toggle visibility Search & Display Options

Select All    Deselect All
 |   | 
Details
   print
  Records Links
Author van den Heiligenberg, S.; Deprés-Brummer, P.; Barbason, H.; Claustrat, B.; Reynes, M.; Lévi, F. url  doi
openurl 
  Title The tumor promoting effect of constant light exposure on diethylnitrosamine-induced hepatocarcinogenesis in rats Type Journal Article
  Year 1999 Publication (up) Life Sciences Abbreviated Journal Life Sciences  
  Volume 64 Issue 26 Pages 2523-2534  
  Keywords Human Health  
  Abstract  
  Address  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0024-3205 ISBN Medium  
  Area Expedition Conference  
  Notes Approved no  
  Call Number LoNNe @ kagoburian @ Serial 827  
Permanent link to this record
 

 
Author Touitou, Y.; Reinberg, A.; Touitou, D. url  doi
openurl 
  Title Association between light at night, melatonin secretion, sleep deprivation, and the internal clock: Health impacts and mechanisms of circadian disruption Type Journal Article
  Year 2017 Publication (up) Life Sciences Abbreviated Journal Life Sci  
  Volume 173 Issue Pages 94-106  
  Keywords Human Health; Review  
  Abstract Exposure to Artificial Light At Night (ALAN) results in a disruption of the circadian system, which is deleterious to health. In industrialized countries, 75% of the total workforce is estimated to have been involved in shift work and night work. Epidemiologic studies, mainly of nurses, have revealed an association between sustained night work and a 50-100% higher incidence of breast cancer. The potential and multifactorial mechanisms of the effects include the suppression of melatonin secretion by ALAN, sleep deprivation, and circadian disruption. Shift and/or night work generally decreases the time spent sleeping, and it disrupts the circadian time structure. In the long run, this desynchronization is detrimental to health, as underscored by a large number of epidemiological studies that have uncovered elevated rates of several diseases, including cancer, diabetes, cardiovascular risks, obesity, mood disorders and age-related macular degeneration. It amounts to a public health issue in the light of the very substantial number of individuals involved. The IARC has classified shift work in group 2A of “probable carcinogens to humans” since “they involve a circadian disorganization”. Countermeasures to the effects of ALAN, such as melatonin, bright light, or psychotropic drugs, have been proposed as a means to combat circadian clock disruption and improve adaptation to shift and night work. We review the evidence for the ALAN impacts on health. Furthermore, we highlight the importance of an in-depth mechanistic understanding to combat the detrimental properties of exposure to ALAN and develop strategies of prevention.  
  Address UHSA – Groupe Hospitalier Paul Guiraud, 54, avenue de la Republique, 94806 Villejuif, France  
  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 0024-3205 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:28214594 Approved no  
  Call Number GFZ @ kyba @ Serial 2455  
Permanent link to this record
 

 
Author Molcan, L.; Sutovska, H.; Okuliarova, M.; Senko, T.; Krskova, L.; Zeman, M. url  doi
openurl 
  Title Dim light at night attenuates circadian rhythms in the cardiovascular system and suppresses melatonin in rats Type Journal Article
  Year 2019 Publication (up) Life Sciences Abbreviated Journal Life Sci  
  Volume 231 Issue Pages 116568  
  Keywords Animals  
  Abstract AIMS: Cardiovascular parameters exhibit significant 24-h variability, which is coordinated by the suprachiasmatic nucleus (SCN), and light/dark cycles control SCN activity. We aimed to study the effects of light at night (ALAN; 1-2lx) on cardiovascular system control in normotensive rats. MAIN METHODS: Heart rate (HR) and blood pressure (BP) were measured by telemetry during five weeks of ALAN exposure. From beat-to-beat telemetry data, we evaluated spontaneous baroreflex sensitivity (sBRS). After 2 (A2) and 5 (A5) weeks of ALAN, plasma melatonin concentrations and the response of BP and HR to norepinephrine administration were measured. The expression of endothelial nitric oxide synthase (eNOS) and endothelin-1 was determined in the aorta. Spontaneous exploratory behaviour was evaluated in an open-field test. KEY FINDINGS: ALAN significantly suppressed the 24-h variability in the HR, BP, and sBRS after A2, although the parameters were partially restored after A5. The daily variability in the BP response to norepinephrine was reduced after A2 and restored after A5. ALAN increased the BP response to norepinephrine compared to the control after A5. Increased eNOS expression was found in arteries after A2 but not A5. Endothelin-1 expression was not affected by ALAN. Plasma melatonin levels were suppressed after A2 and A5. Spontaneous exploratory behaviour was reduced. SIGNIFICANCE: ALAN decreased plasma melatonin and the 24-h variability in the haemodynamic parameters and increased the BP response to norepinephrine. A low intensity ALAN can suppress circadian control of the cardiovascular system with negative consequences on the anticipation of a load.  
  Address Department of Animal Physiology and Ethology, Faculty of Natural Sciences, Comenius University, Bratislava, Slovakia  
  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 0024-3205 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:31202842 Approved no  
  Call Number GFZ @ kyba @ Serial 2548  
Permanent link to this record
 

 
Author Russart, K.L.G.; Chbeir, S.A.; Nelson, R.J.; Magalang, U.J. url  doi
openurl 
  Title Light at night exacerbates metabolic dysfunction in a polygenic mouse model of type 2 diabetes mellitus Type Journal Article
  Year 2019 Publication (up) Life Sciences Abbreviated Journal Life Sci  
  Volume 231 Issue Pages 116574  
  Keywords Animals; diabetes; human health; mouse models; Type 2 diabetes; Insulin Resistance  
  Abstract AIMS: Electric lighting is beneficial to modern society; however, it is becoming apparent that light at night (LAN) is not without biological consequences. Several studies have reported negative effects of LAN on health and behavior in humans and nonhuman animals. Exposure of non-diabetic mice to dim LAN impairs glucose tolerance, whereas a return to dark nights (LD) reverses this impairment. We predicted that exposure to LAN would exacerbate the metabolic abnormalities in TALLYHO/JngJ (TH) mice, a polygenic model of type 2 diabetes mellitus (T2DM). MATERIALS AND METHODS: We exposed 7-week old male TH mice to either LD or LAN for 8-10weeks in two separate experiments. After 8weeks of light treatment, we conducted intraperitoneal glucose tolerance testing (ipGTT) followed by intraperitoneal insulin tolerance testing (ipITT). In Experiment 1, all mice were returned to LD for 4weeks, and ipITT was repeated. KEY FINDINGS: The major results of this study are i) LAN exposure for 8weeks exacerbates glucose intolerance and insulin resistance ii) the effects of LAN on insulin resistance are reversed upon return to LD, iii) LAN exposure results in a greater increase in body weight compared to LD exposure, iv) LAN increases the incidence of mice developing overt T2DM, and v) LAN exposure decreases survival of mice with T2DM. SIGNIFICANCE: In conclusion, LAN exacerbated metabolic abnormalities in a polygenic mouse model of T2DM, and these effects were reversed upon return to dark nights. The applicability of these findings to humans with T2DM needs to be determined.  
  Address Department of Neuroscience, The Ohio State University Wexner Medical Center, Columbus, OH 43210, USA; Department of Internal Medicine, The Ohio State University Wexner Medical Center, Columbus, OH 43210, USA  
  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 0024-3205 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:31207311 Approved no  
  Call Number GFZ @ kyba @ Serial 2549  
Permanent link to this record
Select All    Deselect All
 |   | 
Details
   print

Save Citations:
Export Records: