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Author |
Walker, W.H. 2nd; Melendez-Fernandez, O.H.; Nelson, R.J. |
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Title |
Prior exposure to dim light at night impairs dermal wound healing in female C57BL/6 mice |
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Journal Article |
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Year |
2019 |
Publication |
Archives of Dermatological Research |
Abbreviated Journal |
Arch Dermatol Res |
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Volume |
311 |
Issue |
7 |
Pages |
573-576 |
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Keywords  |
Animals; mouse models; Skin; Human Health |
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Abstract |
Artificial light at night (LAN) is a pervasive phenomenon in today's society, and the detrimental consequences of LAN exposure are becoming apparent. LAN is associated with the increased incidence of metabolic disorders, cancers, mood alterations, and immune dysfunction in mammals. Consequently, we examined the effects of dim LAN (DLAN) on wound healing. Female C57BL/6 mice were housed for 3 weeks in DLAN or LD conditions prior to wounding. Following wounding, mice were maintained in either their previous light conditions or switched to the opposite lighting conditions for 3 weeks. DLAN prior to wounding impaired healing; specifically, mice in DLAN/DLAN had significantly larger wounds on day 8. Additionally, mice in DLAN/LD had significantly larger wounds on days 5, 7, 8, and 9, and increased average time to closure. These data demonstrate a potential harmful effect of DLAN on wound healing that should be considered and may represent a target for therapeutic intervention. |
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Rockefeller Neuroscience Institute, West Virginia University, Morgantown, WV, 26506, USA |
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0340-3696 |
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PMID:31144020 |
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Call Number |
GFZ @ kyba @ |
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2515 |
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Author |
Kyba, C.C.M.; Aronson, K.J. |
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Title |
Assessing Exposure to Outdoor Lighting and Health Risks |
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Journal Article |
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Year |
2015 |
Publication |
Epidemiology |
Abbreviated Journal |
Epidemiology |
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Volume |
26 |
Issue |
4 |
Pages |
e50 |
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Keywords |
Commentary, Human Health |
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1044-3983 |
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LoNNe @ christopher.kyba @ |
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1164 |
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Author |
Burne, B.H. |
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Title |
Pollution By Light |
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Journal Article |
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Year |
1972 |
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The Lancet |
Abbreviated Journal |
The Lancet |
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Volume |
299 |
Issue |
7751 |
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642 |
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Commentary, Human Health |
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0140-6736 |
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LoNNe @ christopher.kyba @ |
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1191 |
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LeGates, T.A.; Kvarta, M.D. |
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Title |
Illuminating a path from light to depression |
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Journal Article |
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Year |
2020 |
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Nature Neuroscience |
Abbreviated Journal |
Nat Neurosci |
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in press |
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Commentary; Animals; Human Health |
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Our light environment can strongly influence our mental health. Kai An and colleagues dissect the neuronal circuit mediating depression-related behaviors induced by mistimed light input in mice, implicating the nucleus accumbens as the downstream target of the neural pathway between intrinsically photosensitive retinal ganglion cells and the perihabenular nucleus. |
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Department of Psychiatry, University of Maryland School of Medicine, Baltimore, MD, USA |
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1097-6256 |
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PMID:32555525 |
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no |
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Call Number |
GFZ @ kyba @ |
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3015 |
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Author |
Reiter, R.J.; Sharma, R.; Ma, Q. |
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Title |
Switching diseased cells from cytosolic aerobic glycolysis to mitochondrial oxidative phosphorylation: A metabolic rhythm regulated by melatonin? |
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Journal Article |
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Year |
2021 |
Publication |
Journal of Pineal Research |
Abbreviated Journal |
J Pineal Res |
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70 |
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1 |
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e12677 |
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Keywords |
Commentary; Animals; Human Health; Alzheimer disease; Warburg metabolism; cancer; circadian rhythm; fibrosis; mitochondria |
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This commentary reviews the concept of the circadian melatonin rhythm playing an essential role in reducing the development of diseases such as solid tumors which adopt cytosolic aerobic glycolysis (Warburg effect) to support their enhanced metabolism. Experimental data show that solid mammary tumors depend on aerobic glycolysis during the day but likely revert to mitochondrial oxidative phosphorylation at night for ATP production. This conversion of diseased cells during the day to a healthier phenotype at night occurs under control of the circulating melatonin rhythm. When the nocturnal melatonin rise is inhibited by light exposure at night, cancer cells function in the diseased state 24/7. The ability of melatonin to switch cancer cells as well as other diseased cells, for example, Alzheimer disease, fibrosis, hyperactivation of macrophages, etc, from aerobic glycolysis to mitochondrial oxidative phosphorylation may be a basic protective mechanism to reduce pathologies. |
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Department of Cell Systems and Anatomy, UT Health Science Center at San Antonio, San Antonio, TX, USA |
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0742-3098 |
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PMID:32621295 |
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Call Number |
GFZ @ kyba @ |
Serial |
3221 |
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