Objective:To observe the inhibited effect and its mechani sm of estro gen on lightinduced apoptosis of retinal photoreceptor cells. Methods:Twenty female Sprague-Dawley rats were randomly divided into two groups: ovariectomized (OV) group and OV and estrogen (E2) replacement (OV+E2) group, with 10 rats in each group. All of the rats were exposed to the cyclic illumination under 12 hou r light and 12 hour dark condition with the light intensity of (600plusmn;35.4) lx ( a total of 14 times). All of the right eyes were extracted and the thickness of r etinal outer nuclear layer (ONL) was measured. Terminal deoxynucleotidyl Transfe rasemediated dUTP nick end labeling (TUNEL) method was used to evaluate positi v e apoptosis cells in ONL. The expression of nitric oxide synthase (NOS) in retin al cells was detected by immunohistochemistry with image analysis method. Results:The thickness of ONL in OV group was obviously thinner than that in the OV+ E2 group. The number of positive apoptosis of the cells was (0.0275plusmn;0.0069) c el ls/mu;m2 in OV group and (0.0162plusmn;0.0054) cells/mu;m2 in OV+E2group; the di fferen ce between the two groups was significant (t=4.1370，P=0.0012). The values o f in tegral optical density of NOS positively stained cells in retinal inner nuclear layer was (0.3675plusmn;0.0662) in the OV group and (0.2941plusmn;0.0350) in OV+E2 group ; the difference between the two groups was significant (t=3.4885, P=0.0031). Conclusion:Estrogen can protect retina from light injuries by regu lating NOS synthesis and inhibiting apoptosis of photoreceptor cells.
Illumimaton intensities of 6 indirect opthalmoscopes and 5 slit lamps were measured and calculated. The results showed the retinal irradiance from these instruments is quite high with dilated pupils ahd clear media. Although such illuminating intensity is a potential risk factor for the human retina, with careful use and reduced intensity, they are relatively safe. We suggest that ophthalmologists try their best to avoid using brighter source beyond useful illumination and unnecessary wide slit. （Chin J Ocul Fundus Dis,1992,8:133-137）
Aminoadipic acid(AAA) is known to damage retinal glia cells primarily when it is given to animals intravitreally. The present study is to demonstrate marked increase of retinal susceptibility to photic damage following administration of sub-thres-hold doses of this agent to albino rats. Right eyes were intravitreally injected with 10 ?l of 10 mM AAA, a dose which caused transient swelling of Muller cell nucleiimmediately after treatment, and total recovery by 24 hours. These rats were exposed to fluorescent light at 150 f.c. for one hour three days after injection. The left eyes were injected with the same amount of physiologic saline solution and exposed to light with an identical time schedule. The animals were killed at the 24th hour,third and seventh day, following light exposure. Cytologic changes in the retinae of both eyes were compared light microscopically. The light exposed left eyes showed mild disorganization of photoreceptor outer segements. Usually this change disappeared by the seventh day. AAA-injected right eyes showed marked destruction in the photoreceptor cell layer. The change in the photoreceptor cells was progressive and disappearance of outer segments and degeneration of numerous nuclei occurred during the following period. （Chin J Ocul Fundus Dis,1992,8:17-19）