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Alaimo, A., Linares, G. G., Bujjamer, J. M., Gorojod, R. M., Alcon, S. P., Martinez, J. H., et al. (2019). Toxicity of blue led light and A2E is associated to mitochondrial dynamics impairment in ARPE-19 cells: implications for age-related macular degeneration. Arch Toxicol, 93(5), 1401–1415.
Abstract: Age-related macular degeneration (AMD) is a multifactorial retinal disease characterized by a progressive loss of central vision. Retinal pigment epithelium (RPE) degeneration is a critical event in AMD. It has been associated to A2E accumulation, which sensitizes RPE to blue light photodamage. Mitochondrial quality control mechanisms have evolved to ensure mitochondrial integrity and preserve cellular homeostasis. Particularly, mitochondrial dynamics involve the regulation of mitochondrial fission and fusion to preserve a healthy mitochondrial network. The present study aims to clarify the cellular and molecular mechanisms underlying photodamage-induced RPE cell death with particular focus on the involvement of defective mitochondrial dynamics. Light-emitting diodes irradiation (445 +/- 18 nm; 4.43 mW/cm(2)) significantly reduced the viability of both unloaded and A2E-loaded human ARPE-19 cells and increased reactive oxygen species production. A2E along with blue light, triggered apoptosis measured by MC540/PI-flow cytometry and activated caspase-3. Blue light induced mitochondrial fusion/fission imbalance towards mitochondrial fragmentation in both non-loaded and A2E-loaded cells which correlated with the deregulation of mitochondria-shaping proteins level (OPA1, DRP1 and OMA1). To our knowledge, this is the first work reporting that photodamage causes mitochondrial dynamics deregulation in RPE cells. This process could possibly contribute to AMD pathology. Our findings suggest that the regulation of mitochondrial dynamics may be a valuable strategy for treating retinal degeneration diseases, such as AMD.
Keywords: Vision; age-related macular degeneration; Eye; Eye Diseases; blue light
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Anisimov, V. N., Vinogradova, I. A., Panchenko, A. V., Popovich, I. G., & Zabezhinskii, M. A. (2012). Light-at-Night-Induced Circadian Disruption, Cancer and Aging. Current Aging Science, 5(3), 170–177.
Abstract: Light-at-night has become an increasing and essential part of the modern lifestyle and leads to a number of health problems, including excessive body mass index, cardiovascular diseases, diabetes, and cancer. The International Agency for Research on Cancer (IARC) Working Group concluded that “shift-work that involves circadian disruption is probably carcinogenic to humans†(Group 2A) [1]. According to the circadian disruption hypothesis, light-at-night might disrupt the endogenous circadian rhythm and specifically suppress nocturnal production of the pineal hormone melatonin and its secretion into the blood. We evaluated the effect of various light/dark regimens on the survival, life span, and spontaneous and chemical carcinogenesis in rodents. Exposure to constant illumination was followed by accelerated aging and enhanced spontaneous tumorigenesis in female CBA and transgenic HER-2/neu mice. In male and female rats maintained at various light/dark regimens (standard 12:12 light/dark [LD], the natural light [NL] of northwestern Russia, constant light [LL], and constant darkness [DD]) from the age of 25 days until natural death, it was found that exposure to NL and LL regimens accelerated age-related switch-off of the estrous function (in females), induced development of metabolic syndrome and spontaneous tumorigenesis, and shortened life span both in male and females rats compared to the standard LD regimen. Melatonin given in nocturnal drinking water prevented the adverse effect of the constant illumination (LL) and natural light (NL) regimens on the homeostasis, life span, and tumor development both in mice and rats. The exposure to the LL regimen accelerated colon carcinogenesis induced by 1,2-dimethylhydrazine (DMH) in rats, whereas the treatment with melatonin alleviated the effects of LL. The maintenance of rats at the DD regimen inhibited DMH-induced carcinogenesis. The LL regimen accelerated, whereas the DD regimen inhibited both mammary carcinogenesis induced by N-nitrosomethylurea and transplacental carcinogenesis induced by N-nitrosoethylurea in rats. Treatment with melatonin prevented premature aging and tumorigenesis in rodents. The data found in the literature and our observations suggest that the use of melatonin would be effective for cancer prevention in humans at risk as a result of light pollution.
Keywords: Animals; Light-at-night; aging; cancer; cardiovascular diseases; circadian; circadian rhythm; diabetes; disruption; melatonin; shift-work
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Barclay, J. L., Husse, J., Bode, B., Naujokat, N., Meyer-Kovac, J., Schmid, S. M., et al. (2012). Circadian desynchrony promotes metabolic disruption in a mouse model of shiftwork. PLoS One, 7(5), e37150.
Abstract: Shiftwork is associated with adverse metabolic pathophysiology, and the rising incidence of shiftwork in modern societies is thought to contribute to the worldwide increase in obesity and metabolic syndrome. The underlying mechanisms are largely unknown, but may involve direct physiological effects of nocturnal light exposure, or indirect consequences of perturbed endogenous circadian clocks. This study employs a two-week paradigm in mice to model the early molecular and physiological effects of shiftwork. Two weeks of timed sleep restriction has moderate effects on diurnal activity patterns, feeding behavior, and clock gene regulation in the circadian pacemaker of the suprachiasmatic nucleus. In contrast, microarray analyses reveal global disruption of diurnal liver transcriptome rhythms, enriched for pathways involved in glucose and lipid metabolism and correlating with first indications of altered metabolism. Although altered food timing itself is not sufficient to provoke these effects, stabilizing peripheral clocks by timed food access can restore molecular rhythms and metabolic function under sleep restriction conditions. This study suggests that peripheral circadian desynchrony marks an early event in the metabolic disruption associated with chronic shiftwork. Thus, strengthening the peripheral circadian system by minimizing food intake during night shifts may counteract the adverse physiological consequences frequently observed in human shift workers.
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Behar-Cohen, F., Martinsons, C., Vienot, F., Zissis, G., Barlier-Salsi, A., Cesarini, J. P., et al. (2011). Light-emitting diodes (LED) for domestic lighting: any risks for the eye? Prog Retin Eye Res, 30(4), 239–257.
Abstract: Light-emitting diodes (LEDs) are taking an increasing place in the market of domestic lighting because they produce light with low energy consumption. In the EU, by 2016, no traditional incandescent light sources will be available and LEDs may become the major domestic light sources. Due to specific spectral and energetic characteristics of white LEDs as compared to other domestic light sources, some concerns have been raised regarding their safety for human health and particularly potential harmful risks for the eye. To conduct a health risk assessment on systems using LEDs, the French Agency for Food, Environmental and Occupational Health & Safety (ANSES), a public body reporting to the French Ministers for ecology, for health and for employment, has organized a task group. This group consisted physicists, lighting and metrology specialists, retinal biologist and ophthalmologist who have worked together for a year. Part of this work has comprised the evaluation of group risks of different white LEDs commercialized on the French market, according to the standards and found that some of these lights belonged to the group risk 1 or 2. This paper gives a comprehensive analysis of the potential risks of white LEDs, taking into account pre-clinical knowledge as well as epidemiologic studies and reports the French Agency's recommendations to avoid potential retinal hazards.
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Bijveld, M. M. C., van Genderen, M. M., Hoeben, F. P., Katzin, A. A., van Nispen, R. M. A., Riemslag, F. C. C., et al. (2013). Assessment of night vision problems in patients with congenital stationary night blindness. PLoS One, 8(5), e62927.
Abstract: Congenital Stationary Night Blindness (CSNB) is a retinal disorder caused by a signal transmission defect between photoreceptors and bipolar cells. CSNB can be subdivided in CSNB2 (rod signal transmission reduced) and CSNB1 (rod signal transmission absent). The present study is the first in which night vision problems are assessed in CSNB patients in a systematic way, with the purpose of improving rehabilitation for these patients. We assessed the night vision problems of 13 CSNB2 patients and 9 CSNB1 patients by means of a questionnaire on low luminance situations. We furthermore investigated their dark adapted visual functions by the Goldmann Weekers dark adaptation curve, a dark adapted static visual field, and a two-dimensional version of the “Light Lab”. In the latter test, a digital image of a living room with objects was projected on a screen. While increasing the luminance of the image, we asked the patients to report on detection and recognition of objects. The questionnaire showed that the CSNB2 patients hardly experienced any night vision problems, while all CSNB1 patients experienced some problems although they generally did not describe them as severe. The three scotopic tests showed minimally to moderately decreased dark adapted visual functions in the CSNB2 patients, with differences between patients. In contrast, the dark adapted visual functions of the CSNB1 patients were more severely affected, but showed almost no differences between patients. The results from the “2D Light Lab” showed that all CSNB1 patients were blind at low intensities (equal to starlight), but quickly regained vision at higher intensities (full moonlight). Just above their dark adapted thresholds both CSNB1 and CSNB2 patients had normal visual fields. From the results we conclude that night vision problems in CSNB, in contrast to what the name suggests, are not conspicuous and generally not disabling.
Keywords: Vision; Adolescent; Adult; Case-Control Studies; Child; *Dark Adaptation; Electroretinography; Eye Diseases, Hereditary/*physiopathology; Female; Genetic Diseases, X-Linked/*physiopathology; Humans; Light; Male; Middle Aged; Myopia/*physiopathology; Night Blindness/*physiopathology; *Night Vision; *Pattern Recognition, Visual; Surveys and Questionnaires; *Visual Acuity; Visual Fields
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