Production of nitric oxide in the retina after continuous illumination.

PIEHL LL., FACORRO GB.; CAPANI F., LÓPEZ EM., HAGER AA., COIRINI H., AND LÓPEZ COSTA JJ

Buenos Aires

Congreso; . 12th Biennial Meeting of the Society for Free Radical Research International (SFFR 2004).; 2004

Society for Free Radical Research International

Continuous illumination induces severe ultrastructural damage in retinal photoreceptors that is reversible after an adequate period of darkness. In previous studies, we observed the increase ofNADPH diaphorase reactivity in choroids after 7 days of continuous illumination and the decrease in number and optical density of reactive amacrine cells during regeneration. The aim of this work was to evaluate nitric oxide (NO) production by ESR during retina illumination. Sprague Dawley rats were continuously illuminated for 2, 24, 48 hours and 7 days. Control rats were subjected to 12/12 hours light/dark cycles. After illumination, animals were treated with: a) intraperitonela sodium nitroprusiate (1 mg/kg), b) intraperitoneal sodium diethyldithiocarbamate (DETC) (500 mg/kg), c) subcutaneous ferrous sulphate (37.5 mg/kg) in citrate solution, and d) DETC and ferrous sulphate intravitreous injection. Retinas were removed and forzen at - 20 C in a quartz tube. The paramagnetic signal of the Fe-DETC-NO complex was recorded using a Brucker ECS 106 spectrometer. We observed an increase in the ESR signal within 24 hours of illumination. ESR signal intensities after 7 days of illumination were similar to the controls. No differences were observed between female and male rats. Photoreceptor degeneration could be due to the neurotoxic effect of the excess of NO produced during continuous illumination.