Objective To investigate the risk factors and treatment of silicone oil glaucoma (SOG). Methods Ninety-five eyes of 93 patients who underwent pars plana vitrectomy and silicone oil tamponade were evaluated in this study. The lens was removed in 58 eyes in which intraocular lens (IOL) was implanted in 10 eyes, so 48 eyes were aphakic. Silicone oil tamponade time was le;6 months in 32 eyes, and ＞6 months in 63 eyes. The follow-up time ranged from 2 to 25 months, with a mean of (9.5plusmn;5.1) months. The fundus and intraocular pressure (IOP) were evaluated at 1 week, 2 weeks and 1 month after surgery. The diagnosis of SOG was established if the onemonth postoperative IOP＞21 mm Hg （1 mm Hg=0.133 kPa）, and primary and neovascular glaucoma were excluded. After the diagnosis of SOG, carteolol hydrochloride and brinzolamide solution were immediately applied to the eye, and intravenous mannitol infusion was performed. If the IOP still can not be controlled after 1 week of such treatment, silicone oil removal surgery will be performed. If removal of silicone oil can not control the IOP, trabeculectomy surgery will be performed. Results SOG occurred in 21 eyes (22.1%), including 5 phakic eyes (10.6% of 47 phakic eyes) and 16 aphakic eyes (33.3% of 48 aphakic eyes), 3 eyes (9.4% of 32 eyes) with short tamponade time (le;6 months) and 18 eyes (28.6% of 63 eyes) with long tamponade time (＞6 months). The average silicone oil tamponade time was (10.8plusmn;5.1) months. Emulsification of the silicone oil occurred in 17 eyes (81.0%). After silicone oil removed, IOP was controlled in 17 eyes (81.0%) within one week. Conclusions Aphakic eye and the duration of silicone oil tamponade are the risk factors of SOG. Emulsification of silicone oil is the main cause. Silicone oil removal is an effective way to treat SOG.
Objective To observe the effect of visible light (white light, red light, blue light) on the expression of reactive oxygen species (ROS), 8-OHdG and hOGG1 in cultured human retinal pigment epithelial (RPE) cells. Methods Cultured human RPE-19 cells (4th-6th generations) were divided into white light, red light, blue light and control group. The illumination was 600 Lux. The cells of experimental groups were exposed to white light or red light for 6, 12, 24 and 48 hours, and exposed to blue light for 1, 3, 6 and 12 hours, while cells of the control group were cultured in foil packaged dishes to avoid light. The levels of ROS expression were detected by 2prime;,7-dichlorofluorescin-diacetate (DCFH-DA), the levels of 8-OHdG protein expression were observed by immunocytochemistry (ICC), and the levels of hOGG1 were measured by western blot. Results Compared to the control group, the ROS expression in RPE cells were increased in white and red light group after 12, 24 and 48 hours and in blue light group after 1, 3, 6 and 12 hours (Fwhite light=11.611, Fred light=6.706, Fblue light=23.259; P＜0.05 ). Additionally, the ROS expression had a tendency to increase gradually along with exposure time. Compared to the control group, the 8-OHdG expression in RPE cells were increased significantly in both white and red light group after 12, 24 and 48 hours and in blue light group after 1, 3, 6 and 12 hours (Fwhite light=16.032,Fred light=6.378, Fblue light=19.484;P＜0.05). Additionally, the 8-OHdG expression in white and red light group were increased gradually with exposure time but decreased when exposure time was up to 48 hours, while that in blue light group was increased firstly though it started to decrease when exposure time was up to 6 hours. Compared to the control group, the hOGG1 expression in RPE cells were increased in white and red light group after 12, 24 and 48 hours and in blue light group after 6 and 12 hours (Fwhite light=15.121,Fred lig=21.041,Fblue light=12.479;P＜0.05). Conclusions Exposure to white, red or blue light could induce ROS production and DNA oxidative damage in RPE cells in a time-dependent way. Exposure to visible light could switch on self-protection of RPE cells against DNA oxidative damage by up-regulating of the hOGG1 expression.