AIMS/HYPOTHESIS: The aim of this study was to verify whether retinal photoreceptors, like other tissues, are subject to oxidative stress during diabetes. METHODS: Oxidative stress was monitored by the oxidation of preloaded dehydrorhodamine 123 into fluorescent rhodamine 123, during a period of intense illumination of isolated rod retinal receptor cells. These were obtained from 22 Syrian hamsters injected with streptozotocin (50 mg/kg body weight., intraperitoneal route) 90 days before the study began. Eleven hamsters were treated daily with melatonin (0.4 mg/kg body wt., per os), an antioxidant synthesized within photoreceptors. Isolated photoreceptors were bathed on the stage of a Leitz Orthoplan microscope, where the fluorescent lamp also served as the light stimulus (485 nm). Fluorescence irradiance was measured by photometry and stored in a personal computer for further analysis. RESULTS: The light-induced oxidant production greatly decreased and was also delayed in the streptozotocin-injected hamsters compared with the control hamsters matched for age. Similar effects were obtained in control photoreceptors after 40 min incubation with 2-2'-azobis (2-amidinopropane) dihydrochloride, a potent lipoperoxidation inducer. The effect of melatonin was to partially restore the light-induced fluorescence response. CONCLUSION/INTERPRETATION: The depression of the light-induced oxidative response in diabetic photoreceptors could be ascribed to a hyperglycaemia-induced background of oxidative stress whereby the light-oxidizable substrate is actually lowered. Melatonin induces a larger fluorescence response during illumination, probably as a consequence of its antioxidant effect during diabetes, which would provide more oxidizable lipids.
Retinal photoreceptors of Syrian hamsters undergo oxidative stress during streptozotocin-induced diabetes
LONGONI, BIANCAMARIA;MARCHIAFAVA, PIER LORENZO
2002-01-01
Abstract
AIMS/HYPOTHESIS: The aim of this study was to verify whether retinal photoreceptors, like other tissues, are subject to oxidative stress during diabetes. METHODS: Oxidative stress was monitored by the oxidation of preloaded dehydrorhodamine 123 into fluorescent rhodamine 123, during a period of intense illumination of isolated rod retinal receptor cells. These were obtained from 22 Syrian hamsters injected with streptozotocin (50 mg/kg body weight., intraperitoneal route) 90 days before the study began. Eleven hamsters were treated daily with melatonin (0.4 mg/kg body wt., per os), an antioxidant synthesized within photoreceptors. Isolated photoreceptors were bathed on the stage of a Leitz Orthoplan microscope, where the fluorescent lamp also served as the light stimulus (485 nm). Fluorescence irradiance was measured by photometry and stored in a personal computer for further analysis. RESULTS: The light-induced oxidant production greatly decreased and was also delayed in the streptozotocin-injected hamsters compared with the control hamsters matched for age. Similar effects were obtained in control photoreceptors after 40 min incubation with 2-2'-azobis (2-amidinopropane) dihydrochloride, a potent lipoperoxidation inducer. The effect of melatonin was to partially restore the light-induced fluorescence response. CONCLUSION/INTERPRETATION: The depression of the light-induced oxidative response in diabetic photoreceptors could be ascribed to a hyperglycaemia-induced background of oxidative stress whereby the light-oxidizable substrate is actually lowered. Melatonin induces a larger fluorescence response during illumination, probably as a consequence of its antioxidant effect during diabetes, which would provide more oxidizable lipids.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
