotes aggregation of sub-pathological Abeta42 in Wistar rats Type Journal Article
Year 2020 Publication Pharmacology, Biochemistry, and Behavior Abbreviated Journal Pharmacol Biochem Behav
Volume in press Issue Pages 172892
Keywords Animals; Amyloid beta; Behavior, fluoxetine, rifampicin; Oxidative stress
Abstract Constant exposure to light is prevalent in modern society where light noise, shift work, and jet lag is common. Constant light exposure disrupts circadian rhythm, induces stress and thus influences memory performance. We subjected adult male Wistar rats to a two-month exposure to constant light (LL), constant dark or normal light-dark cycles. Significant cognitive impairment and oxidative stress were observed in LL rats without a significant elevation in soluble Abeta1-42 levels. Next, we examined whether long-term exposure to constant light may accelerate dementia in a sub-pathological Abeta model of rats. Normal control rats received ACSF, AD rats received 440pmol, and sub-pathological Abeta rats (Abeta(s)) received 220pmol of human Abeta42 peptide in a single unilateral ICV administration. Sub-pathological Abeta rats exposed to constant light (LL+Abeta(s)) show significant memory deficits and oxidative damage, although not significantly different from LL rats. Additionally, constant light promoted aggregation of exogenous Abeta42 in LL+Abeta(s) rats shown by the presence of congophilic plaques. Furthermore, chronic fluoxetine treatment (5mg/kg/day) rescued rats from the behavioral deficits, oxidative damage and amyloid aggregation. Whereas, rifampicin treatment (20mg/kg/day) did not reverse the behavioral deficits or oxidative stress but rescued rats from amyloid plaque formation. It was concluded that constant light for two months induces behavioral deficits, oxidative stress, and accelerates aggregation of sub-pathological concentrations of human-Abeta42 peptides in Wistar rats, which is reversed by daily fluoxetine administration.
Address Neuropharmacology Laboratory, School of Pharmaceutical Sciences, Shoolini University, Solan 173 212, Himachal Pradesh, India. Electronic address: rohitgoyal@shooliniuniversity.com
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Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0091-3057 ISBN Medium
Area Expedition Conference
Notes PMID:32142744 Approved no
Call Number (up) GFZ @ kyba @ Serial 2841
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Author Cope, K.L.; Schook, M.W.; Benard, M.F.
Title Exposure to artificial light at night during the larval stage has delayed effects on juvenile corticosterone concentration in American toads, Anaxyrus americanus Type Journal Article
Year 2020 Publication General and Comparative Endocrinology Abbreviated Journal Gen Comp Endocrinol
Volume in press Issue Pages 113508
Keywords Animals; amphibian; anthropogenic light; carry-over effects; environmental stressor; glucocorticoid; predation
Abstract Artificial Light At Night (ALAN) is an environmental stressor that can disrupt individual physiology and ecological interactions. Hormones such as corticosterone are often responsible for mediating an organism's response to environmental stressors. We investigated whether ALAN was associated with a corticosterone response and whether it exacerbated the effects of another common stressor, predation. We tested for consumptive, non-consumptive, and physiological effects of ALAN and predator presence (dragonfly larvae) on a widespread amphibian, the American toad (Anaxyrus americanus). We found predators had consumptive (decreased survival) and non-consumptive (decreased growth) effects on larval toads. ALAN did not affect larval toads nor did it interact with the predator treatment to increase larval toad predation. Despite the consumptive and non-consumptive effects of predators, neither predators nor ALAN affected corticosterone concentration in the larval and metamorph life-stages. In contrast to studies in other organisms, we did not find any evidence that suggested ALAN alters predator-prey interactions between dragonfly larvae and toads. However, there was an inverse relationship between corticosterone and survival that was exacerbated by exposure to ALAN when predators were absent. Additionally, larval-stage exposure to ALAN increased corticosterone concentration in juvenile toads. Our results suggest the physiological effects of ALAN may not be demonstrated until later life-stages.
Address Department of Biology, Case Western Reserve University, 10900 Euclid Ave., Cleveland, OH 44016, USA. Electronic address: mfb38@case.edu
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Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0016-6480 ISBN Medium
Area Expedition Conference
Notes PMID:32442544 Approved no
Call Number (up) GFZ @ kyba @ Serial 2931
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Author Navara, K.J.; Nelson, R.J.
Title The dark side of light at night: physiological, epidemiological, and ecological consequences Type Journal Article
Year 2007 Publication Journal of Pineal Research Abbreviated Journal J Pineal Res
Volume 43 Issue 3 Pages 215-224
Keywords Animals; Biological Clocks; *Darkness; Disease; Ecology; Humans; Oxidative Stress; Work
Abstract Organisms must adapt to the temporal characteristics of their surroundings to successfully survive and reproduce. Variation in the daily light cycle, for example, acts through endocrine and neurobiological mechanisms to control several downstream physiological and behavioral processes. Interruptions in normal circadian light cycles and the resulting disruption of normal melatonin rhythms cause widespread disruptive effects involving multiple body systems, the results of which can have serious medical consequences for individuals, as well as large-scale ecological implications for populations. With the invention of electrical lights about a century ago, the temporal organization of the environment has been drastically altered for many species, including humans. In addition to the incidental exposure to light at night through light pollution, humans also engage in increasing amounts of shift-work, resulting in repeated and often long-term circadian disruption. The increasing prevalence of exposure to light at night has significant social, ecological, behavioral, and health consequences that are only now becoming apparent. This review addresses the complicated web of potential behavioral and physiological consequences resulting from exposure to light at night, as well as the large-scale medical and ecological implications that may result.
Address Department of Psychology, Institute for Behavioral Medicine Research, The Ohio State University, Columbus, OH, USA. knavara@gmail.com
Corporate Author Thesis
Publisher Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0742-3098 ISBN Medium
Area Expedition Conference
Notes PMID:17803517 Approved no
Call Number (up) IDA @ john @ Serial 17
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