Exposure to a solar eclipse causes neuronal death in the retina

被引:18
作者
Thanos, S [1 ]
Heiduschka, P [1 ]
Romann, I [1 ]
机构
[1] Univ Munster, Sch Med, Dept Expt Ophthalmol, D-48149 Munster, Germany
关键词
D O I
10.1007/s004170100362
中图分类号
R77 [眼科学];
学科分类号
100212 ;
摘要
Background: A solar eclipse was observed in Europe on 11 August 1999. Several individuals suffered from transient or persisting retinal damage, caused by gazing at the eclipse without adequate eye protection. Retinal damage is the most serious hazard of exposure to light, but the mechanisms by which this type of exposure produces retinal damage and its cellular correlates are not yet established. We used an animal model to monitor the mechanisms of retinal damage following excessive light exposure, and in particular to study whether observation of the eclipse induces death of retinal cells. Methods: In the geographic area where the experiment was conducted, a partial (90%) solar eclipse was observed. Experimental albino rats were exposed to these eclipse conditions, and control rats were exposed to normal sunlight. Another group of control animals was exposed to the same conditions, but was provided with protective light filters of the type recommended for human use. The DNA fragmentation in retinal sections of the various groups was analysed by terminal deoxynucleotidyl-transferase-mediated dUTP nick-end labelling. This analysis revealed that exposure to both normal sunlight and to the eclipse resulted in neuronal apoptosis. Immunohistochemical techniques were used to evaluate possible glial-vascular alterations. Results: Dying cells could first be detected 24 It after exposure, the largest number of which were found 6 days later in the photoreceptor layer. Control levels were attained 14 days after the exposure. Retinal ganglion cells underwent apoptosis in both groups (normal sunlight and eclipse exposure). whereas i n the neuroglial cells there was an up-regulation of the intermediate filament content. The number of dying cells in both groups was greater in animals whose pupils had been dilated pharmacologically during exposure. On the other hand, the protective filters were effective in preserving the rat retinal cells from apoptosis. Conclusions: These result,, show, for the first time, that the cellular correlates of solar retinopathy are neuronal apoptosis accompanied by glio-vascular responses. Cellular apoptosis is an irreversible process, which could manifest itself as permanent visual impairment. The activation of non-neuronal cells, such as glial and endothelial cells, could be responsible for the more transient clinical symptoms.
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页码:794 / 800
页数:7
相关论文
共 22 条
[1]  
[Anonymous], LASERS LIGHT OPHTHAL
[2]   Retinal cell death by light damage [J].
Aonuma, H ;
Yamazaki, R ;
Watanabe, I .
JAPANESE JOURNAL OF OPHTHALMOLOGY, 1999, 43 (03) :171-179
[3]   Temporal sequence of changes in rat retina after UV-A and blue light exposure [J].
Busch, EM ;
Gorgels, TGMF ;
van Norren, D .
VISION RESEARCH, 1999, 39 (07) :1233-1247
[4]   SUNLIGHT AND AGE-RELATED MACULAR DEGENERATION - THE BEAVER DAM EYE STUDY [J].
CRUICKSHANKS, KJ ;
KLEIN, R ;
KLEIN, BEK .
ARCHIVES OF OPHTHALMOLOGY, 1993, 111 (04) :514-518
[5]   Microperimetry and reading saccades in solar retinopathy. Follow-up study with the scanning laser ophthalmoscope [J].
Ehrt, O ;
Tavcar, J ;
Eckl-Titz, G .
OPHTHALMOLOGE, 1999, 96 (05) :325-331
[6]  
GLADSTONE GJ, 1978, ARCH OPHTHALMOL-CHIC, V96, P1368
[7]   RETINAL DAMAGE BY VISIBLE LIGHT [J].
GORN, RA ;
KUWABARA, T .
ARCHIVES OF OPHTHALMOLOGY, 1967, 77 (01) :115-&
[8]   Differential DNA binding activities of the transcription factors AP-1 and Oct-1 during light-induced apoptosis of photoreceptors [J].
Hafezi, F ;
Marti, A ;
Grimm, C ;
Wenzel, A ;
Remé, CE .
VISION RESEARCH, 1999, 39 (15) :2511-2518
[9]  
LAWWILL T, 1973, INVEST OPHTH VISUAL, V12, P45
[10]   VISUAL PROGNOSIS AFTER SOLAR RETINOPATHY [J].
MACFAUL, PA .
BRITISH JOURNAL OF OPHTHALMOLOGY, 1969, 53 (08) :534-&