Retinal nitric oxide and malonyldialdehyde levels following photodynamic therapy.

Background: To determine the retinal nitric oxide (NO) and malonyldialdehyde (MDA) levels following photodynamic therapy (PDT). Materials and Methods: Seven Dutch-belted rabbits received dextrose, while seven others received 2 mg/kg verteporfin infusion over a period of 15 minutes in a dim-lit room. Irradiation to a 1.5 mm diameter intact chorioretinal area in the right eye of verteporfin-infused rabbits, was started 5 minutes after the end of infusion. Three groups were control (dextrose infusion), infusion with verteporfin (left eyes were not irradiated), and irradiation after verteporfin injection (right eyes were irradiated). On the fifth day of the experiment, the eyes were enucleated. The retinas were subsequently frozen and homogenized. Nitrite, a stable end-product of NO and MDA, was measured using the spectrophotometer. Protein concentrations were measured by the Lowry method. Tissue NO and MDA levels were expressed as μmol/gprt and nmol/mgprt, respectively. Results: The mean retinal NO and MDA levels of the control, infusion, and irradiation groups were 24.67 ± 6.66, 0.11 ± 0.02; 45.90 ± 15.52, 0.21 ± 0.09; and 84.43 ± 14.96 μmol/gprt, 0.58 ± 0.14 nmol/mgprt, respectively. The mean retinal NO levels were significantly elevated in the infusion and irradiation groups compared with the control group (P:0.004; P:0.001). The mean retinal MDA levels were significantly elevated in the infusion and irradiation groups compared to the control one (P:0.026; P:0.001). Also the mean retinal NO and MDA levels in the irradiation group were found to be significantly higher than the infusion group (P:0.018; P:0.018). Conclusion: Not only PDT, but also verteporfin infusion alone resulted in NO and MDA level increments in the retina, which might be toxic.

The effect of infliximab, cyclosporine A and recombinant IL-10 on vitreous cytokine levels in experimental autoimmune uveitis.

BACKGROUND: To identify the effect of infliximab, cyclosporine A and recombinant IL-10 in experimental autoimmune uveitis. MATERIALS AND METHODS: Sixty male rats were assigned to five groups of 12 each. All the groups (except the control group) were administered 30 microg retinal-S antigen intraperitoneally. On the 14th day, after confirmation of uveitis with histopathological study, daily cyclosporine A injection was given in cyclosporine A treatment group and physiological serum in the uveitis-induced placebo treatment and control groups. In the infliximab treatment group, infliximab was administered on the 14th, 15th, 17th, 19th and 21st days. In the recombinant IL-10 treatment group, three doses of recombinant IL-10 were given four hours and a half hours before and eight hours after retinal-S antigen administration. On the 21st day of the study, all rats were sacrificed and vitreous cytokine levels (IL-1, IL-6, IL-8 and TNF-alpha) were studied with ELISA. RESULTS: In the treatment groups, cytokine levels (IL-1, IL-6 and TNF-alpha) were significantly lower than the uveitis-induced placebo treatment group. Compared with the control group, there was no significant difference with respect to TNF-alpha and IL-8 in the infliximab treatment group; IL-8 in the cyclosporine A treatment group; IL-6 and IL-8 in the recombinant IL-10 treatment group. The drugs used did not significantly differ in respect to their effects on vitreous IL-6, IL-8 and TNF-alpha levels. CONCLUSION: Cyclosporine A, infliximab and recombinant IL-10 reduce the vitreous cytokines levels. Among these drugs, recombinant IL-10, which is still in its experimental phase, might be considered as a new therapeutic agent.